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Archive - Aug 2017

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August 15th

Compounds in Desert Creosote Bush Could Be Used to Treat Giardia and “Brain-Eating” Amoeba Infections

Researchers at Skaggs School of Pharmacy and Pharmaceutical Sciences at University of California San Diego and the University of Colorado Anschutz Medical Campus have found that compounds produced by the creosote bush, a desert plant common to the southwestern United States, exhibit potent anti-parasitic activity against the protozoa responsible for giardia infections and an amoeba that causes an often-lethal form of encephalitis. The findings, published online on August 9, 2017 in PLOS Neglected Tropical Diseases, offer a starting point for widening the arsenal of antimicrobial agents, effective against deadly parasitic infections, scientists said. The open-access article is titled “Larrea tridentata: A novel source for anti-parasitic agents active against Entamoeba histolytica, Giardia lamblia and Naegleria fowleri.” The World Health Organization estimates that giardiasis, a diarrheal illness, is linked to approximately 846,000 deaths around the world each year. Infection usually occurs through ingestion of contaminated water or food. Though rarely lethal in the U.S., it's estimated there are more than 1 million cases of giardiasis in the country annually. Standard treatment usually involves antibiotics and anti-parasitic drugs. "The significance and intrigue of our study is that it shows the value of prospecting for new medicines from plants traditionally used by indigenous people as medicine," said co-principal investigator Anjan Debnath, PhD, an Assistant Adjunct Professor at Skaggs School of Pharmacy and Pharmaceutical Sciences at UC San Diego. The creosote bush (Larrea tridentata), also known as greasewood, or gobernadora in Spanish, is a tough evergreen bush with small waxy leaves, yellow flowers, and a distinctive turpentine-like scent. Native Americans in both the U.S.

August 15th

Artificial Intelligence and Blockchain Companies Partner to Advance Healthcare Research

On August 15, 2017, Insilico Medicine, Inc, a Baltimore-based next-generation artificial intelligence (AI) company today announced a research collaboration with The Bitfury Group, the world's leading full-service blockchain technology conglomerate, to develop novel solutions for healthcare applications. The companies signed a memorandum of understanding (MOU) to collaborate in the academic and commercial settings to develop AI on blockchain solutions for the healthcare industry. "Blockchain can secure and streamline our medical systems, while AI has the potential to revitalize data management and machine learning to help identify trends and diseases," said Valery Vavilov, Founder and CEO of The Bitfury Group. "By partnering with Insilico, we will be able to combine their expertise in deep learning and bioinformatics with our blockchain proficiency and real-time solutions to create bespoke and innovative new products for the healthcare sector." "The Bitfury Group is one of the most reputable companies in blockchain, developing their own semiconductors and end-to-end blockchain solutions trusted by the major corporations and governments worldwide. We are happy to enter into a research collaboration with Bitfury to develop innovative solutions that may save lives and extend human healthspan,” said Alex Zhavoroknov, PhD, Founder and CEO of Insilico Medicine, Inc. [Editor’s Note. The following excerpt from an article (http://mitsloan.mit.edu/newsroom/articles/blockchain-explained/) from the MIT Sloan School of Management provides some insight into blockchain technology: Blockchain is a term widely used to represent an entire new suite of technologies. There is substantial confusion around its definition because the technology is early-stage, and can be implemented in many ways depending on the objective.

Therapeutic Fusion Protein (ApoM-Fc) Could Mitigate Blood Vessel Damage from Cardiovascular Disease

