June 22, 2017 The fungus Aspergillus fumigatus (in red) produces a sticky sugar molecule (in green) to make a biofilm that is important for its virulence. It covers the fungus and allows it to stick to surfaces and tissues, making it difficult to remove and treat patients. Researchers developed a new innovative technique aimed at destroying biofilms. Credit: Brendan Snarr, McGill University Health Centre

Have you ever heard of biofilms? They are slimy, glue-like membranes that are produced by microbes, like bacteria and fungi, in order to colonize surfaces. They can grow on animal and plant tissues, and even inside the human body on medical devices such as catheters, heart valves, or artificial hips. Biofilms protect microbes from the body's immune system and increase their resistance to antibiotics. They represent one of the biggest threats to patients in hospital settings. But there is good news - a research team led by the Research Institute of the McGill University Health Centre (RI-MUHC) and The Hospital for Sick Children (SickKids) has developed a novel enzyme technology that prevents the formation of biofilms and can also break them down.

This finding, recently published in Proceedings of the National Academy of Sciences (PNAS), creates a promising avenue for the development of innovative strategies to treat a wide variety of diseases and hospital-acquired infections like pneumonia, bloodstream and urinary tract infection. Biofilm-associated infections are responsible for thousands of deaths across North America every year. They are hard to eradicate because they secrete a matrix made of sugar molecules which form a kind of armour that acts as a physical and chemical barrier, preventing antibiotics from reaching their target sites within microbes.

"We were able to use the microbe's own tools against them to attack and destroy the sugar molecules that hold the biofilm together," says the study's co-principal investigator, Dr. Don Sheppard, director of the Division of Infectious Diseases at the MUHC and scientist from the Infectious Diseases and Immunity in Global Health Program at the RI-MUHC. "Rather than trying to develop new individual 'bullets' that target single microbes we are attacking the biofilm that protects those microbes by literally tearing down the walls to expose the microbes living behind them. It's a completely new and novel strategy to tackle this issue."

This work is the result of a four-year successful collaboration between Dr. Sheppard's team and scientists in the laboratory of Dr. P. Lynne Howell, senior scientist in the Molecular Medicine program at SickKids. They have been working to combat biofilms for several years, focusing on two of the most common organisms responsible for lung infections: a bacterium called Pseudomonas aeruginosa and a fungus called Aspergillus fumigatus. Infections with these organisms in patients with chronic lung diseases like cystic fibrosis represent an enormous challenge in medical therapy.

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While studying machinery that these organisms use to make their biofilms, the scientists discovered enzymes that cut up the sugar molecules, which glue biofilms together. "Microbes use these enzymes to move sugar molecules around and cut them into pieces in order to build and remodel the biofilm matrix," says Dr. Sheppard, who is also a professor in the departments of Medicine and Microbiology and Immunology at McGill University. The researchers found a way to use these enzymes to degrade the sugar armour, exposing the microbe to antibiotics and host defenses.

"We made these enzymes into a biofilm destroying machine that we can use outside the microbe where the sugar molecules are found," explains co-first study author Brendan Snarr, a PhD student in Dr. Sheppard's laboratory. "These enzymes chew away all of the sugar molecules in their path and don't stop until the matrix is destroyed."

"Previous attempts to deal with biofilms have had only limited success, mostly in preventing biofilm formation. These enzymes are the first strategy that has ever been effective in eradicating mature biofilms, and that work in mouse models of infection," adds Dr. Sheppard.

"When we took the enzymes from bacteria and applied them to the fungi, we found that they worked in the same way on the fungi biofilm; which was surprising," says the study's co-principal investigator, Dr. P. Lynne Howell, who is also a professor in the Department of Biochemistry at the University of Toronto. "What's key is that this approach could be a universal way of being able to leverage the microbes' own systems for degrading biofilms. This has bigger implications across many microbes, diseases and infections."

"Over 70 percent of hospital-acquired infections are actually associated with biofilms and we simply lack tools to treat them!" states Dr. Sheppard. According to both lead scientists, the potential of this novel therapy is enormous and they hope to commercialize it in the coming years.

Explore further: Scientists uncover interactions between bacteria that infect the lungs in cystic fibrosis

More information: Microbial glycoside hydrolases as antibiofilm agents with cross-kingdom activity, biorxiv.org/content/early/2017/03/04/113696

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Great find. And because these enzymes are used by the bacteria, they can not so easily become resistant to them. Or somehow develop ways to stop them from working.

Getting 'black gunk' out of the soap & softener dispensers in our laundry machine is a real battle. At least I can take out their tray, dunk it in bleach and scrub unto clean. The gunk in the duct beyond has resisted anything that won't corrode the equipment or gas the operator...

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June 22, 2017 10:30 ET | Source: Tempus

CHICAGO, June 22, 2017 (GLOBE NEWSWIRE) -- Tempus, a technology company focused on helping doctors personalize cancer care by collecting, sorting and analyzing clinical and molecular data, and pancreatic cancer specialists at the University of Chicago Medicine, announce a new collaboration aimed at accelerating the pace of discovery and, over time, improving treatment of pancreatic cancer.

Pancreatic cancer is the third leading cause of cancer-related death in the United States. It has a five-year survival rate of just nine percent. Lack of effective treatments and early detection methods contribute to this grim prognosis. Personalized approaches to match a patients genomic information to therapies have led to improvements in treatment of other cancer types. None of the genetic mutations commonly seen in pancreatic cancer, however, have druggable targets.

As part of the research collaboration, Tempus will work directly with a team of researchers and clinicians from the Chicago Pancreatic Cancer Initiative (CPCI), led by Ralph Weichselbaum, MD, professor and chairman of the Department of Radiation Oncology at the University of Chicago. The CPCI has collected genomic data, biospecimens and clinical information from more than 300 patients with pancreatic cancer. Tempus will compile this data with their existing robust database to apply machine learning and advanced bioinformatics to analyze them. Tempus will also produce additional genomic data using their platform.

The goal is to help cancer specialists and research teams uncover novel patterns in clinical and molecular data, in order to better predict how patients will respond to treatment.

The University of Chicago and Tempus share a commitment to accelerate pancreatic cancer research and identify treatments that can improve the lives of those diagnosed, said Weichselbaum. We are optimistic that this collaboration can make a difference in the lives of those diagnosed and treated for pancreatic cancer.

A tremendous amount of work and effort across hospital systems, academic institutions and research consortia has been done to help improve the odds of patients diagnosed with pancreatic cancer and yet the outlook is still grim for those battling the disease, said Eric Lefkofsky, Co-founder and CEO at Tempus. We are pleased to support the team at the University of Chicago by bringing technology and analytics to our common quest for improved patient outcomes.

The University of Chicago Medicine Comprehensive Cancer Center, which includes CPCI investigators, is one of only 48 Comprehensive Cancer Centers in the U.S. designated by the National Cancer Institute.

In 2016, the University of Chicago Medicine was selected as a Pancreatic Cancer Action Network (PanCAN) Precision Promise Consortium site. Under the leadership of oncologist and CPCI investigator, Hedy Kindler, MD, professor of medicine and medical director of the gastrointestinal oncology and the mesothelioma programs at the University, the program will advance clinical trial options for pancreatic cancer patients.

Tempus and the University of Chicago Medicine are currently involved in another research project focusing on improving outcomes for breast cancer patients.

About Tempus: Tempus is a technology company that is building the worlds largest library of molecular and clinical data and an operating system to make that data accessible and useful. We enable physicians to deliver personalized cancer care for patients through our interactive analytical and machine learning platform. We provide genomic sequencing services and analyze molecular and therapeutic data to empower physicians to make real-time, data-driven decisions. Our goal is for each patient to benefit from the treatment of others who came before by providing physicians with tools that learn as we gather more data. For more information, visit tempus.com and follow us on Facebook (Tempus Labs) and Twitter (@TempusLabs). For more information on Eric Lefkofsky, visit lefkofsky.com.

About the University of Chicago Medicine: The University of Chicago Medicine & Biological Sciences is one of the nations leading academic medical institutions. It comprises the Pritzker School of Medicine, a top U.S. medical school; the University of Chicago Biomedical Sciences Division; and the University of Chicago Medical Center. Twelve Nobel Prize winners in physiology or medicine have been affiliated with the University of Chicago Medicine.

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Long typecast as the strong silent type, bones are speaking up.

In addition to providing structural support, the skeleton is a versatile conversationalist. Bones make hormones that chat with other organs and tissues, including the brain, kidneys and pancreas, experiments in mice have shown.

The bone, which was considered a dead organ, has really become a gland almost, says Beate Lanske, a bone and mineral researcher at Harvard School of Dental Medicine. Theres so much going on between bone and brain and all the other organs, it has become one of the most prominent tissues being studied at the moment.

At least four bone hormones moonlight as couriers, recent studies show, and there could be more. Scientists have only just begun to decipher what this messaging means for health. But cataloging and investigating the hormones should offer a more nuanced understanding of how the body regulates sugar, energy and fat, among other things.

Of the hormones on the list of bones messengers osteocalcin, sclerostin, fibroblast growth factor 23 and lipocalin2 the last is the latest to attract attention. Lipocalin 2, which bones unleash to stem bacterial infections, also works in the brain to control appetite, physiologist Stavroula Kousteni of Columbia University Medical Center and colleagues reported in the March 16 Nature.

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After mice eat, their bone-forming cells absorb nutrients and release a hormone called lipocalin 2 (LCN2) into the blood. LCN2 travels to the brain, where it gloms on to appetite-regulating nerve cells, which tell the brain to stop eating, a recent study suggests.

Researchers previously thought that fat cells were mostly responsible for making lipocalin 2, or LCN2. But in mice, bones produce up to 10 times as much of the hormone as fat cells do, Kousteni and colleagues showed. And after a meal, mices bones pumped out enough LCN2 to boost blood levels three times as high as premeal levels. Its a new role for bone as an endocrine organ, Kousteni says.

