A team of UCLA Health System brain specialists implanted a brain pacemaker in a 39-year-old man on Thursday. It was the 500th such procedure the team had completed, but the first time the group had invited followers to observe the procedure on Twitter. Updates with Instagram photos and short video clips were posted using the hashtag #UCLAORLive.

 

The procedure stimulates an area of the brain and implants a brain pacemaker to treat Parkinson's disease and essential tremors. During Thursday's operation, which was overseen by Dr. Nader Pouratian, the patient was awakened and asked to play a guitar to assist the team in placing electrodes into position. Dr. Pouratian is director of the UCLA Functional and Movement Disorder Program.

 

Brad Carter, the patient, is a Los Angeles-based actor, musician and stand-up comedian who developed hand tremors in 2006. He had lost the ability to perform, but after the brain stimulation portion of the surgery, his detxerity on the guitar was much improved. Carter gave his authorization for the surgery to be shared via Twitter and the social media outlet's Vine video application.

 

UCLA live-tweeted the surgery with the hope that it would help alleviate future patients' fear of the procedure. About 10 million Americans live with essential tremors and more than 1 million suffer from Parkinson’s disease. Many UCLA patients have found deep brain stimulation beneficial in stopping the tremors and helpful in enabling them to lead normal lives.

 

Before the procedure began, the patient explained what notes he would be playing on the guitar.

 

 

 

He was prepared for the surgery, which would open his brain while he was under anesthesia.

 

 

 

After the brain was exposed, the patient was awakened so that the team could precisely position electrodes.

 

 

 

His guitar playing sounded good in the operating room.

 

 

 

The patient's tremors were already much improved during the surgery.

 

 

 

About six hours after Carter was prepped, the procedure was over.

 

 

 

 

However, the team found that even today, with these significant improvements, one-third of patients don't survive more than three years after being diagnosed with advanced disease. Heart failure is increasingly common, affecting close to 6 million individuals in the United States alone.

 

"We are doing a good job of ensuring that patients receive the latest therapies for heart failure, but we still have a lot more work to do," said senior author Dr. Tamara Horwich, an assistant professor of cardiology at the David Geffen School of Medicine at UCLA. "It is very sobering that despite recent improvements, a third of advanced heart-failure patients aren't surviving past three years."

 

The findings are published in the May issue of the journal Circulation–Heart Failure.

 

The study focused on heart failure patients referred to UCLA, a major center for advanced heart failure management and heart transplants. The researchers examined outcomes in 2,507 adults who had "heart failure with reduced ejection fraction," which is characterized by a weak heart muscle. 

 

Patients were divided into three six-year eras, based on when they received care: (1) 1993–98, (2) 1999–2004 and (3) 2005–10. Researchers looked at patient outcomes for each of the groups at one-, two- and three-year follow-up points after diagnosis.

 

Significant differences emerged between the eras. In the second and third eras, the team found greater use of therapies that help prolong life, including medications such as beta-blockers and aldosterone antagonists and devices that help control and stabilize irregular heart rhythms, including implantable cardioverter defibrillators and biventricular pacemakers. For example, beta-blocker usage in the first era was only 15.5 percent, but by the third era, a full 87.1 percent of patients received the medication.

 

Researchers believe the increased use of these therapies in later eras is due to the completion of clinical trials — and the publication of results — that demonstrated their benefit, as well as the inclusion of these therapies in national treatment guidelines developed by organizations like the American Heart Association and the American College of Cardiology.

 

The team also found that sudden cardiac death occurred significantly less often in the later eras. At the three-year follow-up point for patients, sudden death declined from 10.1 percent in the first era to 6.4 percent in the second era and 4.6 percent in the third.

 

"The decline in sudden cardiac death is most likely due to increased use of medications and devices like defibrillators," said first author John Loh, a medical student at the Geffen School of Medicine.

 

There was also a decrease in overall mortality rates in the later eras, Loh noted. Specifically, after adjusting for multiple risk factors like age and gender, researchers found that second-era patients were 13 percent less likely to die from any cause than first-era patients. Third-era patients were 42 percent less likely than those in the first era to die from any cause.

 

Although there was a reduction in overall mortality, there was a shift in the mode of death seen over time. The study found that patient mortality from progressive heart failure had increased from 11.6 percent in the first era to 19.9 percent in the third. The need for urgent heart transplants was also up in later years. According to the researchers, this shift in mode of death may result from a modest increase in progressive heart-failure death or the need for trannsplants in patients who might have died suddenly in earlier eras, before the widespread use of implantable cardioverter defibrillators.

 

"For patients with the most advanced heart failure, treatment options used to be limited to heart transplantation — or face early death," said study author Dr. Gregg C. Fonarow, UCLA's Eliot Corday Professor of Cardiovascular Medicine and Science and director of the Ahmanson–UCLA Cardiomyopathy Center. "This study demonstrates that with improvements in medical therapy and availability of implanted devices, survival for these patients has improved considerably. What was once considered an end-stage, terminal disease state has, through implementation of innovative treatments, evolved into a manageable, but still challenging, condition."  

 

In addition, although the overall mortality rate for all patients at the three-year follow-up point fell from 36.4 percent in the first era to 31.5 percent in the third era — a statistically significant reduction that represents thousands of patients — the researchers note that this is still too high.

 

"Despite a dramatic improvement in some outcomes, we still need to gear up and continue to investigate new modalities of treatment for heart failure patients," Fonarow added.

 

According to the researchers, the study provides a "real-world" view of advanced heart failure patients and the impact of implementing the latest treatments and devices.

 

The study was supported in part by the National Institutes of Health (grant 1K23HL085097). Disclosures are included in the manuscript.

 

Other authors included Julie Creaser, Darlene A. Rourke, Nancy Livingston, Tamara K. Harrison, Elizabeth Vandenbogaart, Jaime Moriguchi, Michele A. Hamilton and Chi-Hong Tseng.

 

For more news, visit the UCLA Newsroom and follow us on Twitter.

 

 

May 23: Dr. John Stobo, UC senior vice president for health sciences and services, issued this statement, at the end of the strike at UC medical centers.

 

May 21, 8:40 a.m.: The UCLA Health System issued the following statement: "Despite a strike by two unions, both the Westwood and Santa Monica campuses of the UCLA Health System are open and providing the safest and highest quality care to our patients. With careful planning and the professionalism and dedication of many union employees who put patients first and came to work today, the UCLA Health System is taking care of the health care needs of our community."

 

May 20: UCLA Health System has taken steps in anticipation of a strike, including postponment of surgeries and reducing the patient census at hospitals. Full statement.

 

May 20: UC announced that in response to a request filed by the California Public Employment Relations Board (PERB), Sacramento Superior Court Judge David l. Brown issued an injunction limiting the number of union employees that may strike UC medical centers (see copy of injunction).

 

May 17: UC announced that the California Public Employment Relations Board (PERB) will seek a temporary restraining order in Sacramento Superior Court on Monday, May 20, to curtail the number striking employees represented by two unions at UC's five medical centers.

 

May 17: UC issued a statement by Dr. John Stobo, UC senior vice president for health sciences and services, about the human impact of the strike scheduled for May 21–22 at UC medical centers.

May 10: UC announced it would seek a restraining order against the AFSCME, in response to an announcement from the union that it was asking UC patient care and service employees to strike at UC medical centers May 21–22.

 

May 8: The UCLA Health System issued a statement regarding AFSCME's announcement that it would ask the UC patient care and service employees it represents at UCLA Health System hospitals and clinics to strike. (Statement updated May 14.)

 

 

 

In anticipation that hundreds of AFSCME and UPTE employees would not come to work, the UCLA Health System postponed twenty-five percent of the surgeries scheduled for Tuesday and Wednesday. In addition, the patient census, which is normally at or above 100 percent of capacity, has been lowered to about 80 percent. Approximately 550 replacement workers and redeployed administration staff will fill in for striking workers in positions ranging from housekeeping staff to respiratory therapists and nursing assistants. The estimated cost of the two-day strike to UCLA is more than $5 million, which reflects lost revenue and expenditures for replacement workers.

Patient care areas that would be impacted include Ronald Reagan UCLA Medical Center, UCLA Medical Center, Santa Monica, UCLA’s Resnick Neuropsychiatric Hospital, the David Geffen School of Medicine, Mattel Children’s Hospital UCLA and its community and outpatient clinics.
"We sincerely regret any inconvenience this strike may cause our patients, their families and friends," said Dr. Tom Rosenthal, chief medical officer, UCLA Hospital Systems. "However, every effort is being made to ensure that the hospitals and clinics that are part of the UCLA Health System remain open and continue to deliver the highest level of patient care and safety through the duration of the strike."

The American Federation of State, County, and Municipal Employees (AFSCME) and the University Professional and Technical Employees (UPTE) represent about 5,000 UCLA Health System employees.

On May 20, the California Superior Court issued an injunction, which prohibits a very limited number of union employees at UCLA from striking because of the threat to public health and safety. The highest priority at UCLA Health System’s hospitals and clinics is to provide patients with safe, high quality care.

 

Related: Latest news on strike by patient-care workers unions at UC, UCLA

 

The study reports 14-year survival outcomes for 3,000 men diagnosed with prostate cancer between 1994 and 1995. The results suggest that older patients with low- or intermediate-risk prostate cancer who have at least three underlying health problems, or comorbidities, are much more likely to die of something other than their cancer.

 

"For men with low-to-intermediate–risk disease, prostate cancer is an indolent disease that doesn't pose a major risk to survival," said the study's first author, Dr. Timothy Daskivich, a UCLA Robert Wood Johnson fellow. "The take-home point from this study is that older men with multiple underlying health problems should carefully consider whether they should treat these tumors aggressively, because that treatment comes with a price."

 

Aggressive treatments for prostate cancer, including surgery, external radiation and radioactive seed implants, can result in major side effects, including erectile dysfunction, urinary incontinence and bowel problems. Also, the survival advantage afforded by these treatments does not develop until approximately eight to 10 years after treatment.

 

In many cases, Daskivich said, either "watchful waiting" or active surveillance — monitoring the patient's cancer very closely with regular biopsies and intervening with surgery or radiation if the disease progresses — is better than hitting the disease with everything in the treatment arsenal.

 

The study appears May 21 in the early online issue of the peer-reviewed journal Annals of Internal Medicine.

 

The study looked at men diagnosed with prostate cancer in two age ranges: those between 61 and 74, and those 75 and older. The men completed surveys within six months of their diagnoses, documenting the other medical conditions they had at that time. Researchers then determined survival outcomes 14 years after diagnosis using information from the Surveillance, Epidemiology and End Results database. 

 

"This was a great opportunity to get a glimpse at the long-term outcomes of these men diagnosed with prostate cancer in the mid-1990s," Daskivich said. "What we were most interested in was their survival outcomes. We wanted to prove that in older men with other health problems, the risk of dying from their cancer paled in comparison to the risk that they'd die from something else."

 

The study examined patients who had three or more comorbidities, such as diabetes, hypertension, congestive heart failure and arthritis. The researchers found that the 10-year risk of dying from causes other than prostate cancer was 40 percent in men aged 61 to 74, and 71 percent in men 75 or older. In comparison, the 14-year risks of dying from low- or intermediate-risk prostate cancer were 3 percent for and 7 percent, respectively, which Daskivich characterized as low.

 

"If you're very unlikely to benefit from treatment, then don't run the risk and end up dealing with side effects that can significantly impact quality of life," he said. "It's important for these men to talk to their doctors about the possibility of forgoing aggressive treatment. We're not talking about restricting care, but the patient should be fully informed about their likelihood of surviving long enough to benefit from treatment."

 

However, Daskivich said, older men with high-risk, aggressive prostate cancers may benefit from treatment so that they don't die of their cancers. The risk of death from high-risk prostate cancer was 18 percent over the 14 years of this study.

 

Daskivich said that prior to this study, there was very little long-term data on which patients could base these crucial decisions. The study will result in patients who are much better informed on the risks and benefits of treatment, he said.

 

As they age, many men will develop prostate cancer and not know it because it's slow growing and causes no symptoms. Autopsy studies of men who died from other causes have shown that almost 30 percent over the age of 50 have histological evidence of prostate cancer, according to a study published in 2008 in the journal Urology.

 

In 2013, prostate cancer will strike 238,590 men, killing 29,720. It is the most frequently diagnosed cancer in men aside from skin cancer.

 

The study was funded by the Robert Wood Johnson/VA Clinical Scholars Program, the Urology Care Foundation of the American Urologic Association, the American Cancer Society, and the National Institutes of Health.

 

For more news, visit the UCLA Newsroom and follow us on Twitter.

 

The research, conducted by UCLA's Michael Fanselow and Moriel Zelikowsky in collaboration with Bryce Vissel, a group leader of the neuroscience research program at Sydney's Garvan Institute of Medical Research, appears this week in the early online edition of the journal Proceedings of the National Academy of Sciences.

 

The researchers found that parts of the prefrontal cortex take over when the hippocampus, the brain's key center of learning and memory formation, is disabled. Their breakthrough discovery, the first demonstration of such neural-circuit plasticity, could potentially help scientists develop new treatments for Alzheimer's disease, stroke and other conditions involving damage to the brain.

 

For the study, Fanselow and Zelikowsky conducted laboratory experiments with rats showing that the rodents were able to learn new tasks even after damage to the hippocampus. While the rats needed more training than they would have normally, they nonetheless learned from their experiences — a surprising finding.

 

"I expect that the brain probably has to be trained through experience," said Fanselow, a professor of psychology and member of the UCLA Brain Research Institute, who was the study's senior author. "In this case, we gave animals a problem to solve."

 

After discovering the rats could, in fact, learn to solve problems, Zelikowsky, a graduate student in Fanselow's laboratory, traveled to Australia, where she worked with Vissel to analyze the anatomy of the changes that had taken place in the rats' brains. Their analysis identified significant functional changes in two specific regions of the prefrontal cortex.

 

"Interestingly, previous studies had shown that these prefrontal cortex regions also light up in the brains of Alzheimer's patients, suggesting that similar compensatory circuits develop in people," Vissel said. "While it's probable that the brains of Alzheimer's sufferers are already compensating for damage, this discovery has significant potential for extending that compensation and improving the lives of many."

 

The hippocampus, a seahorse-shaped structure where memories are formed in the brain, plays critical roles in processing, storing and recalling information. The hippocampus is highly susceptible to damage through stroke or lack of oxygen and is critically inolved in Alzheimer's disease, Fanselow said.

 

"Until now, we've been trying to figure out how to stimulate repair within the hippocampus," he said. "Now we can see other structures stepping in and whole new brain circuits coming into being."

 

 Zelikowsky said she found it interesting that sub-regions in the prefrontal cortex compensated in different ways, with one sub-region — the infralimbic cortex — silencing its activity and another sub-region — the prelimbic cortex — increasing its activity.

 

"If we're going to harness this kind of plasticity to help stroke victims or people with Alzheimer's," she said, "we first have to understand exactly how to differentially enhance and silence function, either behaviorally or pharmacologically. It's clearly important not to enhance all areas. The brain works by silencing and activating different populations of neurons. To form memories, you have to filter out what's important and what's not."

 

Complex behavior always involves multiple parts of the brain communicating with one another, with one region's message affecting how another region will respond, Fanselow noted. These molecular changes produce our memories, feelings and actions.

 

"The brain is heavily interconnected — you can get from any neuron in the brain to any other neuron via about six synaptic connections," he said. "So there are many alternate pathways the brain can use, but it normally doesn't use them unless it's forced to. Once we understand how the brain makes these decisions, then we're in a position to encourage pathways to take over when they need to, especially in the case of brain damage.

 

"Behavior creates molecular changes in the brain; if we know the molecular changes we want to bring about, then we can try to facilitate those changes to occur through behavior and drug therapy," he added. I think that's the best alternative we have. Future treatments are not going to be all behavioral or all pharmacological, but a combination of both."

  

Fanselow and Vissel have worked closely over the last several years. For more information on Fanselow's research, visit the Fanselow Lab website. For more on the Garvan Institute of Medical Research, visit their website.

 

The research was funded by the National Institute of Mental Health (grant MH 62122), part of the National Institutes of Health, and by the National Science Foundation (EAPSI award 0914307 to Zelikowsky).

 

UCLA is California's largest university, with an enrollment of more than 40,000 undergraduate and graduate students. The UCLA College of Letters and Science and the university's 11 professional schools feature renowned faculty and offer 337 degree programs and majors. UCLA is a national and international leader in the breadth and quality of its academic, research, health care, cultural, continuing education and athletic programs. Six alumni and six faculty have been awarded the Nobel Prize.

 

For more news, visit the UCLA Newsroom and follow us on Twitter.

 

In addition to changing HDL from "good" to "bad," the inhalation of emissions activates other components of oxidation, the early cell and tissue damage that causes inflammation, leading to hardening of the arteries, according to the research team, which included scientists from UCLA and other institutions.

 

The findings of this early study, done in mice, are available in the online edition of the journal Arteriosclerosis, Thrombosis and Vascular Biology, a publication of the American Heart Association, and will appear in the journal's June print edition.

 

Emission particles such as those from vehicles are major pollutants in urban settings. These particles are coated in chemicals that are sensitive to free radicals, which have been known to cause oxidation. The mechanism behind how this leads to atherosclerosis, however, has not been well understood.

 

In the study, the researchers found that after two weeks of exposure to vehicle emissions, mice showed oxidative damage in the blood and liver — damage that was not reversed after a subsequent week of receiving filtered air. Altered HDL cholesterol may play a key role in this damaging process, they said.

"This is the first study showing that air pollutants promote the development of dysfunctional, pro-oxidative HDL cholesterol and the activation of an internal oxidation pathway, which may be one of the mechanisms in how air pollution can exacerbate clogged arteries that lead to heart disease and stroke," said senior author Dr. Jesus Araujo, an associate professor of medicine and director of environmental cardiology at the David Geffen School of Medicine at UCLA. 

 

For the study, one group of mice was exposed to vehicle emissions for two weeks and then filtered air for one week, a second was exposed to two weeks of emissions with no filtered air, and a third was exposed to only clean, filtered air for two weeks. This part of the collaborative research took place at the Northlake Exposure Facility at the University of Washington, headed by study author Michael E. Rosenfeld.

 

"The biggest surprise was finding that after two weeks of exposure to vehicle emissions, one week of breathing clean filtered air was not enough to reverse the damage," said Rosenfeld, a professor of environmental and occupational health sciences and pathology at the University of Washington.

