Public smoking bans linked with rapid fall in preterm births, child hospital visits for asthma

The introduction of laws banning smoking in public places and workplaces in North America and Europe has been quickly followed by large drops in rates of preterm births and children attending hospital for asthma, according to the first systematic review and meta-analysis examining the effect of smoke-free legislation on child health, published in The Lancet.The analysis of 11 studies done in North America and Europe, involving more than 2.5 million births, and nearly 250 000 asthma exacerbations, showed that rates of both preterm births and hospital attendance for asthma were reduced by 10% within a year of smoke-free laws coming into effect.Currently only 16% of the world’s population is covered by comprehensive smoke-free laws, and 40% of children worldwide are regularly exposed to second-hand smoke. To date, most studies have looked at the impact of smoking bans on adult outcomes, but children account for more than a quarter of all deaths and over half of all healthy years of life lost due to exposure to second-hand smoke.After searching systematically for both published and unpublished studies over 38 years (1975-2013) reporting on the impact of public smoking restrictions on health outcomes in children aged 12 years or younger, Dr Jasper Been from the Maastricht University Medical Centre, in the Netherlands, and colleagues identified 11 suitable studies — five North American studies describing local bans and six European studies looking at national bans.”Our research found significant reductions in preterm birth and severe asthma attacks in childhood, as well as a 5% decline in children being born very small for gestational age after the introduction of smoke-free laws,” says Dr Been.”Together with the known health benefits in adults, our study provides clear evidence that smoking bans have considerable public health benefits for perinatal and child health, and provides strong support for WHO recommendations to create smoke-free public environments on a national level.”*”This research has demonstrated the very considerable potential that smoke-free legislation offers to reduce preterm births and childhood asthma attacks,” says study co-author Professor Aziz Sheikh, of Brigham and Women’s Hospital, USA, and the University of Edinburgh, UK. “The many countries that are yet to enforce smoke-free legislation should in the light of these findings reconsider their positions on this important health policy question.”*Writing in a linked Comment, Sara Kalkhoran and Stanton Glantz from the University of California San Francisco in the USA point out that, “Medical expenses for asthma exceeded US$50 billion in the USA in 2007, and US$20 billion in Europe in 2006. If asthma emergency department visits and admissions to hospital decreased by even 10%, the savings in the USA and Europe together would be US$7 billion annually.”They conclude, “The cigarette companies, their allies, and the groups they sponsor have long used claims of economic harm, particularly to restaurants, bars, and casinos, to oppose smoke-free laws despite consistent evidence to the contrary. By contrast, the rapid economic benefits that smoke-free laws and other tobacco control policies bring in terms of reduced medical costs are real. Rarely can such a simple intervention improve health and reduce medical costs so swiftly and substantially.”Story Source:The above story is based on materials provided by The Lancet. Note: Materials may be edited for content and length.

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New and improved laser and light treatments take aim at cellulite, fat, tattoos, wrinkles and sagging skin

As more people look for ways to turn back the clock or improve their appearance, dermatologists are pioneering many of the newest aesthetic laser technologies — from tattoo removal to erasing fine lines and wrinkles to reducing fat or cellulite. Before considering any cosmetic procedure, dermatologists recommend that consumers do their homework to better understand the best technologies available for their specific needs.Information was provided by board-certified dermatologist M. Christine Lee, MD, FAAD, assistant clinical professor of dermatologic surgery at the University of California, San Francisco and director of a private practice in Walnut Creek, Calif.Treatments for Cellulite, Excess Fat Now Produce Long-Lasting ResultsCellulite and excess fat are two of the biggest hurdles that many women face in their quest to improve their appearance. While diet and exercise can help reduce body fat, cellulite is resistant to these types of lifestyle changes. Unique to women, Dr. Lee estimates that cellulite affects 80 percent of women regardless of their body weight. Until now, no cellulite treatment could dramatically change the appearance of cellulite, and any results were temporary.1440 Nanometer Laser• First minimally invasive laser treatment to treat cellulite approved by the Food and Drug Administration (FDA) in 2012 and provides long-lasting, dramatic results.• Surgical procedure involves inserting a tiny fiber optic beneath the skin to break the fiber bands responsible for cellulite in women. The laser releases the skin and allows the depressions (or dimpling that gives cellulite its appearance) to rise to the surface of the skin. Once the laser beam severs the fiber bands, the blood supply to this area is cut off so the bands do not regrow, and collagen production is stimulated.• Multiple areas can be treated with only one session, and the most common treatment areas are the buttocks, hips and thighs.• Some downtime is required after the procedure, due to bruising and swelling that can take one to two weeks to resolve.Cryolipolysis• Non-invasive procedure approved by the FDA to remove localized areas of fat in the lower abdomen and along the sides of the body.• Works by freezing the lipids in fat cells, which then slowly dissolve without injuring surrounding tissues.• Typically, three treatments are needed to dissolve an inch of fat.• Results are not immediate, as it takes three to four months to see a noticeable improvement.Ultrasound• Non-invasive procedure approved by the FDA uses high-intensity, focused ultrasound energy to destroy or melt targeted fat without harming surrounding skin.• Used to reduce fat bulges in the abdomen, with the average reduction of about an inch per treatment session. Can also be used on the thighs or other large areas of fat.• Results are not immediate, requiring two to three months.• An added benefit is noticeable improvement in the appearance of cellulite in the months following the procedure.These newer treatments provide alternatives to liposuction, which has been used to remove pockets of fat for decades but is more invasive and requires more downtime. …