Clifford Rosen, a bone endocrinologist at the Center for Molecular Medicine in Scarborough, Maine, is excited by this new bone-brain connection. It makes sense physiologically that there are bidirectional interactions between bone and other tissues, Rosen says. You have to have things to regulate the fuel sources that are necessary for bone formation.

Bones constantly reinvent themselves through energy-intensive remodeling. Cells known as osteoblasts make new bone; other cells, osteoclasts, destroy old bone. With such turnover, the skeleton must have some fine-tuning mechanism that allows the whole body to be in sync with whats happening at the skeletal level, Rosen says. Osteoblasts and osteoclasts send hormones to do their bidding.

Scientists began homing in on bones molecular messengers a decade ago (SN: 8/11/07, p. 83). Geneticist Gerard Karsenty of Columbia University Medical Center found that osteocalcin made by osteoblasts helps regulate blood sugar. Osteocalcin circulates through the blood, collecting calcium and other minerals that bones need. When the hormone reaches the pancreas, it signals insulin-making cells to ramp up production, mouse experiments showed. Osteocalcin also signals fat cells to release a hormone that increases the bodys sensitivity to insulin, the bodys blood sugar moderator, Karsenty and colleagues reported in Cell in 2007. If it works the same way in people, Karsenty says, osteocalcin could be developed as a potential diabetes or obesity treatment.

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Bones produce hormones that go to work in other organs. Some of those functions are known, but researchers are finding new ways these hormones may work.

Blood sugar and insulin metabolism

Memory and mood

Testosterone production

Pancreas and fat tissue

Brain

Testicles

Their data is fairly convincing, says Sundeep Khosla, a bone biologist at the Mayo Clinic in Rochester, Minn. But the data in humans has been less than conclusive. In observational studies of people, its hard to say that osteocalcin directly influences blood sugar metabolism when there are so many factors involved.

More recent mouse data indicate that osteocalcin may play a role in energy metabolism. After an injection of the hormone, old mice could run as far as younger mice. Old mice that didnt receive an osteocalcin boost ran about half as far, Karsenty and colleagues reported last year in Cell Metabolism. As the hormone increases endurance, it helps muscles absorb more nutrients. In return, muscles talk back to bones, telling them to churn out more osteocalcin.

There are hints that this feedback loop works in humans, too. Womens blood levels of osteocalcin increased during exercise, the team reported.

Mounting evidence from the Karsenty lab suggests that osteocalcin also could have more far-flung effects. It stimulates cells in testicles to pump out testosterone crucial for reproduction and bone density and may also improve mood and memory, studies in mice have shown. Bones might even use the hormone to talk to a fetuss brain before birth. Osteocalcin from the bones of pregnant mice can penetrate the placenta and help shape fetal brain development, Karsenty and colleagues reported in 2013 in Cell. What benefit bones get from influencing developing brains remains unclear.

Another emerging bone messenger is sclerostin. Its day job is to keep bone growth in check by telling bone-forming osteoblasts to slow down or stop. But bones may dispatch the hormone to manage an important fuel source fat. In mice, the hormone helps convert white (or bad) fat into more useful energy-burning beige fat, molecular biologist Keertik Fulzele of Boston University and colleagues reported in the February Journal of Bone and Mineral Research.

Osteocalcin, sclerostin and LCN2 offer tantalizing clues about bones communication skills. Another hormone, fibroblast growth factor 23, or FGF-23, may have more immediate medical applications.

Bones use FGF-23 to tell the kidneys to shunt extra phosphate that cant be absorbed. In people with kidney failure, cancer or some genetic diseases, including an inherited form of rickets called X-linked hypophosphatemia, FGF-23 levels soar, causing phosphate levels to plummet. Bones starved of this mineral become weak and prone to deformities.

In the case of X-linked hypophosphatemia, or XLH, a missing or broken gene in bones causes the hormone deluge. Apprehending the molecular accomplice may be easier than fixing the gene.

In March, researchers, in collaboration with the pharmaceutical company Ultragenyx, completed the first part of a Phase III clinical trial in adults with XLH the final test of a drug before federal approval. The scientists tested an antibody that latches on to extra FGF-23 before it can reach the kidneys. Structurally similar to the kidney proteins where FGF-23 docks, the antibody is like a decoy in the blood, says Lanske, who is not involved in the trial. Once connected, the duo is broken down by the body.

Traditionally, treating XLH patients has been like trying to fill a bathtub without a plug. The kidney is peeing out the phosphorus, and were pouring it in the mouth as fast as we can so bones mineralize, says Suzanne Jan De Beur, a lead investigator of the clinical trial and director of endocrinology at Johns Hopkins Bayview Medical Center. Success is variable, and debilitating side effects often arise from long-term treatment, she says. The antibody therapy should help restore the bodys ability to absorb phosphate.

Unpublished initial results indicate that the antibody works. Of 68 people taking the drug in the trial, over 90 percent had blood phosphate levels reach and stay in the normal range after 24 weeks of treatment, Ultragenyx announced in April. People taking the antibody also reported less pain and stiffness than those not on the drug.

Osteocalcin, sclerostin and LCN2 might also be involved in treating diseases someday, if results in animals apply to people.

In the study recently published in Nature, Koustenis team found that boosting LCN2 levels in mice missing the LCN2 gene tamed their voracious feeding habits. Even in mice with working LCN2 genes, infusions of the hormone reduced food intake, improved blood sugar levels and increased insulin sensitivity.

Researchers traced the hormones path from the skeleton to the hypothalamus a brain structure that maintains blood sugar levels and body temperature and regulates other processes. Injecting LCN2 into mices brains suppressed appetite and decreased weight gain. Once the hormone crosses the blood-brain barrier and reaches the hypothalamus, it attaches to the surface of nerve cells that regulate appetite, the team proposed.

Mice with defective LCN2 docking stations on their brain cells, however, overate and gained weight just like mice that couldnt make the hormone in the first place. Injections of LCN2 didnt curb eating or weight gain.

(Two mouse studies by another research group published in 2010, however, found that LCN2 had no effect on appetite. Kousteni and colleagues say that inconsistency could have resulted from a difference in the types of mice that the two groups used. Additional experiments by Koustenis lab still found a link between LCN2 and appetite.)

In a small group of people with type 2 diabetes, those who weighed more had less LCN2 in their blood, the researchers found. And a few people whose brains had defective LCN2 docking stations had higher blood levels of the hormone.

If the hormone suppresses appetite in people, it could be a great obesity drug, Rosen says. Its still too early, though, to make any definitive proclamations about LCN2 and the other hormones side hustles, let alone medical implications. Theres just all sorts of things that we are uncovering that weve ignored, Rosen says. But one thing is clear, he says: The era of bone as a silent bystander is over.

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Bones make hormones that communicate with the brain and other organs - Science News Magazine

A new study has identified for the first time how a common process in cancer might be involved in the development of autoimmunediseases.

Researchers at the University of Helsinki and the Institute for Molecular Medicine Finland have found that the accumulation of mutations in mature immune cells could drive rheumatoid arthritis in a similar way to how somatic mutations drive cancer. This phenomenon has been extensively studied in tumors, but this study is the first to investigate it in other diseases.

The results,published today in Nature Communications, revealed 30 mutations in CD8+ cytotoxic T cells of 5out of 25 patients with rheumatoid arthritis, versus a single mutation in one out of 20 healthy patients.The mutations were found in genes linked with the regulation of immunity and cell proliferation, and the clones of those cells with mutations appeared in much larger quantities that T cell clones without the mutations.

Interestingly, all the mutations were found incytotoxic CD8+ T cells, and none in helper CD4+ T cells. Given both cell types have a common origin, it was determined that the mutations appeared in mature cells and were not related to genetic defects in the stem cells that produce new immune cells every day.

Counterintuitively, none of the mutations identified were found in other 82 rheumatoid arthritis patients, indicating that rather than beingdriven by any specific genes, the process would depend on the accumulation of nonspecific mutations.

The prevalence of these types of mutations in hematopoietic cells increases with age,a process that has been extensively linked to an increased risk of cancer, and particularly blood cancer. These results indicate that the same process could also be behind a higher risk of suffering from an autoimmune disease.

For now, there is no certainty on how these mutations affect the regulation of chronic inflammations, says Professor Satu Mustjoki, one of theprojects leaders. They may be, for lack of a better word, genomic scars formed as a result of the activation of the immune defense system. In any case, this research project revealed a new connection on the molecular level between autoimmune diseases and cancer, which brings us one step closer to understanding these diseases.

After this first step, further studies with larger patients cohorts are definitely needed to confirm the results and gain a deeper insight into the mechanisms by which these mutations result in autoimmune disease. As Mustjoki stated, his group is planning to continue investigating the phenomenon in several inflammatory conditions.

Images via nobeastsofierce / Shutterstock;P Savola et al. Nature Communications 8, 15869 (2017)

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Finnish Researchers find Similar Mutation Patterns to Cancer in ... - Labiotech.eu (blog)

June 21, 2017 by Becky Freemal Treatments targeting a gene known as NLRX1 could help provide relief to the estimated 1.6 million Americans currently suffering from inflammatory bowel disease. Credit: Virginia Tech

Researchers at the Biocomplexity Institute of Virginia Tech have discovered a new therapeutic target for inflammatory bowel diseaseand it's right inside our immune cells.

The research at the Nutritional Immunology and Molecular Medicine Laboratory (NIMML), at the Biocomplexity Institute of Virginia Tech, targeted the gene known as NLRX1 as one that has potential therapeutic effects to aid in the treatment of gastrointestinal inflammation.

