Secretary Shinseki – Please Notify Veterans There’s No Waiting List at the Zumwalt Mesothelioma Treatment Program in Los Angeles

The mesothelioma treatment team at the West LA VA Medical Center would love to have a list of veterans to treat. But there’s no list, no waiting list and no effort to educate our war heroes stricken with asbestos cancer that help is available.You’ve read about the double digit number of veterans who have allegedly died whilewaiting to be treated. We may never know how many veterans with mesothelioma have died after receiving no or sub-standard treatment.According to the popular literature, about 4,000 Americans are diagnosed with mesothelioma each year. Of those, roughly a third were exposed to asbestos while serving in the Navy. It’s not a stretch to surmise that at least 600 Navy veterans are diagnosed with mesothelioma every year–a diagnosis that carries …

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Dr. Robert Cameron Chairs International Panel of Medical Specialists at 4th Annual Symposium on Lung-Sparing Therapies for Malignant Pleural…

Dr. Robert Cameron ThePacific Meso Center, in conjunction with The Office of Continuing Medical Education of the David Geffen School of Medicine at UCLA, held the 4th International Symposium on Lung-SparingTherapies for Malignant Pleural Mesothelioma on June 7, 2014 in Santa Monica, California. TheWorthington & Caron Law Firmwas proud to once again be a platinum sponsor of this unique medical seminar focusing on rational treatment options for patients with pleural mesothelioma.As in years past, the course organizer and chair of the symposium was thoracic surgeon and pleural mesothelioma specialist,Dr. Robert Cameron. An ardent supporter of rational lung-sparing treatments for pleural mesothelioma, and innovator of thepleurectomy/decortication(“PD”) surgical procedure, Dr. Cameron is the founder and director of both theComprehensive Mesothelioma Programat the UCLA Medical Center and…

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Brain scans show we take risks because we can’t stop ourselves

A new study correlating brain activity with how people make decisions suggests that when individuals engage in risky behavior, such as drunk driving or unsafe sex, it’s probably not because their brains’ desire systems are too active, but because their self-control systems are not active enough.This might have implications for how health experts treat mental illness and addiction or how the legal system assesses a criminal’s likelihood of committing another crime.Researchers from The University of Texas at Austin, UCLA and elsewhere analyzed data from 108 subjects who sat in a magnetic resonance imaging (MRI) scanner — a machine that allows researchers to pinpoint brain activity in vivid, three-dimensional images — while playing a video game that simulates risk-taking.The researchers used specialized software to look for patterns of activity across the whole brain that preceded a person’s making a risky choice or a safe choice in one set of subjects. Then they asked the software to predict what other subjects would choose during the game based solely on their brain activity. The software accurately predicted people’s choices 71 percent of the time.”These patterns are reliable enough that not only can we predict what will happen in an additional test on the same person, but on people we haven’t seen before,” said Russell Poldrack, director of UT Austin’s Imaging Research Center and professor of psychology and neuroscience.When the researchers trained their software on much smaller regions of the brain, they found that just analyzing the regions typically involved in executive functions such as control, working memory and attention was enough to predict a person’s future choices. Therefore, the researchers concluded, when we make risky choices, it is primarily because of the failure of our control systems to stop us.”We all have these desires, but whether we act on them is a function of control,” said Sarah Helfinstein, a postdoctoral researcher at UT Austin and lead author of the study that appears online this week in the journal Proceedings of the National Academy of Sciences.Helfinstein said that additional research could focus on how external factors, such as peer pressure, lack of sleep or hunger, weaken the activity of our brains’ control systems when we contemplate risky decisions.”If we can figure out the factors in the world that influence the brain, we can draw conclusions about what actions are best at helping people resist risks,” said Helfinstein.To simulate features of real-world risk-taking, the researchers used a video game called the Balloon Analogue Risk Task (BART) that past research has shown correlates well with self-reported risk-taking such as drug and alcohol use, smoking, gambling, driving without a seatbelt, stealing and engaging in unprotected sex.While playing the BART, the subject sees a balloon on the screen and is asked to make either a risky choice (inflate the balloon a little and earn a few cents) or a safe choice (stop the round and “cash out,” keeping whatever money was earned up to that point). Sometimes inflating the balloon causes it to burst and the player loses all the cash earned from that round. After each successful balloon inflation, the game continues with the chance of earning another standard-sized reward or losing an increasingly large amount. Many health-relevant risky decisions share this same structure, such as when deciding how many alcoholic beverages to drink before driving home or how much one can experiment with drugs or cigarettes before developing an addiction.The data for this study came from the Consortium for Neuropsychiatric Phenomics at UCLA, which recruited adults from the Los Angeles area for researchers to examine differences in response inhibition and working memory between healthy adults and patients diagnosed with bipolar disorder, schizophrenia, or adult attention deficit hyperactivity disorder (ADHD). Only data collected from healthy participants were included in the present analyses.Other researchers on the study include: Tom Schonberg and Jeanette A. Mumford at The University of Texas at Austin; Katherine H. Karlsgodt at Zucker Hillside Hospital and the Feinstein Institute for Medical Research; Eliza Congdon, Fred W. …