 

Mice were exposed for a few hours, several days a week, to whole diesel exhaust at a particulate mass concentration within the range of what mine workers usually are exposed to.

 

After the exposures, UCLA scientists analyzed blood and tissue specimens and checked to see if the protective antioxidant and anti-inflammatory properties of HDL, known as "good" cholesterol, were still intact. They used special analytical laboratory procedures originally developed by study author Mohamad Navab at UCLA to evaluate how "good" or "bad" HDL had become. The team found that many of the positive properties of HDL were markedly altered after the air-pollutant exposure.

 

For example, the HDL of mice exposed to two weeks of vehicle emissions, including those that received a subsequent week of filtered air, had a much-decreased ability to protect against oxidation and inflammation induced by low-density lipoprotein (LDL) cholesterol, known as "bad" cholesterol, than the mice that had only been exposed to filtered air.

 

According to researchers, without HDL's ability to inhibit LDL, along with other factors, the oxidation process may run unchecked. Moreover, not only was the HDL of the mice exposed to diesel exhaust unable to protect against oxidation, but, in fact, it further enhanced the oxidative process and even worked in tandem with the LDL to promote even more oxidative damage.

 

Researchers also found a twofold to threefold increase of additional oxidation products in the blood of mice exposed to vehicle emissions, as well as activation of oxidation pathways in the liver. The degree of HDL dysfunction was correlated with the level of these oxidation markers.

 

"We suggest that people try to limit their exposure to air pollutants, as they may induce damage that starts during the exposure and continues long after it ends," said first author Fen Yin, a researcher in the division of cardiology at the Geffen School of Medicine. 

 

The current research builds on the team's previous findings that ambient ultrafine particles commonly found in air pollution, including vehicle emissions, enhance the build-up of cholesterol plaques in the arteries and that HDL may play a role. 

 

"Our research helps confirm that the functionality of HDL may be as important to check as the levels," said study author Dr. Alan Fogelman, executive chair of the department of medicine and director of the atherosclerosis research unit at the Geffen School of Medicine.

 

The study was funded by the National Institute of Environmental Health Sciences; the National Heart, Lung and Blood Institute; and the U.S. Environmental Protection Agency.

 

Additional authors included Akeem Lawal, Jerry Ricks, Julie R. Fox and Tim Larson.

 

For more news, visit the UCLA Newsroom and follow us on Twitter.

 

Their discovery shows the positive effects of drugs that may lead to effective new treatments for the neurodegenerative disease. iPS cells are made from patients' skin cells, rather than from embryos, and they can become any type of cells, including brain cells, in the laboratory. The study appears online ahead of print in the journal Nature Communications.

 

People with A-T begin life with neurological deficits that become devastating through progressive loss of function in a part of the brain called the cerebellum, which leads to severe difficulty with movement and coordination. A-T patients also suffer frequent infections due to their weakened immune systems and have an increased risk for cancer. The disease is caused by lost function in a gene, ATM, that normally repairs damaged DNA in the cells and preserves normal function.

 

Developing a human neural cell model to understand A-T's neurodegenerative process — and create a platform for testing new treatments — was critical because the disease presents differently in humans and laboratory animals. Scientists commonly use mouse models to study A-T, but mice with the disease do not experience the more debilitating effects that humans do. In mice with A-T, the cerebellum appears normal and they do not exhibit the obvious degeneration seen in the human brain.

Lee and colleagues used iPS cell–derived neural cells developed from skin cells of A-T patients with a specific type of genetic mutation to create a disease-in-a-dish model. In the laboratory, researchers were able to model the characteristics of A-T, such as the cell's lack of ATM protein and its inability to repair DNA damage. The model also allowed the researchers to identify potential new therapeutic drugs, called small molecule read-through (SMRT) compounds, that increase ATM protein activity and improve the model cells' ability to repair damaged DNA.

 

"A-T patients with no ATM activity have severe disease but patients with some ATM activity do much better," Lee said. "This makes our discovery promising, because even a small increase in the ATM activity induced by the SMRT drug can potentially translate to positive effects for patients, slowing disease progression and hopefully improving their quality of life."

 

These studies suggest that SMRT compounds may have positive effects on all other cell types in the body, potentially improving A-T patients' immune function and decreasing their susceptibility to cancer.

Additionally, the patient-specific iPS cell–derived neural cells in this study combined with the SMRT compounds can be an invaluable tool for understanding the development and progression of A-T. This iPS cell–neural cell A-T disease model also can be a platform to identify more potent SMRT drugs. The SMRT drugs identified using this model can potentially be applied to most other genetic diseases with the same type of mutations.

 

This research was supported by training and research grants from the California Institute of Regenerative Medicine, the National Institutes of Health, APRAT, A-T Ease and Scott Richards Foundation.

 

The Eli and Edythe Broad Center of Regenerative Medicine and Stem Cell Research: UCLA's stem cell center was launched in 2005 with a UCLA commitment of $20 million over five years. A $20 million gift from the Eli and Edythe Broad Foundation in 2007 resulted in the renaming of the center. With more than 200 members, the Broad Stem Cell Research Center is committed to a multidisciplinary, integrated collaboration among scientific, academic and medical disciplines for the purpose of understanding adult and human embryonic stem cells. The center supports innovation, excellence and the highest ethical standards focused on stem cell research with the intent of facilitating basic scientific inquiry directed toward future clinical applications to treat disease. The center is a collaboration of the David Geffen School of Medicine at UCLA, UCLA's Jonsson Cancer Center, the UCLA Henry Samueli School of Engineering and Applied Science and the UCLA College of Letters and Science.

 

 

UCLA’s Laboratory of Neuro Imaging (LONI) has been an international pioneer in enhancing the understanding of human brain structure and function. I am proud of UCLA’s role in supporting the lab’s many positive impacts so, naturally, I was disappointed to learn that the lab plans to end its affiliation with the campus. I want to stress, though, that the exceptional drive and ingenuity of our faculty, staff and students and the quality of our research infrastructure ensures our continued strength, especially in the field of neuroscience. UCLA is among the world’s great research enterprises, testing boundaries and producing new knowledge on a daily basis, and the departure of one lab will not diminish our impact.

Two professors from the David Geffen School of Medicine at UCLA have been elected by their peers to the prestigious National Academy of Sciences in recognition of their distinguished and continuing achievements in original research.

 

Election to the academy is considered one of the highest honors presented to scientists in the U.S.; its membership includes Albert Einstein, Robert Oppenheimer, Thomas Edison, Orville Wright and Alexander Graham Bell. 

 

The UCLA professors are among 84 new members of the academy from across the U.S. and 21 foreign associates from 14 countries. Their election brings the number of current UCLA academy members to 43. The new UCLA members are:

 

Dr. Edward De Robertis, Norman Sprague Professor of Biological Chemistry and a Howard Hughes Medical Institute investigator. De Robertis is a member of the Pontifical Academy of Sciences and the Latin American Academy of Sciences, as well as a fellow of the American Academy of Arts and Sciences. His research focuses on the way that cells communicate with each other. 

 

De Robertis' isolation of genes that control head-to-tail and back-to-belly patterning in early frog and mouse embryos led to the discovery that all animals' development is controlled by an ancient genetic toolkit. In particular, he carried out the molecular dissection of the process of embryonic induction, in which groups of cells called "organizers" control tissue differentiation. This work is aimed at understanding cell signaling, a fundamental problem in stem cell biology and cancer. De Robertis has been a member of the Jonsson Comprehensive Cancer Center at UCLA since 1985. 

 

Ernest Wright, distinguished professor of physiology and Sherman M. Mellinkoff Distinguished Professor in Medicine. Wright was named a fellow of the British Royal Society in 2005, an honor considered one of the highest accolades a scientist can achieve next to the Nobel Prize, and in 2006 he was elected to the German Academy of Sciences Leopoldina. His research focuses on the structure, function and genetics of membrane transport proteins, which act as the gatekeepers for the body by carrying essential molecules in and out of cells.

 

Research in Wright's laboratory on the cloning and function of glucose transporters has already led to the development of new drugs to control diabetes. 

 

The National Academy of Sciences rolls currently list 2,179 active academy members, and 437 foreign associates.

 

The National Academy of Sciences was established in 1863 by a congressional act of incorporation signed by Abraham Lincoln that calls on the academy to act as an official adviser to the federal government, upon request, in any matter of science or technology. The academy is a private organization of scientists and engineers dedicated to the advancement of science and its use for the general welfare. 

 

The David Geffen School of Medicine at UCLA has more than 2,000 full-time faculty members, almost 1,300 residents, more than 750 medical students, and almost 400 Ph.D. candidates, and ranks in the top tier of research institutions funded by the National Institutes of Health.

 

For more news, visit the UCLA Newsroom and follow us on Twitter. 

The study, published online May 8 in the journal Nature, is the first to identify the strategy by which bacteria form the micro-colonies that become biofilms, which can cause lethal infections. The research may have significant implications for battling stubborn bacterial infections that do not respond to antibiotics.

 

Bacteria in biofilms behave very differently from free-swimming bacteria. Within biofilms, bacteria change their gene expression patterns and are far more resistant to antibiotics and the body's immune defenses than individual, free-swimming bacteria, because they mass together and are protected by a matrix of proteins, DNA and long, chain-like sugar molecules called polysaccharides. This makes seemingly routine infections potentially deadly.

 

Gerard Wong, professor of bioengineering at the UCLA Henry Samueli School of Engineering and Applied Science, member of the California NanoSystems Institute, and professor of chemistry and biochemstry at UCLA; Erik Luijten, professor of materials science and engineering and of applied mathematics at Northwestern University; and Matthew R. Parsek, professor of microbiology at the University of Washington, led a team of researchers who elucidated the early formation of biofilms by developing algorithms that describe the movements of the different strains of the bacterium Pseudomonas aeruginosa and by conducting computer simulations to map the bacteria's movements. P. aeruginosa can cause lethal, difficult-to-treat infections, including those found in cystic fibrosis and AIDS patients.

 

Surprisingly, the researchers found that the individual bacteria that start the formation of micro-colonies have no special, inherent qualities. As bacteria move across a surface, they leave trails composed of a specific type of polysaccharide called Psl. "Some of the bacteria remained fixed in position," Parsek said. "But some moved around on the surface, apparently randomly, but leaving a trail that influenced the surface behavior of other bacteria that encountered it."

 

Bacteria arriving later also lay trails, but their movements tend to be guided by the trails from the pioneers. This network of trails creates a process of positive feedback and enables bacteria to organize into micro-colonies that mature into biofilms. By being at the right place at the right time, and by using communally produced polysaccharides, a small number of lucky cells — often ones that come later — become the first to form micro-colonies. Cells in micro-colonies have many survival advantages over other bacteria.

 

Interestingly, these biofilms develop in accordance with Zipf's Law, which has been used to describe the phenomenon of a small portion of a population controlling the majority of that population's wealth. "It turns out bacteria do something similar," Wong said. "A small number of bacteria have the best access to the lion's share of communally produced polysaccharides."

 

Wong said the research may provide insight into how to fight antibiotic-resistant bacteria. "Typically, when we want to get rid of bacteria, we just kill them with antibiotics," he said. "As a result, they develop defense mechanisms and grow stronger. Maybe that's not always the best way to treat biofilms. Perhaps we can regulate bacterial communities the way we regulate economies. Our work suggests that new treatment options may use incentives and communications, as well as punishment, to control bacterial communities."

 

Luijten said that the group's findings were possible because the researchers drew knowledge from their various individual disciplines. "Only through combination of the totally different types of expertise of three different research groups has it been possible to disentangle what is going on, and how polysaccharides influence the organization of bacteria into micro-colonies."

 

Postdoctoral researcher Kun Zhao of UCLA's Department of Bioengineering and senior fellow Boo Shan Tseng of the University of Washington are the paper's lead authors. The principal investigators are Wong, Parsek and Luijten. Other authors include Joe Harrison of the University of Washington, Professor Fan Jin of the University of Science and Technology of China in Hefei, Northwestern University graduate student Bernard Beckerman and UCLA graduate student Maxsim Gibiansky. Harrison is now an assistant professor at the University of Calgary.

 

The research was supported by the National Institutes of Health, the National Science Foundation, the Cystic Fibrosis Foundation, the Natural Sciences and Engineering Research Council of Canada and a UCLA Transdisciplinary Research Grant.

 

The UCLA Henry Samueli School of Engineering and Applied Science, established in 1945, offers 28 academic and professional degree programs and has an enrollment of more than 5,000 students. The school's distinguished faculty are leading research to address many of the critical challenges of the 21st century, including renewable energy, clean water, health care, wireless sensing and networking, and cyber-security. Ranked among the top 10 engineering schools at public universities nationwide, the school is home to eight multimillion-dollar interdisciplinary research centers in wireless sensor systems, wireless health, nanoelectronics, nanomedicine, renewable energy, customized computing, the smart grid, and the Internet, all funded by federal and private agencies and individual donors.

 

For more news, visit the UCLA Newsroom and follow us on Twitter.

[This statement was updated May 14 to reflect new developments.]

 

On May 10, the American Federation of State, County and Municipal Employees (AFSCME) union announced that it had asked the UC patient care and service employees it represents at UCLA Health System hospitals and clinics to strike from 4 a.m. on Tuesday, May 21, until 4 a.m. on Thursday, May 23.   

 

In response, the University of California announced May 10 that it will seek a restraining order against the AFSCME union. Strikes that pose a substantial and imminent threat to public health or safety are illegal under state law. UC believes a strike targeting UC medical centers would pose an imminent threat to public health and safety and would improperly withhold health care from members of the public.

It is very disappointing that AFSCME is threatening services to patients as a tactic in negotiations that are mainly about pension benefits — our patients are not bargaining chips.

 

The first priority at UCLA Health System's hospitals is to provide patients with safe, high-quality care. In anticipation of a possible strike, UCLA Health System staff has been meeting daily to make contingency plans so that it can continue to serve the public's health needs.

 

A strike by AFSCME patient care and service workers could possibly involve more than 4,000 UCLA Health System and medical school employees, the majority of whom take care of patients and their families. They include patient care assistants, respiratory therapists, hospital lab and imaging technicians, custodians and food service workers. Patient care areas that would be impacted include Ronald Reagan UCLA Medical Center, UCLA Medical Center, Santa Monica, UCLA's Resnick Neuropsychiatric Hospital, the David Geffen School of Medicine at UCLA, Mattel Children's Hospital UCLA, and UCLA's community and outpatient clinics.

 

The cost of bringing in replacement workers to provide medical care safely and effectively would be millions of dollars, and the strike would place an undue burden on our non-striking employees.

 

 

The dedication and hard work of employees at UCLA Health System, including AFSCME members, allow us to provide the best patient care in the country. In return, UC provides competitive compensation and benefits.

 

To continue to provide world-class care and service, UC needs thoughtful engagement from the union leadership of AFSCME.

 

• Details about UC-AFSCME negotiations

 

Chancellor Gene Block and UCLA staff members gathered today for 10 minutes of exercise to honor Dr. Antronette (Toni) Yancey, a professor at the UCLA Fielding School of Public Health and advocate for health equity and proponent of "Instant Recess." She died April 23 following a battle with lung cancer. The 1 p.m. tribute at UCLA's CHS Plaza coincided with "Instant Recess" events by public health professionals and supporters across the United States.

 

FINDINGS:  

IMPACT:
Human squamous cell carcinoma is highly invasive and frequently spreads to cervical lymph nodes. Understanding the molecular and epigenetic mechanisms that control the metastasis of squamous cell carcinoma in humans will help scientists develop new therapies for treating cancer.  

 

AUTHORS:

FUNDING:
This work was supported in part by grants from the National Institute of Dental and Craniofacial Research of the National Institutes of Health and the Shapiro Family Charitable Foundation.

JOURNAL:
Wang's new research is published in Science Signaling — a peer-reviewed scientific journal published by the American Association for the Advancement of Science.

 

The gene, called parkin, serves at least two vital functions: It marks damaged proteins so that cells can discard them before they become toxic, and it is believed to play a key role in the removal of damaged mitochondria from cells.

 

"Aging is a major risk factor for the development and progression of many neurodegenerative diseases," said David Walker, an associate professor of integrative biology and physiology at UCLA and senior author of the research. "We think that our findings shed light on the molecular mechanisms that connect these processes."

 

In the research, published today in the early online edition of the journal Proceedings of the National Academy of Sciences, Walker and his colleagues show that parkin can modulate the aging process in fruit flies, which typically live less than two months. The researchers increased parkin levels in the cells of the flies and found that this extended their life span by more than 25 percent, compared with a control group that did not receive additional parkin.

 

"In the control group, the flies are all dead by Day 50," Walker said. "In the group with parkin overexpressed, almost half of the population is still alive after 50 days. We have manipulated only one of their roughly 15,000 genes, and yet the consequences for the organism are profound."

 

"Just by increasing the levels of parkin, they live substantially longer while remaining healthy, active and fertile," said Anil Rana, a postdoctoral scholar in Walker's laboratory and lead author of the research. "That is what we want to achieve in aging research — not only to increase their life span but to increase their health span as well."

 

Treatments to increase parkin expression may delay the onset and progression of Parkinson's disease and other age-related diseases, the biologists believe. (If parkin sounds related to Parkinson's, it is. While the vast majority of people with the disease get it in older age, some who are born with a mutation in the parkin gene develop early-onset, Parkinson's-like symptoms.)

 

"Our research may be telling us that parkin could be an important therapeutic target for neurodegenerative diseases and perhaps other diseases of aging," Walker said. "Instead of studying the diseases of aging one by one — Parkinson's disease, Alzheimer's disease, cancer, stroke, cardiovascular disease, diabetes — we believe it may be possible to intervene in the aging process and delay the onset of many of these diseases. We are not there yet, and it can, of course, take many years, but that is our goal."

 

 

To function properly, proteins must fold correctly, and they fold in complex ways. As we age, our cells accumulate damaged or misfolded proteins. When proteins fold incorrectly, the cellular machinery can sometimes repair them. When it cannot, parkin enables cells to discard the damaged proteins, said Walker, a member of UCLA's Molecular Biology Institute.

 

"If a protein is damaged beyond repair, the cell can recognize that and eliminate the protein before it becomes toxic," he said. "Think of it like a cellular garbage disposal. Parkin helps to mark damaged proteins for disposal. It's like parkin places a sticker on the damaged protein that says 'Degrade Me,' and then the cell gets rid of this protein. That process seems to decline with age. As we get older, the garbage men in our cells go on strike. Overexpressed parkin seems to tell them to get back to work."

