Microscopic organism plays a big role in ocean carbon cycling

It’s broadly understood that the world’s oceans play a crucial role in the global-scale cycling and exchange of carbon between Earth’s ecosystems and atmosphere. Now scientists at Scripps Institution of Oceanography at UC San Diego have taken a leap forward in understanding the microscopic underpinnings of these processes.When phytoplankton use carbon dioxide to make new cells, a substantial portion of that cellular material is released into the sea as a buffet of edible molecules collectively called “dissolved organic carbon.” The majority of these molecules are eventually eaten by microscopic marine bacteria, used for energy, and recycled back into carbon dioxide as the bacteria exhale. The amount of carbon that remains as cell material determines the role that ocean biology plays in locking up atmospheric carbon dioxide in the ocean.Thus, these “recycling” bacteria play an important role in regulating how much of the planet’s carbon dioxide is stored in the oceans. The detailed mechanisms of how the oceans contribute to this global carbon cycle at the microscopic scale, and which microbes have a leadership role in the breakdown process, are complex and convoluted problems to solve.In a study published in the Proceedings of the National Academy of Sciences, Scripps scientists have pinpointed a bacterium that appears to play a dominant role in carbon consumption. Scripps’s Byron Pedler, Lihini Aluwihare, and Farooq Azam found that a single bacterium called Alteromonas could consume as much dissolved organic carbon as a diverse community of organisms.”This was a surprising result,” said Pedler. “Because this pool of carbon is composed of an extremely diverse set of molecules, we believed that many different microbes with complementary abilities would be required to breakdown this material, but it appears that individual species may be pulling more weight than others when it comes to carbon cycling.”Pedler, a marine biology graduate student at Scripps, spent several years working with Scripps marine microbiologist Azam and chemical oceanographer Aluwihare in designing a system that would precisely measure carbon consumption by individual bacterial species. Because carbon in organic matter is essentially all around us, the most challenging part of conducting these experiments is avoiding contamination.”Much of the carbon cycling in the ocean happens unseen to the naked eye, and it involves a complex mix of processes involving microbes and molecules,” said Azam, a distinguished professor of marine microbiology. “The complexity and challenge is not just that we can’t see it but that there’s an enormous number of different molecules involved. The consequences of these microbial interactions are critically important for the global carbon cycle, and for us.”By demonstrating that key individual species within the ecosystem can play a disproportionally large role in carbon cycling, this study helps bring us a step closer to understanding the function these microbes play in larger questions of climate warming and increased acidity in the ocean.”In order to predict how ecosystems will react when you heat up the planet or acidify the ocean, we first need to understand the mechanisms of everyday carbon cycling — who’s involved and how are they doing it?” said Pedler. “Now that we have this model organism that we know contributes to ocean carbon cycling, and a model experimental system to study the process, we can probe further to understand the biochemical and genetic requirements for the breakdown of this carbon pool in the ocean.”While the new finding exposes the unexpected capability of a significant species in carbon cycling, the scientists say there is much more to the story since whole communities of microbes may interact together or live symbiotically in the microscopic ecosystems of the sea.Pedler, Aluwihare, and Azam are now developing experiments to test other microbes and their individual abilities to consume carbon.The study was supported by the Gordon and Betty Moore Foundation Marine Microbiology Initiative through grant GBMF2758 and the National Science Foundation.Story Source:The above story is based on materials provided by University of California – San Diego. …

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Computers see through faked expressions of pain better than people