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Biologists use sound to identify breeding grounds of endangered whales

Remote acoustic monitoring among endangered whales is the subject of a major article by two doctoral students in The College of Arts and Sciences.Leanna Matthews and Jessica McCordic, members of the Parks Lab in the Department of Biology, have co-authored “Remote Acoustic Monitoring of North Atlantic Right Whales Reveals Seasonal and Diel Variations in Acoustic Behavior.” The article appears in the current issue of PLOS ONE, an inclusive, peer-reviewed, open-access resource from the Public Library of Science in San Francisco.Susan Parks, assistant professor of biology for whom the lab is named, says the article confirms what many conservationists fear — that Roseway Basin, a heavily traveled shipping lane, off the coast of Nova Scotia, is a vital habitat area for the endangered North Atlantic right whale.”Remote acoustic monitoring is an important tool for understanding patterns in animal communication, and studies on the seasonality of context-specific acoustic signals allow inferences to be made about the behavior and habitat use of certain species,” says Parks, an expert in behavioral ecology, acoustic communication and marine science. “Our results support the hypothesis that the North Atlantic right whale’s breeding season occurs mostly from August to November and that this basin is a widely used habitat area.”More than 30 percent of all right whales use Roseway Basin, part of a larger geological formation called the Scotian Shelf, throughout the year. With only 400-500 in existence, these whales, says Parks, must congregate in the basin to feed and find mates.Already, the U.S. and Canadian governments have taken steps to redirect shipping traffic, in response to several fatal collisions with right whales.Matthews, whose research includes animal behavior and physiology, says the object of the article is to determine how and when Roseway Basin is used for male breeding activities.”Part of the answer lies in a loud ‘gunshot’ sound, made by the male whale,” says Matthews, the article’s lead author. “We’re not exactly sure what the gunshot is, but we think it may be a male-to-male antagonistic signal or an advertisement to females. … During a two-year period, we used non-invasive acoustic monitoring to analyze gunshots at two locations on the Scotian Shelf. The resultant data has provided tremendous insights into the whales’ feeding and mating habits.”Matthews and her team found that gunshot sound production occurred mainly in the autumn and, more often than not, at night. Researchers say this kind of information is essential to not only the individual fitness of each whale, but also the survival of the species, in general.McCordic, whose research spans animal behavior and communication, says the observed seasonal increase in gunshot sound production is consistent with the current understanding of the right whale breeding season.”Our results demonstrate that detection of gunshots with remote acoustic monitoring can be a reliable way to track shifts in distribution and changes in acoustic behavior, including possible mating activities,” she says, acknowledging David Mellinger, associate professor of marine bioacoustics at Oregon State University, who collected and provided access to the recordings used in the study. “It also provides a better understanding of right whale behavior and what needs to be done with future conservation efforts.”Parks, who assisted with the article, is proud of her students’ accomplishments.”Right whales are increasingly rare, and Leanna’s and Jessica’s research helps us understand how to better protect them,” she says. “By identifying potential breeding areas, we might be able to save this critically endangered species.”Story Source:The above story is based on materials provided by Syracuse University. …

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It slices, it dices, and it protects the body from harm: 3-D structure of enzyme that helps defend against bacteria

An essential weapon in the body’s fight against infection has come into sharper view. Researchers at Princeton University have discovered the 3D structure of an enzyme that cuts to ribbons the genetic material of viruses and helps defend against bacteria.The discovery of the structure of this enzyme, a first-responder in the body’s “innate immune system,” could enable new strategies for fighting infectious agents and possibly prostate cancer and obesity. The work was published Feb. 27 in the journal Science.Until now, the research community has lacked a structural model of the human form of this enzyme, known as RNase L, said Alexei Korennykh, an assistant professor of molecular biology and leader of the team that made the discovery.”Now that we have the human RNase L structure, we can begin to understand the effects of carcinogenic mutations in the RNase L gene. For example, families with hereditary prostate cancers often carry genetic mutations in the region, or locus, encoding RNase L,” Korennykh said. The connection is so strong that the RNase L locus also goes by the name “hereditary prostate cancer 1.” The newly found structure reveals the positions of these mutations and explains why some of these mutations could be detrimental, perhaps leading to cancer, Korennykh said. RNase L is also essential for insulin function and has been implicated in obesity.The Princeton team’s work has also led to new insights on the enzyme’s function.The enzyme is an important player in the innate immune system, a rapid and broad response to invaders that includes the production of a molecule called interferon. Interferon relays distress signals from infected cells to neighboring healthy cells, thereby activating RNase L to turn on its ability to slice through RNA, a type of genetic material that is similar to DNA. The result is new cells armed for destruction of the foreign RNA.The 3D structure uncovered by Korennykh and his team consists of two nearly identical subunits called protomers. The researchers found that one protomer finds and attaches to the RNA, while the other protomer snips it.The initial protomer latches onto one of the four “letters” that make up the RNA code, in particular, the “U,” which stands for a component of RNA called uridine. …

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Huntington’s disease: Hot on the trail of misfolded proteins’ toxic modus operandi