 

Rana focused on the effects of increased parkin activity at the cellular and tissue levels. Do flies with increased parkin show fewer damaged proteins at an advanced age? "The remarkable finding is yes, indeed," Walker said.

 

Parkin has recently been shown to perform a similarly important function with regard to mitochondria, the tiny power generators in cells that control cell growth and tell cells when to live and die. Mitochandria become less efficient and less active as we age, and the loss of mitochondrial activity has been implicated in Alzheimer's, Parkinson's and other neurodegenerative diseases, as well as in the aging process, Walker said.

 

Parkin appears to degrade the damaged mitochondria, perhaps by marking or changing their outer membrane structure, in effect telling the cell, "This is damaged and potentially toxic. Get rid of it."

 

 

While the researchers found that increased parkin can extend the life of fruit flies, Rana also discovered that too much parkin can have the opposite effect — it becomes toxic to the flies. When he quadrupled the normal amount of parkin, the fruit flies lived substantially longer, but when he increased the amount by a factor of 30, the flies died sooner.

 

"If you bombard the cell with too much parkin, it could start eliminating healthy proteins," Rana said.

 

In the lower doses, however, the scientists found no adverse effects. Walker believes the fruit fly is a good model for studying aging in humans — who also have the parkin gene — because scientists know all of the fruit fly's genes and can switch individual genes on and off.

 

Previous research has shown that fruit flies die sooner when you remove parkin, Walker noted.

 

Walker and Rana do not know what the optimal amount of parkin would be in humans.

 

While the biologists increased parkin activity in every cell in the fruit fly, Rana also conducted an experiment in which he increased parkin expression only in the nervous system. That, too, was sufficient to make the flies live longer.

 

"This tells us that parkin is neuroprotective during aging," Walker said. "However, the beneficial effects of parkin are greater — twice as large — when we increased its expression everywhere."

 

"We were excited about this research from the beginning but did not know then that the life span increase would be this impressive," Rana said.

  

The image that accompanies this news release shows clumps or aggregates of damaged proteins in an aged brain from a normal fly (left panel) and an age-matched brain with increased neuronal parkin levels (right panel). As can be seen, increasing parkin levels in the aging brain reduces the accumulation of aggregated proteins.

 

Scientists have found that this kind of protein aggregation occurs in mammals as well, including humans, Rana said.

 

"Imagine the damage the accumulation of protein trash is doing to the cell," Walker said. "With increased Parkin, the trash has been collected. Without it, the garbage that should be discarded is accumulating in the cells."

 

Walker's research was funded by the National Institutes of Health's National Institute on Aging (grants R01 AG037514 and R01 AG040288) and the Ellison Medical Foundation. Rana was supported by a Rubicon fellowship from the Organization for Scientific Research in the Netherlands, where he earned his doctorate (University of Groningen). Michael Rera, a UCLA postdoctoral scholar in Walker's laboratory, is a co-author of the PNAS research.

 

UCLA is California's largest university, with an enrollment of more than 40,000 undergraduate and graduate students. The UCLA College of Letters and Science and the university's 11 professional schools feature renowned faculty and offer 337 degree programs and majors. UCLA is a national and international leader in the breadth and quality of its academic, research, health care, cultural, continuing education and athletic programs. Six alumni and six faculty have been awarded the Nobel Prize.

 

For more news, visit the UCLA Newsroom and follow us on Twitter.

 

UCLA staff affectionately dubbed the 5'5", 176-pound robot "EVA," for executive virtual attending physician. Unlike earlier models that physicians steered via a computer-linked joystick, this version drives on auto-pilot, freeing doctors to devote more time to patient care.

 

"During a stroke, the loss of a few minutes can mean the difference between preserving or losing brain function," said Dr. Paul Vespa, director of neurocritical care at Ronald Reagan UCLA Medical Center and a professor of neurosurgery and neurology at the David Geffen School of Medicine at UCLA. "This new advance enables me to concentrate on caring for my patients without being distracted by the need to set up and manage its technological features."

 

With a simple push of an iPad button, Vespa can send the robot gliding down the hall to a patient's room. Equipped with 30 sensors that enable the it to "see" when its route is blocked by a gurney or curious bystander, EVA possesses the intelligence to self-correct and plot a detour to its destination.

 

After the robot reaches a patient's bedside, Vespa can examine the patient in real time. A two-way video monitor in EVA's "face" enables the patient and doctor to see and hear each other. A 120x zoom capacity allows Vespa to magnify a single word on the patient's chart or zero in on the patient's eyes to check for dilated pupils.

 

"The robot is the next best thing to having a doctor come and talk to you," said Kevin Sittner, a former neuro-ICU patient at Ronald Reagan UCLA Medical Center. "You see each other's faces, and it feels like you're actually talking to the doctor. It was added comfort to me as a patient knowing I could get care whenever I needed it."

 

Jointly developed by InTouch Health and iRobotCorp, EVA's software creates a map of the neuro-ICU floor that is integrated with hospital records, informing the robot where to go when a physician selects a patient on an iPad. Saved in EVA's memory bank, the map constantly refreshes as patients are admitted and discharged.

 

In the neuro-ICU, where "time is brain," EVA enables neurosurgeons and neurologists to connect with patients and their family members at a moment's notice, regardless of where they are. The robot also allows specialists to offer lifesaving consultations on complex cases worldwide at hospitals without neurocritical-care expertise. Encrypted patient data and medical images are easily downloaded from a cloud-based network.

 

"Consumers nationwide are facing long delays in medical delivery, largely because the health care system can't provide enough physicians in enough locations," Vespa said. "We need new technologies that revolutionize physicians' capacity to see more patients and greatly expand patients' access to specialized care."

 

The UCLA Department of Neurosurgery is committed to providing the most comprehensive patient care through innovative clinical programs in minimally invasive brain and spinal surgery; neuroendoscopy; neuro-oncology for adult and pediatric brain tumors; cerebrovascular surgery; stereotactic radiosurgery for brain and spinal disorders; surgery for movement disorders such as Parkinson's disease; and epilepsy surgery. For 21 consecutive years, the department has been ranked among the top neurosurgery programs in the nation by U.S. News & World Report, including No. 1 in Los Angeles and No. 2 on the West Coast.

 

For more news, visit the UCLA Newsroom and follow us on Twitter.

 

Plastic surgeons have been leaders among medical specialists in the development of interactive websites to promote their practices and educate patients, said the study's principal investigator and senior author, Dr. Reza Jarrahy, an associate clinical professor of plastic and reconstructive surgery at Ronald Reagan UCLA Medical Center. But until now, there there had been surprisingly little information on whether and how they are using social media.

 

In the study, published in the May issue of Plastic and Reconstructive Surgery, the official medical journal of the American Society of Plastic Surgeons (ASPS), approximately 50 percent of plastic surgeons polled said they use Facebook, Twitter and other social media platforms to help market their professional practice.

 

"Social media platforms represent a dynamic and powerful tool to educate, engage, market to and directly communicate with patients and professional colleagues," said Jarrahy, who is a member of ASPS and vice president of communications for the American Society of Maxillofacial Surgeons. "However, for plastic surgeons, the potential benefits associated with using this tool must be balanced against its potential pitfalls."

 

The researchers sent an anonymous survey to more than 5,000 ASPS member surgeons. Responses from 500 of them provided information on their use of social media in their plastic surgery practice, their reasons for using it and the perceived benefits and risks.

 

Just more than half said they regularly use social media for their professional practice. Facebook was by far the most popular platform, followed by LinkedIn, Twitter and YouTube. The poll also showed that surgeons who primarily perform cosmetic plastic surgery and who are in private practice were more likely to use social media.

 

When asked their reasons for using these tools, most responded that incorporating social media into medical practice was inevitable. About half said that social media was an effective marketing tool and a useful forum for patient education.

 

About one-third of plastic surgeons saw positive effects from using social media, saying they felt it provided an effective, low-cost means of advertising and increased the exposure of their practice. Roughly half believed that engaging in social media led to increased patient referrals and positive feedback.

 

A small proportion of plastic surgeons (1.5 percent) reported that using social media had a negative effect on their practice. Yet while some surgeons had received criticism or negative commentary from patients via social media, most thought these criticisms had not harmed their practice.

 

Those plastic surgeons who didn't use social media cited a number of reasons why, including a desire to maintain a sense of professionalism, protecting patient confidentiality and concerns about becoming too accessible.

 

Approximately one-fourth of respondents felt that ASPS and other governing bodies should provide some oversight and monitoring of plastic surgeons' use of social medial to ensure ethical online behavior.

 

The new study shows that many plastic surgeons have joined the social media revolution and believe it has benefited their practice in various ways. However, they also perceive a need for standards of practice and oversight to ensure appropriate and ethical use.

 

"Because of our current level of engagement with existing online content, plastic surgeons are uniquely poised to become leaders in developing the future of social media architecture to the maximum benefit of practitioners and patients alike," Jarrahy said.

 

Additional study authors, all from UCLA, included Dr. Andrew J. Vardanian, Nicholas Kusnezov, Dr. Daniel D. Im and James C. Lee.

 

The study was funded in part by the Annenberg Fund for Craniofacial Surgery and Research at UCLA.

 

The authors have no financial ties to disclose. Jarrahy participates in oversight of the ASMS website and social media development.

 

For more information on the American Society of Plastic Surgeons, visit at www.plasticsurgery.org.

 

For more information on the division of plastic and reconstructive surgery at Ronald Reagan UCLA Medical Center, visit www.plasticsurgery.ucla.edu.

 

For more news, visit the UCLA Newsroom and follow us on Twitter.

 

Take one step out the front door, and an individual brain cell fires. Pass by your rose bush on the way to the car, another specific neuron fires. And so it goes. Ultimately, the brain constructs its own pinpoint geographical chart that is far more precise than anything you'd find on Google Maps.

 

But just how neurons make these maps of space has fascinated scientists for decades. It is known that several types of stimuli influence the creation of neuronal maps, including visual cues in the physical environment — that rose bush, for instance — the body's innate knowledge of how fast it is moving, and other inputs, like smell. Yet the mechanisms by which groups of neurons combine these various stimuli to make precise maps are unknown.

 

To solve this puzzle, UCLA neurophysicists built a virtual-reality environment that allowed them to manipulate these cues while measuring the activity of map-making neurons in rats. Surprisingly, they found that when certain cues were removed, the neurons that typically fire each time a rat passes a fixed point or landmark in the real world instead began to compute the rat's relative position, firing, for example, each time the rodent walked five paces forward, then five paces back, regardless of landmarks. And many other mapping cells shut down altogether, suggesting that different sensory cues strongly influence these neurons.

 

Finally, the researchers found that in this virtual world, the rhythmic firing of neurons that normally speeds up or slows down depending on the rate at which an animal moves, was profoundly altered. The rats' brains maintained a single, steady rhythmic pattern.

 

The findings, reported in the May 2 online edition of the journal Science, provide further clues to how the brain learns and makes memories.

 

 

"Place cells" are individual neurons located in the brain's hippocampus that create maps by registering specific places in the outside environment. These cells are crucial for learning and memory. They are also known to play a role in such conditions as post-traumatic stress disorder and Alzheimer's disease when damaged.

 

For some 40 years, the thinking had been that the maps made by place cells were based primarily on visual landmarks in the environment, known as distal cues — a tall tree, a building — as well on motion, or gait, cues. But, as UCLA neurophysicist and senior study author Mayank Mehta points out, other cues are present in the real world: the smell of the local pizzeria, the sound of a nearby subway tunnel, the tactile feel of one's feet on a surface. These other cues, which Mehta likes to refer to as "stuff," were believed to have only a small influence on place cells.

 

Could it be that these different sensory modalities led place cells to create individual maps, wondered Mehta, a professor with joint appointments in the departments of neurology, physics and astronomy. And if so, do these individual maps cooperate with each other, or do they compete? No one really knew for sure.

 

 

To investigate, Mehta and his colleagues needed to separate the distal and gait cues from all the other "stuff." They did this by crafting a virtual-reality maze for rats in which odors, sounds and all stimuli, except distal and gait cues, were removed. As video of a physical environment was projected around them, the rats, held by a harness, were placed on a ball that rotated as they moved. When they ran, the video would move along with them, giving the animals the illusion that they were navigating their way through an actual physical environment.

 

As a comparison, the researchers had the rats — six altogether — run a real-world maze that was visually identical to the virtual-reality version but that included the additional "stuff" cues. Using micro-electrodes 10 times thinner than a human hair, the team measured the activity of some 3,000 space-mapping neurons in the rats' brains as they completed both mazes.

 

What they found intrigued them. The elimination of the "stuff" cues in the virtual-reality maze had a huge effect: Fully half of the neurons being recorded became inactive, despite the fact that the distal and gate cues were similar in the virtual and real worlds. The results, Mehta said, show that these other sensory cues, once thought to play only a minor role in activating the brain, actually have a major influence on place cells.

 

And while in the real world, place cells responded to fixed, absolute positions, spiking at those same positions each time rats passed them, regardless of the direction they were moving — a finding consistent with previous experiments — this was not the case in the virtual-reality maze.

 

"In the virtual world," Mehta said, "we found that the neurons almost never did that. Instead, the neurons spiked at the same relative distance in the two directions as the rat moved back and forth. In other words, going back to the front door-to-car analogy, in a virtual world, the cell that fires five steps away from the door when leaving your home would not fire five steps away from the door upon your return. Instead, it would fire five steps away from the car when leaving the car. Thus, these cells are keeping track of the relative distance traveled rather than absolute position. This gives us evidence for the individual place cell's ability to represent relative distances."

 

Mehta thinks this is because neuronal maps are generated by three different categories of stimuli — distal cues, gait and "stuff" — and that all are competing for control of neural activity. This competition is what ultimately generates the "full" map of space.

 

"All the external stuff is fixed at the same absolute position and hence generates a representation of absolute space," he said. "But when all the stuff is removed, the profound contribution of gait is revealed, which enables neurons to compute relative distances traveled."

 

The researchers also made a new discovery about the brain's theta rhythm. It is known that place cells use the rhythmic firing of neurons to keep track of "brain time," the brain's internal clock. Normally, Mehta said, the theta rhythm becomes faster as subjects run faster, and slower as running speed decreases. This speed-dependent change in brain rhythm was thought to be crucial for generating the 'brain time' for place cells. But the team found that in the virtual world, the theta rhythm was uninfluenced by running speed.

 

"That was a surprising and fascinating discovery, because the 'brain time' of place cells was as precise in the virtual world as in the real world, even though the speed-dependence of the theta rhythm was abolished," Mehta said. "This gives us a new insight about how the brain keeps track of space-time."

 

The researchers found that the firing of place cells was very precise, down to one-hundredth of a second, "so fast that we humans cannot perceive it but neurons can," Mehta said. "We have found that this very precise spiking of neurons with respect to 'brain-time' is crucial for learning and making new memories."

 

Mehta said the results, taken together, provide insight into how distinct sensory cues both cooperate and compete to influence the intricate network of neuronal activity. Understanding how these cells function is key to understanding how the brain makes and retains memories, which are vulnerable to such disorders as Alzheimer's and PTSD.

 

"Ultimately, understanding how these intricate neuronal networks function is a key to developing therapies to prevent such disorders," he said.

 

In May, Mehta joined 100 other scientists in Washington, D.C., to help shape President Obama's BRAIN Initiative (Brain Research through Advancing Innovative Neurotechnologies), with the goal of trying to tease out how this most complicated of organs works.

 

Other authors of the study included Pascal Ravassard, Ashley Kees and Bernard Willers, all lead authors, and David Ho, Daniel A. Aharoni, Jesse Cushman and Zahra M. Aghajan of UCLA. Funding was provided by the W.M. Keck foundation, a National Science Foundation career award grant and a National Institutes of Health grant (5R01MH092925-02).

 

The UCLA Department of Neurology, with over 100 faculty members, encompasses more than 20 disease-related research programs, along with large clinical and teaching programs. These programs cover brain mapping and neuroimaging, movement disorders, Alzheimer's disease, multiple sclerosis, neurogenetics, nerve and muscle disorders, epilepsy, neuro-oncology, neurotology, neuropsychology, headaches and migraines, neurorehabilitation, and neurovascular disorders. The department ranks in the top two among its peers nationwide in National Institutes of Health funding.

 

For more news, visit the UCLA Newsroom and follow us on Twitter.

 

Research has shown that stroke risk can be substantially lowered by increasing physical activity, controlling blood pressure, adopting a healthy diet, quitting smoking, lowering cholesterol and, for certain individuals, taking medication like aspirin.

 

However, the underserved populations targeted by this research program are frequently prevented from achieving these health goals by a variety barriers, including a lack of transportation for doctor visits, an inability to afford medication, insufficient knowledge about how to change their lifestyle, living in neighborhoods where infrastructure or safety concerns prevent walking, and an inability to read food labels in English, among others.

 

The Los Angeles Stroke Prevention/Intervention Research Program in Health Disparities is a multi-partner research center funded by the National Institutes of Health that will conduct two randomized, controlled, community-based trials of stroke-prevention interventions. One will measure how much the risk of recurrent stroke is lowered by teaming community health workers with physicians and nurses at Los Angeles medical centers serving low-income populations.

 

"These community health workers will conduct home visits to outreach to patients with a recent stroke," said the research center's director, Dr. Barbara Vickrey, vice chair and professor of neurology at the David Geffen School of Medicine at UCLA. "They will use mobile health technology to help them educate and empower these patients to make changes in their diet and physical activity and to promote the use of home blood-pressure monitors and medications that substantially lower the risk of another stroke."

 

A second trial will assess the impact and sustainability of a culturally tailored behavioral intervention designed to provide stroke risk–factor education and increase physical activity, primarily walking. This program will be delivered by staff at senior centers serving African American, Latino, Chinese and Korean communities in Los Angeles and is designed to be self-sustained after the study is over.

 

An additional study will analyze several decades of data from the National Health and Nutrition Examination Survey to identify changes in biological and social risk factors for stroke over time across different racial and ethnic groups. Hopefully, Vickrey said, this research will identify new risk factors that can be controlled through future interventions.

 

"The goal of the program is to learn what is effective in reducing stroke risk in underserved minority populations, which are at higher risk and have worse outcomes," Vickrey said. "We know that we have effective treatments to control risk factors for stroke, and now we need to create and test effective and sustainable ways for patients to access medications and to succeed in lifestyle changes that will prevent stroke. What we learn from the center's research could improve stroke prevention for those in Los Angeles County and also could be exported to communities with underserved populations across the country."