A joint study by researchers at the University of California, San Diego and the University of Toronto has found that a computer system spots real or faked expressions of pain more accurately than people can.The work, titled “Automatic Decoding of Deceptive Pain Expressions,” is published in the latest issue of Current Biology.”The computer system managed to detect distinctive dynamic features of facial expressions that people missed,” said Marian Bartlett, research professor at UC San Diego’s Institute for Neural Computation and lead author of the study. “Human observers just aren’t very good at telling real from faked expressions of pain.”Senior author Kang Lee, professor at the Dr. Eric Jackman Institute of Child Study at the University of Toronto, said “humans can simulate facial expressions and fake emotions well enough to deceive most observers. The computer’s pattern-recognition abilities prove better at telling whether pain is real or faked.”The research team found that humans could not discriminate real from faked expressions of pain better than random chance — and, even after training, only improved accuracy to a modest 55 percent. The computer system attains an 85 percent accuracy.”In highly social species such as humans,” said Lee, “faces have evolved to convey rich information, including expressions of emotion and pain. And, because of the way our brains are built, people can simulate emotions they’re not actually experiencing — so successfully that they fool other people. The computer is much better at spotting the subtle differences between involuntary and voluntary facial movements.””By revealing the dynamics of facial action through machine vision systems,” said Bartlett, “our approach has the potential to elucidate ‘behavioral fingerprints’ of the neural-control systems involved in emotional signaling.”The single most predictive feature of falsified expressions, the study shows, is the mouth, and how and when it opens. Fakers’ mouths open with less variation and too regularly.”Further investigations,” said the researchers, “will explore whether over-regularity is a general feature of fake expressions.”In addition to detecting pain malingering, the computer-vision system might be used to detect other real-world deceptive actions in the realms of homeland security, psychopathology, job screening, medicine, and law, said Bartlett.”As with causes of pain, these scenarios also generate strong emotions, along with attempts to minimize, mask, and fake such emotions, which may involve ‘dual control’ of the face,” she said. “In addition, our computer-vision system can be applied to detect states in which the human face may provide important clues as to health, physiology, emotion, or thought, such as drivers’ expressions of sleepiness, students’ expressions of attention and comprehension of lectures, or responses to treatment of affective disorders.”Story Source:The above story is based on materials provided by University of California – San Diego. The original article was written by Paul K. …

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Costly cigarettes and smoke-free homes

Oct. 17, 2013 — Researchers at the University of California, San Diego School of Medicine say high-priced cigarettes and smoke-free homes effectively reduce smoking behaviors among low-income individuals — a demographic in which tobacco use has remained comparatively high.Writing in the October 17, 2013 issue of the American Journal of Public Health, principal investigator John P. Pierce, PhD, professor and director of population sciences at UC San Diego School of Medicine, and colleagues found that expensive cigarettes — $4.50 or more per pack — were associated with lower consumption across all levels.”Living in a state where the average price paid for cigarettes is low ($3.20 or less per pack) means that all smokers, regardless of income, will smoke a lot more than those who live in a state with higher prices,” said Pierce. “This is the case for those living below the federal poverty level as well as for the wealthy.”When smokers agreed to a smoke-free home, not only were they more likely to reduce their smoking but, in addition, if they quit, they were less likely to relapse.”Price is a deterrent to smoking,” said Pierce, “but successful quitting (90 or more days) was associated in this study only with a smoke-free home.”The challenge to anti-smoking groups is that low-income smokers are less likely to adopt a smoke-free home environment. Pierce offered several possible explanations: “First, there’s a higher prevalence of smoking in people with lower incomes, which means that there will be more spouses who smoke as well. When both adults smoke, there is much lower motivation to introduce a smoke-free home. Also, social norms against smoking have historically been lower in those with lower incomes.”No one is mandating a smoke-free home,” Pierce continued. “We are telling people that if they really want to quit, then introducing a smoke-free home will help them be successful. This study supports the current policy of increasing (cigarette) prices and building social norms that protect against secondhand smoke. These policies will reduce consumption among all smokers — reducing potential harm — and the ensuing smoke-free homes will help smokers quit successfully.”The findings are derived from the 2006-2007 Tobacco Use Supplement to the Current Population Survey, a monthly nationally representative cross-sectional survey conducted by the U.S. …

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Touch goes digital: Electronic recording and replay of human touch demonstrated