Scientists from Boston Children's Hospital Vascular Biology Program have revealed an engineered fusion protein that could recover blood vessel health following the onset of hypertension, atherosclerosis, stroke, heart attack, and other cardiovascular diseases. The findings were published on August 14, 2017 in Science Signaling. The article is titled “An Engineered S1P Chaperone Attenuates Hypertension and Ischemic Injury.” On average, each person has 60,000 miles of blood vessels coursing through his or her body. There are a number of mechanisms that the body uses to keep its vast vascular network healthy, including a tiny fat molecule, a lipid called S1P, that plays a particularly important role. S1P receptors dot the surface of the endothelium, a layer of cells that line the inside of all the body's blood cells. Together, these so-called endothelial cells form a barrier between the body's circulating blood and surrounding tissue. When S1P molecules activate their receptors, that suppresses endothelial inflammation and generally helps regulate cardiovascular health. Now, researchers led by Timothy Hla, PhD, from the Boston Children's Vascular Biology Program, have designed a novel therapeutic fusion that could trigger increased S1P receptor activity and recover blood vessel health following the onset of a range of cardiovascular diseases. As crucial as S1P is to our health, it cannot do its job alone. Instead, S1P relies on another set of the body's molecules to ferry it through the bloodstream so that it can find and bind with its cell receptors on the endothelium. "High density cholesterol (HDL) -- also known as good cholesterol -- carries a protein called ApoM, which in turn attracts and binds S1P in its cargo," says Dr. Hla, an investigator in the Vascular Biology Program, Patricia K.

Possible Metabolic Treatment for Pancreatic Cancer Would Target an Enzyme (Arginase 2) That Helps Dispose of Excess Nitrogen

Pancreatic cancer is now the third leading cause of cancer mortality. Its incidence is increasing in parallel with the population increase in obesity, and its five-year survival rate still hovers at just 8 to 9 percent. Research led by Nada Kalaany, PhD, at Boston Children's Hospital and the Broad Institute of MIT and Harvard, now suggests a novel approach to treating this deadly cancer: targeting an enzyme that tumors use to get rid of nitrogen. The study, published online on August 14, 2017 in Nature Communications, provides evidence that targeting the enzyme arginase 2 (ARG2) (image) can curb the growth of pancreatic tumors, especially in people who are obese. The open-access article is titled “Critical Role for Arginase 2 in Obesity-Associated Pancreatic Cancer." The researchers began by introducing human pancreatic tumors into obese and lean mice. They then analyzed what genes the tumors turned on and what metabolic products they were producing. They found that tumors in obese mice had enhanced expression of many genes involved in metabolizing nitrogen, a natural byproduct of cells when proteins are broken down. Until now, how nitrogen excess affects tumor growth has been largely unknown. "We found that highly malignant pancreatic tumors are very dependent on the nitrogen metabolism pathway," says Dr. Kalaany, a researcher in Boston Children's Division of Endocrinology and an Assistant Professor at Harvard Medical School. Pancreatic tumors grew faster in obese mice than in lean mice and produced increased amounts of ARG2, an enzyme that helps dispose of excess nitrogen by breaking down ammonia, as part of the urea cycle. Dr.

Scientists Identify Weight-Gain Receptor Linked to Atypical Antipsychotic Drugs (Olanzapine)

Many schizophrenic and depressed patients experience weight gain and type 2 diabetes in their quests for the life-changing benefits of a major class of antipsychotic drugs. University of Texas (UT) Southwestern Medical Center researchers identified a cellular receptor central to these undesirable effects. They then eliminated most of these metabolic changes in mice co-treated with a weight-loss drug that targets the serotonin 2c receptor. "Atypical antipsychotics are essential medications for millions of schizophrenia patients worldwide and they are increasingly being prescribed for bipolar disorder, major depressive disorder, and autism," said Dr. Chen Liu, an Assistant Professor of Internal Medicine and Neuroscience and co-corresponding author of an August 14, 2017 Journal of Clinical Investigation study along with Dr. Joel Elmquist, Director of the Division of Hypothalamic Research and a Professor of Internal Medicine, Pharmacology, and Psychiatry. The open-access article is titled “The Atypical Antipsychotic Olanzapine Causes Weight Gain by Targeting Serotonin Receptor 2C.” "Most members of this class of antipsychotics are linked to a drug-induced metabolic syndrome characterized by excessive weight gain, blood fat abnormalities, and type 2 diabetes. Obesity and diabetes often develop shortly after treatment begins," added Dr. Liu, who is also in the Division of Hypothalamic Research. The researchers found that six weeks of exposure to the antipsychotic drug olanzapine caused weight gain - particularly in female mice - due to increased fat rather than muscle. "Similar to treatment in humans, mice given olanzapine showed significant weight gain, higher food intake, and metabolic changes associated with insulin resistance and diabetes," said Dr.