 

The multi-disciplinary, collaborative center builds on UCLA's established partnerships with other health care systems, including Rancho Los Amigos National Rehabilitation Center, Harbor–UCLA Medical Center, Olive View–UCLA Medical Center and the University of Southern California. Partnerships also include many local community organizations, such as Healthy African American Families, the Watts Labor Community Action Committee and multiple senior centers, as well as the American Heart Association and the City of Los Angeles Department of Aging.

 

A central component of the program will be the creation of a community action panel made up of individuals representing the racial and ethnic diversity of Los Angeles. This group will formally and regularly review and present advice on the work in progress and the products of the center overall, promote ways to effectively disseminate the work in the targeted communities, and provide feedback to investigators at every stage of the research. An annual symposium also will be held to engage community members and academic investigators in Los Angeles and foster the sharing of knowledge.

 

"At the end of five years, we'll know we're successful if our interventions are effective and if we can identify new targets for future interventions to reduce disparities in stroke risk," Vickrey said.

 

She added that they also will be identifying and educating future investigators and research staff, many of whom may be from these minority communities, to continue in disparities-intervention research in the future.

 

For more news, visit the UCLA Newsroom and follow us on Twitter.

 

Results from the study, conducted by the UCLA Center for Behavioral and Addiction Medicine and the community-based substance abuse treatment program Behavioral Health Services Inc., are published in the April edition of the Journal of Adolescent Health. 

 

"The greater severity of methamphetamine problems in adolescent girls compared to boys, combined with results of studies in adults that also found women to be more susceptible to methamphetamine than men, suggests that the gender differences in methamphetamine addiction observed in adults may actually begin in adolescence," said the study's lead author, Dr. Keith Heinzerling, a health sciences assistant clinical professor of family medicine at the David Geffen School of Medicine at UCLA.

 

The clinical trial focused on use of the antidepressant bupropion for treating methamphetamine addiction. Nineteen adolescents — nine boys and 10 girls — with meth addiction who were receiving counseling at Behavioral Health Services were given either bupropion or placebo pills. The average age of participants was approximately 17.5 years.

 

The researchers found that the study subjects who received the antidepressant provided significantly fewer meth-free urine samples than those who were given placebos, suggesting that bupropion was an ineffective treatment for addiction in this small sample.

 

Overall, boys in both groups provided more than twice as many meth-free urine drug tests during treatment as girls in both groups. 

 

While the results did not support continued research into the use of bupropion for methamphetamine addiction, they did suggest the need for research to develop new interventions to improve the outcomes of treatment for addiction in adolescent girls, the researchers said.

 

Heinzerling noted the importance of collaborations such as the one between UCLA and Behavioral Health Services.

 

"It shows that partnerships between researchers and community organizations are critical to insuring that research is translated into improvements in the health of real people," he said.

 

Additional researchers on the study included Janette Gadzhyan, James McCracken and Steven Shoptaw, all of UCLA, and Henry van Oudheusden and Felipe Rodriguez of Behavioral Health Services Inc.

 

The research was funded by the National Institute on Drug Abuse (grant 5 R21 DA26513).

Behavioral Health Services Inc. is a not-for-profit community-based health care organization providing substance abuse, mental health, drug-free transitional living, older adult, HIV/AIDS education and prevention, and related health services to the residents of Southern California.

 

The UCLA Center for Behavioral and Addiction Medicine aims to advance the prevention and treatment of chronic illnesses, especially in communities with health care disparities. This includes internationally recognized research to advance the science behind addiction medicine in order to develop safer and more effective treatments for addiction. Treatment for methamphetamine addiction is available through the center at its clinics in Santa Monica and Hollywood.

 

The UCLA Department of Family Medicine provides comprehensive primary care to entire families from newborns to seniors. It provides low risk obstetrical services and prenatal and inpatient care at UCLA Medical Center Santa Monica, and outpatient care at the University Family Health Center in Santa Monica and the Mid-Valley Family Health Center, which is located in a Los Angeles County Health Center in Van Nuys, Calif. The department is also a leader in family medicine education, for both medical students and residents, and houses a significant research unit focusing on health care disparities among immigrant families and minority communities and other underserved populations in Los Angeles and California.

 

For more news, visit the UCLA Newsroom and follow us on Twitter.

 

 

Sepulveda, the former director of the National Institutes of Health of Mexico and executive director of UC San Francisco Global Health Sciences, will discuss financing mechanisms to improve health in Latin America.

 

Other speakers and panelists will include:

 

Director of the UCLA Blum Center and professor of family medicine

 

RAND Center for Latin American Social Policy

 

Dr. Timothy Brewer
UCLA vice provost for interdisciplinary and cross-campus affairs

 

Director of the UCLA Center for World Health

 

Director of UCLA's Labor Occupational Safety and Health program

 

Dean of the social sciences division, UCLA College of Letters and Science

 

Director of the North American Integration and Development Center, UCLA Luskin School of Public Affairs

 

UCLA interim vice provost for international studies

 

Director of UCLA's Center for the Study of Latino Health and Culture

 

Dean of the UCLA Fielding School of Public Health

 

UCLA distinguished professor of sociology

 

Chair of community health sciences, UCLA Fielding School of Public Health

 

UCLA executive vice chancellor and provost

 

  

 

The UCLA Blum Center takes an interdisciplinary approach toward analyzing the key factors that influence poverty and the social determinants of health in Latin America, including government practices and policies, community action, social justice, human rights, race, ethnicity, socioeconomic status, religion, foreign policies and more. The center draws on the expertise of schools and colleges across UCLA, including the humanities and social sciences divisions of the College of Letters and Science, the David Geffen School of Medicine, the Fielding School of Public Health, the Graduate School of Education and Information Studies, the Luskin School of Public Affairs, the School of Dentistry, the School of Law, the School of Nursing, and the Department of Sociology, as well as, the UCLA Center for World Health, the UC Center of Expertise in Women's Health and Empowerment, the UC Center of Expertise on Migration and Health, UCLA's Chicano Studies Research Center, the UCLA Latin American Institute, and the UCLA Program on International Migration.

Parking will available in Structure DD, 409 Charles E. Young Dr. West (map).

Call media contact for parking instructions.

Enrique Rivero, UCLA Health Sciences Media Relations

erivero@mednet.ucla.edu | 310-794-2273 | on day of event: 310-597-5768 (cell)      

 

Dr. Jamie Feusner, the study's senior author and a UCLA associate professor of psychiatry, and his colleagues report that individuals with BDD have, in essence, global "bad wiring" in their brains — that is, there are abnormal network-wiring patterns across the brain as a whole.

 

And in line with earlier UCLA research showing that people with BDD process visual information abnormally, the study discovered abnormal connections between regions of the brain involved in visual and emotional processing.

 

The findings, published in the May edition of the journal Neuropsychopharmacology, suggest that these patterns in the brain may relate to impaired information processing.

 

"We found a strong correlation between low efficiency of connections across the whole brain and the severity of BDD," Feusner said. "The less efficient patients' brain connections, the worse the symptoms, particularly for compulsive behaviors, such as checking mirrors."

 

People suffering from BDD tend to fixate on minute details, such as a single blemish on their face or body, rather than viewing themselves in their entirety. They become so distressed with their appearance that they often can't lead normal lives, are fearful of leaving their homes and occasionally even commit suicide. Patients frequently have to be hospitalized. BDD affects approximately 2 percent of the population and is more prevalent than schizophrenia or bipolar disorder. Despite its prevalence and severity, scientists know relatively little about the neurobiology of BDD.

 

In the current study, Feusner and his colleagues performed brain scans of 14 adults diagnosed with BDD and 16 healthy controls. The goal of the study was to map the brain's connections to examine how the white-matter networks are organized. White matter is made up of nerve cells that carry impulses from one part of the brain to another.

 

To do this, they used a sensitive form of brain imaging called diffusion tensor imaging, or DTI. DTI is a variant of magnetic resonance imaging that can measure the structural integrity of the brain's white matter. From these scans, they were able to create whole brain "maps" of reconstructed white-matter tracks. Next, they used a form of advanced analysis called graph theory to characterize the patterns of connections throughout the brains of people with BDD and then compared them with those of healthy controls.

 

The researchers found people with BDD had a pattern of abnormally high network "clustering" across the entire brain. This suggests that these individuals may have imbalances in how they process "local" or detailed information. The researchers also discovered specific abnormal connections between areas involved in processing visual input and those involved in recognizing emotions.

 

"How their brain regions are connected in order to communicate about what they see and how they feel is disturbed," said Feusner, who also directs the Adult Obsessive-Compulsive Disorder Program and the Body Dysmorphic Disorder Research Program at UCLA.

 

"Their brains seem to be fine-tuned to be very sensitive to process minute details, but this pattern may not allow their brains to be well-synchronized across regions with different functions," he said. "This could affect how they perceive their physical appearance and may also result in them getting caught up in the details of other thoughts and cognitive processes."

 

The study, Feusner noted, advances the understanding of BDD by providing evidence that the "hard wiring" of patients' brain networks is abnormal.

 

"These abnormal brain networks could relate to how they perceive, feel and behave," he said. "This is significant because it could possibly lead to us being able to identify early on if someone is predisposed to developing this problem."

 

Other authors on the study included Jesse A Brown, Liang Zhan and Sarit Hovav, all from UCLA, and Donatello Arienzo, Alex Leow and Johnson GadElkarim from the University of Illinois. The authors declare no conflict of interest.

 

The research was supported by grants from the National Institute of Mental Health (K23 MH079212 and R01MH093535).

 

The UCLA Department of Psychiatry and Biobehavioral Sciences is the home within the David Geffen School of Medicine at UCLA for faculty who are experts in the origins and treatment of disorders of complex human behavior. The department is part of the Semel Institute for Neuroscience and Human Behavior at UCLA, a world-leading interdisciplinary research and education institute devoted to the understanding of complex human behavior and the causes and consequences of neuropsychiatric disorders.

 

For more news, visit the UCLA Newsroom and follow us on Twitter.

UCLA has formed the UCLA Blum Center on Poverty and Health in Latin America, where faculty and students from multiple disciplines will work with other institutions to conduct research, develop training programs and promote innovative policy solutions aimed at addressing key social and health-related issues in the region. 

 

"As a public university, UCLA has a duty to address the world's challenges, and our cross-disciplinary strengths in medicine, public health, humanities, social sciences, research and public policy position us to make a difference," said UCLA Executive Vice Chancellor and Provost Scott Waugh. "We have strong ties to Latin America and welcome the opportunity to strengthen our collaborations with other academic institutions, nonprofit groups and nongovernmental organizations in the region. The UCLA Blum Center is a team effort that draws faculty and students from across campus who are committed to redressing issues of poverty and health in Latin America."     

 

Dr. Michael Rodriguez, professor and vice chair of research in the department of family medicine at the David Geffen School of Medicine at UCLA, will serve as the center's director. 

 

"The programs of this new center reflect our mission to work collaboratively with a wide range of UCLA disciplines, as well as Latin American partnering institutions, to identify and promote solutions in health policy and practice," Rodriguez said. "We expect to build the center into a preeminent authority in our three focus areas — research, policy and training on the social determinants contributing to health inequalities in Latin American populations." 

 

The center's inaugural event, a symposium titled "Informing Responses to Reduce Poverty and Improve Health in Latin America," will be held on campus on Wednesday, May 1. The symposium will feature speakers and panels examining the social and economic factors that contribute to stratification and subsequent health inequalities; differences in approaches to these inequalities; innovative policy and programmatic solutions to reduce poverty and health inequalities; and potential areas for government investments in public health expenditures. 

 

Symposium details and registration information are available on the UCLA Blum Center website. 

 

The center's educational programs — a core component of its mission — to date include the UCLA Freshman Cluster Program "Poverty and Health in Latin America," which enrolled more than 70 undergraduates for its three-quarter series that began last fall, and the UCLA Blum Center Summer Intern Scholar Program, which offers eight-week internships for both undergraduate and graduate students, who participate in Los Angeles–based and Latin American–based field experiences. Researchers with the Blum Center are continuing to develop and refine its research programs and policy efforts. 

 

The new center is named for Richard Blum, a University of California regent whose generosity also made possible the Blum Center for Developing Economies at both UC Berkeley and at UC Davis. Blum provided $1 million to start the UCLA center. 

 

The UCLA Blum Center on Poverty and Health in Latin America takes an interdisciplinary approach toward analyzing the key factors that influence poverty and the social determinants of health in Latin America, including: government practices and policies, community action, social justice, human rights, race, ethnicity, socioeconomic status, religion, foreign policies and more. The center draws on the expertise of professional schools and academic units across campus, including the divisions of social sciences and humanities in the College of Letters and Science, the David Geffen School of Medicine, the Fielding School of Public Health, the Graduate School of Education and Information Studies, the Luskin School of Public Affairs, the School of Dentistry, the School of Law, the School of Nursing and many others. 

 

For more news, visit the UCLA Newsroom and follow us on Twitter.

 

UCLA researchers will create and lead a network of U.S. academic centers that will carry out early "high risk/high reward" studies of experimental medications over a three-year period. The goal of the project, New Experimental Medicine Studies: Fast–Fail Trials in Autism Spectrum Disorders, is to determine within weeks rather than years ("fast") if a particular pharmacological compound is working or not ("fail").

 

Recent progress in identifying the genes and biological components involved in autism spectrum disorders (ASD) holds great promise for the identification of life-changing treatments for individuals of all ages, said the project's principal investigator, Dr. James McCracken, a professor of psychiatry and director of the division of child and adolescent psychiatry at the Semel Institute for Neuroscience and Human Behavior at UCLA.

 

"Current medical treatments are commonly prescribed by physicians for ASD but only to manage difficult behaviors, like aggressiveness, hyperactivity and self-injury," McCracken said. "Such treatments can be important and helpful, but they do not impact the core problems of the disorders.

 

"This is definitely the most exciting time yet to be involved in treatment research for ASD," he added. "Our basic science colleagues are generating enormous information on the likely underlying causes of this common and often disabling condition. We are well positioned to apply the basic science and find drugs that make a difference."

 

ASD is increasingly recognized by clinicians. The Centers for Disease Control and Prevention estimates that one in 88 children in the U.S. has been identified with ASD, which is characterized by delays in the development of effective communication and social relationships and which impacts nearly every area of child and adult functioning.

 

Behavioral and developmental interventions, including programs developed at UCLA in the 1980s, offer significant hope of improvement for many, and behavioral and medical interventions can be helpful with behavior problems. But at present, there are no established medical treatments for the core social deficits of ASD, despite its acknowledged genetic and biological basis.

 

"It's a challenge," McCracken said. "There are now so many possible experimental medicines and approaches from basic science for ASD that we find ourselves way behind. We need a new paradigm to test the many possible compounds, and we need to quickly and accurately identify which ones are really ready for 'prime time.'"

 

Currently, McCracken noted, large-scale studies of possible medications take years and can cost upwards of $500 million dollars before yielding an approved, marketed drug. The three-year NIMH contract will support a new approach involving multiple "fast–fail" studies, which could accelerate progress by providing an early "yes or no" assessment of various compounds.

 

The initiative will focus on analyzing how novel molecular and clinical targets for ASD are affected by both new and repurposed compounds. The outcome is expected to lead to an enhanced understanding of the mechanisms that underlay ASD and the development of innovative pharmacological treatment approaches for the disorder.

 

At UCLA, testing will involve scientists and clinicians from the fields of psychiatry, radiology and biostatistics. The UCLA Clinical and Translational Science Institute will use sophisticated measures of brain and behavioral responses to identify signs of successful drug action in key brain regions. Positive findings could then be followed up by other large-scale national and international studies.

 

Ironically, the explosion of basic-science knowledge about ASD and possible drug treatments is emerging at a time when major pharmaceutical companies are canceling drug-development programs for ASD and other mental disorders, citing costs, difficulties and the recent failures of what were deemed good prospects. Many National Institutes of Health officials, research scientists and affected families are fearful that progress in medication development will slow in the face of the industry's retreat from neuroscience drug development.

 

Funding from the NIMH comes under contract No. HHSN-271-2012-00005-I. In addition to McCracken, UCLA collaborators will include Susan Bookheimer, Sandra Loo, Joseph O'Neill and Edythe London from the department of psychiatry; Dr. Albert Thomas from the department of radiological sciences; and Catherine Sugar from the department of biostatistics. Additional colleagues from other institutions around the country are expected to participate in the new network.

 

The UCLA Department of Psychiatry and Biobehavioral Sciences is the home within the David Geffen School of Medicine at UCLA for faculty who are experts in the origins and treatment of disorders of complex human behavior. The department is part of the Semel Institute for Neuroscience and Human Behavior at UCLA, a world-leading interdisciplinary research and education institute devoted to the understanding of complex human behavior and the causes and consequences of neuropsychiatric disorders.

 

For more news, visit the UCLA Newsroom and follow us on Twitter.

 

Because these remaining pluripotent stem cells can subsequently develop into unintended cell types — bone cells among blood, for instance — or form tumors known as teratomas, identifying and separating them from their differentiated progeny is of utmost importance in keeping stem cell–based therapeutics safe.

 

Now, UCLA scientists have discovered a new agent that may be useful in strategies to remove these cells. Their research was published online April 15 in the journal Developmental Cell and will appear in an upcoming print edition of the journal.

 

The study was led by Carla Koehler, a professor of chemistry and biochemistry at UCLA, and Dr. Michael Teitell, a UCLA professor of pathology and pediatrics. Both are members of the Eli and Edythe Broad Center for Regenerative Medicine and Stem Cell Research at UCLA and UCLA's Jonsson Comprehensive Cancer Center.

 

In work using the single-celled microorganism known as baker's yeast, or Saccharomyces cerevisiae, as a model system, Koehler, Teitell and their colleagues had discovered a molecule called MitoBloCK-6, which inhibits the assembly of cells' mitochondria — the energy-producing "power plants" that drive most cell functions. The research team then tested the molecule in a more complex model organism, the zebrafish, and demonstrated that MitoBloCK-6 blocked cardiac development. 

 

However, when the scientists introduced MitoBloCK-6 to differentiated cell lines, which are typically cultured in the lab, they found that the molecule had no effect at all. UCLA postdoctoral fellow Deepa Dabir tested the compound on many differentiated lines, but the results were always the same: The cells remained healthy. 

 

"I was puzzled by this result, because we thought this pathway was essential for all cells, regardless of differentiation state," Koehler said. 