Sep. 6, 2013 — Researchers at the University of California, San Diego report a breakthrough in technology that could pave the way for digital systems to record, store, edit and replay information in a dimension that goes beyond what we can see or hear: touch.”Touch was largely bypassed by the digital revolution, except for touch-screen displays, because it seemed too difficult to replicate what analog haptic devices — or human touch — can produce,” said Deli Wang, a professor of Electrical and Computer Engineering (ECE) in UC San Diego’s Jacobs School of Engineering. “But think about it: being able to reproduce the sense of touch in connection with audio and visual information could create a new communications revolution.”In addition to uses in health and medicine, the communication of touch signals could have far-reaching implications for education, social networking, e-commerce, robotics, gaming, and military applications, among others. The sensors and sensor arrays reported in the paper are also fully transparent which makes it particularly interesting for touch-screen applications in mobile devices.Wang is the senior author on a paper appearing in Nature Publishing Group’s Scientific Reports, published online Aug. 28. Co-authors include 11 researchers at UC San Diego, including fellow ECE professor Truong Nguyen, and UCLA professor Qibing Pei, whose team contributed to the sections on using polymer actuators for analog reproduction of recorded touch.The first authors of this article, Siarhei Vishniakou and Brian Lewis of UCSD and co-authors Paul Brochu and Xiaofan Niu from UCLA, received the Qualcomm Innovation Fellowship (QInF) in 2012. (This project is partially supported by a Qualcomm Innovation Fellowship.)In addition to professors Wang and Nguyen, other researchers on the project affiliated with the Qualcomm Institute at UC San Diego include recent Ph.D., Ke Sun, and Namseok Park, recipients of the institute’s Calit2 Strategic Research Opportunities, or CSRO, Graduate Fellowships in 2010 and in 2012, respectively.”Our sense of touch plays a significant role in our daily lives, particularly in personal interaction, learning and child development, and that is especially true for the development of preemies,” said Nguyen, another senior author of this Scientific Reports paper. “We were approached by colleagues in the UC San Diego School of Medicine’s neonatology group to see if there was a way to record a session of a mother holding the baby, which could be replayed at a different time in an incubator.”In their Scientific Reports paper, the researchers reported the electronic recording of touch contact and pressure using an active-matrix pressure sensor array made of transparent zinc-oxide (ZnO), thin-film transistors (TFTs). The companion tactile feedback display used an array of diaphragm actuators made of an acrylic-based dielectric elastomer with the structure of an interpenetrating polymer network (IPN). The polymer actuators’ actuation — the force and level of displacement — are modulated by adjusting both the voltage and charging time.One of the critical challenges in developing touch systems is that the sensation is not one thing. …

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New and Emerging Biologics– ep. 25 of 32

Dr. Arthur Kavanaugh (University of California San Diego) describes the most recent data on IL-6 and IL-17 inhibition in rheumatoid arthritis.This episode is a part of the Rheumatology Highlights Report Webcast Series of 32 episodes.To claim CME credit visit http://www.ccfcme.org/rhr-33The video was produced by the

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Why don’t we all get Alzheimer’s disease?

Aug. 7, 2013 — Though one might think the brains of people who develop Alzheimer’s disease (AD) possess building blocks of the disease absent in healthy brains, for most sufferers, this is not true. Every human brain contains the ingredients necessary to spark AD, but while an estimated 5 million Americans have AD — a number projected to triple by 2050 — the vast majority of people do not and will not develop the devastating neurological condition.For researchers like Subhojit Roy, MD, PhD, associate professor in the Departments of Pathology and Neurosciences at the University of California, San Diego School of Medicine, these facts produce a singular question: Why don’t we all get Alzheimer’s disease?In a paper published in the August 7 issue of the journal Neuron, Roy and colleagues offer an explanation — a trick of nature that, in most people, maintains critical separation between a protein and an enzyme that, when combined, trigger the progressive cell degeneration and death characteristic of AD.”It’s like physically separating gunpowder and match so that the inevitable explosion is avoided,” said principal investigator Roy, a cell biologist and neuropathologist in the Shiley-Marcos Alzheimer’s Disease Research Center at UC San Diego. “Knowing how the gunpowder and match are separated may give us new insights into possibly stopping the disease.”The severity of AD is measured in the loss of functioning neurons. In pathological terms, there are two tell-tale signs of AD: clumps of a protein called beta-amyloid “plaques” that accumulate outside neurons and threads or “tangles” of another protein, called tau, found inside neurons. Most neuroscientists believe AD is caused by the accumulating assemblies of beta-amyloid protein triggering a sequence of events that leads to impaired cell function and death. This so-called “amyloid cascade hypothesis” puts beta-amyloid protein at the center of AD pathology.Creating beta-amyloid requires the convergence of a protein called amyloid precursor protein (APP) and an enzyme that cleaves APP into smaller toxic fragments called beta-secretase or BACE.”Both of these proteins are highly expressed in the brain,” said Roy, “and if they were allowed to combine continuously, we would all have AD.”But that doesn’t happen. Using cultured hippocampal neurons and tissue from human and mouse brains, Roy — along with first author Utpal Das, a postdoctoral fellow in Roy’s lab, and colleagues — discovered that healthy brain cells largely segregate APP and BACE-1 into distinct compartments as soon as they are manufactured, ensuring the two proteins do not have much contact with each other.”Nature seems to have come up with an interesting trick to separate co-conspirators,” said Roy.The scientists also found that the conditions promoting greater production of beta-amyloid protein boost the convergence of APP and BACE. Specifically, an increase in neuronal electrical activity — known to increase the production of beta-amyloid — also led to an increase in APP-BACE convergence. Post-mortem examinations of AD patients revealed increased physical proximity of the proteins as well, adding support to the pathophysiological significance of this phenomenon in human disease.Das said the findings are fundamentally important because they elucidate some of the earliest molecular events triggering AD and show how a healthy brain naturally avoids them. …