This investigation into how immunology and metabolism interface may hold critical answers for next generation nutritional immunology. The findings from the team's most recent research were published in the Journal of Immunology.

It's this sort of discovery that has the potential to customize healthcare for the individual, from personalized nutrition to precision medicine. The team uncovered new mechanistic insights into the role of NLRX1, targeting cellular metabolism and offering new therapeutic possibilities beyond traditional targets in autoimmune disease treatment.

"For decades, immunologists have applied reductionist approaches to studying the smallest details of the immune response without considering crucial system-wide interactions with nutrition and metabolism," said Josep Bassaganya-Riera, director of NIMML, a professor of immunology, and CEO of BioTherapeutics. "Our laboratory has built predictive computational and mathematical models and artificial intelligence pipelines capable of analyzing complex, massively interacting systems, including interactions between immunity and metabolism. This study not only elucidates novel mechanisms of immunoregulation in IBD, but it also validates transcriptomic and computational modeling studies that predicted the importance of NLRX1 in regulating gastrointestinal inflammation and its potential as a therapeutic target for infectious and immune-mediated diseases."

Due to an incomplete understanding of how NLRX1 works to decrease inflammation, scientific attempts to target this molecule as a treatment for the disease had previously stalled. The lab team's findings provide a deeper understanding of this gene's role in mucosal immunity and metabolism. This levels the playing field for both nutritional interventions that target NLRX1 and the development of NLRX1-based drugs.

"This seminal work, while impactful independently, sets the stage for the next lines of applied investigation on the role of NLRX1 in IBD," said Andrew Leber, scientific director of BioTherapeutics. "It highlights the need to understand not only the immediately relevant pathways for novel immunoregulatory genes, but their global effect on all of the cohesive metabolic and immunological processes within a cell, a goal that we will continue to pursue."

This work builds upon NIMML's successful track record in leading innovative transdisciplinary research at the interface of nutrition, immunity, and metabolism that dates back to its founding in 2002. The NIMML team has been involved in establishing spinoff companies that translate new scientific discoveries into the development of marketable products that address unmet consumer or clinical needs.

Explore further: Solving the immunity puzzle takes collaboration among different fields

More information: Andrew Leber et al. NLRX1 Regulates Effector and Metabolic Functions of CD4T Cells, The Journal of Immunology (2017). DOI: 10.4049/jimmunol.1601547

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Researchers at the Biocomplexity Institute of Virginia Tech have discovered a new therapeutic target for inflammatory bowel diseaseand it's right inside our immune cells.

A subpopulation of immune cells that normally fend off pathogens can turn against the host during certain infections, a new study publishing on June 20 in the open access journal PLOS Biology reveals.

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Researchers target gene to treat inflammatory bowel disease - Medical Xpress

June 20, 2017 by Christina Sumners Credit: Texas A&M University

When hundreds of thousands of American troops deployed to the Persian Gulf in 1990 and 1991 in what is now called the First Gulf War, they were exposed to a variety of chemicals. These chemicalsespecially when coupled with war-related stressseem to still be affecting nearly 200,000 Gulf War veteransor 25 to 32 percent of those who servedmore than 25 years later, and the constellation of resulting symptoms has been termed Gulf War illness (GWI). This condition is characterized by central nervous system impairmentsincluding cognitive and memory problems, mood dysfunction, sleep disorders and chronic fatigueand systemic symptoms such as gastrointestinal problems and hypersensitive skin.

Using an animal model of GWI, researchers at the Texas A&M College of Medicine and the Central Texas Veterans Health Care System were able to demonstrate how GWI occurs, and their findings, which were published in the journal Frontiers in Molecular Neuroscience, hint at possible ways to mitigate some of the symptoms. This work was supported by grants from the Department of Veterans Affairs and Department of Defense and from the Texas Emerging Technology Fund.

The chemicals troops were exposed to in the Persian Gulf included pyridostigmine bromide, which was used as prophylaxis to prevent death in an attack with nerve gas agents. In addition, mosquito repellants, such as DEET, and pesticides, such as permethrin, were sprayed on their clothes and tents to keep potentially disease-carrying insects and rodents at bay. Some troops were also likely exposed to low levels of chemical warfare agents, due to demolition of Iraqi facilities storing those agents, and smoke from oil well fires.

Chemicals like DEET and permethrin can enter the brain through disruption of the blood-brain barrier, where they can inhibit the breakdown of a neurotransmitter called acetylcholine. "Essentially, they cause acetylcholine to build up in the brain, causing hyperexcitability of neurons as well as the death of some neurons, which leads to inflammation in the brain," said Ashok K. Shetty, PhD, a professor in the Department of Molecular and Cellular Medicine at the Texas A&M College of Medicine, associate director of the Institute for Regenerative Medicine, research career scientist at the Olin E. Teague Veterans Medical Center, Central Texas Veterans Health Care System and senior author of the paper. "At the same time, troops were also taking pyridostigmine bromide, which can sequester the enzyme that breaks down acetylcholine, compounding the problem."

To test the effects of such exposure, the researchers must first create an animal model. "We simulate what happened during the war," Shetty said. "We give pyridostigmine bromide orally and apply DEET and permethrin dermally, and then expose them to a mild stressor. When you do that, these animal models develop the symptoms of GWI, such as cognitive and memory problems, and have chronic low-level inflammation in the brain." Six months laterwhich is about 17 years in human termsthere was still evidence of persistent oxidative stress, even though they hadn't been exposed to either chemicals or stress in the interim.

"Our data in animal models matches very well with what has been seen in patients," Shetty said. They both had considerable systemic inflammation, which can be measured by levels of multiple pro-inflammatory cytokines in the blood serum. Pro-inflammatory cytokines circulate all over the body and cause systemic inflammation, which, in turn, can cause considerable problems in certain vulnerable regions of the brain such as the hippocampus. These problems include declined production of new neurons important for making new memories.

"We examined changes in a type of housekeeping cell in the brain, called microglia, and they indicated inflammation, which looked similar to what we see in aging individuals with memory problems and other cognitive impairments," Shetty said. The animal models also had hyper-activated mitochondria (the 'powerhouse' of the cell), implied by increased expression of genes related to mitochondrial respirationthe process by which mitochondria transform stored energy into a form the cell can use. The researchers also found that many genes related to inflammation were upregulated. "Together, these findings raise the possibility that hippocampal dysfunction in GWI is one of the adverse outcomes of persistently elevated oxidative stress and inflammation at the systemic level," he added.

Fortunately, antioxidants and anti-inflammatory compounds may be able to treat systemic inflammation, and it is possible such treatment would improve memory and mood function, Shetty said. The next steps are to test antioxidant and/or anti-inflammatory compounds on human veterans. For this, Shetty has established a collaboration with Dena Davidson, PhD, deputy director of research at the Veterans Integrated Service Network (VISN) 17 Center of Excellence for Research on Returning War Veterans in Waco, Texas, to purse clinical trials in GWI patients. Davidson and her team, along with Shetty, will begin a clinical trial funded by the Department of Defense in September to examine the efficacy of resveratrol in GWI patients. Shetty's earlier research has shown that this compound may be able to help prevent memory loss occurring with aging. Additional studies completed recently in Shetty's laboratory have also shown resveratrol as a promising compound for decreasing systemic and brain inflammation, as well as improving cognitive and memory function in animal models of GWI.

"This really does demonstrate that when someone is exposed concurrently to a whole host of nasty chemicals even at low doses, there are consequences that are not going away," Shetty said. "We hope that our research can help improve the quality of life in these veterans who were exposed while serving our country, and therefore are so deserving of whatever we can do to support them."

Explore further: Compound found in grapes, red wine may help prevent memory loss

More information: Geetha A. Shetty et al. Chronic Oxidative Stress, Mitochondrial Dysfunction, Nrf2 Activation and Inflammation in the Hippocampus Accompany Heightened Systemic Inflammation and Oxidative Stress in an Animal Model of Gulf War Illness, Frontiers in Molecular Neuroscience (2017). DOI: 10.3389/fnmol.2017.00182

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Modeling Gulf War illness: Knowing the cause of brain dysfunction is key to finding a cure - Medical Xpress

DENVER--(BUSINESS WIRE)--CereScan, a leading provider of neuro-diagnostics solutions, presented the newest features, capabilities and use cases of its CereMetrix platform during the Society for Nuclear Medicine and Molecular Imaging (SNMMI) Annual Conference at the Colorado Convention Center last week. CereMetrix is a patented, statistically-correlated, normative and scalable medical database designed to aid in the diagnosis and treatment of the human brain.

CereMetrix will provide the healthcare community with the most robust resource on conditions like traumatic brain injury, toxic brain injury, Alzheimers Disease and other dementias, PTSD, bipolar disorder, ADHD, anxiety, autism and depression. Its a brain focused medical analytics platform that may accelerate the accurate and effective diagnosis of complex brain-related disorders to improve treatment and outcomes for patients.

We see SNMMI members as core stakeholders for CereMetrix and wanted to engage them to both share our vision and get feedback on the solution. Im happy to report that the response was overwhelmingly favorable and we now feel that we are innovating in the right direction, said John Kelley Jr., Chairman and CEO of CereScan.

The key attributes of CereMetrix include:

About CereScan

CereScan combines state-of-the-art brain imaging technologies with a patient-centered model of care to provide the highest level of neuro-diagnostics available. CereScan utilizes state-of-the-art gamma camera technology, new generation imaging software and a proprietary process to produce comprehensive medical reports including voxel level images of brain function and physiology. Our functional brain imaging technologies are the most sophisticated in the world today. Additional information about the company is available at https://cerescan.com.

CereScan and CereMetrix are registered trademark of CereHealth Corp.