Proteins are the workhorses of the cell, and their correctly folded three-dimensional structures are critical to cellular functions. Misfolded structures often fail to properly perform these vital jobs, leading to cellular stress and devastating neurodegenerative disorders such as Alzheimer’s, Parkinson’s and Huntington’s disease.In comparison with the mysteries of Alzheimer’s or Parkinson’s disease, Huntington’s disease has a seemingly simple culprit: an expansion in the polyglutamine (polyQ) tract of a protein called “Huntingtin” (Htt). This polyQ expansion causes the Htt protein to misfold, which triggers a cascade of events — including aggregation of the Htt protein into very stable, fibrillar, amyloid species, and ultimately, neuronal cell death.”Despite the simplicity of the misfolding involved, we understand very little about why Htt — an essential protein expressed ubiquitously in all human tissue — becomes so toxic when misfolded,” said Koning Shen, a grad student working in the Frydman Lab at Stanford University.Shen will describe her team’s multipronged efforts to gain a better understanding of the relationship between protein misfolding, aggregation and cell toxicity at the 58th Annual Biophysical Society Meeting, which takes place Feb. 15-19, 2014, in San Francisco, Calif.The cause of neuronal toxicity in Huntington’s disease remains unknown. Until recently, general consensus had associated fibrillar aggregates with pathogenesis in Huntington’s disease. Newer studies, however, point to transient, intermediate species called “oligomers,” which occur during the aggregation process, as the key players in neurotoxicity, rather than the fibrillar aggregates.”Identifying the toxic perpetrators will help explain the pathogenesis of not only Huntington’s disease, but perhaps Alzheimer’s and Parkinson’s as well,” explained Shen.Shen and colleagues also hope to discover which molecular factors may contribute to or ameliorate Htt toxicity. An extended polyQ region is the molecular signature of Htt aggregation, but regions flanking the polyQ tract can also alter the aggregation pathway.”A molecular chaperone called ‘TRiC’ can suppress Huntington’s disease pathogenesis by binding to one of the polyQ-flanking regions. These flanking regions act as a tool to probe the Htt aggregation pathway to learn how Htt forms toxic aggregate species and how the cell has developed tools to stop it,” Shen said. “Altering the regions flanking the polyQ tract could remarkably impact both the aggregation and toxicity of the Huntingtin protein.”Deletions or mutations within these regions may either exacerbate or alleviate aggregation — despite having the same polyQ length. And, Shen pointed out, “fibrillar aggregation and toxicity don’t go hand-in-hand amongst these flanking mutants. …

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Cochlear implant with no exterior hardware can be wirelessly recharged

Cochlear implants — medical devices that electrically stimulate the auditory nerve — have granted at least limited hearing to hundreds of thousands of people worldwide who otherwise would be totally deaf. Existing versions of the device, however, require that a disk-shaped transmitter about an inch in diameter be affixed to the skull, with a wire snaking down to a joint microphone and power source that looks like an oversized hearing aid around the patient’s ear.Researchers at MIT’s Microsystems Technology Laboratory (MTL), together with physicians from Harvard Medical School and the Massachusetts Eye and Ear Infirmary (MEEI), have developed a new, low-power signal-processing chip that could lead to a cochlear implant that requires no external hardware. The implant would be wirelessly recharged and would run for about eight hours on each charge.The researchers describe their chip in a paper they’re presenting this week at the International Solid-State Circuits Conference. The paper’s lead author — Marcus Yip, who completed his PhD at MIT last fall — and his colleagues Rui Jin and Nathan Ickes, both in MIT’s Department of Electrical Engineering and Computer Science, will also exhibit a prototype charger that plugs into an ordinary cell phone and can recharge the signal-processing chip in roughly two minutes.”The idea with this design is that you could use a phone, with an adaptor, to charge the cochlear implant, so you don’t have to be plugged in,” says Anantha Chandrakasan, the Joseph F. and Nancy P. Keithley Professor of Electrical Engineering and corresponding author on the new paper. “Or you could imagine a smart pillow, so you charge overnight, and the next day, it just functions.”Adaptive reuseExisting cochlear implants use an external microphone to gather sound, but the new implant would instead use the natural microphone of the middle ear, which is almost always intact in cochlear-implant patients.The researchers’ design exploits the mechanism of a different type of medical device, known as a middle-ear implant. Delicate bones in the middle ear, known as ossicles, convey the vibrations of the eardrum to the cochlea, the small, spiral chamber in the inner ear that converts acoustic signals to electrical. In patients with middle-ear implants, the cochlea is functional, but one of the ossicles — the stapes — doesn’t vibrate with enough force to stimulate the auditory nerve. A middle-ear implant consists of a tiny sensor that detects the ossicles’ vibrations and an actuator that helps drive the stapes accordingly.The new device would use the same type of sensor, but the signal it generates would travel to a microchip implanted in the ear, which would convert it to an electrical signal and pass it on to an electrode in the cochlea. …

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Screening mammography every two years for most women recommended