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Efficient model for generating human induced pluripotent stem cells

Aug. 1, 2013 — Researchers at the University of California, San Diego School of Medicine report a simple, easily reproducible RNA-based method of generating human induced pluripotent stem cells (iPSCs) in the August 1 edition of Cell Stem Cell. Their approach has broad applicability for the successful production of iPSCs for use in human stem cell studies and eventual cell therapies.Partially funded by grants from the California Institute for Regenerative Medicine (CIRM) and the National Institutes of Health (NIH), the methods developed by the UC San Diego researchers dramatically improve upon existing DNA-based approaches — avoiding potential integration problems and providing what appears to be a safer and simpler method for future clinical applications.The generation of human iPSCs has opened the potential for regenerative medicine therapies based on patient-specific, personalized stem cells. Pluripotent means that these cells have the ability to give rise to any of the body’s cell types. The human iPSCs are typically artificially derived from a non-pluripotent adult cell, such as a skin cell. They retain the characteristics of the body’s natural pluripotent stem cells, commonly known as embryonic stem cells. Because iPSCs are developed from a patient’s own cells, it was first thought that treatment using them would avoid any immunogenic responses. However, depending on methods used to generate such iPSCs, they may pose significant risks that limit their use. For example, using viruses to alter the cell’s genome could promote cancer in the host cell.Methods previously developed to generate integration-free iPSCs were not easily and efficiently reproducible. Therefore, the UC San Diego researchers focused their approach on developing a self-replicating, RNA-based method (one that doesn’t integrate into the DNA) with the ability to be retained and degraded in a controlled fashion, and that would only need to be introduced once into the cell.Using a Venezuelan equine virus (VEE) with structural proteins deleted, but non-structural proteins still present, the scientists added four reprogramming factors (OCT4, KLF4, SOX2 with either c-MYC or GLIS1). …

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Potential nutritional therapy for childhood neurodegenerative disease

Aug. 1, 2013 — Researchers at the University of California, San Diego School of Medicine have identified the gene mutation responsible for a particularly severe form of pontocerebellar hypoplasia, a currently incurable neurodegenerative disease affecting children. Based on results in cultured cells, they are hopeful that a nutritional supplement may one day be able to prevent or reverse the condition.The study, from a team of international collaborators led by Joseph G. Gleeson, MD — Howard Hughes Medical Institute investigator and professor in the UCSD Departments of Neurosciences and Pediatrics and at Rady Children’s Hospital-San Diego, a research affiliate of UC San Diego — will be published in the August 1 issue of the journal Cell.Pontocerebellar hypoplasia is a group of rare, related genetic neurological disorders characterized by abnormal development of the brain, resulting in disabilities in movement and cognitive function. Most patients do not survive to adulthood.Gleeson and colleagues identified a specific gene mutation that causes pontocerebellar hypoplasia and linked it to an inability of brain cells to generate a form of energy required to synthesize proteins. Without this ability, neurons die, but the researchers also found that bypassing this block with a nutritional supplement restored neuronal survival.”The goal is to one day use this supplement to prevent or reverse the course of neurodegeneration in humans, and thus cure this disease,” said Gleeson.Nucleotides are the main energy source of cells. They exist in two forms: ATP and GTP. While ATP fuels most energy requirements, GTP is the source for protein synthesis. Mutations in the gene AMPD2 lead to the accumulation of ATP, and the subsequent depletion of GTP. The result, said Gleeson, is an imbalance in the cell’s energy source, which prevents protein synthesis and causes neurodegeneration.”These patients have what is described in medical textbooks as an untreatable disease, yet show mutations in a neuronal pathway that should be amenable to medication,” said study co-author Naiara Akizu, PhD, a member of Gleeson’s lab. …

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App to protect private data on iOS devices finds almost half of other apps access private data