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Psychologists report new insights on human brain, consciousness

Oct. 17, 2013 — UCLA psychologists have used brain-imaging techniques to study what happens to the human brain when it slips into unconsciousness. Their research, published Oct. 17 in the online journal PLOS Computational Biology, is an initial step toward developing a scientific definition of consciousness.”In terms of brain function, the difference between being conscious and unconscious is a bit like the difference between driving from Los Angeles to New York in a straight line versus having to cover the same route hopping on and off several buses that force you to take a ‘zig-zag’ route and stop in several places,” said lead study author Martin Monti, an assistant professor of psychology and neurosurgery at UCLA.Monti and his colleagues used functional magnetic resonance imaging (fMRI) to study how the flow of information in the brains of 12 healthy volunteers changed as they lost consciousness under anesthesia with propofol. The participants ranged in age from 18 to 31 and were evenly divided between men and women.The psychologists analyzed the “network properties” of the subjects’ brains using a branch of mathematics known as graph theory, which is often used to study air-traffic patterns, information on the Internet and social groups, among other topics.”It turns out that when we lose consciousness, the communication among areas of the brain becomes extremely inefficient, as if suddenly each area of the brain became very distant from every other, making it difficult for information to travel from one place to another,” Monti said.The finding shows that consciousness does not “live” in a particular place in our brain but rather “arises from the mode in which billions of neurons communicate with one another,” he said.When patients suffer severe brain damage and enter a coma or a vegetative state, Monti said, it is very possible that the sustained damage impairs their normal brain function and the emergence of consciousness in the same manner as was seen by the life scientists in the healthy volunteers under anesthesia.”If this were indeed the case, we could imagine in the future using our technique to monitor whether interventions are helping patients recover consciousness,” he said.”It could, however, also be the case that losing consciousness because of brain injury affects brain function through different mechanisms,” said Monti, whose research team is currently addressing this question in another study.”As profoundly defining of our mind as consciousness is, without having a scientific definition of this phenomenon, it is extremely difficult to study,” Monti noted. This study, he said, marks an initial step toward conducting neuroscience research on consciousness.The research was conducted at Belgium’s University Hospital of Liege.Monti’s expertise includes cognitive neuroscience, the relationship between language and thought, and how consciousness is lost and recovered after severe brain injury. He was part of a team of American and Israeli brain scientists who used fMRI on former Israeli Prime Minister Ariel Sharon in January 2013 to assess his brain responses.Surprisingly, Sharon, who was presumed to be in a vegetative state since suffering a brain hemorrhage in 2006, showed significant brain activity, Monti and his colleagues reported.The former prime minister was scanned to assess the extent and quality of his brain processing, using methods recently developed by Monti and his colleagues. The scientists found subtle but encouraging signs of consciousness.

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New approach to remedying childhood visual disorders

Aug. 26, 2013 — By discovering the role of key neurons that mediate an important part of vision development, UC Irvine and UCLA neurobiologists have revealed a new approach to correcting visual disorders in children who suffer from early cataracts or amblyopia, also known as lazy eye.Such youngsters can have permanent defects in vision, even after surgery to remove cataracts or correct lazy eye. These flaws are often a result of improper brain development due to visual deprivation during childhood. In contrast, when cataracts in adults are surgically corrected, normal vision is usually restored.Xiangmin Xu, assistant professor of anatomy & neurobiology at UC Irvine, and Josh Trachtenberg, associate professor of neurobiology at UCLA, found that this phenomenon is caused by a specific class of inhibitory neurons that control the time window, or “critical period,” in early vision development, generally before age 7. The results of their study appeared online Aug. 25 in Nature.The researchers discovered that improper functioning of these key neurons during the critical period of development is responsible for these vision defects. Additionally, in tests on mice, they used an experimental drug compound to reopen this critical-period window and treat the neuronal defects associated with temporary loss of vision in one eye during early development.Their work suggests that drugs targeted to the critical period-regulating neurons can correct central vision disorders in children who’ve suffered from amblyopia or early cataracts.”The specific type of neurons that mediate the critical-period window during childhood development have not been well understood until now,” Xu said. “Our breakthrough outlines a new path for treatments that can restore normal vision in children who have had early vision disorders.”