Adoption of new guidelines recommending screening mammography every two years for women ages 50 to 74 would result in breast cancer screening that is equally effective, while saving the United States $4.3 billion a year in health care costs, according to a study led by UC San Francisco.The study compares three possible mammography screening strategies with a model of current U.S. screening practices.The article appears on February 4, 2014 in Annals of Internal Medicine.The authors call for the adoption of guidelines developed in 2009 by the U.S. Preventive Services Task Force (USPSTF). Under those guidelines, in addition to biennial screening for women age 50 to 74, women age 40 to 49 would be screened according to other risk factors, and women 75 and older would be screened depending on the presence or absence of other diseases.The study was led by Laura J. Esserman, MD, MBA, professor of surgery and radiology at UCSF and an internationally known leader in the field of breast cancer.”The USPSTF guidelines are based on the best scientific evidence to date,” said Esserman, director of the Carol Franc Buck Breast Care Center at the UCSF Helen Diller Family Comprehensive Cancer Care Center. “What we need now is a better way to assess breast cancer risk and implement a more risk-based approach to screening. We have demonstrated that the resources for doing this are already in the system. We should redirect them to learning, enabling change, and improving outcomes.”According to the authors’ estimate, approximately 70 percent of women in the U.S. were screened for breast cancer in 2010, at a cost of $7.8 billion. Some women are screened annually, some biennially, and some are screened on an irregular basis.The scientists compared this current picture of breast cancer screening with three simulated models: annual screening of 85 percent of women age 40 to 84, in accordance with recommendations from the American Cancer Society and many other policymaking organizations, at an annual estimated cost of $10.1 billion; biennial screening of 85 percent of women age 50 to 70, in line with guidelines used in many European countries, at an annual estimated cost of $2.6 billion; and screening in accordance with USPSTF recommendations, which the authors estimate would cost $3.5 billion per year at a screening rate of 85 percent.”Over the last decade, in study after study, it has become very clear that — apart from limited, specific high risk groups — biennial screening is as effective as annual screening mammography,” said Esserman. …

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Revealing how the brain recognizes speech sounds

UC San Francisco researchers are reporting a detailed account of how speech sounds are identified by the human brain, offering an unprecedented insight into the basis of human language. The finding, they said, may add to our understanding of language disorders, including dyslexia.Scientists have known for some time the location in the brain where speech sounds are interpreted, but little has been discovered about how this process works.Now, in Science Express (January 30th, 2014), the fast-tracked online version of the journal Science, the UCSF team reports that the brain does not respond to the individual sound segments known as phonemes — such as the b sound in “boy” — but is instead exquisitely tuned to detect simpler elements, which are known to linguists as “features.”This organization may give listeners an important advantage in interpreting speech, the researchers said, since the articulation of phonemes varies considerably across speakers, and even in individual speakers over time.The work may add to our understanding of reading disorders, in which printed words are imperfectly mapped onto speech sounds. But because speech and language are a defining human behavior, the findings are significant in their own right, said UCSF neurosurgeon and neuroscientist Edward F. Chang, MD, senior author of the new study.”This is a very intriguing glimpse into speech processing,” said Chang, associate professor of neurological surgery and physiology. “The brain regions where speech is processed in the brain had been identified, but no one has really known how that processing happens.”Although we usually find it effortless to understand other people when they speak, parsing the speech stream is an impressive perceptual feat. Speech is a highly complex and variable acoustic signal, and our ability to instantaneously break that signal down into individual phonemes and then build those segments back up into words, sentences and meaning is a remarkable capability.Because of this complexity, previous studies have analyzed brain responses to just a few natural or synthesized speech sounds, but the new research employed spoken natural sentences containing the complete inventory of phonemes in the English language.To capture the very rapid brain changes involved in processing speech, the UCSF scientists gathered their data from neural recording devices that were placed directly on the surface of the brains of six patients as part of their epilepsy surgery.The patients listened to a collection of 500 unique English sentences spoken by 400 different people while the researchers recorded from a brain area called the superior temporal gyrus (STG; also known as Wernicke’s area), which previous research has shown to be involved in speech perception. The utterances contained multiple instances of every English speech sound.Many researchers have presumed that brain cells in the STG would respond to phonemes. But the researchers found instead that regions of the STG are tuned to respond to even more elemental acoustic features that reference the particular way that speech sounds are generated from the vocal tract. “These regions are spread out over the STG,” said first author Nima Mesgarani, PhD, now an assistant professor of electrical engineering at Columbia University, who did the research as a postdoctoral fellow in Chang’s laboratory. “As a result, when we hear someone talk, different areas in the brain ‘light up’ as we hear the stream of different speech elements.””Features,” as linguists use the term, are distinctive acoustic signatures created when speakers move the lips, tongue or vocal cords. …

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Making sense of conflicting advice on calcium intake

Oct. 17, 2013 — In recent years, studies have reported inconsistent findings regarding whether calcium supplements used to prevent fractures increase the risk of heart attack.Now, in an assessment of the scientific literature, reported as a perspective piece in the October 17, 2013 issue of the New England Journal of Medicine, a UC San Francisco researcher says patients and health care practitioners should focus on getting calcium from the diet, rather than supplements, when possible.”Osteoporosis may result from inadequate calcium intake and it’s quite common for certain segments of our population, such as the elderly, to consume less than the recommend amount,” said Douglas C. Bauer, MD, UCSF professor of Medicine, Epidemiology and Biostatistics. “But a high calcium diet should be the preferred method to receive adequate amounts of the nutrient. The Institute of Medicine’s recommended dosage for post-menopausal women over the age of 50 and men over 70 is 1,200 mg per day.”If it is not possible to consume enough calcium from the diet, the use of calcium supplements is most likely safe and not associated with cardiovascular outcomes,” he said.Calcium supplements are known to have several side effects, the most common being indigestion and minor constipation, and kidney stones are a rare complication. However, several recent studies have suggested that calcium supplements can also lead to an increase risk of heart attacks.A 2010 British Medical Journal study, which pooled nearly a dozen randomized trials, concluded that calcium supplements “are associated with an increased risk of myocardial infarction [heart attacks]” and went on to say, ” As calcium supplements are widely used, these modest increases in risk of cardiovascular disease might translate into a large burden of disease in the population.”A 2013 JAMA Internal Medicine non-randomized study examined 11,778 cardiovascular-related deaths and found an increased risk with calcium supplement use. The authors concluded, “high intake of supplemental calcium is associated with an excess risk of CVD (cardiovascular disease) death in men but not in women.”However, several other studies have shown no relationship between the use of calcium supplements and cardiovascular events.For example, a 2010 meta-analysis that included all of the Women’s Health Initiative (WHI) trial participants showed “no significant relationship between supplementation and cardiovascular events” in three trials of calcium supplements alone.Bauer recommends consuming dairy products to increase one’s dietary intake of calcium as well as food products that are fortified with extra calcium, such as kale, broccoli and Bok Choy.