June 20, 2013 — Almost half of the mobile apps running on Apple’s iOS operating system access the unique identifier of the devices where they’re downloaded, computer scientists at the University of California, San Diego, have found. In addition, more than 13 percent access the devices’ location and more than 6 percent the address book. The researchers developed a new app that detects what data the other apps running on an iOS device are trying to access.The findings are based on a study of 130,000 users of jailbroken iOS devices, where users have purposefully removed restrictions that keep apps from accessing the iPhone’s operating system. Most apps in the study were downloaded from Apple’s App Store and access the same type of information on unlocked, jailbroken, phones and on locked phones, said Yuvraj Agarwal, a research scientist in the Department of Computer Science and Engineering at UC San Diego, who co-authored the study with fellow researcher Malcolm Hall. Agarwal will present the findings at ACM MobiSys, the premier mobile systems conference, which takes place June 25 to 28 in Taipei, Taiwan.The findings suggest that although Apple’s App Store no longer accepts new apps or app updates that access the unique identifier as of March of this year, many apps can still get a hold of that information. The unique identifier allows app vendors and advertisers to track users’ behaviors across all the different apps on their devices, including iPhones, iPads and iPods. In addition, some apps can associate the unique identifier with the user’s email and other personal information.The researchers believe that it’s the first time anyone has done such an extensive privacy study focused on iOS-based apps across a large user population.The ProtectMyPrivacy AppTo carry out their study, researchers developed an app of their own, called ProtectMyPrivacy, or PMP. It lets users know what personal information the other apps on their devices are trying to access. PMP enables users to selectively allow or deny access to this information on an app-by-app basis, based on whether they feel the apps need the information to function properly — for example, a map app needs to access the location of a device to provide driving directions. iOS devices currently notify users when apps try to access location, photos and contacts. …

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Developmental protein plays role in spread of cancer

June 14, 2013 — A protein used by embryo cells during early development, and recently found in many different types of cancer, apparently serves as a switch regulating the spread of cancer, known as metastasis, report researchers at the University of California, San Diego School of Medicine and UC San Diego Moores Cancer Center in the June 15, 2013 issue of the journal Cancer Research.Metastasis is responsible for 90 percent of cancer-related deaths. More than 575,000 Americans die of cancer each year, the second leading cause of death in the United States after cardiovascular disease.The scientists, led by principal investigator Thomas Kipps, MD, PhD, Evelyn and Edwin Tasch Chair in Cancer Research at UC San Diego, discovered an association between the protein, called Receptor-tyrosine-kinase-like Orphan Receptor 1 or ROR1, and the epithelial-mesenchymal transition (EMT), a process that occurs during embryogenesis when cells migrate and then grow into new organs during early development.In research published in 2012, Kipps and colleagues reported for the first time that ROR1 is expressed during embryogenesis and by many different types of cancers, but not by normal post-partum tissues. They also discovered that silencing the protein impaired the growth and survival of human breast cancer cells.In their latest work, the scientists found that high-level expression of ROR1 in breast cancer cells correlates to higher rates of relapse and metastasis in patients with breast adenocarcinoma, a type of cancer that originates in glandular tissue. Conversely, silencing expression of ROR1 reverses EMT and inhibits the metastatic spread of breast cancer cells in animal models. Moreover, the researchers found that treatment with a monoclonal antibody targeting ROR1 also could inhibit the growth and spread of highly metastatic tumors that express ROR1.”We might think of ROR1 as an oncogene,” said study co-author Bing Cui, PhD, a postdoctoral fellow in Kipps’ lab. “This means ROR1 has some tumor initiation functions. However, ROR1 also appears to allow transformed cells to invade other tissues and to promote tumor expansion in both the primary tumor site and in distant organs.”Because ROR1 is expressed only in cancer cells, Kipps’ team says it presents a singular, selective target for anti-cancer therapies that would leave normal cells unaffected. It’s not yet clear how the monoclonal antibody approach, tested thus far only in culture and animal models, impacts primary tumors, said Cui, but it does offer promise for inhibiting the spread of cancer. The researchers are developing a humanized monoclonal antibody for potential clinical studies in patients with cancers that express ROR1.Co-authors are Suping Zhang, Liguang Chen, Jianqiang Yu, George F. Widhopf II, Jessie F. …

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Pilot program to decrease emergency room wait times