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CereScan Demos CereMetrix at Society for Nuclear Medicine ... - Business Wire (press release)

News / Published: 19 June 2017

Several members of the Wellcome community have been named in the Queens Birthday Honours list. The list, which was announced over the weekend, includes over 1,000 people who are recognised for their achievements and contributions to society.

Members of the Wellcome community recognised in the honours list include:

Our warmest congratulations to all those who have been honoured this year.

Dr Jeremy Farrar, Wellcomes Director, said: "The Queens Birthday Honours is a wonderful way to celebrate the achievements and contribution to society of so many from Wellcomes broad community. I am delighted for everyone who was recognised, but a very special mention and congratulations to Beth Thompson who led Wellcomes work on EU data protection, which allowed critical research to proceed, ensured cross border collaboration and protected individual privacy. A huge achievement!"

A full list of all those who have been recognised can be found on the Government website.

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Awards for the Wellcome community in the Queen's Birthday Honours - Wellcome Trust

Newswise DETROIT The medical journal publishing original research in the field of obstetrics and gynecology with the highest impact factor is edited on the campus of the Wayne State University School of Medicine.

Thomson Reuters announced June 14 the 2016 impact factor of biomedical journals on its Journal Citation Reports, the world's most influential resource for evaluating peer-reviewed publications and the authoritative source of annual journal metrics, including the renowned Impact Factor of Journals.

The American Journal of Obstetrics & Gynecology ranked second in the discipline of obstetrics and gynecology with an impact factor of 5.574. Human Reproduction Update, which publishes only reviews and not original research, ranked first; therefore, for all intents and purposes, the American Journal of Obstetrics & Gynecology is the leading journal in impact factor in obstetrics and gynecology publishing original research.

Roberto Romero, M.D., D.Med.Sci., chief of the Perinatology Research Branch of the Eunice Kennedy Shriver National Institute of Child Health and Human Development/National Institutes of Health, is editor in chief for Obstetrics of the American Journal of Obstetrics & Gynecology. The journal, the oldest in obstetrics and gynecology, which celebrates its 150th anniversary in 2019, is edited at the PRB, on the campus of the WSU School of Medicine and the Detroit Medical Center.

The American Journal of Obstetrics & Gynecology has the highest number of citations of any journal in obstetrics and gynecology, said Dr. Romero, who also serves as director of the Division of Obstetrics and Maternal-Fetal Medicine for the NIH and is a professor of Molecular Obstetrics and Genetics in the Center of Molecular Medicine and Genetics for Wayne State University.

Throughout its distinguished history, the journal has changed the lives of women and their families, and the practice of obstetrics and gynecology.

Dr. Romero offered numerous examples of landmark papers published on the pages of the journal, including:

The impact factor, published independently by Thomson Reuters, is used to assess a journal's standing in scholarly literature through the objective evaluation of quantifiable, statistical information. The analysis comprises citation data, impact and influence metrics, and millions of cited and citing journal data points from the Web of Science, the industry's leading citation indices in the sciences, social sciences, and arts and humanities.

The American Journal of Obstetrics & Gynecology, Dr. Romero noted, has introduced innovations in biomedical publishing and is committed to bringing information to physicians, scientists, midwives, nurses and patients, and has promoted changes to favor wide dissemination of its content with videos, PowerPoint presentations and other features. The journal has a new section to celebrate Giants in Obstetrics and Gynecology, recognizing the protagonists of the field and the stories behind the headlines.

The journal is published by Elsevier, the largest publisher in the world. The American Journal of Obstetrics & Gynecology has a printed circulation of 42,000 in the United States, and is present in every major biomedical library and maternity hospital around the world. Its electronic presence and international footprint and influence have made it the premier academic journal in obstetrics and gynecology.

###

About Wayne State University

Wayne State University is one of the nations pre-eminent public research universities in an urban setting. Through its multidisciplinary approach to research and education, and its ongoing collaboration with government, industry and other institutions, the university seeks to enhance economic growth and improve the quality of life in the city of Detroit, state of Michigan and throughout the world. For more information about research at Wayne State University, visit research.wayne.edu.

The rest is here:

Top Biomedical Journal Is Edited at Wayne State University and the Perinatology Research Branch of NICHD/NIH - Newswise (press release)

In 2010, Sonia Vallabh watched her mom, Kamni Vallabh, die in a really horrible way.

First, her mom's memory started to go, then she lost the ability to reason. Sonia says it was like watching someone get unplugged from the world. By the end, it was as if she was stuck between being awake and asleep. She was confused and uncomfortable all the time.

"Even when awake, was she fully or was she really? And when asleep, was she really asleep?" says Sonia.

The smart, warm, artistic Kamni just 51 years old was disappearing into profound dementia.

"I think until you've seen it, it's hard to actually imagine what it is for a person to be alive and their body is moving around, but their brain is not there anymore," says Eric Minikel, Sonia's husband.

In less than a year, Sonia's mom died.

An autopsy showed Kamni had died from something rare -- a prion disease. Specifically, one called fatal familial insomnia because in some patients it steals the ability to fall asleep.

Basically, certain molecules had started clumping together in Kamni's brain, killing her brain cells. It was all because of one tiny error in her DNA an "A" where there was supposed to be a "G," a single typo in a manuscript of 6 billion letters.

Sonia sent a sample of her own blood to a lab, where a test confirmed she inherited the same mutation. The finding threw the family into grief all over again.

"But that grieving period sort of started to resolve within about a week or so," she says. "And we weren't in crisis anymore. We were finding our way toward a new normal, where this was something that we were going to have to live with and deal with and learn more about."

Today, Sonia and her husband live and work in Cambridge, Mass., where they are both doctoral students in the lab of Stuart Schreiber, a Harvard professor of chemistry and chemical biology. Over the past several years, the couple has completely redirected their careers and their lives toward this single goal: to prevent prion disease from ever making Sonia sick.

The two wear bright colors and laugh easily. When they answer my questions, they look at each other instead of at me. They like complicated board games, urban walks and efficient cooking. They are thinkers and problem solvers, which is why, when Sonia got her genetic test results, it changed everything.

The change

"It didn't happen all at once," Sonia says. "There wasn't a day when we woke up and said, 'OK let's change everything about our lives.'"

At the time, Sonia, who has a Harvard law degree, had just started a new job as a legal consultant. Eric was a transportation analyst.

But they couldn't stop thinking about Sonia's test result. They started researching prion diseases online, and invited over friends who are biologists and chemists, to help them understand the science.

"And around that time," Sonia says, "we both enrolled in night classes as well," in subjects like biology and neuroscience.

They were hungry to learn more as quickly as possible; the night classes weren't enough.

"I was basically fresh out of law school and started walking into classes at MIT during the day because this was kind of all I could think about," says Sonia, who at the time wore sneakers every day so that she could rush between work, classes, and a neuroscience lab at Massachusetts General Hospital. She'd started volunteering there, thanks to a professor from one of her classes, and mentors in the lab who helped her learn everything from how to use a pipette to how to work with human brain cells.

"And from there, this is where things happened surprisingly quickly," Sonia says.

The couple started a nonprofit, Prion Alliance, in hopes of raising money for research. Sonia left her legal job to work in the Mass General lab full-time as a technician. Then, Eric left his job and joined a genetics lab, applying his skills in coding to analyzing genetic data, rather than transportation data.

"I was getting left behind!" he says. "Sonia was out there doing all this science. It was her day job now and I was still in my old career and, you know, it was a good job and all, it was meaningful, but it wasn't the mission that it was increasingly clear that we were going to be on."

Just months after they'd finished grad school in law and urban planning, the pair went back to graduate school, this time in biomedical sciences to study prion diseases.

"You are talking to two third-year graduate students," says Eric.

Life as scientists

The two now share an office and a lab bench, under Schreiber's supervision, at the Broad Institute of MIT and Harvard.

"There's a date in the future when Sonia will get the first dose of the drug that's going to save her life," Eric says. "What can I do today that brings that date closer to the present?"

A posted printout of an email says: "Let's just blast forward and solve problems as they become real and as they need immediate solutions." It's a note Schreiber sent the pair at one point when they were worrying about bureaucratic hoops they had to jump through.

"I thought it was a good philosophy, so we printed it out and put it on the wall," says Eric.

Sonia and Eric are "the best of humanity" Schreiber tells Shots. "Their story is, of course, remarkable, and they personify the concept of patientscientists. But their deep understanding of science and ability to innovate and execute on one of the hardest challenges in biomedical science are breathtaking."

Schreiber says that his lab, like many others in biomedicine, has long included researchers who are physicians as well as scientists; that dual training and experience brings an important perspective to the research, he says.

"But the last decade has seen the emergence of patientscientists including Sonia and Eric, but also others in my lab," he says. "And this has had an even greater impact on the lab. They remind us of our mission to understand and treat human disease."

Still, it's really hard to cure diseases especially conditions like this one, because the usual way scientists look for a treatment isn't going to work.

Sonia is 33 years old. On average, people with the kind of genetic mutation she has usually start to show symptoms at age 50. But they could surface at any time. Symptoms of fatal familial insomnia have set in as early as age 12 and as late as 84. Once they do, it's a rapid decline like Alzheimer's disease on fast-forward.

"You're healthy, you're healthy, you're healthy and then you're falling off a cliff," says Sonia. "You wait a little bit too long, and that patient is gone. We need to get out ahead of it aggressively."

The challenge

They need to keep Sonia from getting sick in the first place. And they need to do it quickly. But right now, Sonia appears to be just fine, and that's actually one of the first obstacles.

Across medicine, there is an understandable resistance to testing experimental drugs on healthy people. That's why, traditionally, drug trials go something like this: Take a group of people who are sick, give some of them an experimental medicine, and wait to see if it makes them get better, live longer, or decline more slowly than people who didn't get the drug.

But Sonia has to convince the medical establishment that, especially in the age of genetics, some people who seem perfectly healthy should be considered patients.