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Cell growth discovery has implications for targeting cancer

Oct. 11, 2013 — The way cells divide to form new cells — to support growth, to repair damaged tissues, or simply to maintain our healthy adult functioning — is controlled in previously unsuspected ways UC San Francisco researchers have discovered. The findings, they said, may lead to new ways to fight cancer.The steps leading a quiet cell to make and divvy up new parts to form daughter cells rely on some of the cell’s most complex molecular machines. Different machines play key roles at different stages of this cell cycle. Each of these cellular machines consists of many proteins assembled into a functioning whole. They carry out such tasks as repairing DNA in the newly replicated gene-bearing chromosomes, for instance, or helping pull the chromosomes apart so that they can be allocated to daughter cells.In a study published online on October 10, 2013 in the journal Molecular Cell, UCSF researchers led by molecular biologist Davide Ruggero, PhD, associate professor of urology, and computational biologist Barry Taylor, PhD, assistant professor of epidemiology and biostatistics, found that the production of entire sets of proteins that work together to perform such crucial tasks is ramped up together, all at once — not due to the transcription of genes into messenger RNA, a phenomenon scientists often study to sort out cellular controls — but at a later stage of gene expression that occurs within the cell’s protein-making factories, called ribosomes.”We have found that these proteins are regulated specifically and exquisitely during the cell cycle,” Ruggero said. When this regulation falters, it wreaks havoc in the cell, he added. “Cell-cycle control is a process that is most often misregulated in human disease,” he said.More specifically, the researchers found that this coordinated timing of protein production during the cell cycle is largely governed at the tail end of gene expression, within the ribosome, where cellular machinery acts on messenger RNA to churn out the chains of amino acids that eventually fold into functional form as proteins.In 2010 Ruggero reported key evidence suggesting that this stage of protein production, called “translation,” might be an often-neglected process in many tumors, ranging from lymphomas, multiple myeloma and prostate cancer.In the new study, the researchers examined translation of messenger RNA into protein at the classic phases of the cell cycle, before the cell actually divides. These are the G1 phase, when cells grow and make lots of proteins before replicating their DNA; the S phase, when cells replicate their DNA; and the G2 phase, when cells make internal components known as organelles, which they divvy up along with the chromosomes when the cell actually divides during mitosis.The scientists used a technique know as ribosome profiling, originally developed for yeast cells in the lab of Jonathan Weismann, PhD, Howard Hughes Investigator at UCSF and professor of cellular and molecular pharmacology, to figure out which messenger RNA was being translated into protein by the ribosome during human cell division. They then used computational techniques developed by Taylor’s lab team along with the lab team of Adam Olshen, PhD, professor of epidemiology and biostatistics, to better quantify which genes had been translated into proteins.By conducting a genome-wide investigation of translation and interrogating the data with sophisticated computer algorithms, the researchers discovered that different groups of protein were made in abundance at a particular phase, only to be quieted during another phase of the cell cycle. …

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Severity of sleep apnoea predicts aggressiveness of melanoma

Sep. 9, 2013 — The severity of sleep apnoea can independently predict the aggressiveness of malignant skin melanoma, according to a new study.The research, presented today at the European Respiratory Society (ERS) Annual Congress, adds new evidence to a number of studies that have found a link between cancer and the sleep disorder.Previous studies have looked at a link between sleep apnoea and both mortality and incidence rates from cancer. Some experimental studies in mice have also shown that reduced oxygen levels in the blood, which is common in sleep apnoea, enhanced tumour growth. This is the first study in humans to look at the link between a specific type of cancer (skin melanoma) and sleep apnoea.Researchers studied 56 patients diagnosed with malignant skin melanomas. They measured the aggressiveness of the cancer along with the presence and severity of sleep apnoea.60.7% of the patients had sleep apnoea and 14.3% had severe sleep apnoea. The results found that the melanoma was more aggressive as the severity of sleep apnoea increased. This was the case for all three measurements for sleep apnoea severity. The severity measurements were also linked with other factors of aggressiveness, including the growth rate or the depth of invasion of the tumour.Lead author, Dr Francisco Campos-Rodriguez, from the Hospital de Valme in Seville, Spain, said: “This is the first study in a human sample to show that sleep apnoea can worsen the outcomes of melanoma. The findings are from a preliminary small sample, but if the results are confirmed in larger studies, this would have important clinical implications, particularly as sleep apnoea can be easily treated and this could open up new therapeutic possibilities for people with both conditions. We have just begun a bigger prospective trial enrolling 450 patients with cutaneous melanoma to analyse this link further.”