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Researchers find essential brain circuit in visual development

Aug. 25, 2013 — A study in mice reveals an elegant circuit within the developing visual system that helps dictate how the eyes connect to the brain. The research, funded by the National Institutes of Health, has implications for treating amblyopia, a vision disorder that occurs when the brain ignores one eye in favor of the other.Amblyopia is the most common cause of visual impairment in childhood, and can occur whenever there is a misalignment between what the two eyes see — for example, if one eye is clouded by a cataract or if the eyes are positioned at different angles. The brain at first has a slight preference for the more functional eye, and over time — as that eye continues to send the brain useful information — the brain’s preference for that eye gets stronger at the expense of the other eye.Patching the strong eye can help correct amblyopia. But if the condition isn’t caught and corrected during childhood, visual impairment in the weaker eye is likely to persist into adulthood.”Our study identifies a mechanism for visual development in the young brain and shows that it’s possible to turn on the same mechanism in the adult brain, thus offering hope for treating older children and adults with amblyopia,” said Joshua Trachtenberg, Ph.D., an associate professor of neurobiology at the David Geffen School of Medicine, University of California, Los Angeles (UCLA). The study was published in Nature.Within the brain, cells in a limited region called the binocular zone can receive input from both eyes. During brain development, the eyes compete to connect within this zone, and sometimes one eye prevails — a process known as ocular dominance.Ocular dominance is a normal process and is an example of the brain’s ability to adapt based on experience — called plasticity. But it can also set the stage for amblyopia. If one eye is impaired and can’t effectively compete, it will lose space in the binocular zone to the other eye. Also, this competition takes place during a limited time called the critical period. …

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Scientists analyze genetic makeup of human and mouse embryos in amazing detail

July 31, 2013 — UCLA scientists, in collaboration with teams in China, have used the powerful technology of single-cell RNA sequencing to track the genetic development of a human and a mouse embryo at an unprecedented level of accuracy.The technique could lead to earlier and more accurate diagnoses of genetic diseases, even when the embryo consists of only eight cells.The study was led by Guoping Fan, professor of human genetics and molecular biology and member of both the Jonsson Comprehensive Cancer Center and the Eli and Edythe Broad Center of Regenerative Medicine and Stem Cell Research. The findings were published in the online edition of the journal Nature and will appear later in the print edition.Single-cell RNA sequencing allows researchers to determine the precise nature of the total gene transcripts, or all of the genes that are actively expressed in a particular cell.”The advantages of this technique are twofold,” Fan said. “It is a much more comprehensive analysis than was achievable before and the technique requires a very minimal amount of sample material — just one cell.”Besides its implications for genetic diagnoses — such as improving scientists’ ability to identify genetic mutations like BRCA1 and BRCA2, which predispose women to breast cancer and ovarian cancer, or genetic diseases that derive from protein dysfunction, such as sickle cell disease — the technology may also have important uses in reproductive medicine.The technique marks a major development in genetic diagnoses, which previously could not be conducted this early in embryonic development and required much larger amounts of biological material.”Previous to this paper we did not know this much about early human development,” said Kevin Huang, the study’s co-first author and a postdoctoral scholar in Fan’s laboratory. “Now we can define what ‘normal’ looks like, so in the future we will have a baseline from which to compare possible genetic problems. This is our first comprehensive glance at what is normal.”With single-cell RNA sequencing, much more gene transcription was detected than before. “The question we asked is, ‘How does the gene network drive early development from one cell to two cells, two cells to four cells, and so on?'” Fan said. “Using the genome data analysis methods developed by co-author Steve Horvath at UCLA, we have uncovered crucial gene networks and we can now predict possible future genetic disorders at the eight-cell stage.”The research was supported by the Chinese Ministry of Science and Technology, the International Science and Technology Cooperation Program of China, and the National Natural Science Foundation of China.

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Scientists ID compounds that target amyloid fibrils in Alzheimer’s, other brain diseases