"We have to be willing to act upstream of what we would traditionally call 'illness'," she says.

It's a shift in mindset that she had to come to grips with, personally.

"I feel very lucky to be healthy today," she says. "But I hold a sort of dual reality understanding of my own health, which is that I'm healthy today but very seriously at risk for a very serious disease."

Others in the medical field, like Dr. Reisa Sperling, who studies Alzheimer's disease, are making the same mental shift as they think about the best time to intervene.

"Alzheimer's disease is a terrible disease. Many people fear it more than cancer," says Sperling, a neurologist with Brigham and Women's Hospital and Massachusetts General Hospital.

Like Sonia and Eric, she, too, is on a quest to prevent even the first symptoms of a terrible brain disease.

Sperling is now enrolling people whose brain scans show they might be in the very early stages of Alzheimer's in a clinical trial to test an experimental drug treatment. And she's planning another study in people as young as 50 who have no noticeable symptoms, but are at high risk of developing them.

"It really does primarily come down to thinking about disease as beginning years before symptoms," says Sperling. "If we can shift that thinking not just in Alzheimer's disease, but in rarer diseases like prion diseases I think this is the way we win the war."

But before any of that can happen with a prion disease, there's the problem of actually doing the science to find a good candidate drug.

The plan

Researchers don't have one in hand yet, but they have a clear idea of what it should look like, based on studies in mice. Sonia and Eric already are talking to pharmaceutical companies that may be involved in running human trials in the future, and have requested a meeting with the Food and Drug Administration to talk about what a trial should involve.

Other efforts at treating prion disease have focused on preventing the misfolded proteins from killing brain cells, or on preventing them from accumulating. Sonia and Eric have a different approach.

"We're really interested in preventing the misfolding in the first place," says Sonia.

"Sonia's brain is producing this mutant protein," Eric says. "But as far as we know it's not misfolded yet, and the disease process hasn't started. I want her brain to be producing half or less of the amount of that protein as she is [producing] right now, because we know that less is better."

Essentially, they want to muffle the faulty gene in order to reduce the amount of prion protein floating around in Sonia's brain.

But a key question right now is this: Say they make the right drug and give it to Sonia and others with her type of mutation. If the goal is to change nothing about her current health, then how will they know it's actually working?

A traditional clinical trial is out of the question, Eric says.

It would be unethical and untenable he says, to "just treat half of the people with a drug and half with placebo and then wait 30 years to see when they die."

Not only would that kind of experiment condemn some patients to terrible death, it would also be wildly expensive and require thousands of participants. There are only a few hundred people in the U.S. with prion disease mutations.

"Instead, we need a biomarker," Eric says. "We need some laboratory test that we can run on a living human to see if the drug is having its effect."

The answer, Sonia and Eric hope, could be in a very cold refrigerator in the lab where they work. It's full of samples of spinal fluid. In mouse studies, at least, reducing prion protein in the brain seems to delay disease progression.

So, Sonia and Eric are now studying samples of spinal fluid from all sorts of people from people who already have symptoms of prion disease, from others like Sonia (who have mutations for prion disease but no symptoms yet) and from healthy controls. The aim is to establish how the levels of protein in the samples change over time, to figure out if protein levels would be a good enough measure to say, "Yes, this drug works."

"We have strong evidence that 50 percent [reduction] if we could achieve that would be protective," says Sonia, based on preliminary findings in mice.

Others are optimistic, too

Sonia and Eric are organized, hardworking, and efficient. Ultimately, for them, failure is not an option. But on a day-to-day basis, failure is what science is all about.

"In biology, if everything you did one day goes wrong, and then you figure out why it went wrong, that was a good day," says Eric, who chronicles their struggles on a blog.

It's an achingly slow process. But Eric thinks they will do it they'll find a drug.

"I'm an optimist that we'll get there in our lifetime," he says, "but not this year and not next year."

He's not alone in his optimism. Sonia and Eric have some powerful colleagues who believe the couple can pull it off colleagues like Eric Lander, a renowned mathematician, geneticist and molecular biologist. He started the Human Genome Project and founded the Broad Institute where Sonia and Eric now work.

"This is not pie in the sky," says Lander. "I see a path forward for multiple shots on goal. All you have to do is get one through."

Fifteen years ago, he says, solving this puzzle would have seemed impossible. But now he believes the science, the technology, and the knowledge about what certain mutations mean for a person's health have made defeating prion disease possible.

"Human genetics and molecular medicine are reaching a point of maturity where they're becoming much more powerful," he says. "It's exciting and important and there's nobody who's more motivated than somebody who's going to be affected by the disease themselves."

One small success

In one way, Sonia and Eric have already stopped the disease in its tracks.

Sonia is very pregnant. She's due in July to have a daughter a daughter without a mutation for prion disease. That's something the couple made sure of by screening embryos after in vitro fertilization.

So, they've stopped the transmission of prion disease in Sonia's line of the family. And in a way, that's a gift from Sonia's mom, Kamni, the couple says.

"If my mom was still alive, we wouldn't know any of this and we wouldn't have had the opportunity to choose to have a mutation-negative baby," says Sonia. "But, tragically, it also means that they'll never meet."

Sonia and Eric hope that, by the time their daughter is in elementary school, Sonia will be taking an experimental drug that could keep her as healthy as she is today.

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A Couple's Quest To Stop A Rare Disease Before It Takes One Of Them - Maine Public

June 19, 2017 by Joseph Bonner The top image shows the movement of a mouse in a behavioral test that measures social interaction. The blue to green color represents least to most time spent interacting with another mouse. The bottom set of images measures anxiety-like behavior exhibited by a mouse. The amount of filling in the vertical bars represents levels of anxiety. Credit: Dr. Zeeba Kabir/Weill Cornell Medicine

A calcium-dependent molecular mechanism discovered in the brain cells of mice by Weill Cornell Medicine investigators may underlie the impaired social interactions and anxiety found in neuropsychiatric disorders including schizophrenia and autism.

The study, published June 6 in Molecular Psychiatry, reports that reduced function of a calcium channel at synapses, the site of contact essential for communication between neurons, impairs social behavior and heightens anxiety. The findings also illuminate how this occurs: overactivation of a molecule within protrusions in neurons, called spines, which receive communicating signals from adjacent neurons. Blocking the action of this molecule in adult mice repaired the abnormal social interactions and elevated anxiety, a finding that may lead to the development of new treatments for patients with certain neuropsychiatric and anxiety disorders.

"Our study suggests that if we can repair malfunctioning synapses in humans, we can reverse behavioral abnormalities and potentially treat specific symptoms, such as social impairment and anxiety, in patients with these neuropsychiatric disorders," said senior study author Anjali Rajadhyaksha, associate professor of neuroscience in pediatrics and of neuroscience in the Feil Family Brain and Mind Research Institute, and director of the Weill Cornell Autism Research Program at Weill Cornell Medicine. "We believe that targeting this molecule and its pathway may provide us with a molecular framework for future exploration of treatment of patients."

Rajadhyaksha and her colleagues focused on a calcium channel gene called CACNA1C that has emerged as a significant risk gene across major forms of neuropsychiatric disorders: schizophrenia, bipolar disorder, major depressive disorder, autism spectrum disorders and attention deficit hyperactivity disorder. Impaired social behavior and elevated anxiety are common symptoms observed in patients with these disorders.

Studies using mice lacking CACNA1C production in neurons in a part of the brain, called the prefrontal cortex, which is responsible for cognition, personality and decision-making, made mice less social and more anxious. This finding seemingly confirms those of human studies, which suggests that defects in protein production may underlie the symptoms of patients with neuropsychiatric disorders and autism.

The investigators then identified the culprit for the social impairments and elevated anxiety: increased activity of a molecule called eIF2alpha that has been linked to cognitive deficits in neurodegenerative disorders like Alzheimer's disease.

Zeeba Kabir, the study's first author and a postdoctoral researcher in Rajadhyaksha's lab, tested a small molecule called ISRIB, which had previously been shown to block the action of eIF2alpha and improve learning and memory in mice, in rodents missing the CACNA1C gene. ISRIB reversed the aberrant behavior found in these mice, improving their social interactions and reducing anxiety.

"Some studies have revealed that ISRIB has side effects that may be harmful to human cells," Rajadhyaksha said, "but research shows that there are two alternative small molecule inhibitors of eIF2alpha that may be safer for use in humans. A next step is to study these ISRIB alternatives in mice to determine whether they have a similar effect."

"Neuropsychiatric disorders are complex and treatments remain suboptimal," Rajadhyaksha said. "To be able to treat specific symptoms that are common across multiple disorders is an exciting possibility. We would also like to determine whether alterations in the eIF2alpha pathway are held in common among other rodent models displaying social deficits and anxiety that result from risk genes other than CACNA1C. If so, molecules like ISRIB could be widely applicable for treating these symptoms, in general."

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Molecular mechanism underlies anxiety, autism - Medical Xpress

The WNT1 ligand has previously been identified in bone disease, but its role in bone homeostasis, its cellular source and targets in bone have only just recently been identified.The research, led by Dr. Brendan Lee at Baylor College of Medicine, appears in the Journal of Clinical Investigation.

To determine the bone-specific function of WNT1, the mutation that has been associated with recessive forms of Osteogenesis Imperfecta (OI) and other forms of early-onset osteoporosis, Lee, chair of the Department of Molecular and Human Genetics at Baylor, generated mouse models to study the consequences of both the loss and gain of WNT1 function in a specialized bone cell called the osteocyte.

This research builds on previous work that identified WNT1s role in coordination and its known effect on brain development. Now, we understand how this molecule works in bone, and this paper tells us that WNT1 is produced by osteocytes to control the activity of the bone-forming cell, the osteoblast, said Lee, also the Robert and Janice McNair Endowed Chair and professor of molecular and human genetics at Baylor.