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Toward an early diagnostic tool for Alzheimer’s disease

Aug. 29, 2013 — Despite all the research done on Alzheimer’s, there is still no early diagnostic tool for the disease. By looking at the brain wave components of individuals with the disease, Professor Tiago H. Falk of INRS’s Centre Énergie Matériaux Télécommunications has identified a promising avenue of research that may not only help diagnose the disease, but also assess its severity.Share This:This non-invasive, objective method is the subject of an article in the journal PLOS ONE.Patients with Alzheimer’s disease currently undergo neuropsychological testing to detect signs of the disease. The test results are difficult to interpret and are insufficient for making a definitive diagnosis. But as scientists have already discovered, activity in certain areas of the cerebral cortex is affected even in the early stages of the disease. Professor Falk, who specialises in biological signal acquisition, examined this phenomenon and compared the electroencephalograms (EEGs) of healthy individuals (27), individuals with mild Alzheimer’s (27), and individuals with moderate cases of the disease (22). He found statistically significant differences across the three groups.In collaboration with neurologists and Francisco J. Fraga, an INRS visiting professor specializing in biological signals, Professor Falk used an algorithm that dissects brain waves of varying frequencies. “What makes this algorithm innovative is that it characterizes the changes in temporal dynamics of the patients’ brain waves,” explains Professor Falk. …

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Thyroid cancer biopsy guidelines should be simplified, researchers say

Aug. 26, 2013 — A team led by UC San Francisco researchers has called for simplified guidelines on when to biopsy thyroid nodules for cancer, which they say would result in fewer unnecessary biopsies.Their recommendation, based on a retrospective study published online on August 26, 2013 in JAMA Internal Medicine, is to biopsy patients only when imaging reveals a thyroid nodule with microcalcifications — tiny flecks of calcium — or one that is over two centimeters in diameter and completely solid. Any other findings represent too low a risk to require biopsy or continued surveillance for cancer, the scientists concluded.More than 98 percent of detected nodules in the study were benign, not malignant cancers.”Compared with other existing guidelines, many of which are complicated to apply, following these simple, evidence-based guidelines would substantially decrease the number of unnecessary thyroid biopsies in the United States,” said lead author Rebecca Smith-Bindman, MD, a UCSF School of Medicine professor with the Department of Radiology and Biomedical Imaging and the Department of Epidemiology and Biostatistics. “Right now, we’re doing far too many thyroid biopsies in patients who are really at very low risk of having thyroid cancer,” she said.The research team analyzed the medical records of 8,806 patients who underwent 11,618 thyroid ultrasound examinations at a UCSF inpatient or outpatient facility from January 2000 through March 2005. The patients did not have a diagnosis of thyroid cancer at the time of the ultrasound, but were referred to ultrasound for a variety of reasons, such as a physician’s suspicion that a patient had a nodule, an abnormal thyroid function test or a CT or MRI examination that revealed the presence of at least one nodule.The researchers linked the patients with the California Cancer Registry and identified 105 who were diagnosed with thyroid cancer. The cancer patients were matched with a group of cancer-free control subjects from the same cohort, based on factors such as gender, age and the year of the ultrasound exam.Six of the paper’s eight authors then reviewed those patients’ ultrasound images without knowing whether the image came from a cancer patient or a control, and characterized what the thyroid looked like based on 11 characteristics, including the presence and appearance of nodules, blood flow and calcifications.The authors found that while 97 percent of the cancer patients had at least one nodule, 56 percent of patients without cancer had nodules as well. “Thus, it turns out that most patients have thyroid nodules,” said Smith-Bindman.Ultimately, the researchers identified only three significant ultrasound imaging findings that indicated an increased chance of thyroid cancer: microcalcification, a nodule diameter greater than two centimeters, and a nodule that was solid rather than cyst-like.”If there’s a large solid nodule, or if there are any nodules with microcalcification, the likelihood of cancer increases by fivefold or tenfold, depending on the finding, and I would do a biopsy,” said Smith-Bindman. “If you have all three characteristics together, it’s almost certainly cancer. On the other hand, without these characteristics, you are at very low risk — less than one half of one percent — and a biopsy is not necessary. Nor is continued surveillance.”The time has come, she said, to “start doing diagnostic tests and procedures more selectively and prudently, as there are harms to doing unnecessary tests and procedures.” In medicine, she explained, “We tend to focus on the individual patient who is front of us. …

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Cocaine use linked to new brain structures: Possible mechanism for drug-seeking behavior in humans identified