July 26, 2013 — UCLA chemists and molecular biologists have for the first time used a “structure-based” approach to drug design to identify compounds with the potential to delay or treat Alzheimer’s disease, and possibly Parkinson’s, Lou Gehrig’s disease and other degenerative disorders.All of these diseases are marked by harmful, elongated, rope-like structures known as amyloid fibrils, linked protein molecules that form in the brains of patients.Structure-based drug design, in which the physical structure of a targeted protein is used to help identify compounds that will interact with it, has already been used to generate therapeutic agents for a number of infectious and metabolic diseases.The UCLA researchers, led by David Eisenberg, director of the UCLA-Department of Energy Institute of Genomics and Proteomics and a Howard Hughes Medical Institute investigator, report the first application of this technique in the search for molecular compounds that bind to and inhibit the activity of the amyloid-beta protein responsible for forming dangerous plaques in the brain of patients with Alzheimer’s and other degenerative diseases.In addition to Eisenberg, who is also a professor of chemistry, biochemistry and biological chemistry and a member of UCLA’s California NanoSystems Institute, the team included lead author Lin Jiang, a UCLA postdoctoral scholar in Eisenberg’s laboratory and Howard Hughes Medical Institute researcher, and other UCLA faculty.The research was published July 16 in eLife, a new open-access science journal backed by the Howard Hughes Medical Institute, the Max Planck Society and the Wellcome Trust.A number of non-structural screening attempts have been made to identify natural and synthetic compounds that might prevent the aggregation and toxicity of amyloid fibrils. Such studies have revealed that polyphenols, naturally occurring compounds found in green tea and in the spice turmeric, can inhibit the formation of amyloid fibrils. In addition, several dyes have been found to reduce amyloid’s toxic effects, although significant side effects prevent them from being used as drugs.Armed with a precise knowledge of the atomic structure of the amyloid-beta protein, Jiang, Eisenberg and colleagues conducted a computational screening of 18,000 compounds in search of those most likely to bind tightly and effectively to the protein.Those compounds that showed the strongest potential for binding were then tested for their efficacy in blocking the aggregation of amyloid-beta and for their ability to protect mammalian cells grown in culture from the protein’s toxic effects, which in the past has proved very difficult. Ultimately, the researchers identified eight compounds and three compound derivatives that had a significant effect.While these compounds did not reduce the amount of protein aggregates, they were found to reduce the protein’s toxicity and to increase the stability of amyloid fibrils — a finding that lends further evidence to the theory that smaller assemblies of amyloid-beta known as oligomers, and not the fibrils themselves, are the toxic agents responsible for Alzheimer’s symptoms.The researchers hypothesize that by binding snugly to the protein, the compounds they identified may be preventing these smaller oligomers from breaking free of the amyloid-beta fibrils, thus keeping toxicity in check.An estimated 5 million patients in the U.S. suffer from Alzheimer’s disease, the most common form of dementia. Alzheimer’s health care costs in have been estimated at $178 billion per year, including the value of unpaid care for patients provided by nearly 10 million family members and friends.In addition to uncovering compounds with therapeutic potential for Alzheimer’s disease, this research presents a new approach for identifying proteins that bind to amyloid fibrils — an approach that could have broad applications for treating many diseases.Co-authors on the research included Cong Liu, David Leibly, Meytal Landau, Minglei Zhao and Michael Hughes.The research was funded by the Howard Hughes Medical Institute and the National Institute of Aging, part of the National Institutes of Health (grant AG-029430).

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Is sexual addiction the real deal?

July 19, 2013 — Controversy exists over what some mental health experts call “hypersexuality,” or sexual “addiction.” Namely, is it a mental disorder at all, or something else? It failed to make the cut in the recently updated Diagnostic and Statistical Manual of Mental Disorders, or DSM-5, considered the bible for diagnosing mental disorders. Yet sex addiction has been blamed for ruining relationships, lives and careers.Now, for the first time, UCLA researchers have measured how the brain behaves in so-called hypersexual people who have problems regulating their viewing of sexual images. The study found that the brain response of these individuals to sexual images was not related in any way to the severity of their hypersexuality but was instead tied only to their level of sexual desire.In other words, hypersexuality did not appear to explain brain differences in sexual response any more than simply having a high libido, said senior author Nicole Prause, a researcher in the department of psychiatry at the Semel Institute for Neuroscience and Human Behavior at UCLA.”Potentially, this is an important finding,” Prause said. “It is the first time scientists have studied the brain responses specifically of people who identify as having hypersexual problems.”The study appears in the current online edition of the journal Socioaffective Neuroscience and Psychology.A diagnosis of hypersexuality or sexual addiction is typically associated with people who have sexual urges that feel out of control, who engage frequently in sexual behavior, who have suffered consequences such as divorce or economic ruin as a result of their behaviors, and who have a poor ability to reduce those behaviors.But, said Prause and her colleagues, such symptoms are not necessarily representative of an addiction — in fact, non-pathological, high sexual desire could also explain this cluster of problems.One way to tease out the difference is to measure the brain’s response to sexual-image stimuli in individuals who acknowledge having sexual problems. If they indeed suffer from hypersexuality, or sexual addiction, their brain response to visual sexual stimuli could be expected be higher, in much the same way that the brains of cocaine addicts have been shown to react to images of the drug in other studies.The study involved 52 volunteers: 39 men and 13 women, ranging in age from 18 to 39, who reported having problems controlling their viewing of sexual images. They first filled out four questionnaires covering various topics, including sexual behaviors, sexual desire, sexual compulsions, and the possible negative cognitive and behavioral outcomes of sexual behavior. Participants had scores comparable to individuals seeking help for hypersexual problems.While viewing the images, the volunteers were monitored using electroencephalography (EEG), a non-invasive technique that measures brain waves, the electrical activity generated by neurons when they communicate with each other. Specifically, the researchers measured event-related potentials, brain responses that are the direct result of a specific cognitive event.”The volunteers were shown a set of photographs that were carefully chosen to evoke pleasant or unpleasant feelings,” Prause said. “The pictures included images of dismembered bodies, people preparing food, people skiing — and, of course, sex. …