 

The team then decided to test MitoBloCK-6 on human pluripotent stem cells. Postdoctoral fellow Kiyoko Setoguchi showed that MitoBloCK-6 caused the pluripotent stem cells to die by triggering apoptosis, a process of programmed cell suicide.

 

Because the tissue-specific daughter cells became resistant to death shortly after their differentiation, the destruction of the pluripotent stem cells left a population of only the differentiated cells. Why this happens is still unclear, but the researchers said that this ability to separate the two cell populations could potentially reduce the risk of teratomas and other problems in regenerative medicine treatment strategies.

 

"We discovered that pluripotent stem cell mitochondria undergo a change during differentiation into tissue-specific daughter cells, which could be the key to the survival of the differentiated cells when the samples are exposed to MitoBloCK-6," Teitell said. "We are still investigating this process in mitochondria, but we now know that mitochondria have an important role in controlling pluripotent stem cell survival."                        

 

MitoBloCK-6 is what is known as a "small molecule," which can easily cross cell membranes to reach mitochondria. This quality makes MitoBloCK-6 — or a derivative compound with similar properties — ideal for potential use as a drug, because it can function in many cell types and species and can alter the function of mitochondria in the body for therapeutic effects.

 

"It is exciting that our research in the one-cell model baker's yeast yielded an agent for investigating and controlling mitochondrial function in human pluripotent stem cells," Koehler said. "This illustrates that mitochondrial function is highly conserved across organisms and confirms that focused studies in model systems provide insight into human stem-cell biology. When we started these experiments, we did not predict that we would be investigating and controlling mitochondrial function in pluripotent stem cells."

 

The research was supported by the California Institute for Regenerative Medicine, the National Institutes of Health, the United Mitochondrial Disease Foundation, and the Development and Promotion of Science and Technology Talents Project of the Royal Thai Government.

 

The Eli and Edythe Broad Center of Regenerative Medicine and Stem Cell Research: UCLA's stem cell center was launched in 2005 with a UCLA commitment of $20 million over five years. A $20 million gift from the Eli and Edythe Broad Foundation in 2007 resulted in the renaming of the center. With more than 200 members, the Broad Stem Cell Research Center is committed to a multidisciplinary, integrated collaboration among scientific, academic and medical disciplines for the purpose of understanding adult and human embryonic stem cells. The center supports innovation, excellence and the highest ethical standards focused on stem cell research with the intent of facilitating basic scientific inquiry directed toward future clinical applications to treat disease. The center is a collaboration of the David Geffen School of Medicine at UCLA, UCLA's Jonsson Cancer Center, the UCLA Henry Samueli School of Engineering and Applied Science and the UCLA College of Letters and Science.

 

UCLA's Jonsson Comprehensive Cancer Center has more than 240 researchers and clinicians engaged in disease research, prevention, detection, control, treatment and education. One of the nation's largest comprehensive cancer centers, the Jonsson center is dedicated to promoting research and translating basic science into leading-edge clinical studies. In July 2012, the Jonsson Cancer Center was once again named among the nation's top 10 cancer centers by U.S. News & World Report, a ranking it has held for 12 of the past 13 years.

For more news, visit the UCLA Newsroom and follow us on Twitter.

The UCLA Henry Samueli School of Engineering and Applied Science presents its annual Tech Forum. This year's free daylong conference, "The Future of Engineering Research in the United States," brings together many of the top engineering minds in California.

 

Event highlights include a keynote address by Neil Siegel, vice president and chief engineer of Northrop Grumman Information Systems; a panel discussion with industry experts forecasting research trends; and more than 40 talks by distinguished engineers, entrepreneurs and UCLA Engineering faculty on their cutting-edge research. Talks will cover such areas as the use of nanotechnology in the fields of health care, renewable energy and mobile devices; the development of sustainable fuels, better drinking water supplies and treatments for toxic groundwater; and new materials for construction, aviation and space exploration. 

 

In addition, UCLA Engineering students will host a poster session, displaying information and answering questions about ongoing research in their laboratories.

 

Sponsors of the Tech Forum include satellite communications firm ViaSat, networking equipment manufacturer Cisco Systems and intellectual property law firm Cislo & Thomas.

 

To register for the free event; find detailed information about the schedule, speakers and topics; or get directions and parking information for the conference site at UCLA's Covel Commons, visit the Tech Forum page at www.engineer.ucla.edu/techforum/index.html. 

 

10 a.m. to 5 p.m. on Wednesday, May 8

 

(A wine-and-cheese reception will follow, where guests can talk with faculty, students, guest speakers and industry leaders.)

 

Covel Commons, on the UCLA campus (map)

WHO:
Forum speakers will include:

 

Vijay K. Dhir (welcoming remarks)

Dhir is the dean of the UCLA Henry Samueli School of Engineering and Applied Science.

 

Neil Siegel (keynote address)

Siegel is vice president and chief engineer of Northrop Grumman Information Systems and an adjunct professor of engineering at UCLA. A member of the National Academy of Engineering, he oversees research programs at Northrop Grumman and leads a team of more than 14,000 engineering and technology professionals working with industrial, intelligence, military and other clients.

 

The following experts from top engineering firms will participate in a panel discussion titled "The Future of Engineering Research in the United States":

 

Dwight Streit (moderator)

Streit, the chair of the 2013 Tech Forum, is a professor at the UCLA Henry Samueli School of Engineering and Applied Science and a member of the National Academy of Engineering.

Conilee Kirkpatrick (panelist)

Kirkpatrick is vice president of HRL Laboratories, a Malibu-based aviation, aerospace and automotive engineering firm.

 

Cary Nachenberg (panelist)

Nachenberg is a fellow at the Mountain View–based security software firm Symantec Corp. and chief architect of Symantec's office of the chief technology officer.

 

Muddu Sudhakar (panelist)

Sudhakar is vice president of VMware Inc., a Palo Alto–based cloud computing information technology firm.

 

Rachel Vandenberg (panelist)

Vandenberg is vice president of intermodal practice for the global engineering and design firm AECOM.

 

 

Bill Kisliuk | 310-206-0540 | bkisliuk@support.ucla.edu

 

Now, a new study led by Dr. Patricia Ganz, director of cancer prevention and control research at UCLA's Jonsson Comprehensive Cancer Center, demonstrates a significant correlation between poorer performance on neuropsychological tests and memory complaints in post-treatment, early-stage breast cancer patients — particularly those who have undergone combined chemotherapy and radiation.

 

"The study is one of the first to show that such patient-reported cognitive difficulties — often referred to as 'chemo brain' in those who have had chemotherapy — can be associated with neuropsychological test performance," said Ganz, who is also a professor of health policy and management at UCLA's Fielding School of Public Health and a professor of medicine at the David Geffen School of Medicine at UCLA.

 

The study was published April 18 in the online edition of the Journal of the National Cancer Institute and will appear in an upcoming print edition of the journal.

 

Ganz and her colleagues looked at 189 breast cancer patients, who enrolled in the study about one month after completing their initial breast cancer treatments and before beginning endocrine hormone-replacement therapy (70 percent planned to undergo hormone therapy). Two-thirds of the women had had breast-conserving surgery, more than half had received chemotherapy, and three-quarters had undergone radiation therapy. The average age of study participants was 52.

 

Because cognitive complaints following cancer treatment have often been associated with anxiety and depressive symptoms, limiting confidence that "chemo brain" and similar difficulties reflect a cancer treatment toxicity, the researchers excluded women with serious depressive symptoms. They also took careful account of the cancer treatments used and whether or not menopause and hormonal changes could be influencing the cognitive complaints. A sample of age-matched healthy women who did not have breast cancer was used as a control group.

 

The researchers provided a self-reporting questionnaire to the women and found that those with breast cancer reported, on the whole, more severe complaints than normal; 23.3 percent of these patients had higher complaints about their memory, and 19 percent reported higher complaints about higher-level cognition (problem-solving, reasoning, etc.). Significantly, those breast cancer patients who reported more severe memory and higher-level cognition problems were more likely to have undergone both chemotherapy and radiation.

 

While earlier studies had not identified a consistent association between cognitive complaints and neuropsychological testing abnormalities, the UCLA research team found that even when patients reported subtle changes in their memory and thinking, neuropsychological testing showed detectable differences.

 

In particular, they discovered that poorer performance on the neuropsychological test was associated both with higher levels of cognitive complaints and with combined radiation-and-chemotherapy treatment, as well as with symptoms related to depression.

 

"In the past, many researchers said that we can't rely on patients' self-reported complaints or that they are just depressed, because previous studies could not find this association between neuropsychological testing and cognitive complaints," Ganz said. "In this study, we were able to look at specific components of the cognitive complaints and found they were associated with relevant neuropsychological function test abnormalities."

 

The findings are part of an ongoing study that seeks to examine the extent to which hormone therapy contributes to memory and thinking problems in breast cancer survivors, and this pre-hormone therapy assessment was able to separate the effects of initial treatments on these problems. Earlier post-treatment studies of breast cancer patients were difficult to interpret, as they included women already taking hormone therapy.

 

"As we provide additional reports on the follow-up testing in these women, we will track their recovery from treatment, as well as determine whether hormone therapy contributes to worsening complaints over time," Ganz said.

 

This research was supported by the National Cancer Institute and the Breast Cancer Research Foundation, and by funding from the National Institutes of Health to the Cousins Center for Psychoneuroimmunology.

 

UCLA's Jonsson Comprehensive Cancer Center has more than 240 researchers and clinicians engaged in disease research, prevention, detection, control, treatment and education. One of the nation's largest comprehensive cancer centers, the Jonsson center is dedicated to promoting research and translating basic science into leading-edge clinical studies. In July 2012, the Jonsson Cancer Center was once again named among the nation's top 10 cancer centers by U.S. News & World Report, a ranking it has held for 12 of the past 13 years.

For more news, visit the UCLA Newsroom and follow us on Twitter.

 

Their findings are the result of 10 years of UCLA research on kidney cancers at the genetic and molecular levels, with scientists conducting chromosomal analyses in an effort to identify what mutations may be causing and affecting the behavior of the malignancies. Thousands of tumors removed at UCLA have been studied, said Dr. Allan Pantuck, a professor of urology and director of genitourinary oncology at UCLA's Jonsson Comprehensive Cancer Center.

 

Traditionally, pathologists study tumors under the microscope and attempt to predict their behavior by the way they look. However, tumors that appear the same often behave differently, and oncologists need to know which are lower risk, which are more aggressive and which are more likely to spread, making the cancer much more difficult to treat.

 

"Pathologists can give us some important information, but similar-appearing tumors often can and do behave differently," said Pantuck, the senior author of the study. "Our findings have us heading further in the direction of personalized medicine based on the molecular signature of an individual's tumor. We still have a lot to learn, but we're now a step closer."

 

The study appears April 16 in the early online edition of Cancer, a peer-reviewed journal of the American Cancer Society.

 

The study findings were made in a type of kidney cancer called clear cell renal carcinoma. The researchers identified two new subtypes of this cancer: one in which there is the deletion of the short arm of chromosome 3 (known as 3p) and one in which both the short arm of chromosome 3 and the long arm of chromosome 14 (known as 14q) are deleted.

 

This is significant because the short arm 3p harbors a tumor-suppressor gene. In the case of 14q, its deletion results in the additional loss of a hypoxia-inducible factor 1 (HIF1) alpha gene, which lessens the effects of hypoxia, the state of low oxygen concentration, on the cell; tumors need oxygen so they can grow and spread.

 

The researchers found that the loss of 3p was associated with improved survival, meaning patients with this subtype of cancer might not need to be treated as aggressively as those with tumors that still have 3p. In elderly patients with this subtype, tumors could perhaps be monitored aggressively for evidence of progression in lieu of immediate treatment, the researchers said. The study authors are not yet sure why the loss of the the tumor-suppressor gene associated with 3p does not correlate with worse outcomes.

 

Patients with tumors in which both 3p and 14q were deleted had much worse outcomes.

 

"The results of this study support the hypothesis that the HIF1 alpha gene functions as another important tumor-suppressor gene," Pantuck said. "With this finding, we can now decide to treat these patients with more aggressive therapies."

 

Going forward, Pantuck and his team will work to identify more subtypes of kidney cancer. The findings of this study come from a single center, so they will also need to be reproduced by other scientists in other locations, he said.

 

This year alone, kidney cancer will strike more than 65,000 Americans, killing more than 13,000. Finding new and more effective therapies is vital to reducing the number of deaths.

 

Dr. Arie Belldegrun, director of UCLA's Institute of Urologic Oncology, characterized the finding as significant.

 

"Kidney cancer is not a single disease, and it can now be further subdivided based on a clearly defined molecular profile. These researchers have identified unique molecular patterns in patients with various stages of the disease," he said. "These findings have important implications to the surgical and medical treatment of kidney cancer. It is one important step to individualize kidney cancer therapy and move away from the 'one size fits all' approach."

 

UCLA's Kidney Cancer Program is world-renowned, dedicated to providing the highest quality patient care, research, training and education for the past 21 years. In that time, more than 5,000 patients with all stages of kidney cancer, including the most complicated and challenging surgical cases, were treated at UCLA. The program has long utilized a pioneering multidisciplinary approach to treating kidney cancer patients that includes urologists, medical oncologists, radiation oncologists, pathologists, radiologists and clinical trial nurses that allows for specialized perspectives when deciding on the best option for each individual patient.

 

For more news, visit the UCLA Newsroom and follow us on Twitter.

 

But cancers in one of the four groups — called "basal-like" or "triple-negative" breast cancer (TNBC) — have been particularly tricky to treat because they usually don't respond to the "receptor-targeted" treatments that are often effective in treating other types of breast cancer. TNBC tends to be more aggressive than the other types and more likely to recur, and can also have a higher mortality rate.

 

Fortunately, better drug therapies may be on the horizon. UCLA researchers and collaborators led by Dean Ho, a professor at the UCLA School of Dentistry and co-director of the school's Jane and Jerry Weintraub Center for Reconstructive Biotechnology, have developed a potentially more effective treatment for TNBC that uses nanoscale, diamond-like particles called nanodiamonds.

 

Nanodiamonds are between 4 and 6 nanometers in diameter and are shaped like tiny soccer balls. Byproducts of conventional mining and refining operations, the particles can form clusters following drug binding and have the ability to precisely deliver cancer drugs to tumors, significantly improving the drugs' desired effect. In the UCLA study, the nanodiamond delivery system has been able to home in on tumor masses in mice with triple negative breast cancer.

 

Findings from the study are published online April 15 in the peer-reviewed journal Advanced Materials.

 

"This study demonstrates the versatility of the nanodiamond as a targeted drug-delivery agent to a tumor site," said Ho, who is also a member of the California NanoSystems Institute at UCLA, UCLA's Jonsson Comprehensive Cancer Center and the UCLA Department of Bioengineering. "The agent we've developed reduces the toxic side effects that are associated with treatment and mediates significant reductions in tumor size."

 

The team combined several important cancer-fighting components on the nanodiamond surface, including Epirubicin, a highly toxic but widely used chemotherapy drug that is often administered in combination with other cancer drugs. The new compound was then bound to a cell-membrane material coated with antibodies that were targeted toward the epidermal growth factor receptor, which is highly concentrated on the surfaces of TNBC cells. The resulting agent is a drug-delivery system called a nanodiamond-lipid hybrid compound, or NDLP.

 

When tested on mice, the agent was shown to notably decrease tumor growth and eliminate the devastating side effects of cancer treatment.

 

Because of its toxicity, Epirubicin, when administered alone can cause serious side effects, such as heart failure and reduced white blood cell count, and it has been linked to an increased risk for leukemia. In the study, all of the mice that were given Epirubicin alone died well before the completion of the study. But all the mice given Epirubicin through the targeted NDLPs survived the treatment, and some of the tumors even regressed until they were no longer visible.

 

"Triple-negative breast cancer is often very aggressive and hard to treat, making aggressive chemotherapy a requirement," said Dr. Edward K. Chow, co-first author of the study and an assistant professor at the Cancer Science Institute of Singapore. "The targeting and therapeutic efficiency of the nanodiamond-lipid agents were quite remarkable. The simultaneous tumor regression and improved drug tolerance are promising indicators for the continued development of the nanodiamonds toward clinical translation."

 

The research team is now studying the efficacy and safety of the NDLPs in larger animals. Additional research objectives include determining whether nanodiamonds can enhance the tolerance of a wide spectrum of highly toxic drug compounds, which may improve current treatment options and outcomes. These discoveries will serve as precursors for human trials, the researchers said.

 

"The nanodiamond-lipid hybrid developed in this study is a modular platform," said Laura Moore, a graduate student in Ho's laboratory and a co-first author of the study. "Therefore, we can easily bind a wide spectrum of targeting antibodies and drug compounds to address several diseases."

 

Dr. No-Hee Park, dean of the UCLA School of Dentistry, noted that the research will provide a foundation for future clinical applications.

 

"This pioneering study conducted by Dean Ho and his team provides a better understanding of the capabilities of the nanodiamond material to address several diseases," Park said. "Their work is of paramount importance."

 

Other authors of the study were Professor Eiji Osawa of the NanoCarbon Research Institute in Nagano, Japan, and Professor J. Michael Bishop of UC San Francisco. Laura Moore is currently at Northwestern University.

 

The study was supported by the National Cancer Institute, the National Science Foundation, the Wallace H. Coulter Foundation, the V Foundation for Cancer Research, the Society for Laboratory Automation and Screening, the George Williams Hooper Foundation, the American Cancer Society, Beckman Coulter, the European Commission, the Cancer Science Institute of Singapore, and the Singapore Ministry of Education Academic Research Fund.

 

The UCLA School of Dentistry is dedicated to improving the oral and systemic health of the people of California, the nation and the world through its teaching, research, patient care and public service initiatives. The School of Dentistry provides education and training programs that develop leaders in dental education, research, the profession and the community. The School of Dentistry also conducts research programs that generate new knowledge, promote oral health and investigate the cause, prevention, diagnosis and treatment of oral disease in an individualized disease-prevention and management model; and delivers patient-centered oral health care to the community and the state.

 

For more news, visit the UCLA Newsroom and follow us on Twitter.

 

In preliminary results from a phase 2 study, patients with advanced breast cancer that was estrogen-receptor positive (ER+) and HER2-negative (HER2-) and who were given the investigational drug palbociclib (PD 0332991) — which was discovered and is being developed by Pfizer Inc. — in addition to the standard anti-estrogen treatment of letrozole had significantly higher progression-free survival than patients taking letrozole alone.