Aug. 25, 2013 — Mice given cocaine showed rapid growth in new brain structures associated with learning and memory, according to a research team from the Ernest Gallo Clinic and Research Center at UC San Francisco. The findings suggest a way in which drug use may lead to drug-seeking behavior that fosters continued drug use, according to the scientists.The researchers used a microscope that allowed them to peer directly into nerve cells within the brains of living mice, and within two hours of giving a drug they found significant increases in the density of dendritic spines — structures that bear synapses required for signaling — in the animals’ frontal cortex. In contrast, mice given saline solution showed no such increase.The researchers also found a relationship between the growth of new dendritic spines and drug-associated learning. Specifically, mice that grew the most new spines were those that developed the strongest preference for being in the enclosure where they received cocaine rather than in the enclosure where they received saline. The team published its findings online in Nature Neuroscience on August 25, 2013.”This gives us a possible mechanism for how drug use fuels further drug-seeking behavior,” said principal investigator Linda Wilbrecht, PhD, a Gallo investigator now at UC Berkeley, but who led the research while she was on the UCSF faculty.”It’s been observed that long-term drug users show decreased function in the frontal cortex in connection with mundane cues or tasks, and increased function in response to drug-related activity or information,” Wilbrecht said. “This research suggests how the brains of drug users might shift toward those drug-related associations.”In all living brains there is a baseline level of creation of new spines in response to, or in anticipation of, day-to-day learning, Wilbrecht said. By enhancing this growth, cocaine might be a super-learning stimulus that reinforces learning about the cocaine experience, she said.The frontal cortex, which Wilbrecht called the “steering wheel” of the brain, controls functions such as long-term planning, decision-making and other behaviors involving higher reasoning and discipline.The brain cells in the frontal cortex that Wilbrecht and her team studied regulate the output of this brain region, and may play a key role in decision-making. “These neurons, which are directly affected by cocaine use, have the potential to bias decision-making,” she said.Wilbrecht said the findings could potentially advance research in human addiction “by helping us identify what is going awry in the frontal cortexes of drug-addicted humans, and by explaining how drug-related cues come to dominate the brain’s decision-making processes.”In the first of a series of experiments, the scientists gave cocaine injections to one group of mice and saline injections to another. The next day, they observed the animals’ brain cells using a 2-photon laser scanning microscope. …

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Mending a broken heart? Non-beating human cells transformed into heart-muscle cells

Aug. 22, 2013 — In the aftermath of a heart attack, cells within the region most affected shut down. They stop beating. And they become entombed in scar tissue. But now, scientists at the Gladstone Institutes have demonstrated that this damage need not be permanent — by finding a way to transform the class of cells that form human scar tissue into those that closely resemble beating heart cells.Last year, these scientists transformed scar-forming heart cells, part of a class of cells known as fibroblasts, into beating heart-muscle cells in live mice. And in the latest issue of Stem Cell Reports, researchers in the laboratory of Gladstone Cardiovascular and Stem Cell Research Director Deepak Srivastava, MD, reveal that they have done the same to human cells in a petri dish.”Fibroblasts make up about 50% of all cells in the heart and therefore represent a vast pool of cells that could one day be harnessed and reprogrammed to create new muscle,” said Dr. Srivastava, who is also a professor at the University of California, San Francisco, with which Gladstone is affiliated. “Our findings here serve as a proof of concept that human fibroblasts can be reprogrammed successfully into beating heart cells.”In 2012, Dr. Srivastava and his team reported in the journal Nature that fibroblasts could be reprogrammed into beating heart cells by injecting just three genes, together known as GMT, into the hearts of live mice that had been damaged by a heart attack. They reasoned that the same three genes could have the same effect on human cells. …

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Psychiatric patients given smoking-cessation treatment less likely to be rehospitalized

Aug. 15, 2013 — Patients who participated in a smoking-cessation program during hospitalization for mental illness were able to quit smoking and were less likely to be hospitalized again for their psychiatric conditions, according to a new study led by a Stanford University School of Medicine scientist.The findings counter a longstanding assumption, held by many mental-health experts, that smoking serves as a useful tool in treating some psychiatric patients.Smoking among such patients has been embedded in the culture for decades, with cigarettes used as part of a reward system. Indeed, clinicians sometimes smoke alongside patients as a way of creating a rapport with them, said Judith Prochaska, PhD, MPH, associate professor of medicine at the Stanford Prevention Research Center and lead author of the study.The result is that psychiatric patients are among the country’s most prolific smokers and among those most likely to die of smoking-related ailments, Prochaska said. Nearly half of the cigarettes sold in the United States are to people with psychiatric or addictive disorders, according to data from the U.S. Centers for Disease Control and Prevention. The average life expectancy for people with severe mental illness is 25 years less than that of the general population, and their leading cause of death is chronic illness, mostly tobacco-related.Prochaska said it has long been thought that if these patients quit smoking, it would be detrimental to their recovery — that they would lose a critical crutch for coping with stress. However, she pointed out that the daily cycle of nicotine withdrawal a smoker experiences creates a great deal of stress, and that mental-health providers are well-equipped to assist patients with developing healthier forms of coping.The new study showed that a simple intervention that included periodic contact with a counselor, written and computerized materials, and the use of nicotine patches could support, rather than harm, the patients’ mental health, she said.”This is a very low-cost, brief intervention that helped patients quit smoking and offers evidence that it may have helped their mental health recovery,” said Prochaska, who focuses on developing interventions to treat tobacco dependence in people with mental illness or addictive disorders.She said the study, done in collaboration with researchers at UC-San Francisco, is the first to examine the impact of a stop-smoking intervention in adult psychiatric patients. It will be published online Aug. 15 in the American Journal of Public Health.Michael Fiore, MD, MPH, director of the University of Wisconsin Center for Tobacco Research and Intervention and a leader in national policy for tobacco treatment who was not involved in the study, said the paper “provides powerful evidence that evidence-based tobacco dependence treatments can substantially increase quit rates among psychiatric inpatients. We know that psychiatric patients smoke at very high rates and are at tremendous risk from their smoking. …

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A new wrinkle in Parkinson’s disease research: Skin cream ingredient may stop effects of Parkinson’s on brain cells