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New clue to cause of human narcolepsy

July 3, 2013 — In 2000, researchers at the UCLA Center for Sleep Research published findings showing that people suffering from narcolepsy, a disorder characterized by uncontrollable periods of deep sleep, had 90 percent fewer neurons containing the neuropeptide hypocretin in their brains than healthy people. The study was the first to show a possible biological cause of the disorder.Subsequent work by this group and others demonstrated that hypocretin is an arousing chemical that keeps us awake and elevates both mood and alertness; the death of hypocretin cells, the researchers said, helps explain the sleepiness of narcolepsy. But it has remained unclear what kills these cells.Now the same UCLA team reports that an excess of another brain cell type — this one containing histamine — may be the cause of the loss of hypocretin cells in human narcoleptics.UCLA professor of psychiatry Jerome Siegel and colleagues report in the current online edition of the journal Annals of Neurology that people with the disorder have nearly 65 percent more brain cells containing the chemical histamine. Their research suggests that this excess of histamine cells causes the loss of hypocretin cells in human narcoleptics.Narcolepsy is a chronic disorder of the central nervous system characterized by the brain’s inability to control sleep-wake cycles. It causes sudden bouts of sleep and is often accompanied by cataplexy, an abrupt loss of voluntary muscle tone that can cause a person to collapse. According to the National Institutes of Health, narcolepsy is thought to affect roughly one in every 3,000 Americans. Currently, there is no cure.Histamine is a body chemical that works as part of the immune system to kill invading cells. When the immune system goes awry, histamine can act on a person’s eyes, nose, throat, lungs, skin or gastrointestinal tract, causing the symptoms of allergy that many people are familiar with. But histamine is also present in a type of brain cell.For the study, researchers examined five narcoleptic brains and seven control brains from human cadavers. Prior to death, all the narcoleptics had been diagnosed by a sleep disorder center as having narcolepsy with cataplexy. …

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Curcumin may protect premature infants’ lungs

July 2, 2013 — Turmeric, a key ingredient in spicy curry dishes, has long been known to have medicinal values. Now new research finds a substance in turmeric, curcumin, may provide lasting protection against potentially deadly lung damage in premature infants.Share This:Premature infants often need the assistance of ventilators and forced oxygen therapy because they’re frequently born with inadequate lung function. These therapies can cause the infants to suffer lasting lung damage and even death. Researchers at Los Angeles Biomedical Research Institute at Harbor-UCLA Medical Center (LA BioMed), using disease models, found curcumin provided long-term protection against this damage.Their study, published online by the American Journal of Physiology, Lung Cellular and Molecular Physiology, found curcumin provided protection against bronchopulmonary dysplasia (BDP), a condition characterized by scarring and inflammation, and against hyperoxia, in which too much oxygen enters the body through the lungs, for up to 21 days after birth. A previous LA BioMed study found curcumin provided protection for up to seven days after birth.”This is the first study to find long-term benefits of using curcumin to protect lung function in premature infants,” said Virender K. Rehan, MD, the LA BioMed lead researcher who authored the study. “Curcumin is known to have potent antioxidant, anti-inflammatory and anti-microbial properties, making it a promising therapy for premature infants who require oxygen therapy after birth.”BDP is now the most common chronic lung disease of infancy in the U.S. With more premature babies surviving because of improvements in neonatal care, the cases of BPD have increased. A 2010 study found 67.3% of babies born at 22-25 weeks of gestation developed BPD, compared to 36.6% of infants born at 26-30 weeks of gestation.Share this story on Facebook, Twitter, and Google:Other social bookmarking and sharing tools:|Story Source: The above story is reprinted from materials provided by Los Angeles Biomedical Research Institute at Harbor-UCLA Medical Center (LA BioMed), via EurekAlert!, a service of AAAS. Note: Materials may be edited for content and length. …

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How did a third radiation belt appear in the Earth’s upper atmosphere?