June 11, 2013 — Emergency department (ED) overcrowding has been a major issue nationally for 20 years and continues to increase in severity. To address this issue, a pilot study has been launched at UC San Diego Health System’s ED to use telemedicine as a way to help address crowding and decrease patient wait times. The study is the first of its kind in California to use cameras to bring on-call doctors who are outside of the hospital to the patient in need.”This telemedicine study will determine if we can decrease wait times while reducing the number of patients who leave the ED without being seen by a physician,” said David Guss, MD, principal investigator and chair of the department of emergency medicine at UC San Diego School of Medicine. “With the ED physicians on site and an added telemedicine physician, patient care may be significantly expedited. If the use of a telemedicine evaluation can be shown to be safe and effective, it may shift how care in the emergency department is delivered.”The study, called Emergency Department Telemedicine Initiative to Rapidly Accommodate in Times of Emergency (EDTITRATE), brings telemedicine doctors to patients when the ED becomes busy. An offsite doctor is paged who then remotely links to a telemedicine station to see patients. With the aide of an ED nurse, these patients are seen based on arrival time and level of medical need. All patients must sign a consent form to participate in the study.Guided by high fidelity sound and video, the telemedicine physician can examine a patient’s eyes, ears, nose, throat and skin, as well as listen to heart and lung sounds through the module. Laboratory and imaging tests can be ordered and results reviewed. Physician ordering and documentation is accomplished through an electronic medical record. …

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Herpes virus exploits immune response to bolster infection

June 6, 2013 — Researchers at the University of California, San Diego School of Medicine and colleagues report that the herpes simplex virus type-1 (HSV-1), which affects an estimated 50 to 80 percent of all American adults, exploits an immune system receptor to boost its infectivity and ability to cause disease.The findings are published in the June 6, 2013 issue of Nature Communications.HSV-1 is a persistent and problematic pathogen. Typically, it infects victims through oral secretions (kissing, sharing a contaminated toothbrush) or through openings in the skin. In healthy people, the result may be cold sores or fever blisters. In people with compromised immune systems, HSV-1 can pose more serious and chronic health problems. It can spread, for example, to organs like the brain, lungs and liver, where the infection may become life-threatening. Some patients, such as those with atopic dermatitis — a common form of eczema that accounts for roughly 20 percent of all dermatologic referrals, are especially vulnerable to serious complications stemming from an HSV-1 infection.Led by principal investigator Richard L. Gallo, MD, PhD, professor of medicine and chief of UC San Diego’s Division of Dermatology, the scientists found that HSV-1 launches an infection by binding to receptors on the surface of skin cells. Ordinarily, if a cell recognizes the virus as an invader, an immune response is immediately triggered, which includes a group of proteins called scavenger receptors that help identify and remove harmful viruses.But sometimes the process goes awry. While studying HSV-1 and scavenger receptors in cultured human skin cells, Gallo and colleagues in the Atopic Dermatitis Research Network, funded by the National Institute of Allergy and Infectious Diseases, discovered that the virus strongly interacts with a particular receptor called a macrophage receptor with collagenous structure or MARCO, which it uses to gain entry into cells.In tests comparing mice expressing normal levels of MARCO with mice genetically engineered to lack the receptor, the scientists found that MARCO enhanced the virus’ ability to infect cells. Mice lacking the receptor suffered dramatically smaller skin lesions than normal mice with normal levels of MARCO. …

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Altered neural circuitry may lead to anorexia and bulimia

June 4, 2013 — Anorexia nervosa and bulimia nervosa -disorders characterized by extreme eating behavior and distorted body image — are among the deadliest of psychiatric disorders, with few proven effective treatments.A landmark study, with first author Tyson Oberndorfer, MD, and led by Walter H. Kaye, MD, professor of psychiatry at the University of California, San Diego School of Medicine, suggests that the altered function of neural circuitry contributes to restricted eating in anorexia and overeating in bulimia. The research, published June 4 in the early on-line edition of the American Journal of Psychiatry, may offer a pathway to new and more effective treatments for these serious eating disorders.”It has been unknown whether individuals with anorexia or bulimia have a disturbance in the system that regulates appetite in the brain, or whether eating behavior is driven by other phenomena, such as an obsessional preoccupation with body image,” said Kaye, director of the UCSD Eating Disorders Treatment and Research Program. “However, this study confirms earlier studies by our group and others that establish a clear link between these disorders and neural processes in the insula, an area of the brain where taste is sensed and integrated with reward to help determine whether an individual hungry or full.”The UC San Diego study used functional MRI to test this neurocircuitry by measuring the brain response to sweet tastes in 28 women who had recovered from either anorexia or bulimia.Relative to a cohort of 14 women who had never suffered from either disorder, those recovered from anorexia had significantly diminished, and those recovered from bulimia, significantly elevated responses to the taste of sucrose in the right anterior insula.”One possibility is that restricted eating and weight loss occurs in anorexia because the brain fails to accurately recognize hunger signals,” said Oberndorfer. “Alternately, overeating in bulimia could represent an exaggerated perception of hunger signals.”A recent complementary study that investigated brain structure in anorexia and bulimia nervosa (Frank et al 2013) similarly highlights that the insula could be an integral part of eating disorder pathology.The researchers added that such studies could have very important implications for treatment, and that identifying abnormal neural substrates could help to reformulate the basic pathology of eating disorders and offer new targets for treatment.”It may be possible to modulate the experience by, for example, enhancing insula activity in individuals with anorexia or dampening the exaggerated or unstable response to food in those with bulimia,” said Kaye. Studies indicate that healthy subjects can use real-time fMRI, biofeedback or mindfulness training to alter the brain’s response to food stimuli. For patients with anorexia who have an overly active satiety signal in response to palatable foods, the researchers suggest bland or even slightly aversive foods might prevent the brain’s overstimulation. Medications may also be found that enhance the reward response to food, or decrease inhibition to food consumption in the brain’s reward circuitry.This study was supported in part by grants from the National Institute of Mental Health (grants MH46001, MH42984, K05-MD01894 and training grant T32-MH18399) and by the Price Foundation.Additional contributors to the study include Guido K.W. Frank, MD; Alan N. Simmons, PhD; Angela Wagner, MD, PhD; Danyale McCurdy, PhD; Julie L. …