Aug. 15, 2013 — The active ingredient in an over-the-counter skin cream might do more than prevent wrinkles. Scientists have discovered that the drug, called kinetin, also slows or stops the effects of Parkinson’s disease on brain cells.Scientists identified the link through biochemical and cellular studies, but the research team is now testing the drug in animal models of Parkinson’s. The research is published in the August 15, 2013 issue of the journal Cell.”Kinetin is a great molecule to pursue because it’s already sold in drugstores as a topical anti-wrinkle cream,” says HHMI investigator Kevan Shokat of the University of California, San Francisco. “So it’s a drug we know has been in people and is safe.”Parkinson’s disease is a degenerative disease that causes the death of neurons in the brain. Initially, the disease affects one’s movement and causes tremors, difficulty walking, and slurred speech. Later stages of the disease can cause dementia and broader health problems. In 2004, researchers studying an Italian family with a high prevalence of early-onset Parkinson’s disease discovered mutations in a protein called PINK1 associated with the inherited form of the disease.Since then, studies have shown that PINK1 normally wedges into the membrane of damaged mitochondria inside cells that causes another protein, Parkin, to be recruited to the mitochondria, which are organelles responsible for energy generation. Neurons require high levels of energy production, therefore when mitochondrial damage occurs, it can lead to neuronal death. However, when Parkin is present on damaged mitochondria, studding the mitochondrial surface, the cell is able to survive the damage. …

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Largest study of epilepsy patients ever conducted reveals new and surprising genetic risk factors

Aug. 12, 2013 — Neurologists and epilepsy researchers from NYU Langone Medical Center were among scientists who have 329 random genetic mutations associated with two of the most severe forms of epilepsy, according to a paper published today in Nature. Though well-known that many forms of epilepsy are strongly influenced by genetics, there has been relatively little progress in identifying the genetic differences that contribute to most forms of epilepsy. This study sheds light on why some with an elevated risk for epilepsy never get the disease and why certain medications work better for some patients than others.”For generations we have been treating most forms of generalized epilepsies with no idea what causes the disease. Now, for the first time, we have identified clear genetic risk factors in patients with severe epilepsy,” says study co-author Ruben Kuzniecky, MD, professor of neurology at NYU Langone Medical Center, where he serves as co-director of the NYU Comprehensive Epilepsy Center and director of epilepsy research.The findings are the first to emerge from the largest investigation into the genetics of epilepsy ever conducted. The study, known as the “Epilepsy Phenome/Genome Project” (EPGP) and representing a consortium of 27 medical centers from around the world, is led by Dr. Kuzniecky and Daniel Lowenstein, MD, professor and vice chair of the Department of Neurology at the University of California, San Francisco (UCSF), and director of the UCSF Epilepsy Center. Since 2007, when the project began, its team of several hundred physicians and staff has collected blood samples and clinical information from more than 4,000 patients with epilepsy and their family members. NYU Langone contributed data for 430 patients, representing the largest enroller in the study. The researchers expect the project’s unprecedented dataset to yield results for several years to come.”This project is one of the most ambitious undertakings in our field,” Dr. …

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Newly identified genetic factors drive severe childhood epilepsies

Aug. 11, 2013 — Researchers have identified two new genes and implicated 25 distinct mutations in serious forms of epilepsy, suggesting a new direction for developing tailored treatments of the neurological disorders.The findings by an international research collaboration, which includes investigators from Duke Medicine, appear Aug. 11 in the journal Nature.Epileptic encephalopathies are a devastating group of severe brain disorders characterized by the onset of seizures at an early age. The seizures are often accompanied by cognitive and behavioral issues, which can hinder the quality of life of affected children and their families.The cause of epileptic encephalopathies is largely unknown; while genes are believed to play an important role, specific genes have only been identified in a small number of cases.”One important aspect of the study is that we identified an unusually large number of distinct disease-causing mutations — 25 in total, all of which were de novo mutations. These mutations will be an invaluable resource to scientists working to elucidate the underlying causes of the epilepsies,” said study author David Goldstein, PhD, director of the Duke Center for Human Genome Variation.A de novo mutation is a new alteration in a gene that appears for the first time in a family, and results from a genetic mutation in a parent’s germ cell (egg or sperm).Learning more about the disorders’ origin will guide development of effective therapies, which is the goal of Epi4K, an international research consortium funded by the National Institute of Neurological Diseases and Stroke (NINDS).”This research focusing on epileptic encephalopathies is the first large-scale project of Epi4K,” said study author Erin Heinzen, PhD, assistant professor of medicine in the Division of Medical Genetics at Duke. “The study was designed to identify de novo mutations and search for ones that contribute to risk.”The Epi4K researchers partnered with the Epilepsy Phenome/Genome Project, another NINDS-funded group working to unlock the mysteries of epilepsy. Led by Daniel Lowenstein, M.D., professor of neurology at the University of California, San Francisco, the researchers in the Epilepsy Phenome/Genome Project gathered genetic information on 264 children with epileptic encephalopathies and their parents.The Epi4K researchers then focused on identifying all new mutations in the children using next-generation sequenced data, which looks at the part of genome that encodes protein. The Center for Human Genome Variation at Duke conducted this analysis, and confirmed 329 de novo mutations. Most of these mutations had no connection to the risk of disease, but the researchers showed that a fraction of them strongly influence risk.The researchers saw that the genes already known to cause epileptic encephalopathies carried multiple de novo mutations. However, they found multiple de novo mutations in two additional genes- GABRB3 and ALG13 — not previously connected to epileptic encephalopathies. …

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