June 20, 2013 — Since the discovery of the Van Allen radiation belts in in Earth’s upper atmosphere in 1958, space scientists have believed that these belts consisted of two doughnut-shaped rings of highly charged particles — an inner ring of high-energy electrons and energetic positive ions, and an outer ring of high-energy electrons.However, in February of this year, a team of scientists reported in the journal Science the surprising discovery of a previously unknown third radiation ring. This narrow ring had briefly circled Earth between the inner and outer rings in September 2012 and then almost completely disappeared.How did this temporary radiation belt appear and dissipate?In new research, the radiation belt group in the UCLA Department of Atmospheric and Oceanic Sciences explains the development of this third belt and its decay over a period of slightly more than four weeks. The research is available in the online edition of the journal Geophysical Research Letters and will be published in an upcoming print edition.By performing a “quantitative treatment of the scattering of relativistic electrons by electromagnetic whistler-mode waves inside the dense plasmasphere,” the investigators were able to account for the “distinctively slow decay of the injected relativistic electron flux” and demonstrate why this unusual third radiation belt is observed only at energies above 2 mega-electron-volts.Understanding the processes that control the formation and ultimate loss of such relativistic electrons is a primary science objective of the NASA Van Allen Probe Mission and has important practical applications, because the enormous amounts of radiation the Van Allen belts generate can pose a significant hazard to satellites and spacecraft, as well to astronauts performing activities outside a spacecraft.The current research was funded by the NASA, which launched the twin Van Allen probes in the summer of 2012.The lead author of the research is Richard Thorne, a UCLA professor of atmospheric and oceanic sciences, who was a co-author of the Feb. 28 research paper in Science. Co-authors of the new research include Wen Li, a graduate student who works in Thorne’s laboratory; Binbin Ni, a postdoctoral scholar who works in Thorne’s laboratory; Jacob Bortnik, a researcher with the UCLA Department of Atmospheric and Oceanic Sciences; Daniel Baker, a professor at the University of Colorado’s Laboratory for Atmospheric and Space Physics and lead author of the February Science paper; and Vassilis Angelopoulos, a UCLA professor of Earth and space sciences.

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Scientists unexpectedly discover stress-resistant stem cells in fat tissue removed during liposuction

June 5, 2013 — Researchers from the UCLA Department of Obstetrics and Gynecology have isolated a new population of primitive, stress-resistant human pluripotent stem cells easily derived from fat tissue that are able to differentiate into virtually every cell type in the human body without genetic modification.The cells, called Multi-lineage Stress-Enduring (Muse-AT) stem cells from fat, or adipose, tissue, were discovered by “scientific accident” when a piece of equipment failed in the lab, killing all the stem cells in the experiment except for the Muse-AT cells. The research team further discovered that not only are Muse-AT cells able to survive severe stress, they may even be activated by it, said study senior author Gregorio Chazenbalk, an associate researcher with UCLA Obstetrics and Gynecology.These pluripotent cells, isolated from fat tissue removed during liposuction, expressed many embryonic stem cell markers and were able to differentiate into muscle, bone, fat, cardiac, neuronal and liver cells. An examination of their genetic characteristics confirmed their specialized functions, as well as their capacity to regenerate tissue when transplanted back into the body following their “awakening.””This population of cells lies dormant in the fat tissue until it is subjected to very harsh conditions. These cells can survive in conditions in which usually only cancer cells can live,” Chazenbalk said. “Upon further investigation and clinical trials, these cells could prove a revolutionary treatment option for numerous diseases, including heart disease, stroke and for tissue damage and neural regeneration.”The results of the two-year study are published June 5, 2013 in the peer-reviewed journal PLOS ONE.Purifying and isolating Muse-AT cells does not require the use of a cell sorter or other specialized, high-tech devices. They are able to grow either in suspension, forming cell spheres, or as adherent cells, forming cell aggregates very similar to human embryonic stem cell-derived embryoid bodies.”We have been able to isolate these cells using a simple and efficient method that takes about six hours from the time the fat tissue is harvested,” said Chazenbalk,a scientist with the Eli and Edythe Broad Center of Regenerative Medicine and Stem Cell Research. “This research offers a new and exciting source of fat stem cells with pluripotent characteristics, as well as a new method for quickly isolating them. These cells also appear to be more primitive than the average fat stem cells, making them potentially superior sources for regenerative medicine.”Currently, embryonic stem cells and induced pluripotent stem cells — skin cells turned into embryonic-like cells — are the two main sources of pluripotent cells. However, both types can exhibit an uncontrolled capacity for differentiation and proliferation, leading to the formation of unwanted teratoma, or tumors. Little progress has been made in resolving that defect, Chazenbalk said.Muse cells originally were discovered by a research group at Tokohu University in Japan and were derived from bone marrow and skin, rather than fat. …

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New single virus detection techniques for faster disease diagnosis

May 30, 2013 — To test the severity of a viral infection, clinicians try to gauge how many viruses are packed into a certain volume of blood or other bodily fluid. This measurement, called viral load, helps doctors diagnose or monitor chronic viral diseases such as HIV/AIDS and hepatitis. However, the standard methods used for these tests are only able to estimate the number of viruses in a given volume of fluid. Now two independent teams have developed new optics-based methods for determining the exact viral load of a sample by counting individual virus particles. These new methods are faster and cheaper than standard tests and they offer the potential to conduct the measurements in a medical office or hospital instead of a laboratory.