 

Enacted as part of the 2012 FDA Safety and Innovation Act, the breakthrough therapy designation was created by the agency to expedite the development and review of a potential new medicine if it is "intended, alone or in combination with one or more other drugs, to treat a serious of life-threatening disease or condition and preliminary clinical evidence indicates that the drug may demonstrate substantial improvement over existing therapies on one or more clinically significant endpoints."

 

Dr. Richard S. Finn, associate professor of medicine at the Jonsson Cancer Center, initially reported the preliminary phase 2 clinical data supporting the designation in December 2012 at the CTRC-AACR San Antonio Breast Cancer Symposium (SABCS). The clinical study was built on laboratory work from the Translational Oncology Research Laboratory directed by Dr. Dennis Slamon, professor of medicine at UCLA and director of the Jonsson Cancer Center's Revlon/UCLA Women's Cancer Research Program.

 

In preclinical work, palbociclib was tested in a panel of human breast cancer cells growing in culture dishes and showed very encouraging activity, specifically against ER+ cancer cells. These preclinical observations were then moved into phase 1 clinical studies. Led by Finn and Slamon at UCLA, the studies were designed to determine the doses and safety of a combination with letrozole, a commonly used drug for ER+ breast cancer.

 

Once the phase 1 studies were completed, the phase 2 studies were performed in 165 patients with breast cancer with ER+ disease. The interim data presented at SABCS showed that the median progression-free survival of patients given the palbociclib-letrozole combination was 26.1 months, compared with 7.5 months for those given letrozole alone. Among patients with measurable disease, 45 percent receiving the combination had confirmed responses, compared with 31 percent for letrozole alone, and the clinical benefit rates (tumor shrinkage and/or stable disease for a minimum of six months) were 70 percent for those receiving the combination therapy, versus 44 percent for letrozole only.

 

"This drug combination demonstrated a dramatic and clinically meaningful effect on progression-free survival in women with ER+ breast cancer," Finn said. "These results confirm the preclinical work we began at the Translational Lab."

In collaboration with Finn and colleagues, Pfizer has initiated a randomized, multicenter, double-blind phase 3 study to evaluate palbociclib combined with letrozole, compared with letrozole alone, as a first-line treatment for post-menopausal patients with ER+, HER2-, locally advanced or metastatic breast cancer. 

 

Slamon said the phase 2 study results validate the Translational Laboratory's approach.

 

"By identifying the correct targets for treatment in the right patient population, we move forward with personalized oncology that we hope will greatly improve the outcomes for this group of breast cancer patients," he said. "These results are as exciting as the initial results we saw for trastuzumab (Herceptin) in HER2+ breast cancers but represent a new approach for a different and larger subset of breast cancers, namely those that are ER+."

 

Slamon said the researchers are working diligently to enroll the phase 3 validation study as quickly and safely as possible.

 

UCLA's Jonsson Comprehensive Cancer Center has more than 240 researchers and clinicians engaged in disease research, prevention, detection, control, treatment and education. One of the nation's largest comprehensive cancer centers, the Jonsson center is dedicated to promoting research and translating basic science into leading-edge clinical studies. In July 2012, the Jonsson Cancer Center was once again named among the nation's top 10 cancer centers by U.S. News & World Report, a ranking it has held for 12 of the past 13 years.

For more news, visit the UCLA Newsroom and follow us on Twitter.

 

The research team studied type-1 interferons (IFN-1), proteins released by cells in response to disease-causing organisms. These proteins enable cells to talk to each other and orchestrate an immune response against infection. Constant IFN-1 signaling is also a trademark of chronic viral infection and disease progression, particularly in HIV.

 

"When cells confront viruses, they produce type-1 interferons, which trigger the immune system's protective defenses and set off an alarm to notify surrounding cells," said principal investigator David Brooks, an assistant professor of microbiology, immunology and molecular genetics at UCLA's David Geffen School of Medicine and the UCLA College of Letters and Science. "Type-1 interferon is like the guy in the watchtower yelling 'red alert' when the marauders try to raid the castle." 

 

Scientists have long viewed IFN-1 as beneficial, because it stimulates antiviral immunity and helps control acute infection. Blocking IFN-1 activity, they reasoned, would allow infection to run rampant through the immune system.

 

On the other hand, prolonged IFN-1 signaling is linked to many chronic immune problems. The research team wondered whether obstructing the signaling pathway would enable the immune system to recover enough to fight off chronic infection.

 

To test this theory, Brooks and his colleagues injected mice suffering from chronic viral infection with an antibody that temporarily blocked IFN-1 activity. 

 

Much to their surprise, they discovered that giving the immune system a holiday from IFN-1 boosted the body's ability to fight the virus. Stunningly, the respite also reversed many of the immune problems that result from chronic infection, such as a rise in proteins that suppress immune response, continuous activation of the immune system and disruption of lymph tissue. 

 

The findings fly in the face of past studies that suggest eliminating IFN-1 activity in mice leads to severe, lifelong infection. 

 

"What we saw was entirely illogical," Brooks admitted. "We'd blocked something critical for infection control and expected the immune system to lose the fight against infection. Instead, the temporary break in IFN-1 signaling improved the immune system's ability to control infection. Our next step will be to figure out why and how to harness it for therapies to treat humans."

 

"We suspect that halting IFN-1 activity is like pushing the refresh button," said first author Elizabeth Wilson, a UCLA postdoctoral researcher. "It gives the immune system time to reprogram itself and control the infection." 

 

Uncovering this mechanism could offer potential for new therapies to tackle viruses like HIV and hepatitis C, according to Brooks. The team's next step will be to pinpoint how to sustain IFN-1's control of the virus while blocking the negative impact that chronic IFN-1 activity wreaks on the immune system.

 

The National Institute of Allergy and Infectious Diseases and the UCLA Center for AIDS Research supported the research. 

 

Additional co-authors included Douglas Yamada, Heidi Elsaesser, Jonathan Herskovitz, Jane Deng and Genhong Cheng, all of UCLA; Bruce Aronow of the University of Cincinnati; and Christopher Karp of the University of Cincinnati and the Bill and Melinda Gates Foundation.

 

For more news, visit the UCLA Newsroom and follow us on Twitter.

 

Just as arteries to the heart can become clogged with plaque, causing a blockage, so can the two carotid arteries that supply blood to the brain. Every year, more than 300,000 people in the U.S. are diagnosed with such blockages, which, if left untreated, can reduce or even stop blood flow to the brain, causing a potentially disabling stroke. 

 

Current treatment options include the traditional "open" surgery approach to clean out the carotid artery and a minimally invasive alternative that uses a stent to keep the artery open.

 

Each of these options has some limitations. Traditional surgery involves making a large incision along the neck and carries the risk of surgical complications. While less invasive, the stent procedure requires the insertion of a catheter through an artery in the groin to guide the stent into place, which can potentially dislodge plaque; loose plaque can travel through the bloodstream and cause a blockage. Some studies have indicated that the stent procedure carries a higher risk of stroke than the surgical procedure. 

 

The new technique and device system being tested at UCLA is called transcarotid stenting with dynamic flow reversal, or the Silk Road Procedure, which allows physicians to deliver a stent directly into the carotid artery from the neck, offering a shorter, potentially safer route than the typical stent procedure.

 

A unique aspect of the new system is the ability to temporarily divert blood flow away from the plaque during the procedure to help ensure that a patient's brain is fully protected from plaque debris at all times. Physicians redirect blood flow from the carotid artery where the team is working into tubing set up outside the body and then back into the body through the femoral vein, near the groin.

 

Ronald Reagan UCLA Medical Center is one of 25 centers around the world participating in the clinical study, called the ROADSTER trial, which is designed for high–surgical risk patients who may be older or have especially narrowed arteries.

 

"We're always seeking new options for patients with the ultimate goal of treating these carotid artery blockages with the least procedural risk," said Dr. Wesley Moore, UCLA study investigator and a professor emeritus of vascular surgery at the David Geffen School of Medicine at UCLA. "We look forward to contributing to this important research."

 

The study is funded by Silk Road Medical, developers of the transcarotid stenting with dynamic flow reversal system. 

 

For more information on the clinical trial at UCLA, please call 310-206-1115.  

 

For more news, visit the UCLA Newsroom and follow us on Twitter.

 

Proceeds support UCLA's mobile blood-donation program, which collects 22,000 units of blood a year, supplying half the transfusions for patients at UCLA Health System hospitals. Last year's event raised $73,500 for the center.  

A finish-line festival, featuring a free lunch catered by Sharky's Woodfired Mexican Grill and the raffle of a VW Beach Cruiser bicycle, a carbon-fiber Super Bike and many more prizes, will conclude the event, which is sponsored by Volkswagen, KHS Bicycles, Pace Sportswear and the Los Angeles Police Revolver and Athletic Club. 

WHO:
A young UCLA patient who benefited from blood donations will kick off the race by driving the pace car with her fiancé and parents:

 

Golden, 21, of Las Vegas, is a college student with cystic fibrosis who underwent a rare double-organ transplant to replace her infected lungs and deteriorating liver at Ronald Reagan UCLA Medical Center in 2011. Her life was sustained during her 13-hour surgery by lifesaving donations of 12 units of blood, 11 units of plasma and one unit of platelets from 24 anonymous donors. 

 

 

WHEN:
Sunday, April 14

 

6 a.m.: check-in

 

7:25 a.m.: Jennifer Golden introduced to crowd before revving up pace car

 

7:30 a.m.: advanced ride starts

 

7:50 a.m.: recreational ride starts

 

9:30 a.m.: UCLA blood drive*

 

11 a.m.: lunch and finish-line festival 

 

* Those interested in donating blood at the blood drive should call 310-825-0888, Ext. 2, to reserve a slot.

 

WHERE:
The start/finish line is at the Los Angeles Police Academy, 1880 Academy Dr., Elysian Park 90012 (map)

MEDIA CONTACT:
Elaine Schmidt, UCLA Health Sciences Media Relations

eschmidt@mednet.ucla.edu | 310-794-2272 or 310-597-5767 (Sunday only)

FUN RIDE CONTACT:
Peter Heumann, Heumann Powered Productions

peter@coafunride.com | 818-825-7383

 

At a special state-of-the-science panel on Saturday, April 13, UCLA professor Lynn V. Doering will present a review of gender differences in identification, treatment and outcomes for cardiovascular disease, with a focus on coronary atherosclerosis, heart failure and stroke. During the same panel, UCLA professor JoAnn Eastwood will introduce her novel study in which she is partnering with a community organization and using mobile health technologies to reduce cardiac risk factors among young minority women.  

 

"Cardiovascular disease is the No. 1 killer of women and accounts for more female deaths than all cancers and lung disease combined," Doering said. "Heart disease — particularly its symptoms — presents differently in women, and it is not so obvious in current testing, so it is harder to diagnose. The cutting-edge work that is being presented will provide critical information on diagnosis, treatment and prevention of cardiovascular disease in women."

 

Also during the three-day conference, UCLA School of Nursing faculty and doctoral students will present symposia on health care and nursing education for vulnerable populations and on the behavioral symptoms of dementia.

 

During the symposium "Cultivating Nurse Leaders: A Framework for Nursing Education in Vulnerable Populations" on Friday, April 12, three UCLA nursing researchers will discuss their work on finding ways to eliminate the cultural, financial and language barriers that impact health care delivery. Health disparities continue to exist among vulnerable populations, the researchers stress, and addressing inequities requires mentoring and guiding new nurse–scientists to conduct research in this important area.

 

On Saturday, April 13, "Promoting the Health of Vulnerable Populations" will take a look at the challenges of meeting the health care needs of four vulnerable populations: homeless men on parole, homeless men and women who suffer from frailty, methamphetamine users who are mothers, and American Indians suffering effects of abuse.

 

With an aging population, the prevalence of dementia is increasing, creating an impending health care crisis. A report last week in the New England Journal of Medicine revealed that dementia care is projected to double by 2040. During their April 12 symposium, "Detecting and Characterizing Patterns of Behavioral Symptoms of Dementia," UCLA nursing researchers will discuss current interventions and effective treatments for this behavioral challenge.

 

The Western Institute of Nursing is a professional organization of registered nurses and other healthcare professionals dedicated to advancing nursing science, education and practice to improve healthcare outcomes.

 

The UCLA School of Nursing is redefining nursing through the pursuit of uncompromised excellence in research, education, practice, policy and patient advocacy.

 

For more news, visit the UCLA Newsroom and follow us on Twitter.

 

The results of their study — the first to examine air pollution from traffic and a number of rarer childhood cancers — were presented on April 9 in an abstract at the annual meeting of the American Association for Cancer Research in Washington, D.C.

 

For the study, the UCLA researchers utilized data on 3,950 children who were enrolled in the California Cancer Registry and who were born in the state between 1998 and 2007. They estimated the amount of local traffic the children had been exposed to using California LINE Source Dispersion Modeling, version 4 (CALINE4).

 

Pollution exposure was estimated for the area around each child's home for each trimester of their mother's pregnancy and during their first year of life. The estimates included information on gasoline and diesel vehicles within a 1,500-meter radius buffer, traffic volumes, roadway geometry, vehicle emission rates and weather. Cancer risk was estimated using a statistical analysis known as unconditional logistic regression.

 

The researchers found that heightened exposure to traffic-related air pollution was associated with increases in three rare types of childhood cancer: acute lymphoblastic leukemia (white blood cell cancer), germ-cell tumors (cancers of the testicles, ovaries and other organs) and retinoblastoma (eye cancer), particularly bilateral retinoblastoma, in which both eyes are affected.

 

The pollution-exposure estimates were highly correlated across pregnancy trimesters and the first year of life, meaning that even in areas of high exposure, no particular period stood out as a higher-exposure time. This, the scientists said, made it difficult to determine if one period of exposure was more dangerous than any other.

 

"Much less is known about exposure to pollution and childhood cancer than adult cancers," Heck said. "Our innovation in this study was looking at other, more rare types of childhood cancer, such as retinoblastoma, and their possible connection to traffic-related air pollution."

 

Because these are rare diseases, Heck cautions that the findings need to be replicated in further studies.

 

The UCLA Fielding School of Public Health is dedicated to enhancing the public's health by conducting innovative research; training future leaders and health professionals; translating research into policy and practice; and serving local, national and international communities.

 

UCLA's Jonsson Comprehensive Cancer Center has more than 240 researchers and clinicians engaged in disease research, prevention, detection, control, treatment and education. One of the nation's largest comprehensive cancer centers, the Jonsson Center is dedicated to promoting research and translating basic science into leading-edge clinical studies. In July 2012, the Jonsson Cancer Center was once again named among the nation's top 10 cancer centers by U.S. News & World Report, a ranking it has held for 12 of the last 13 years.

 

For more news, visit the UCLA Newsroom and follow us on Twitter.

 

The new network grant, which will fund collaborative work by Geschwind and experts at other autism centers around the country, is part of the NIH's Autism Centers of Excellence program, which was launched in 2007 to support coordinated research into the causes of autism spectrum disorders (ASD) and the discovery of new treatments.

 

Autism spectrum disorders are complex developmental disorders that affect how a person behaves, interacts with others, communicates and learns. According to the Centers for Disease Control, ASD affects approximately one in 88 children in the U.S.

 

Geschwind's award will allow him to build on his earlier work identifying genetic variants associated with an increased susceptibility to autism while adding an important new emphasis. The research network he leads — which also includes scientists from the Albert Einstein College of Medicine, Emory University, Johns Hopkins University, Washington University and Yale University — aims to recruit at least 600 African American families who have a child diagnosed with an ASD for genetic testing.

 

While nearly all previous research on the genetics of autism has focused on subjects of European descent rather than those of African or other ancestries, it is critical to study different populations to understand if current genetic findings in ASD can be generalized to a broader population, said Geschwind, a professor of neurology, psychiatry and genetics.

 

To that end, he will look for gene variants associated with autism in Americans with African ancestry and then test the genetic risk factors identified in European populations to see what role they may play in the disorder in people of African descent.

 

Because individuals are typically a mix of different ancestries, the research group will use statistical methods that enable them to identify chromosomal markers for different ancestral origins. Genetic data generated by the study will be made available through the Internet to the larger research community.

 

The work will also include an evaluation of disparities in the diagnosis of autism and in access to care. The scientists will be carrying out this study with UCLA as the hub.

 

The award to Geschwind follows on the heels of several large ACE awards to various researchers at UCLA's Center for Autism Research and Treatment (CART) last September. At that time, CART was the only NIH Autism Center of Excellence in the nation to be awarded renewed funding for the next five years. The funding to CART supports ongoing research focused on examining genes' link to behavior, developing clinical interventions for those severely affected by autism, and explaining why autism affects more boys than girls.

 

This network grant will help further the work of CART, in conjunction with other UCLA programs in autism by enabling scientists to approach the study of ASD from both a research and clinical perspective. Together, these ACE grants aim to foster new ways to diagnose patients earlier and tailor treatments to each individual to create the best outcomes.

 

CART and the UCLA Department of Psychiatry and Biobehavioral Sciences are part of the Semel Institute for Neuroscience and Human Behavior, a world leading, interdisciplinary research and education institute devoted to the understanding of complex human behavior and the causes and consequences of neuropsychiatric disorders. The UCLA Department of Neurology, with over 100 faculty members, encompasses more than 20 disease-related research programs, along with large clinical and teaching programs. These programs cover brain mapping and neuroimaging, movement disorders, Alzheimer's disease, multiple sclerosis, neurogenetics, nerve and muscle disorders, epilepsy, neuro-oncology, neurotology, neuropsychology, headaches and migraines, neurorehabilitation, and neurovascular disorders.

 

For more news, visit the UCLA Newsroom and follow us on Twitter.

 

The funds will establish the UCLA–First 5 LA Children's Dental Care Program (CDCP), which will support the delivery of care to children, from birth to age 5, and pregnant women over the next five years. The program will be especially beneficial to those in underserved communities, who are at high risk for dental disease, school officials said.

 

This new award comes on the heels of the $9.23 million that First 5 LA awarded to the dental school last year, bringing the total amount the school has received from the organization to nearly $21 million over the past 12 months.

 

"Our goal, over the next five years, is to develop an integrated health-care delivery system that will provide quality, ongoing dental care to underserved young children and pregnant women in Los Angeles communities," said Dr. James J. Crall, project director of the CDCP. "We hope the Children's Dental Care Program will serve as a prototype for transforming the oral health care system for young children throughout Los Angeles County and beyond."

 

As part of the new program, UCLA faculty members hope to gain a better understanding of the barriers that limit the use of dental care services by underserved groups in order to initiate improvements in care.