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Scarless brain surgery is new option for patients

Sep. 29, 2010 — Surgeons at the University of California, San Diego, School of Medicine and University of Washington Medical Center have determined that transorbital neuroendoscopic surgery (TONES) is a safe and effective option for treating a variety of advanced brain diseases and traumatic injuries. This groundbreaking minimally invasive surgery is performed through the eye socket, thus eliminating the removal of the top of the skull to access the brain. These findings were published in the September issue of Neurosurgery.

“By performing surgery through the eye socket, we eliminate the need for a full craniotomy, gain equivalent or better access to the front of the brain, and eliminate the large ear-to-ear scar associated with major brain surgery,” said Chris Bergeron, MD, assistant professor of Surgery, Division of Head and Neck Surgery, at UC San Diego Health System. “This novel technique is also critical to protecting neurovascular structures such as the optic and olfactory nerves.”

To achieve access, the surgeons make a small incision behind or through the eyelid. A tiny hole is then made through the paper-thin bone of the eye socket to reach the brain. This pathway permits repairs to be made without lifting the brain. The TONES approaches also protect the optic nerves, the nerves for smell, as well as the carotid and ophthalmic arteries.

“This approach has opened a new field of brain surgery,” said study investigator, Kris Moe, MD, chief of the Division of Facial Plastic and Reconstructive Surgery and professor of Otolaryngology at University of Washington Medical Center. “The advantages to this transorbital approach are many, including reduced pain and decreased recovery time for the patient.”

Transnasal surgery, a technique performed through the nose, offers similar access to some areas of the brain but means a more crowded operating environment for the surgeon than TONES. Moe, who pioneered the TONES in 2005, said the novel technique builds on the nasal approach but offers increased maneuverability and visibility for the surgical teams which usually require four sets of hands.

In a traditional craniotomy, a large portion of skull bone is removed. With TONES, the area of bone removed is only two to three centimeters. The operating time is much shorter since the skull does not need to be repaired and there is no need to close a large incision.

Patients underwent the TONES procedure to repair cerebral spinal fluid leaks, optic nerve decompression, repair of cranial base fractures and removal of tumors. Given further research, the surgeons believe that TONES may serve as a means to treat pituitary tumors, meningiomas, and vascular malformations. TONES is currently performed at only two institutions in the world: UC San Diego Medical Center and the University of Washington Medical Center.

Researchers included Kris Moe, MD, Chris Bergeron, MD and Richard Ellenbogen, MD.

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Botox injections now used for severe urinary incontinence

Mar. 13, 2012 — When you think of Botox injections, you probably think of getting rid of unwanted wrinkles around the eyes or forehead, but recently the US Food and Drug Administration (FDA) approved using the injections to help patients with neurological conditions who suffer from incontinence, or an overactive bladder.

Botox injections paralyze the bladder muscle to prevent contractions that cause urgency to urinate or leak. Although medications and behavioral modifications are treatment options, many patients, especially the elderly, do not respond to these methods and need a more aggressive approach.

“About 80 percent of patients with neurological conditions, such as spinal cord injuries, Parkinson’s disease and multiple sclerosis, see improvement after about a week, and the results can last four to nine months,” said Charles Nager, MD, co-director of the UC San Diego Women’s Pelvic Medicine Center at UC San Diego Health System.