The teams will present their latest results at the Conference on Lasers and Electro-Optics (CLEO: 2013), to be held June 9-14, in San Jose, Calif.

One research group, led by electrical engineer and bioengineer Aydogan Ozcan of UCLA, is working to directly image single virus particles using holographic microscopy. The other, led by electrical engineer Holger Schmidt of the University of California, Santa Cruz (UCSC), is detecting single particles tagged with fluorescent labels on a microfluidic chip. Both teams expect to use their work to develop commercial instruments useful for on-site diagnosis and monitoring with rapid results and fast turnaround.

Ozcan’s UCLA team has demonstrated the ability to capture optical images of single viruses and nanoparticles over a comparatively large field of view — about the size of a postage stamp — using nanolenses that self-assemble around the virus particles like little magnifying glasses.

“Because viruses are very small–less than 100 billionths of a meter–compared to the wavelength of light, conventional light microscopy has difficulty producing an image due to weak scattering of sub-wavelength particles,” Ozcan says. When lighted, the team’s new nanolens-nanoparticle assembly projects a hologram that can be recorded using a CMOS imager chip (a type of semiconductor-based light detector) and digitally reconstructed to form an optical image of the particle. “The resulting image improves the field-of-view of a conventional optical microscope by two orders of magnitude,” says Ozcan.

This wide field of view allows the device to form images of many nanoparticles in a single photograph and provides a high-throughput platform for a direct and accurate viral load count. The instrument can be made sufficiently compact and lightweight for field applications and, attached to a cell phone, could become useful even in remote locations.

The UCSC researchers will present the results of a collaborative effort between UCSC, Liquilume Diagnostics Inc., and the groups of infectious disease clinician and virologist Charles Chiu at University of California, San Francisco, and engineer Aaron Hawkins at Brigham Young. While Ozcan’s group visually counts individual viruses, Schmidt’s counts them by detecting their nucleic acids–the genetic makeup of the viruses. The nucleic acids are labeled with a fluorescent dye, and light from the fluorescence is detected as they pass through a channel in a microfluidic chip about the size of a thumbnail.

Current tests for determining viral load generally rely on a technique called polymerase chain reaction (PCR), which amplifies a small sample of nucleic acid, such as DNA, and makes it easier to detect. “The gold standard for viral load detection is PCR, due to its sensitivity and specificity,” Schmidt says, but PCR is limited to merely estimating the number of viruses. In contrast, the new method counts real particles as they pass through the fluorescence detector on the chip. “We have demonstrated actual virus counts of specific nucleic acids in less than 30 minutes with minimal sample workup,” Schmidt says. So far, the group has collected reliable data on samples diluted to a point well within the range required for clinical detection.

Unlike direct visualization techniques, Schmidt’s chip-based method requires that the targeted virus particles be labeled. The labeling technique would allow clinicians to target specific viruses while ignoring unlabeled background material. This makes the process potentially useful in situations where clinicians already know what they are looking for — often the case for viral load tests.

The chip is currently housed in an instrument about one foot square, making the device portable. Along with rapid analysis turnaround, this portability should make the technique useful for point-of-treatment tests. In addition to detecting viruses, the device may also find uses as a sensor for cancer biomarkers, for environmental analyses of chemicals, and even in industrial production monitoring.

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Changing gut bacteria through diet affects brain function

May 28, 2013 — UCLA researchers now have the first evidence that bacteria ingested in food can affect brain function in humans. In an early proof-of-concept study of healthy women, they found that women who regularly consumed beneficial bacteria known as probiotics through yogurt showed altered brain function, both while in a resting state and in response to an emotion-recognition task.

The study, conducted by scientists with UCLA’s Gail and Gerald Oppenheimer Family Center for Neurobiology of Stress and the Ahmanson-Lovelace Brain Mapping Center at UCLA, appears in the June edition of the peer-reviewed journal Gastroenterology.

The discovery that changing the bacterial environment, or microbiota, in the gut can affect the brain carries significant implications for future research that could point the way toward dietary or drug interventions to improve brain function, the researchers said.