The role of osteocytes, blasts and clasts

The over- or underexpression of WNT1 is controlled by osteocytes, or bone embedded cells. The osteocytes produce WNT1 to signal to bone-forming cells called osteoblasts that reside on the surface of bone via a biochemical pathway called mTORC1. When WNT1 is overexpressed by the osteocyte, bone formation is stimulated due to an increase in osteoblast numbers and collagen production following the activation of the mTORC1 pathway in these cells.

Osteocytes are embedded in the bone, with osteoblasts and osteoclasts sitting on the surface adding or removing bone, respectively, explained Lee. It turns out, osteocytes are actually the master controllers of this balance of bone formation and resorption in part by acting as either a receiver or sender of WNT signals.

We knew previously from others work that osteocytes could inhibit bone formation by producing the protein sclerostin, which represses osteoblast function. This research brings the cycle of information full circle by showing that while sclerostin turns the osteoblasts off, WNT1 from osteocytes turns them on, Lee said.

On the other hand, loss of WNT1 function resulted in low bone mass and spontaneous fracturing, similar to that seen in patients with OI. In this case, the osteocyte is not producing WNT1. However, osteocytes also can receive WNT signals themselves, leading them to control the activity of bone-removing cells, the osteoclasts.

Therapeutic impact

Primary therapies traditionally used to treat OI have shown limited efficacy in combating WNT1-related OI and osteoporosis. However, Lee and his research team identified anti-sclerostin antibody (Scl-Ab) treatment is effective in augmenting the action of other WNT ligands to improve bone mass and to significantly decrease the number of fractures in swaying mice, a model of WNT1 related OI and osteoporosis.

The results of this study, while conducted in mice, have important implications for the treatment of OI and osteoporosis in humans down the road, Lee said. By blocking sclerostin, the bone can be repaired effectively in diseases related to loss of WNT1 suggesting a personalized therapy. This is exciting especially as a promising anti-sclerostin drug is already in clinical development.

This work was supported by the Baylor College of Medicine Intellectual and Developmental Disabilities Research Center from the Eunice Kennedy Shriver National Institute of Child Health and Human Development, the Baylor College of Medicine Advance Cores with funding from the National Institutes of Health, the National Institute of Arthritis and Musculoskeletal and Skin Diseases, the Rolanette and Berdon Lawrence Bone Disease of Texas and the Center for Skeletal Medicine and Biology at Baylor College of Medicine.

Other contributors to this work include Kyu Sang Jeong, Yi-Chien Lee, Yuqing Chen, Ming-Ming Jiang and Elda Munivez, all of whom are with Baylor, and Catherine Ambrose with the University of Texas Health Science Center at Houston.

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Research shows bone-building protein can be used in therapy - Baylor College of Medicine News (press release)

Torrance dad David Lau has at least two things in common with Happy Randhawa out in Corona and Yusheng Chen in Chino Hills.

All three are devoted to their childrens education. And, boy, can their kids spell.

Their commitment has helped their children excel in school and taken the dads on trips sometimes more than once to the nations capital as their kids battle it out against the countrys top spellers.

But its the time spent with their kids not chasing the spelling bee crown thats most valuable to these fathers.

This is absolutely the most important job I can have, Randhawa, 43, said of being a father.

All three of them helped and supported their children as they moved through competitions to reach this years Scripps National Spelling Bee in late May.

Jennifer Lau, 14, finished 41st, Daniel Chen, 14, was 23rd, and Aisha Randhawa, 11, came in 35th at the event held outside Washington, D.C.

Being a dad is the hardest job but is the greatest honor and privilege a man could have, said David Lau, a 51-year-old minister at Bread of Life Church in Torrance.

Happy Randhawa encourages other dads to invest in their kids learning. He points out that studies show that having both parents involved leads to less poverty, higher levels of education and other positive outcomes.

The leader of a group that promotes involved fathers agrees.

When men engage themselves in their kids education, whether its at home coaching them academically on a spelling bee or something like that, it serves to further reinforce the work that teachers are doing, said Eric Snow, president and co-founder of Watch D.O.G.S., which stands for Dads of Great Students.

The nonprofit founded in 1998 in Arkansas aims to get fathers to volunteer on school campuses. It has programs in more than 300 schools in California.

Children spend more time working on a math or spelling problem if their father is doing it with them, he said.

The kids are wanting that attention and wanting that connection, Snow said. Its important for the guys to make time to do that.

Heres a look at what makes these dads special:

Lau said he put his golf passion on hold and doesnt watch much TV so he can instead hang out with Jennifer and his 17-year-old son, Timothy. His son also made it to the national spelling bee, finishing 13th in 2014.

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Youve got to prioritize your time, he said. The time your kids are living with you under your roof is pretty limited. The other things can wait.

Lau, who has a background in electrical engineering, uses his math expertise to teach them the underlying concepts of algebra and geometry.

Its not just doing well academically, but having a well-rounded knowledge of all subjects, he said.

To lighten the mood or relieve stress, Lau said he tells corny jokes that often elicit groans from his kids. He occasionally breaks out in song and dance or acts out scenes from their favorite movie, Star Wars, to try to make them laugh.

Chen, 50, a part-time Christian minister who is studying theology, said he tries to set the example for his two sons.

He regularly checks out library books and videos to learn new skills such as plumbing and drywall installation.

The most important thing will be to glorify God, said Chen, who was born in Taiwan and came to the United States in 1991 to pursue a doctorate in molecular medicine at Emory University in Atlanta.

After graduating, he secured a faculty position at the University of Chicago doing research and teaching statistical genetics and advanced molecular neuroscience.

He said he gave up that career when God called him to become a minister.

The one thing I want to teach my kids is its never too late or youre never too old to learn, said Chen, whose other son, Samuel, is 12.

Happy Randhawa has high expectations for his four kids. But he also knows when to let them have fun.

Aisha unwinds from her homework and daily spelling bee preparation by playing basketball and golf with her dad.

I feel like he puts in so much effort to help me, Aisha said. Im so grateful for all the time he puts in every evening. He makes sure Im doing OK and if I ever need anything. I love him so much.

Randhawa tells a story about his late father.

Ajit Randhawa came to the United States from India in 1969 and worked as a microbiology researcher at Loma Linda University. He later opened veterinary clinics in Beaumont and Hemet.

The father liked to garden in his spare time and asked his kids to help. When his son complained about tilling the soil, Ajit Randhawa would give him a choice.

He would say, Is it easier to study or is it easier to dig this dirt up? Randhawa recalls his dad telling him. When I said, its easier to study, he said, Good. Then go do that.

Many years later, Randhawa is passing on the same lessons to his daughters Aisha and Lara, 8, and his 6-year-old twin boys, Avi and Arav.

After becoming a doctor, Randhawa furthered his studies and wanted to become a researcher specializing in diabetes and growth-related disorders in children.

But he abandoned that dream and decided to work in a pediatric practice so he could spend time raising Aisha with his wife, Sundeep, who is also a doctor.

When you get home from work, your job is not over, he said. You have a second job. And that is to sit down with your children and see what theyre doing with their schooling.

Continued here:

Father's Day: These spelling bee helpers love being D-A-D-S - The Daily Breeze

Coronas Happy Randhawa and Yusheng Chen of Chino Hills have at least two things in common.

Theyre devoted to their kids education. And, boy, can their kids spell.

Their commitment has helped their children excel in school and taken the dads on trips sometimes more than once to the nations capitol as their kids battle it out against the countrys top spellers.

But its the time spent with their kids not chasing the spelling bee crown thats most valuable to these fathers.

This is absolutely the most important job I can have, Randhawa, 43, said of being a father.

Both helped and supported their children as they moved through competitions to reach this years Scripps National Spelling Bee in late May.

Daniel Chen, 14, finished 23rd. Aisha Randhawa, 11, came in 35th at the event held outside Washington D.C.

Happy Randhawa encourages other dads to invest in their kids learning. He points out that studies show that having both parents involved leads to less poverty, higher levels of education and other positive outcomes.

The leader of a group that promotes involved fathers agrees.

When men engage themselves in their kids education, whether its at home coaching them academically on a spelling bee or something like that, it serves to further reinforce the work that teachers are doing, said Eric Snow, president and co-founder ofWatch D.O.G.S., whichstands for Dads of Great Students.

The nonprofit founded in 1998 in Arkansas aims to get fathers to volunteer on school campuses. It has programs in more than 300 schools in California, including at least 100 in Riverside and San Bernardino counties.

Children spend more time working on a math or spelling problem if their father is doing it with them, he said.

The kids are wanting that attention and wanting that connection, Snow said. Its important for the guys to make time to do that.

Happy Randhawa has high expectations for his four kids. But he also knows when to let them have fun.

Aisha unwinds from her homework and daily spelling bee preparation by playing basketball and golf with her dad.

I feel like he puts in so much effort to help me, Aisha said. Im so grateful for all the time he puts in every evening. He makes sure Im doing OK and if I ever need anything. I love him so much.

Happy tells a story about his late father.

Ajit came to the United States from India in 1969 and worked as a microbiology researcher at Loma Linda University. He later opened veterinary clinics in Beaumont and Hemet.

Ajit liked to garden in his spare time and asked his kids to help. When his soncomplained about tilling the soil, Ajit would give him a choice.

He would say, Is it easier to study or is it easier to dig this dirt up?'Happy recalls his dad telling him. When I said, its easier to study, he said, Good. Then go do that.

Many years later, Happy is passing on the same lessons to his daughters Aisha and Lara, 8, and his 6-year-old twin boys, Avi and Arav.

After becoming a doctor, Happy furthered his studies and wanted to become a researcher specializing in diabetes and growth-related disorders in children.