"While focusing on dental care for young children, the program is also targeting pregnant women in an effort to provide them with the information and education they need to be able to provide a more positive and healthier approach to oral health for their developing children," Crall said.

 

The program will roll out four major strategies over the next five years to increase access to oral heath care and improve the quality of care for young children and pregnant women: 

"This is a major investment by First 5 LA in Los Angeles County's oral health care delivery system," said No-Hee Park, dean of the UCLA School of Dentistry. "This funding will impact the oral health of tens of thousands of people for the foreseeable future. Greater access to quality oral health care must be addressed. Developing these improved delivery systems in our underserved communities is the best place to start."

 

Crall, the CDCP project director, is a professor and chair of the division of public health and community dentistry at the UCLA School of Dentistry, a member of the UCLA Center for Healthier Children, Families and Communities, and project director for the UCLA–First 5 LA 21st-Century Dental Homes Project.

 

First 5 LA oversees the Los Angeles County allocation of funds from Proposition 10, which added a 50-cent tax on tobacco products sold in California. Funds raised help pay for health care, education and child development programs for children from the prenatal stage to age 5 and their families. First 5 LA's mission is to increase the number of young children who are physically and emotionally healthy, safe and ready to learn.

 

The UCLA School of Dentistry is dedicated to improving the oral health of the people of California, the nation and the world through its teaching, research, patient care and public service initiatives. The School provides education and training programs that develop leaders in dental education, research, the profession and the community; conducts research programs that generate new knowledge, promote oral health and investigate the cause, prevention, diagnosis and treatment of oral disease in an individualized disease-prevention and management model; and delivers patient-centered oral health care to the community and the state.

 

For more news, visit the UCLA Newsroom and follow us on Twitter.

 

The connection between stroke risk and cognitive decline has been well established by previous research. Individuals with higher stroke risk, as measured by factors like high blood pressure, have traditionally performed worse on tests of memory, attention and abstract reasoning.

 

The current small study demonstrated that not only stroke risk, but also the burden of plaques and tangles, as measured by a UCLA brain scan, may influence cognitive decline.

 

The imaging tool used in the study was developed at UCLA and reveals early evidence of amyloid beta "plaques" and neurofibrillary tau "tangles" in the brain — the hallmarks of Alzheimer's disease.

 

The study, published in the April issue of the Journal of Alzheimer's Disease, demonstrates that taking both stroke risk and the burden of plaques and tangles into accout may offer a more powerful assessment of factors determining how people are doing now and will do in the future.

 

"The findings reinforce the importance of managing stroke risk factors to prevent cognitive decline even before clinical symptoms of dementia appear," said first author Dr. David Merrill, an assistant clinical professor of psychiatry and biobehavioral sciences at the Semel Institute for Neuroscience and Human Behavior at UCLA.

 

This is one of the first studies to examine both stroke risk and plaque and tangle levels in the brain in relation to cognitive decline before dementia has even set in, Merrill said.

 

According to the researchers, the UCLA brain-imaging tool could prove useful in tracking cognitive decline over time and offer additional insight when used with other assessment tools.

 

For the study, the team assessed 75 people who were healthy or had mild cognitive impairment, a risk factor for the future development of Alzheimer's. The average age of the participants was 63.

 

The individuals underwent neuropsychological testing and physical assessments to calculate their stroke risk using the Framingham Stroke Risk Profile, which examines age, gender, smoking status, systolic blood pressure, diabetes, atrial fibrillation (irregular heart rhythm), use of blood pressure medications, and other factors.

 

In addition, each participant was injected with a chemical marker called FDDNP, which binds to deposits of amyloid beta plaques and neurofibrillary tau tangles in the brain. The researchers then used positron emission tomography (PET) to image the brains of the subjects — a method that enabled them to pinpoint where these abnormal proteins accumulate.

 

The study found that greater stroke risk was significantly related to lower performance in several cognitive areas, including language, attention, information-processing speed, memory, visual-spatial functioning (e.g., ability to read a map), problem-solving and verbal reasoning.

 

The researchers also observed that FDDNP binding levels in the brain correlated with participants' cognitive performance. For example, volunteers who had greater difficulties with problem-solving and language displayed higher levels of the FDDNP marker in areas of their brain that control those cognitive activities. 

 

"Our findings demonstrate that the effects of elevated vascular risk, along with evidence of plaques and tangles, is apparent early on, even before vascular damage has occurred or a diagnosis of dementia has been confirmed," said the study's senior author, Dr. Gary Small, director of the UCLA Longevity Center and a professor of psychiatry and biobehavioral sciences who holds the Parlow–Solomon Chair on Aging at UCLA's Semel Institute.

 

Researchers found that several individual factors in the stroke assessment stood out as predictors of decline in cognitive function, including age, systolic blood pressure and use of blood pressure–related medications.

 

Small noted that the next step in the research would be studies with a larger sample size to confirm and expand the findings.

 

The study was funded by the National Institutes of Health (grants PO1-AG025831, AG13308, P50 AG 16570, MH/AG58156, MH52453, AG10123 and MO1-RR00865); the UCLA Claude Pepper Older Americans Independence Center, funded by the National Institute on Aging (grant 5P30AG028748); the American Federation for Aging Research; and the John A. Hartford Foundation Centers of Excellence National Program.

 

UCLA owns three U.S. patents on the FDDNP chemical marker. Small and study author Dr. Jorge Barrio are among the inventors. 

 

Additional UCLA authors included Prabha Sidarth, Pushpa V. Rajaa, Nathan Saito, Linda M. Ercoli, Karen J. Miller, Helen Lavretsky, Vladimir Kepe and Susan Y. Bookheimer.

 

For more news, visit the UCLA Newsroom and follow us on Twitter. 

 

For more than 60 years, the faculty and staff at Mattel Children's Hospital UCLA and the department of pediatrics at the David Geffen School of Medicine at UCLA have conducted pioneering research, delivered state-of-the-art patient care and expertly trained future pediatricians. 

 

Now, under the umbrella of the recently launched UCLA Children's Discovery and Innovation Institute, these efforts will have an even bigger and broader impact. By bringing together pediatric physician–scientists and faculty experts from a variety of fields across the UCLA campus, the new institute will drive multidisciplinary research collaborations focused on children's health and disease and will help speed the translation of groundbreaking pediatric research findings into clinical practice — locally, nationally and globally.

 

"We are expanding our well-developed foundation to build a dynamic, interdisciplinary support system for our pediatric physician–scientists that fosters new avenues for innovation," said Dr. Sherin Devaskar, physician-in-chief of Mattel Children's Hospital UCLA and assistant vice chancellor for children's health, who holds the Mattel Executive Endowed Chair in the UCLA Department of Pediatrics. "This new paradigm will lead to advancements that can improve the health of children faster and more efficiently."

 

The institute will pioneer advancements in pediatric medicine in four key research areas: the brain and behavior; nutrition and metabolism; cancer; and inflammation, infection and immunity. Efforts in each area will focus on prevention, screening and treatment, as well as providing training opportunities for the next generation of pediatricians and mentorship programs that enable younger physicians and scientists to learn from UCLA's cadre of experts.

 

Children are not "small adults," pediatricians stress, and they experience illnesses and treatments differently than adults. The UCLA Children's Discovery and Innovation Institute is in a unique position to collaborate with a wide variety of researchers across campus who have expertise not only in science and health but in the unique challenges young people face.

 

"Interdisciplinary research as envisioned by the institute is fundamental to the discoveries that pave the way to major improvements in health," said Dr. Eugene Washington, dean of the David Geffen School of Medicine at UCLA and vice chancellor for health sciences. "Having access to a variety of specialists and experts with different points of view can be invaluable in nurturing innovations that can ultimately benefit children around the world."

 

The institute will hold its inaugural fundraiser, the Kaleidoscope Ball, at the Beverly Hills Hotel on Wednesday, April 17. The sold-out event, hosted by actress Patricia Heaton, will honor philanthropists Heather and Steven Mnuchin and Cameron Cohen and musician and actor LL Cool J. Entertainment will include performances by special guests the Blue Sky Riders, Kenny Loggins, the Georgia Middleman and Gary Burr. 

 

The event will also showcase 10 custom dollhouses created by more than 20 of the most prominent, award-winning visionaries from the world of design and architecture. The dollhouses will be auctioned off, with 100 percent of the proceeds going to support the new institute. 

 

For more information on the UCLA Children's Discovery and Innovation Institute, visit www.uclahealth.org/cdii.

 

For more news, visit the UCLA Newsroom and follow us on Twitter.

  

Also attending from UCLA were Vice Chancellor for Research James Economou; professor Kelsey Martin, chair of biological chemistry and head of a group that is encouraging collaboration among the campus's neuroscience community; Paul Weiss, director of the California NanoSystems Institute at UCLA and a distinguished professor of chemistry and biochemistry and of materials science and engineering; and Anne Andrews, the Richard Metzner Endowed Chair in Clinical Neuropharmacology, and professor of psychiatry and biobehavioral sciences and of chemistry and biochemistry.

 

They were among the invited guests for the president's introduction of the BRAIN Initiative (Brain Research through Advancing Innovative Neurotechnologies), which is intended to help fund research on new ways to treat, cure and prevent brain disorders such as Alzheimer's disease, epilepsy and traumatic brain injury. The president said his proposed 2013–14 budget would include $100 million for the program. (Read the White House's blog post on BRAIN.)

 

UCLA is well positioned to play a significant role in the effort and to secure federal funding because of its strength not only in neuroscience but in nanotechnology, psychology, psychiatry and other academic fields, and because the disciplines at UCLA work closely together.

 

Even before President Obama's announecment, UCLA was in the early stages of developing interdisciplinary teams to address the brain research initiative and other "Grand Challenges" introduced by the White House — national or global research initiatives that are intended to improve lives and spur economic development.

 

 

 

Heart failure, a chronic, progressive disease, affects millions of individuals and results in considerable morbidity, the use of extensive health care resources and substantial costs.

 

Currently online, the study will be published in the April 2 print issue of the Journal of the American College of Cardiology. Researchers studied the incremental health and cost benefits of three common heart failure medications that are recommended by national guidelines developed by organizations like the American College of Cardiology and the American Heart Association.

 

This is one of the first studies analyzing the incremental cost-effectiveness of heart failure medications and taking into account the very latest information, including the lower costs of generic versions of the medications. Researchers found that the combination of these medical therapies demonstrated the greatest gains in quality-adjusted life years for heart failure patients.

 

"We found that use of one or more of these key medications in combination was associated with significant health gains while at the same time being cost-effective or providing a cost savings," said the study's senior author, Dr. Gregg Fonarow, UCLA's Eliot Corday Professor of Cardiovascular Medicine and Science and director of the Ahmanson–UCLA Cardiomyopathy Center at the David Geffen School of Medicine at UCLA. "Our findings demonstrate the importance of prescribing these national guideline–directed medical therapies to patients with heart failure."

 

The study focused on mild to moderate chronic heart-failure patients who had weakening function in the heart's left ventricle and symptoms of heart failure, which occurs when the ventricle can no longer pump enough blood to the body's other organs. With the heart's diminishing function, fluid can build up in the lungs, so most patients take a diuretic.

 

The research team used an advanced statistical model to assess the specific incremental and cumulative health- and cost-benefit contributions of three medications, compared with diuretics alone, in the treatment of heart failure patients. The medications studied included angiotensin-converting enzyme inhibitors, aldosterone antagonists and beta blockers.

 

Researchers found that treatment with one or a combination of these medications was associated with lower costs and higher quality of life when compared to just receiving a diuretic alone. The greatest gain in quality-adjusted life years for patients was achieved when all three guideline-directed medications were provided.

 

The team calculated different scenarios and found that the incremental cost-effectiveness ratio of adding each medication was less than $1,500 per each quality-adjusted life year for patients. In some scenarios, the medications were actually cost-saving, where heart failure patients' lives were prolonged at lower costs to the health care system.

 

The study found that up to $14,000 could be spent over a lifetime on a heart failure disease-management program to improve medication adherence and still be highly cost-effective. 

 

For the study, cost-effective interventions were defined as those providing good value with a cost of less than $50,000 per quality-adjusted life year, which is the general standard, Fonarow said. Cost-saving interventions are those that not only extend life but also actually save money to the health care system. Such interventions are not only more effective but are less costly.

 

Fonarow noted that the costs of not effectively taking these key medications would be higher, due to increased hospitalizations and the need for other interventions.

 

"Given the high health care value provided by these medical therapies for heart failure, reducing patient costs for these medications or even providing a financial incentive to promote adherence is likely to be advantageous to patients as well as the health care system," Fonarow said. "Further resources should be allocated to ensure full adherence to guideline-directed medical therapies for heart failure patients to improve outcomes, provide high-value care and minimize health care costs."

 

The researchers used previous clinical trials and government statistics to help calculate mortality, hospitalization rates and health care costs used in the model.

 

Fonarow noted that the study offers broad insight into the cost-effectiveness of these medications and that a real-world model would provide an additional perspective.

 

The costs used in this study were estimates of true costs, and the actual costs in different health care delivery systems may vary.

 

No outside funding was used for the study. Disclosures are included in the manuscript.

 

Other study authors included Gaurav Banka from the Ahmanson–UCLA Cardiomyopathy Center and Paul A. Heidenreich from the VA Palo Alto Health Care System in Palo Alto, Calif.

 

For more news, visit the UCLA Newsroom and follow us on Twitter.

 

"There are perks to having a park nearby," said Susan Babey, a senior research scientist at the UCLA center and lead author of the study. "And one of the biggest ones for teens seems to be physical activity. Having access to a welcoming green space makes it more likely that teenagers will get up and get moving."

 

The U.S. Department of Health and Human Services recommends at least 60 minutes of daily physical activity for teenagers. In California, only 15 percent of teens meet this recommendation, down from 19 percent in 2007.

While proximity to parks was associated with more physical exercise, the study also found that the perceived safety of neighborhood parks was a significant factor in park use. Low-income teenagers were more likely than teens from higher-income families to report that their neighborhood park was unsafe. Unsurprisingly, low-income teens were less likely to be active for at least one hour daily.

 

"Too many of our youth do not have access to the supports they need to achieve good health," said Dr. Robert K. Ross, CEO and president of The California Endowment, which funded the report. "Access to parks is a necessity, not a luxury. If we are to effectively address the childhood obesity epidemic in California, we must put resources where they are needed. All families, regardless of income, need access to safe parks where children and youth can engage in physical activity."

 

Among the report's findings:

 

Only 34.5 percent of low-income teens were physically active for at least an hour a day on five or more days a week, compared with 40 percent of higher-income teens, whether or not they lived near a park.

 

The percentage of low-income teens reporting that their neighborhood park was unsafe was more than double the percentage for higher-income teens (16.1 percent vs. 5.8 percent.)  

 

Eighty percent of teens who strongly agreed that their neighborhood park was safe reported a recent park visit, compared with just 66 percent of those who thought their nearby park was not safe.

 

 

Regular physical activity is an important factor in preventing obesity and maintaining good health, the study noted. A lack of physical activity contributes to obesity and other chronic health conditions, including diabetes, coronary heart disease and hypertension.

 

Read the policy brief: "Physical Activity, Park Access and Park Use among California Adolescents." 

 

The California Endowment, a private, statewide health foundation, was established in 1996 to expand access to affordable, quality health care for underserved individuals and communities and to promote fundamental improvements in the health status of all Californians.

 

The California Health Interview Survey (CHIS) is the nation's largest state health survey and one of the largest health surveys in the United States.

 

The UCLA Center for Health Policy Research is one of the nation's leading health policy research centers and the premier source of health-related information on Californians.

 

For more news, visit the UCLA Newsroom and follow us on Twitter.

 

The national list, which is compiled every two years by Boston-based Best Doctors Inc., is based on an in-depth, impartial peer survey of doctors working in a variety of specialties. Only the top 5 percent of physicians in the country receive this honor.

 

"Earning a place as one of the Best Doctors in America is a singular honor," said Dr. David Feinberg, president of the UCLA Health System. "This is a testament to our physicians, who provide excellent patient-centered care. We are grateful to our gifted and dedicated medical team throughout the UCLA Health System, which goes the extra mile every day to save lives and deliver compassionate care to patients in our community, one patient at a time."

 

For its list, Best Doctors conducts an exhaustive, peer-reviewed survey of the medical profession, polling more than 50,000 doctors across the U.S. and asking them this question: If you or a loved one needed a doctor in your specialty, to whom would you refer?

 

The doctors surveyed are asked to provide an assessment of the clinical abilities of their peers within more than 400 sub-specialties of medicine. The millions of individual data points collected through this process are compiled using algorithms that correct for statistical bias, yielding the list of the physicians deemed the "best" by their peers. The list identifies specialists who are considered by fellow physicians to be the most skilled in their fields and most qualified for reviewing and treating complex medical conditions.

 

The goal of the Best Doctors in America list is to identify the best trained, most experienced and most skilled specialists, regardless of where they practice, according to Best Doctors Inc.

 

UCLA's world-class specialists made it into every specialty category listed in the Best Doctors database. The UCLA Health System's group of experts listed in the database includes world-class heart, pediatrics, neurology and neurosurgery specialists.

 

Learn more about the Best Doctors list and see the UCLA physicians who made the 2013 list.

 

For further information, visit Best Doctors at www.bestdoctors.com, Twitter, Facebook and LinkedIn, or call 800-223-5003.

 

Best Doctors Inc., founded in 1989 by Harvard Medical School physicians, works with the best 5 percent of doctors, ranked by impartial peer review, to help people get the right diagnosis and right treatment. Gallup has audited and certified Best Doctors Inc.'s database of physicians and its companion Best Doctors in America List as using the highest industry standards survey methodology and processes. The global health solutions company, which has grown to over 30 million members worldwide, uses state-of-the-art technology capabilities to deliver improved health outcomes while reducing costs. Best Doctors seamlessly integrates its trusted health services with large self-insured employers, insurers and other groups in every major region of the world. The company also designs and implements international insurance programs that help people be sure they get the right health solutions. 

 

The UCLA Health System, which comprises the UCLA Hospital System and the UCLA Medical Group and its affiliates, has provided a high quality of health care and the most advanced treatment options to the people of Los Angeles and the world for more than half a century. Ronald Reagan UCLA Medical Center, the Resnick Neuropsychiatric Hospital at UCLA, Mattel Children's Hospital UCLA, and UCLA Medical Center, Santa Monica (which includes the Los Angeles Orthopaedic Hospital) deliver hospital care that is unparalleled in California. Ronald Reagan UCLA Medical Center is consistently ranked one of the top five hospitals in the nation and the best in the western United States by U.S. News & World Report. UCLA physicians and hospitals continue to be world leaders in the full range of care, from maintaining the health of families to the diagnosis and treatment of complex illnesses.