August 14th

UCLA Scientists Identify New Way to Activate Stem Cells to Make Hair Grow; Increasing Lactate Dehydrogenase Activity Is Key

UCLA researchers have discovered a new way to activate the stem cells in the hair follicle to make hair grow. The research, led by scientists Dr. Heather Christofk and Dr. William Lowry, may lead to new drugs that could promote hair growth for people with baldness or alopecia, which is hair loss associated with such factors as hormonal imbalance, stress, aging or chemotherapy treatment. The research was published online on August 14, 2017 in Nature Cell Biology. The article is titled “Lactate Dehydrogenase Activity Drives Hair Follicle Stem Cell Activation.” Hair follicle stem cells are long-lived cells in the hair follicle; they are present in the skin and produce hair throughout a person's lifetime. They are "quiescent," meaning they are normally inactive, but they quickly activate during a new hair cycle, which is when new hair growth occurs. The quiescence of hair follicle stem cells is regulated by many factors. In certain cases, they fail to activate, which is what causes hair loss. In this study, Dr. Christofk and Dr. Lowry, of Eli and Edythe Broad Center of Regenerative Medicine and Stem Cell Research at UCLA, found that hair follicle stem cell metabolism is different from that of other cells of the skin. Cellular metabolism involves the breakdown of the nutrients needed for cells to divide, make energy, and respond to their environment. The process of metabolism uses enzymes that alter these nutrients to produce "metabolites." As hair follicle stem cells consume the nutrient glucose from the bloodstream, they process the glucose to eventually produce a metabolite called pyruvate. The cells then can either send pyruvate to their mitochondria -- the part of the cell that creates energy -- or can convert pyruvate into another metabolite called lactate.

Animal Study Reveals That Secretions (Extracellular Vesicles) from Cardiosphere-Derived Cells Could “Turn Back the Clock” for Age-Related Heart Conditions

Cardiac stem cell infusions could someday help reverse the aging process in the human heart, making older ones behave younger, according to a new study from the Cedars-Sinai Heart Institute. "Our previous lab studies and human clinical trials have shown promise in treating heart failure using cardiac stem cell infusions," said Eduardo Marbán, MD, PhD, Director of the Cedars-Sinai Heart Institute and the primary investigator of the study. "Now we find that these specialized stem cells could turn out to reverse problems associated with aging of the heart." The study was published online on August 14, 2017 in the European Heart Journal. The article is titled “Cardiac and Systemic Rejuvenation After Cardiosphere-Derived Cell Therapy in Senescent Rats.” In the study, investigators injected cardiosphere-derived cells, a specific type of stem cell known as CDCs, from newborn laboratory rats into the hearts of rats with an average age of 22 months, which is considered aged. Other laboratory rats from the same age group were assigned to receive placebo treatment, saline injections instead of stem cells. Both groups of aged rats were compared to a group of young rats with an average age of 4 months. Baseline heart function was measured in all rats, using echocardiograms, treadmill stress tests, and blood analysis. The older rats underwent an additional round of testing one month after receiving cardiosphere-derived cells that came from young rats. "The way the cells work to reverse aging is fascinating," Dr. Marbán said. "They secrete tiny vesicles [extracellular vesicles] that are chock-full of signaling molecules such as RNA and proteins. The vesicles from young cells appear to contain all the needed instructions to turn back the clock."

Brain Scan Study Adds to Evidence That Lower Brain Levels of Serotonin Transporters Are Linked to Dementia; Results Suggest Serotonin Loss May Be a Key Player in Cognitive Decline, Not Just a Side-Effect of Alzheimer's Disease