But he abandoned that dream and decided to work in pediatric practice so he could spend time raising Aisha with his wife, Sundeep, who is also a doctor.

When you get home from work, your job is not over, he said. You have a second job. And that is to sit down with your children and see what theyre doing with their schooling.

Chen, 50, a part-time Christian minister who is studying theology, said he tries to set the example for his two sons.

He regularly checks out library books and videos to learn new skills such as plumbing and drywall installation.

The most important thing will be to glorify God, said Chen, who was born in Taiwan and came to the United States in 1991 to pursue a doctorate in molecular medicine at Emory University in Atlanta.

After graduating, he got a faculty position at the University of Chicago doing research and teaching statistical genetics and advanced molecular neuroscience.

He gave up that career when God called him to become a pastor.

Theone thing I want to teach my kids is its never too late or youre never too old to learn, said Chen, whose other son, Samuel, is 12.

Link:

These spelling bee fathers love being DADS - Press-Enterprise

A calcium-dependent molecular mechanism discovered in the brain cells of mice by Weill Cornell Medicine investigators may underlie the impaired social interactions and anxiety found in neuropsychiatric disorders including schizophrenia and autism.

The study, published June 6 in Molecular Psychiatry, reports that reduced function of a calcium channel at synapses, the site of contact essential for communication between neurons, impairs social behavior and heightens anxiety. The findings also illuminate how this occurs: over-activation of a molecule within protrusions in neurons, called spines, which receive communicating signals from adjacent neurons. Blocking the action of this molecule in adult mice repaired the abnormal social interactions and elevated anxiety, a finding that may lead to the development of new treatments for patients with certain neuropsychiatric and anxiety disorders.

Our study suggests that if we can repair malfunctioning synapses in humans, we can reverse behavioral abnormalities and potentially treat specific symptoms, such as social impairment and anxiety, in patients with these neuropsychiatric disorders, said senior study author Dr. Anjali Rajadhyaksha, an associate professor of neuroscience in pediatrics and of neuroscience in the Feil Family Brain and Mind Research Institute, and director of the Weill Cornell Autism Research Program at Weill Cornell Medicine. We believe that targeting this molecule and its pathway may provide us with a molecular framework for future exploration of treatment of patients.

The top image shows the movement of a mouse in a behavioral test that measures social interaction. The blue to green color represents least to most time spent interacting with another mouse. The bottom set of images measures anxiety-like behavior exhibited by a mouse. The amount of filling in the vertical bars represents levels of anxiety. Dr. Anjali Rajadhyaksha and her team utilized rodent tests that are commonly used to study human disease symptoms, demonstrating that mice that were missing the CACNA1C gene in the brain showed less preference for interactions with another mouse and developed high anxiety. Treatment with the small molecule ISRIB corrected these symptoms. Photo credit: Dr. Zeeba Kabir

Dr. Rajadhyaksha and her colleagues focused on a calcium channel gene called CACNA1C that has emerged as a significant risk gene across major forms of neuropsychiatric disorders: schizophrenia, bipolar disorder, major depressive disorder, autism spectrum disorders and attention deficit hyperactivity disorder. Impaired social behavior and elevated anxiety are common symptoms observed in patients with these disorders.

Studies using mice lacking CACNA1C production in neurons in a part of the brain, called the prefrontal cortex, which is responsible for cognition, personality and decision-making, made mice less social and more anxious. This finding seemingly confirms those of human studies, which suggests that defects in protein production may underlie the symptoms of patients with neuropsychiatric disorders and autism.

The investigators then identified the culprit for the social impairments and elevated anxiety: increased activity of a molecule called eIF2alpha that has been linked to cognitive deficits in neurodegenerative disorders like Alzheimers disease.

Dr. Zeeba Kabir, the studys first author and a postdoctoral researcher in Dr. Rajadhyakshas lab, tested a small molecule called ISRIB, which had previously been shown to block the action of eIF2alpha and improve learning and memory in mice, in rodents missing the CACNA1C gene. ISRIB reversed the aberrant behavior found in these mice, improving their social interactions and reducing anxiety.

Dr. Anjali Rajadhyaksha. Photo by John Abbott

Some studies have revealed that ISRIB has side effects that may be harmful to human cells, Dr. Rajadhyaksha said, but research shows that there are two alternative small molecule inhibitors of eIF2alpha that may be safer for use in humans. A next step is to study these ISRIB alternatives in mice to determine whether they have a similar effect.

Neuropsychiatric disorders are complex and treatments remain suboptimal, Dr. Rajadhyaksha said. To be able to treat specific symptoms that are common across multiple disorders is an exciting possibility. We would also like to determine whether alterations in the eIF2alpha pathway are held in common among other rodent models displaying social deficits and anxiety that result from risk genes other than CACNA1C. If so, molecules like ISRIB could be widely applicable for treating these symptoms, in general.

The research team also included Weill Cornell Medicine researchers Dr. Natalia DeMarco Garcia, an assistant professor of neuroscience, and Dr. Michael Glass, an associate professor of research in neuroscience, both in the Feil Family Brain and Mind Research Institute.

Read more:

New Molecular Pathway Underlies Impaired Social Behavior and ... - Cornell Chronicle

A charity founder, a glassblowing expert and community hero, a world-leading expert diabetes expert, and the man behind some of the millions of government documents written on vellum have all been honoured by the Queen. This year is the centenary of the Queen's Birthday Honours, and five people from Devon have been named.

Ruth Airdie and Norman Veitch has been awarded MBE's, and Brian Medhurst has been awarded a BEM, while Andrew Hattersley, Professor of Molecular Medicine at the University and a diabetes consultant at the Royal Devon & Exeter NHS Foundation Trust, has been awarded a CBE.

Ruth Airdrie, 64, from Aylesbeare, is the founder of Rainbow Living, was awarded an MBE for services to Adults with Learning Disabilities.

In 2006 she raised money to establish Rainbow Living and opened the first home in 2008. She knew other families with similar special needs issues and felt that it would be better if young adults could have secure futures through special accommodation. This also offered parents vital respite from their caring responsibilities. Each young adult has gradually learned to co-habit with the support of the committed staff.

The charity also runs holidays for the residents which enable them to try new activities with support and friends. Such was its success that Rainbow Living opened a second home in 2012 in Torquay and have now bought their third home in Exeter.

She worked for NHS Devon as head of clinical effectiveness. She has secured funding from Sainsbury's and other local businesses and has planned a variety of events including fashion shows at John Lewis, music concert, book sales and other events in Devon. Since the charity was founded it is estimated that she has raised 200,000.

Ruth said: It is a real honour to have been appointed an MBE and I feel truly privileged to have had the opportunity to support learning disabled adults through Rainbow Living's accommodation projects.

I am so proud that the tireless commitment of everyone involved with Rainbow Living has been recognised in this way; our work shows how a group of normal, everyday people can put something back and make a real, lasting and positive difference not only to our Rainbow tenants, but also to their wider families and local communities.

I am overwhelmed by this as it was a bit of a shock, but I am delighted, and I feel honoured that my charity work has been recognised."

Norman Veitch, 70, from Dartington, has been awarded MBE for services to glassblowing.

His contribution to glass art is invaluable. Along with his colleague, Brian Jones, they started work at the Pyrex factory in Sunderland, later known as Corning Glass Works. They were trained in the art of lampworking - the glassblowing technique using a gas burner and worked as glassblowers fabricating complex chemical apparatus for use in laboratories.

When the industry declined around 1980, they found that the properties of the glass made it an excellent medium for complex sculptural work, so they created ornamental glass.

In 1996 they jointly founded Wearside Glass Sculptures. They hold daily demonstrations of lampworking, entertaining visitors and informing them about the properties of glass and the history of glassmaking in Sunderland. Their reputation has attracted commissions from all over the UK, helping artists realise their ideas in glass, to restoring family heirlooms. They have preserved many historical artefacts from the region.

They are also dedicated to teaching their skills to others and generously share their vast experience and knowledge with students. They have dedicated their lives to the pursuit of glass and have adapted their work according to the changing economic climate. As well as being talented creative glassmakers, they have become role models for many young artists.

Brian Medhurst, 82, from Yelverton, has been awarded a BEM for services to the community in Yelverton,

In 1998 he founded the Yelvercare, a system of local volunteers who man a phone and respond to anyone in the catchment area who needs help such as transport, home visits or small DIY projects etc. Since its foundation, Yelvercare has conducted over 8000 tasks and has a volunteer base of 148 volunteers and 130 clients, many of whom are in need of regular use of the service. He has also been involved in the creation of a play park in Yelverton.

His tireless commitment to his community has resulted in children of all ages enjoying the one acre park. Through consultation, he has also established Yelverton's own cinema in the village hall. He sourced the funding of a fully functional cinema which operates throughout the year.

For several years he was also been the trustee of the Fortescue Garden Trust providing invaluable financial and investment advice. He also supports student gardeners and the work he has put in for the trust resulted in the garden being of great importance and benefit to the community, particularly the retired.

Brian said: It is really good news and the icing on the cake for me. I founded the charity 20 years ago, and five years ago we got the Queens Award for voluntary service, so this is the icing on the cake for me really to get this personal honour. The important thing is how much of a success we made this and it has been a great success.

It was a nice surprise to get this award. I am retiring at the end of the year so this has come at the perfect time. It is with great joy and delight that I this award."

A world-leading expert diabetes expert has been awarded the CBE in the Queen's birthday honours list for his work revolutionising diagnosis and treatment of diabetes.

Andrew Hattersley, Professor of Molecular Medicine at the University and a diabetes consultant at the Royal Devon & Exeter NHS Foundation Trust, has won a string of international awards for his work in combining genetic diagnosis with clinical treatment to make a real difference for patients with genetic sub types of diabetes across the world.