 

For more news, visit the UCLA Newsroom and follow us on Twitter.

 

The researchers, from the Larry L. Hillblom Islet Research Center at UCLA and the Diabetes Center at the University of Florida, found that cell mass was increased approximately 40 percent in the pancreases of deceased organ donors who had Type 2 diabetes and who had been treated with incretin therapy. This widely used type of treatment takes advantage of the action of a gut hormone known as glucagon-like peptide 1 (GLP-1) to lower blood sugar in the body.

 

Although there have been conflicting reports on the effects of the incretin class of drugs on the pancreas in animal studies, this is the first study to note such changes in the human pancreas. The research was made possible by a unique research consortium called nPOD (Network for Pancreatic Organ Donors with Diabetes), led by Dr. Mark Atkinson, a professor of pathology and pediatrics at the University of Florida. The network, which is funded by the Juvenile Diabetes Research Foundation, obtains pancreases from deceased organ donors, with permission of their next of kin, to better understand diabetes by investigating tissues of those with the disease.

 

"There is an increasing appreciation that animal studies do not always predict findings in humans," said Dr. Peter Butler, director of UCLA's Hillblom Islet Research Center and chief of the endocrinology, diabetes and hypertension unit. "The nPOD program is therefore a very precious resource."

 

The researchers examined the pancreases of 20 deceased organ donors with Type 2 diabetes. Eight had been treated for at least a year with incretin therapy, while the other 12 had received therapies that didn't include incretin-based drugs. The researchers also evaluated 14 pancreases from a control group of non-diabetic individuals of similar age.

 

The pancreases of the individuals who had been on incretin therapy were larger than those of patients on other types of diabetes therapies, and this larger size was associated with increased cellular proliferation. Incretin-treated individuals showed an increase in pancreas dysplasia, an abnormal form of cell proliferation that is a risk factor for pancreatic cancer, as well as an expansion of alpha cells, endocrine cells that make the hormone glucagon.

 

This latter finding is likely a consequence of GLP-1–based therapies' suppression of the release of glucagon by alpha cells, since decreasing the availability or action of the hormone glucagon has been shown in a variety of prior studies to induce a proliferation of pancreatic alpha cells. This alpha-cell expansion has been associated with the development of pancreatic neuroendocrine tumors. Three of the eight incretin-treated individuals had microadenomas and one has a neuroendocrine tumor composed of alpha cells.

 

Of the eight donors who were on incretin therapy, seven had been taking sitagliptin, sold in pill form as Januvia and marketed by Merck, and one had been on exenatide, sold as Byetta by Bristol-Myers Squibb. These and similar drugs are currently under investigation by the U.S. Food and Drug Administration for their possible links to pancreatitis and pancreatic cancer.

 

"These findings lend additional weight to concerns regarding the effects of long term GLP-1–related therapy, with respect to both unintended proliferative actions on the exocrine pancreas and now also a possible increased risk of neuroendocrine tumors," the researchers write. "In addition to the surveillance previously recommended for the potential association of GLP-1– based therapy and pancreatic cancer risk, the current data imply that surveillance for a possible increased risk of pancreatic neuroendocrine tumors is warranted."

 

Such surveillance approaches might include MRI imaging of the pancreas and screening for neuroendocrine tumors, Butler said.

 

"The present studies are only from a small number of individuals, and while the findings do raise concerns, it will be important that other approaches are now used in a larger group of living individuals to further investigate these findings," he said.

 

A recent study led by Dr. Sonal Singh of Johns Hopkins University School of Medicine and Public Health and published in JAMA Internal Medicine suggested a doubling in the risk of hospitalization for acute pancreatitis with the GLP-1–based therapies and also recommended further research.

 

"Since most risk factors for acute pancreatitis are also linked to an increased risk of pancreatic cancer, these findings of changes in the human pancreas are very concerning," said Singh, an assistant professor of medicine and international health. "Now that GLP-1–based therapies have been shown to increase the risk of pancreatic inflammation and abnormal cell proliferation, further studies are needed to urgently clarify whether these linkages lead to pancreatic cancer with long-term use."

 

Study co-authors, in addition to Butler and Atkinson, are Alexandra E. Butler, Tatyana Gurlo and David W. Dawson, all of UCLA, and Martha Campbell-Thompson of the University of Florida.

 

Grants from National Institute of Diabetes and Digestive and Kidney Diseases (DK059579, DK061539 and DK077967), the Hillblom Foundation, and the Peter and Valerie Kompaniez Foundation funded this study. The Juvenile Diabetes Research Foundation funds the nPOD program.

 

For more news, visit the UCLA Newsroom and follow us on Twitter. 

A new UCLA-led study suggests a way to predict when a woman will have her final menstrual period. The findings, published in the April issue of the peer-reviewed Journal of Clinical Endocrinology and Metabolism, could help women and physicians gauge the onset of menopause-related bone loss, which generally begins a year prior to the last period.

The researchers used women's ages, menstrual bleeding patterns and measurements of hormone levels to estimate the amount of time until they were likely to reach menopause, said the study's lead author, Dr. Gail Greendale, professor of medicine in the division of geriatrics at the David Geffen School of Medicine at UCLA.

 

Greendale said women who are approaching menopause often ask their health care providers when they will be done with their periods, but the information is sometimes more telling than women realize. 

 

"Being able to estimate when the final menstrual period will take place has taken on importance beyond just helping women gauge when they will stop having periods," she said. "We know that potentially deleterious physiological developments, such as the onset of bone loss and an increase in cardiovascular risk factors, precede the final menses by at least a year."

The researchers used data collected annually for up to 11 years on 554 women, including Caucasians, African Americans, Hispanics and those of Chinese and Japanese descent, participating in the multi-site, multi-ethnic Study of Women's Health Across the Nation. At enrollment, the women were between the ages of 42 to 53, had an intact uterus and at least one ovary, were not using medications affecting ovarian function and had experienced at least one menstrual period in the prior three months.

The researchers measured levels of estradiol (E2), a hormone produced by the ovaries, and follicle stimulating hormone (FSH), which comes from the pituitary gland and triggers the production of eggs. FSH starts increasing and E2 starts decreasing about two years prior to the final menstrual period, or about a year before bone loss and cardiovascular risk factors rise.

The study found that the levels of the two hormones could be used to estimate whether women were within two years of beginning their final menstrual period, within one year or beyond their final period.

The study had some limitations, including its modest sample size. In addition, hormone levels were sampled once a year and more frequent sampling might have allowed the researchers to more precisely estimate the woman's place on the timeline.

Study co-authors were Mei-Hua Huang and Dr. Arun Karlamangla of UCLA and Dr. Shinya Ishii of the University of Tokyo.

The Study of Women's Health Across the Nation was funded by the National Institutes of Health through the National Institute on Aging, the National Institute of Nursing Research, and the NIH Office of Research on Women's Health (NR004061, NR004061, AG012505, AG012535, AG012531, AG012539, AG012546, AG012553, AG012554 and AG012495).

The UCLA Division of Geriatrics within the department of medicine at the David Geffen School of Medicine at UCLA offers comprehensive outpatient and inpatient services at several convenient locations and works closely with other UCLA programs that strive to improve and maintain the quality of life of seniors. UCLA geriatricians are specialists in managing the overall health of people age 65 and older and treating medical disorders that frequently affect the elderly, including memory loss and dementia, falls and immobility, urinary incontinence, arthritis, arthritis, high blood pressure, heart disease, osteoporosis and diabetes. As a result of their specialized training, UCLA geriatricians can knowledgably consider and address a broad spectrum of health-related factors — including medical, psychological and social — when treating patients.

For more news, visit the UCLA Newsroom and follow us on Twitter.

 

As children with Type 1 diabetes grow into young adults, they must leave their pediatric health care providers for adult providers. But the timing of this process and its impact on the young people's health had not been fully explored.

 

In a new study published in the April issue of the journal Pediatrics and currently available online, UCLA researchers found that young people with Type 1 diabetes who had transitioned from pediatric to adult care were 2.5 times more likely to have chronically high blood glucose levels, putting them at higher risk for heart attacks, strokes, blindness and kidney failure later in life.

 

The estimated median age of patients when this transition occurred was 20.1 years, the researchers said, and 77 percent had left pediatric care by age 21. 

 

The findings suggest that young adults need additional support and guidance when leaving their pediatric providers to avoid the risk of poor diabetes control.

 

"The transition to adulthood can include changes in health care providers, insurance and often living situations as patients move from high school to college or work," said the study's lead author, Dr. Debra Lotstein, an associate clinical professor of pediatrics at the David Geffen School of Medicine at UCLA and Mattel Children's Hospital UCLA. "These transitions can be challenging for anyone, but youth with a chronic health problem like diabetes are at risk of losing the support of their health care providers and their family that helps them stay healthy. When this transition goes poorly, it increases the risk of worse health outcomes in adulthood."  

 

Previous research on youth with Type 1 diabetes in the U.S. had looked primarily at young people from a single diabetes specialty center or a single geographic area, or it had examined youth at just one point in time — either before or after leaving pediatric care. The current study, however, involved the largest national cohort of youth with Type 1 diabetes in the U.S. to be followed over a period of time.

 

Researchers analyzed data from the multi-center SEARCH for Diabetes in Youth Study, which has tracked children and young adults with diabetes from six centers across the country since 2002. The cohort included 185 adolescents and young adults with Type 1 diabetes who were enrolled in the study in the year after their diabetes was diagnosed. The youth included in these analyses were cared for by pediatric diabetes physicians at the time of their initial study visit and were followed for an average of 4.5 years. 

 

The authors found that a young patient's type of insurance — public versus private insurance, for instance — made no difference in the switch to adult care, but they did observe that older patient age, lower levels of parental education and lower baseline blood-glucose levels were independently associated with increased odds of transitioning to adult care. 

 

"One surprise was that those patients with poor diabetes control were more likely to stay with their pediatric providers, compared to others," Lotstein said. "We theorized that that the doctors have a higher level of concern for those patients with poor control and may care for them longer in an attempt to prevent their condition from worsening."

 

The next stage in the research, the authors said, is to directly follow young adults transitioning to adult care to see what happens as they age and to examine how different types of support aimed at easing the transition affect health outcomes.  

 

The SEARCH for Diabetes in Youth Study is funded by the Centers for Disease Control and Prevention, and National Institutes of Health's National Institute of Diabetes and Digestive and Kidney Diseases.  

 

Additional study authors included Michael Seid (Cincinnati Children's Hospital Medical Center); Dr. Georgeanna Klingensmith (University of Colorado Denver School of Medicine); Doug Case, (Wake Forest University School of Medicine); Jean M. Lawrence, (Kaiser Permanente Southern California); Dr. Cathernine Pihoker (University of Washington); Dr. Dana Dabelea (Colorado School of Public Health); Elizabeth J. Mayer-Davis, (University of North Carolina); Dr. Lisa K. Gilliam (Kaiser Permanente Northern California) Dr. Sarah Corathers (Cincinnati Children's Hospital Medical Center); Dr. Giuseppina Imperatore (Centers for Disease Control and Prevention); Dr. Lawrence Dolan (Cincinnati Children's Hospital Medical Center); Andrea Anderson (Wake Forest University School of Medicine); Ronny A. Bell, (Wake Forest University School of Medicine); and Beth Waitzfelder, (Center for Health Research, Kaiser Permanente, Hawaii).

 

The authors have no financial ties to disclose.

 

For more news, visit the UCLA Newsroom and follow us on Twitter.

 

The research, which appears March 21 in the advance online edition of the journal Cancer Discovery, was led by James Heath, a member of UCLA's Eli and Edythe Broad Center for Regenerative Medicine and Stem Cell Research and UCLA's Jonsson Comprehensive Cancer Center. Heath is a professor of molecular and medical pharmacology at UCLA and also holds the Elizabeth W. Gilloon Chair in Chemistry at Caltech.

 

The melanoma treatment uses T cells — immune cells that play a major role in fighting infection — taken from patients with melanoma. The cells are then genetically modified in the laboratory so that when they are reintroduced into a patient's bloodstream, they specifically attack melanoma tumors. In early clinical trials, this treatment was shown to shrink tumors dramatically in many patients, but the positive effects were often short-lived.

 

The UCLA and Caltech researchers found that after the engineered T cells were returned to patients, their efficacy faded within two to three weeks. Surprisingly, however, once the engineered cells were no longer effective, a new group of non-engineered T cells arose that had a similar tumor-killing effect that lasted even longer, the scientists discovered.

 

Using newly developed nanotechnology chips to perform multidimensional and multiplexed immune-monitoring assays, the researchers were able to examine at high resolution single engineered T cells taken at different times from patients undergoing the therapy, each of whom had a different level of response to the treatment.

 

"The engineered T cells did not recover their tumor-killing effect," Heath said, "but after one month, another group of T cells appeared that did have tumor-killing effects for another 90 days. Those were not the genetically engineered T cells, and they appeared to be a byproduct of a process called 'antigen spreading' by the original engineered cells. After 90 days, those cells lost their tumor-killing ability as well."

 

Antigen spreading is a process by which a T cell that has been engineered to attack a particular tumor expands its immune response to other T cells in the body, which then attack the same tumor but are focused on different antigens. (Antigens are substances that trigger a response by the body's immune system.) Scientists may be able to use this process, Heath stressed, to improve T cell–based treatments for melanoma.

 

"Our results have led us to possible ways to improve the T cell therapy to extend its positive effect," Heath said. "We need to incorporate strategies that maintain the functional properties of the engineered T cells used for therapy. This might include modifying how we grow the T cells in the laboratory to make their tumor-killing effect last longer or make them resistant to the effects of the patient's T cells as they recover from pretreatment chemotherapy conditioning and possibly increase the antigen spreading of anti-tumor T cells."

 

UCLA professor of medicine Dr. Antoni Ribas was one of Heath's key collaborators on the research.

"One of the possible approaches to resolve the problem identified by this study is to use engineered blood stem cells — instead of the peripheral blood used in the original trials — with this therapy in the hope that the engineered blood stem cells will provide a renewable source of engineered T cells," said Ribas, a member of UCLA's Broad Stem Cell Research Center and Jonsson Cancer Center.

 

Caltech’s Chao Ma, the study's first author, said the findings and the use of the new nanotechnology assay process hold promise for treatments of other disease as well.

 

"This study points to the value of these single-cell functional analyses for probing the successes and failures of a sophisticated immunotherapy," he said. "I am excited to see its use as a monitoring tool to understand a spectrum of other cellular immunotherapies in the near future."

 

This research was funded by the National Cancer Institute, the Jean Perkins Foundation, The California Institute for Regenerative Medicine, UCLA's Broad Stem Cell Research Center, the Seaver Institute, the PhaseOne Foundation, the Garcia-Corsini Family Fund, the Caltech/UCLA Joint Center for Translational Medicine, the Melanoma Research Alliance, a Rosen Fellowship and UCLA's Jonsson Comprehensive Cancer Center.

 

The Eli and Edythe Broad Center of Regenerative Medicine and Stem Cell Research: UCLA's stem cell center was launched in 2005 with a UCLA commitment of $20 million over five years. A $20 million gift from the Eli and Edythe Broad Foundation in 2007 resulted in the renaming of the center. With more than 200 members, the Broad Stem Cell Research Center is committed to a multidisciplinary, integrated collaboration among scientific, academic and medical disciplines for the purpose of understanding adult and human embryonic stem cells. The center supports innovation, excellence and the highest ethical standards focused on stem cell research with the intent of facilitating basic scientific inquiry directed toward future clinical applications to treat disease. The center is a collaboration of the David Geffen School of Medicine at UCLA, UCLA's Jonsson Cancer Center, the UCLA Henry Samueli School of Engineering and Applied Science and the UCLA College of Letters and Science.

 

UCLA's Jonsson Comprehensive Cancer Center has more than 240 researchers and clinicians engaged in disease research, prevention, detection, control, treatment and education. One of the nation's largest comprehensive cancer centers, the Jonsson Center is dedicated to promoting research and translating basic science into leading-edge clinical studies. In July 2012, the Jonsson Cancer Center was once again named among the nation's top 10 cancer centers by U.S. News & World Report, a ranking it has held for 12 of the last 13 years.

For more news, visit the UCLA Newsroom and follow us on Twitter.

 

 

The results of a major, multicenter clinical trial to determine the best treatment for younger patients who have strokes that are potentially due to a hole in the upper chambers of the heart has provided suggestive but not definitive evidence of the benefit of a new heart hole–closure device.

 

The trial sought to determine which was the best treatment to prevent further strokes: a combination of closing the hole with a "button" device and anti-clotting medicines, or anti-clotting medicines alone. UCLA was one of the 69 performance sites for the study, called the Recurrent Stroke Comparing PFO Closure to Established Current Standard of Care Treatment (RESPECT).

 

Over eight years, the study enrolled 980 patients between the ages of 18 and 60 (average age 46). All had experienced a stroke of unknown origin and had a hole in the wall of their heart known as a patent foramen ovaleor, or PFO. Nearly half had large strokes as their qualifying stroke event. In up to 10 percent of strokes in the U.S., a PFO is the only identified potential cause.

 

Patients were followed for an average of two-and-a-half years. In the main analysis, patients assigned to receive the button device showed a trend toward having fewer recurrent strokes than those receiving standard care with anti-clotting medications (9 percent versus 16 percent), but the difference did not meet statistical tests for being definite. Further analyses conducted in the subset of patients who adhered to their assigned treatments provided additional evidence that the device was beneficial.

 

Closure-device therapy may be a useful strategy for selected patients with a history of cryptogenic stroke and PFO —a population that is generally younger than the average stroke patient and otherwise facing a lifetime of potentially riskier medications, the UCLA researchers said. The authors said that closing the hole in the heart has also been studied as possibly helping with other health issues, such as migraines.

 

Dr. Jeffrey Saver, director of the UCLA Stroke Center and a professor of neurology, was one of four national principal investigators of the study. Dr. Jonathan Tobis, director of interventional cardiology and professor of medicine at UCLA, was the RESPECT lead cardiology investigator at the UCLA site.

 

Dr. Jeffrey Saver was an author on the paper.

 

The studying findings are published in the March 21 issue of the New England Journal of Medicine.

 

Funding for the study was provided by St. Jude Medical in St. Paul, Minn., maker of the "button" closing device.