In a study examining brain scans of people with mild loss of thought and memory ability, Johns Hopkins researchers report evidence of lower levels of the serotonin transporter -- a natural brain chemical that regulates mood, sleep, and appetite. Previous studies from Johns Hopkins and other centers have shown that people with Alzheimer's disease and severe cognitive decline have severe loss of serotonin neurons, but the studies did not show whether those reductions were a cause or effect of the disease. Results of the new study of people with very early signs of memory decline, the researchers say, suggest that lower levels of serotonin transporters may be drivers of the disease rather than a byproduct. A report on the study, published in the September 2017 issue of Neurobiology of Disease, also suggests that finding ways to prevent the loss of serotonin or introducing a substitute neurotransmitter could slow or stop the progression of Alzheimer's disease and perhaps other dementias. The article is titled “Molecular Imaging of Serotonin Degeneration in Mild Cognitive Impairment." “Now that we have more evidence that serotonin is a chemical that appears affected early in cognitive decline, we suspect that increasing serotonin function in the brain could prevent memory loss from getting worse and slow disease progression," says Gwenn Smith, PhD, Professor of Psychiatry and Behavioral Sciences at the Johns Hopkins University School of Medicine and Director of Geriatric Psychiatry and Neuropsychiatry at Johns Hopkins University School of Medicine. Serotonin levels that are lower and out of balance with other brain chemicals such as dopamine are well known to significantly impact mood, particularly depression, and drugs that block the brain's "reuptake" of serotonin (known as SSRIs) are specific treatments for some major forms of depression and anxiety.

Discovery of New Prostate Cancer Biomarkers Could Improve Precision Therapy; SPOP Mutations Confer Resistance to BET Inhibitors

Mayo Clinic researchers have identified a new cause of treatment resistance in prostate cancer. Their discovery also suggests ways to improve prostate cancer therapy. The findings were published online on August 14, 2017 in Nature Medicine. The article is titled “Prostate Cancer–Associated SPOP Mutations Confer Resistance to BET Inhibitors Through Stabilization of BRD4.” In the publication, the authors explain the role of mutations within the SPOP gene on the development of resistance to one class of drugs. SPOP mutations are the most frequent genetic changes seen in primary prostate cancer. These mutations play a central role in the development of resistance to drugs called BET-inhibitors. BET (bromodomain and extra-terminal domain) inhibitors are drugs that prevent the action of BET proteins. These proteins help guide the abnormal growth of cancer cells. As a therapy, BET-inhibitors are promising, but drug resistance often develops, says Haojie Huang, PhD, senior author and a molecular biologist within Mayo Clinic's Center for Biomedical Discovery. Prostate cancer is among the most frequently diagnosed malignancies in the United States. It is also the third leading cause of cancer death in American men, according to the American Cancer Society. Because of this, says Dr. Huang, improving treatments for prostate cancer is an important public health goal. In the publication, the authors report SPOP mutations stabilize BET proteins against the action of BET-inhibitors. By this action, the mutations also promote cancer cell proliferation, invasion, and survival.

Blood Biopsy Test Reads Platelet-Associated Tumor RNA to Detect Human Lung Cancer; Algorithm Models Swarming Behavior of Birds, Insects, & Fish

Researchers in the Netherlands have designed a different approach to the liquid biopsy. Rather than looking for evidence of cancer DNA or other biomarkers in the blood, their test (called thromboSeq) could diagnose non-small cell lung cancer with close to 90% accuracy by detecting tumor RNA absorbed by circulating platelets, also known as thrombocytes. Non-small cell lung cancers make up the majority of lung cancer cases. The research was published in the August 14, 2017 issue of Cancer Cell. The open-access article is titled “Swarm Intelligence-Enhanced Detection of Non-Small Cell Lung Cancer Using Tumor-Educated Platelets." "Ultimately, the aim of liquid biopsy-based cancer detection is to detect all cancers at once in an early stage; an all-in-one test," says first author Dr. Myron Best, a researcher at the Department of Neurosurgery of the VU University Medical Center in Amsterdam and the Cancer Center Amsterdam. "ThromboSeq might not only provide lung cancer diagnostics, but potentially any other tumor type as well, and may enable tumor-type stratification." Platelets are short-lived blood cells known to form blood clots in response to injury. However, platelets also respond to a range of inflammatory events and cancer. Because platelet cells don't have a nucleus of their own, all RNA found in platelets either comes from megakaryocytes (the cells that form platelets in bone marrow) or from RNA the platelets absorbed while circulating in blood. Platelets in a cancer-free person will contain a different compilation of RNA than platelets that interacted with a tumor, known as tumor-educated platelets.