“Many of us have a container of yogurt in our refrigerator that we may eat for enjoyment, for calcium or because we think it might help our health in other ways,” said Dr. Kirsten Tillisch, an associate professor of medicine at UCLA’s David Geffen School of Medicine and lead author of the study. “Our findings indicate that some of the contents of yogurt may actually change the way our brain responds to the environment. When we consider the implications of this work, the old sayings ‘you are what you eat’ and ‘gut feelings’ take on new meaning.”

Researchers have known that the brain sends signals to the gut, which is why stress and other emotions can contribute to gastrointestinal symptoms. This study shows what has been suspected but until now had been proved only in animal studies: that signals travel the opposite way as well.

“Time and time again, we hear from patients that they never felt depressed or anxious until they started experiencing problems with their gut,” Tillisch said. “Our study shows that the gut-brain connection is a two-way street.”   The small study involved 36 women between the ages of 18 and 55. Researchers divided the women into three groups: one group ate a specific yogurt containing a mix of several probiotics — bacteria thought to have a positive effect on the intestines — twice a day for four weeks; another group consumed a dairy product that looked and tasted like the yogurt but contained no probiotics; and a third group ate no product at all.

Functional magnetic resonance imaging (fMRI) scans conducted both before and after the four-week study period looked at the women’s brains in a state of rest and in response to an emotion-recognition task in which they viewed a series of pictures of people with angry or frightened faces and matched them to other faces showing the same emotions. This task, designed to measure the engagement of affective and cognitive brain regions in response to a visual stimulus, was chosen because previous research in animals had linked changes in gut flora to changes in affective behaviors.

The researchers found that, compared with the women who didn’t consume the probiotic yogurt, those who did showed a decrease in activity in both the insula — which processes and integrates internal body sensations, like those form the gut — and the somatosensory cortex during the emotional reactivity task.

Further, in response to the task, these women had a decrease in the engagement of a widespread network in the brain that includes emotion-, cognition- and sensory-related areas. The women in the other two groups showed a stable or increased activity in this network.

During the resting brain scan, the women consuming probiotics showed greater connectivity between a key brainstem region known as the periaqueductal grey and cognition-associated areas of the prefrontal cortex. The women who ate no product at all, on the other hand, showed greater connectivity of the periaqueductal grey to emotion- and sensation-related regions, while the group consuming the non-probiotic dairy product showed results in between.

The researchers were surprised to find that the brain effects could be seen in many areas, including those involved in sensory processing and not merely those associated with emotion, Tillisch said.

The knowledge that signals are sent from the intestine to the brain and that they can be modulated by a dietary change is likely to lead to an expansion of research aimed at finding new strategies to prevent or treat digestive, mental and neurological disorders, said Dr. Emeran Mayer, a professor of medicine, physiology and psychiatry at the David Geffen School of Medicine at UCLA and the study’s senior author.

“There are studies showing that what we eat can alter the composition and products of the gut flora — in particular, that people with high-vegetable, fiber-based diets have a different composition of their microbiota, or gut environment, than people who eat the more typical

Western diet that is high in fat and carbohydrates,” Mayer said. “Now we know that this has an effect not only on the metabolism but also affects brain function.”

The UCLA researchers are seeking to pinpoint particular chemicals produced by gut bacteria that may be triggering the signals to the brain. They also plan to study whether people with gastrointestinal symptoms such as bloating, abdominal pain and altered bowel movements have improvements in their digestive symptoms which correlate with changes in brain response.

Meanwhile, Mayer notes that other researchers are studying the potential benefits of certain probiotics in yogurts on mood symptoms such as anxiety. He said that other nutritional strategies may also be found to be beneficial.

By demonstrating the brain effects of probiotics, the study also raises the question of whether repeated courses of antibiotics can affect the brain, as some have speculated. Antibiotics are used extensively in neonatal intensive care units and in childhood respiratory tract infections, and such suppression of the normal microbiota may have longterm consequences on brain development.

Finally, as the complexity of the gut flora and its effect on the brain is better understood, researchers may find ways to manipulate the intestinal contents to treat chronic pain conditions or other brain related diseases, including, potentially, Parkinson’s disease, Alzheimer’s disease and autism.

Answers will be easier to come by in the near future as the declining cost of profiling a person’s microbiota renders such tests more routine, Mayer said.

The study was funded by Danone Research. Mayer has served on the company’s scientific advisory board. Three of the study authors (Denis Guyonnet, Sophie Legrain-Raspaud and Beatrice Trotin) are employed by Danone Research and were involved in the planning and execution of the study (providing the products) but had no role in the analysis or interpretation of the results.

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