Incontinence is the seventh condition, including chronic migraines and underarm sweating, that Botox has been approved to treat since the drug first arrived on the market as a wrinkle reducer in 2002.

The outpatient procedure uses a local numbing gel, followed by 15 to 20 injections in different areas of the bladder muscle.

“It can really be life changing for someone with severe incontinence issues,” said Nager who also serves as director of Urogynecology and Reconstructive Pelvic Surgery in the Department of Reproductive Medicine at UC San Diego.

UC San Diego Health System is currently recruiting for a clinical trial to test Botox injections versus sacral nerve stimulation as incontinence treatment options.

Sacral nerve stimulation uses small, electrical impulses to the nerves that control urination. The impulses are generated by a small device surgically placed under the skin. Attached to the device is a thin, electrode-tipped wire that passes under the patient’s skin, carrying impulses to the sacral nerve. The surgery is an outpatient procedure done under local anesthesia.

Patients involved in the clinical trial are required to have tried two drugs that previously failed to treat their incontinence issues.

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Shape-shifting nanoparticles flip from sphere to net in response to tumor signal

May 28, 2013 — Scientists at the University of California, San Diego, have designed tiny spherical particles to float easily through the bloodstream after injection, then assemble into a durable scaffold within diseased tissue. An enzyme produced by a specific type of tumor can trigger the transformation of the spheres into netlike structures that accumulate at the site of a cancer, the team reports in the journal Advanced Materials this week.

Spherical nanoparticles labeled with red or green dye shift their shapes and accumulatte into netlike structures when they encounter a protease secreted by some kinds of cancerous tumors (Click on image for larger view).

Targeting treatments specifically to cancerous or other diseased cells depends on some means of accumulating high levels of a drug or other therapeutic agent at the specific site and keeping it there. Most efforts so far depend on matching a piece of the drug-delivering molecule to specific receptors on the surface of the target cell.

Inspiration for this new strategy came from biological systems that use shape to alter the ability of something to lock in place or slip away and escape, said Nathan Gianneschi, a professor of chemistry and biochemistry, who led the project.

“We wanted to come up with a new approach,” Gianneschi said. “Specifically, we wanted to design switchable materials that we could inject in one shape and have them change to another between the blood and tumors.”

Some cancerous tissues produce high levels of a class of molecules called MMPs, for matrix metalloproteinases. These enzymes change how other proteins behave by altering their molecular configuration, leading to metastasis. Gianneschi and colleagues harnessed this ability to alter their nanoparticles in ways that would cause them to linger at the site of the tumor.

“We figured out how to make an autonomous material that could sense its environment and change accordingly,” Gianneschi said.

Each nanoparticle is made of many detergent-like molecules with one end that mixes readily with water and another that repels it. In solution, they self assemble into balls with the water-repellant ends inside, and in that configuration can easily be injected into a vein.

When mixed with MMPs in vials, the enzymes nicked the peptides on the surface of the spheres, which reassembled into netlike threads.

The team tested the concept further by injecting their new nanoparticles into mice with human fibrosarcomas, a kind of cancer that produces high levels of MMPs.

To mark when the spheres broke down to form other structures, the chemists placed one of two fluorecent dyes, rhodamine or fluorescein, inside the spheres. In close proximity, the dyes interact to create a specific light signal called FRET for Förster Resonance Energy Transfer, when energy jumps from rhodamine to fluorescein.

Within a day they detected FRET signals indicating that the spheres had reassembled at the sites of the tumors, and the signal persisted for at least a week.

The treatment is not inherently toxic. It did not appear to change the tumors in any way, and liver and kidney, the organs most vulnerable to collateral damage from treatments because they clear toxins from the body, were normal and healthy eight days after injection.

Different versions of these nanoparticles could be designed to respond to signals inherent to other types of cancers and inflamed tissue, the authors say. The spheres can also be engineered to carry drugs, or different diagnostic probes.

Right now, this same team is developing nanoparticles that carry an infrared dye, which would enable them to visualize tumors deeper inside the body along with other materials that can be imaged with instruments commonly available in the clinic.

Co-authors include Miao-Ping Chen and Matthew Thompson in Gianneschi’s group, and Christopher Barbak and David Hall in UC San Diego School of Medicine’s Department of Radiology. Funding agencies include National Institutes of Health, Army Research Office and Air Force Office of Scientific Research. Gianneschi was also supported by a New Faculty Award from the Henry and Camille Dreyfus Foundation and a Research Fellowship from the Alfred P. Sloan Foundation.

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