Professor Hattersley and his colleague Professor Sian Ellard set up their molecular genetics laboratory in the Royal Devon and Exeter hospital to do both research and clinical diagnostic resting in 1995, and have built a team that has gained an international reputation for excellence.

Professor Hattersley discovered that some babies with the sub-type neonatal diabetes which is diagnosed before they are six months old - can be treated more effectively with a simple tablet than with daily multiple insulin injections. This discovery has changed international guidelines, and means these patients have better glucose control and better quality of life. In the last week they have received samples from England, Belgium, India and South Africa for this life changing diabetes test.

Professor Hattersley said: "I'm delighted and humbled to receive such a prestigious award. This recognises the outstanding contributions of my talented colleagues here at Exeter both in the diabetes and molecular genetics department at the hospital and in the research departments of the University of Exeter Medical School. . I feel privileged to work with such an excellent team, whose work has benefited tens of thousands of people worldwide."

Professor Sir Steve Smith, Vice-Chancellor and Chief Executive, said: "I cannot think of anyone who deserves such an honour more than Professor Andrew Hattersley. His internationally-renowned research into the genetic causes of diabetes has literally transformed the lives of thousands of patients worldwide through the development of innovative treatments. Andrew is without doubt one of the preeminent clinical scientists in the UK, who has made major contributions in his field, revolutionising treatment. Andrew also nurtures talent in the next generation of researchers. He and his team have trained academics who have won countless awards. The whole University community offers Andrew our heartfelt congratulations."

The man behind some of the millions of government documents written on vellum, is made an MBE.

Wim Visscher, now semi-retired and living in Modbury in Devon, is a partner in the firm of William Cowley Parchment and Vellum Works, in Newport Pagnell, Buckinghamshire, and great-great grandson its founder.

The company Britain's only remaining vellum maker has been in the limelight recently because a parliamentary committee has controversially recommended switching to paper to save money.

Vellum, made from sheepskin, has been used to print the Magna Carta, the Domesday Book and thousands of other historical documents going back a millennium or more.

"Most of the millions of official documents written on vellum are still in good condition," Mr Visscher said.

Vellum and parchment are still used for important documents and high-end bookbinding.

He was nominated for his honour by Heritage Craft Association.

"It was a complete surprise," he said. "You work away in your own little corner of life. Mine is a very unusual business and hardly anyone knows about it."

Visit link:

Queen's Birthday Honours awarded to three deserving Devon heroes - Devon Live

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A noted cancer research has joined AstraZeneca's board of directors.

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AstraZeneca is betting big on its cancer oncology portfolio.(Photo: The News Journal File)Buy Photo

AstraZeneca has named cancer researcher Nazneen Rahman to its board of directors, effective June 1.

Rahman will serve as a non-executive director and will also become a member of the company's Science Committee.

Currently, Rahman is the head of the Division of Genetics and Epidemiology at the Institute of Cancer Research in London, head of the Cancer Genetics Unit at the Royal Marsden NHS Foundation Trustand director of the TGL Clinical Gene Testing Laboratory at the Institute of Cancer Research.

"We are delighted to welcome Professor Rahman to our Board and Science Committee," said Leif Johansson, chairman of AstraZeneca. "She brings world-renowned expertise in genetic research with a focus on cancer, which is a strategic therapy for our business."

Rahmanhas a degree in medicine from Oxford University and holds a doctorate in molecular genetics. Her research focuses on genes predisposed to cancer, and she has discovered genes that cause types of breast, ovarian and childhood cancers.

Elected as a fellow of the Academy of Medical Sciences in 2010, Rahman is a member of the scientific advisory boards of Genomics Plc and the Centre for Molecular Medicine Norway, as well as the advisory board of Wellcome Open Research.

Contact Jeff Mordock at (302) 324-2786, on Twitter @JeffMordockTNJ orjmordock@delawareonline.com.

Read or Share this story: http://www.delawareonline.com/story/money/business/delawareinc/2017/06/16/famed-cancer-researcher-joins-astrazenecas-board/403707001/

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Famed cancer researcher joins AstraZeneca's board - The News Journal

The Queen's Birthday Honour's List recognises the incredible achievements of extraordinary people across the UK.

Keith Palmer, the policeman killed after confronting the Westminster attacker outside Parliament, and Bernard Kenny, the heroic passer-by stabbed trying to protect MP Jo Cox, have been awarded medals for their bravery.

Those honoured from the world of entertainment include chart-topper Ed Sheeran and comedian comedian Billy Connolly, with the committee describing the list as "the most diverse yet".

And Oscar-winner Olivia de Havilland, who turns 101 next month, is the oldest woman to become a dame in the celebration.

In a break with tradition, the Queen's Civilian Gallantry List has been released at the same time as the monarch's birthday honours.

There is a total of 1,109 people on the Honours list, of whom 438 are awarded an MBE, 221 an OBE and 303 a BEM.

Here is the full list of those handed awards for services to their country.

Dame Stephanie "Steve" Shirley is the most successful tech entrepreneur you never heard of. After arriving in Britain as a Kindertransport child refugee in 1939, she went on to found a pioneering all-woman software company. The company, F International, was ultimately valued at $3 billion, making millionaires of 70 of her team members. She now uses the proceeds from the sale of the company for philanthropy.

Sgt Philip Baden Bower. Royal Auxiliary Air Force

Senior AC Shane Victor Staniforth. Royal Auxiliary Air Force Overseas Territories Police and Fire Service Medal

Moustafa Kemal. Chief inspector Sovereign Base Areas Police, Cyprus.

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Queen's Birthday Honours 2017: Full list of great and the good awarded for services to their country - Mirror.co.uk

Dr. Zeeba Kabir/Weill Cornell Medicine

The top image shows the movement of a mouse in a behavioral test that measures social interaction. The blue to green color represents least to most time spent interacting with another mouse. The bottom set of images measures anxiety-like behavior exhibited by a mouse. The amount of filling in the vertical bars represents levels of anxiety.

A calcium-dependent molecular mechanism discovered in the brain cells of mice by Weill Cornell Medicine investigators may underlie the impaired social interactions and anxiety found in neuropsychiatric disorders including schizophrenia and autism.

The study, published June 6 in Molecular Psychiatry, reports that reduced function of a calcium channel at synapses, the site of contact essential for communication between neurons, impairs social behavior and heightens anxiety. The findings also illuminate how this occurs: overactivation of a molecule within protrusions in neurons, called spines, which receive communicating signals from adjacent neurons. Blocking the action of this molecule in adult mice repaired the abnormal social interactions and elevated anxiety, a finding that may lead to the development of new treatments for patients with certain neuropsychiatric and anxiety disorders.

Our study suggests that if we can repair malfunctioning synapses in humans, we can reverse behavioral abnormalities and potentially treat specific symptoms, such as social impairment and anxiety, in patients with these neuropsychiatric disorders, said senior study author Anjali Rajadhyaksha, associate professor of neuroscience in pediatrics and of neuroscience in the Feil Family Brain and Mind Research Institute, and director of the Weill Cornell Autism Research Program at Weill Cornell Medicine. We believe that targeting this molecule and its pathway may provide us with a molecular framework for future exploration of treatment of patients.

Rajadhyaksha and her colleagues focused on a calcium channel gene called CACNA1C that has emerged as a significant risk gene across major forms of neuropsychiatric disorders: schizophrenia, bipolar disorder, major depressive disorder, autism spectrum disorders and attention deficit hyperactivity disorder. Impaired social behavior and elevated anxiety are common symptoms observed in patients with these disorders.

Studies using mice lacking CACNA1C production in neurons in a part of the brain, called the prefrontal cortex, which is responsible for cognition, personality and decision-making, made mice less social and more anxious. This finding seemingly confirms those of human studies, which suggests that defects in protein production may underlie the symptoms of patients with neuropsychiatric disorders and autism.

The investigators then identified the culprit for the social impairments and elevated anxiety: increased activity of a molecule called eIF2alpha that has been linked to cognitive deficits in neurodegenerative disorders like Alzheimers disease.

Zeeba Kabir, the studys first author and a postdoctoral researcher in Rajadhyakshas lab, tested a small molecule called ISRIB, which had previously been shown to block the action of eIF2alpha and improve learning and memory in mice, in rodents missing the CACNA1C gene. ISRIB reversed the aberrant behavior found in these mice, improving their social interactions and reducing anxiety.

Some studies have revealed that ISRIB has side effects that may be harmful to human cells, Rajadhyaksha said, but research shows that there are two alternative small molecule inhibitors of eIF2alpha that may be safer for use in humans. A next step is to study these ISRIB alternatives in mice to determine whether they have a similar effect.

Neuropsychiatric disorders are complex and treatments remain suboptimal, Rajadhyaksha said. To be able to treat specific symptoms that are common across multiple disorders is an exciting possibility. We would also like to determine whether alterations in the eIF2alpha pathway are held in common among other rodent models displaying social deficits and anxiety that result from risk genes other than CACNA1C. If so, molecules like ISRIB could be widely applicable for treating these symptoms, in general.

The research team also included Weill Cornell Medicine researchers Natalia De Marco Garcia, assistant professor of neuroscience, and Michael Glass, associate professor of research in neuroscience, both in the Feil Family Brain and Mind Research Institute.

Joseph Bonner is a freelance writer for Weill Cornell Medicine.

Read the original:

Molecular mechanism underlies anxiety, autism - Cornell Chronicle

Oncology Nurse Advisor

Personalized Medicine and the Role of the Oncology Navigator Oncology Nurse Advisor Nurse navigators must understand which patients require molecular testing to ensure tissue collection and testing, timely results reporting, and education of patients as to the significance of testing results for treatment planning. The navigator may ...

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Personalized Medicine and the Role of the Oncology Navigator - Oncology Nurse Advisor