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Investigating the Effects of Social Support on Aging

Investigating the Effects of Social Support on Aging—Strong social support can protect older adults from cognitive and physical decline. The neural underpinnings of social support’s cognition boost, however, are not well understood. In a study published on February 28 in The Journals of Gerontology: Series B, Helena Blumen, Ph.D., and colleagues identified neural networks associated with social support. The researchers used a computational approach to identify neural networks in elderly study participants and linked those networks to the degree of participants’ social support as measured by the Medical Outcomes Study Social Support Survey. Having broad social support was associated with neural networks involving the prefrontal cortex, hippocampus, cingulate cortex, and thalamus— brain regions known to be involved in memory and executive function. These findings suggest that strengthening social support among elderly people may reduce cognitive decline and dementia. Dr. Blumen is assistant professor of medicine and in the Saul R. Korey Department of Neurology at Einstein.

Monday, March 25, 2019
 
Brain Imaging and Walking

Brain Imaging and Walking—Studies in older adults have found a link between walking speed and executive function (mental skills that help people plan, organize and complete tasks). The brain’s frontal cortex is known to control gait in older adults. In a study published online on January 30 in NeuroImage, Mark Wagshul, Ph.D.,Roee Holtzer, Ph.D.,and colleagues investigated whether changes in frontal-cortex structure influence its activation during walking. In a study of healthy older adults using MRI and functional near-infrared spectroscopy (a technique that can measure blood flow in the brain during walking), they found a clear link between increased brain activation during walking (a known risk for falls) and structural changes in the brain. During complex walking tasks, individuals with smaller frontal cortices required greater activation compared with individuals with larger frontal cortices, possibly an indication of inefficient brain utilization.  The researchers hope to use similar measures to predict the risk of falling in older adults. Dr. Wagshul is an associate professor of radiology and is an assistant professor of physiology & biophysics at Einstein. Dr. Holtzer is a professor in the Saul R. Korey Department of Neurology at Einstein.

Monday, March 25, 2019
 
Insight Into HIV-associated Cardiovascular Disease

Insight Into HIV-associated Cardiovascular Disease—Cardiovascular disease (CVD) is a major health problem for people living with HIV. Antiretroviral drugs, viral load, immune-cell activation and inflammation all contribute to HIV-associated CVD. Biomarkers are needed for predicting CVD risk among these individuals. In a study published online on February 14 in Circulation, Qibin Qi, Ph.D., and Wei Zhao, M.S., found that levels of ceramides (a class of circulating blood lipids) correlate with the risk of developing carotid artery plaque (indicating greater likelihood of CVD events) during the course of HIV-infection and use of antiretroviral drugs. The findings suggest that targeting ceramides among people living with HIV might help to treat CVD or prevent its onset.  Dr. Qi is an associate professor of epidemiology & population health Einstein. Wei Zhao is a medical student at Einstein.

Friday, March 22, 2019
 
Understanding Kidney Cancer Progression

Understanding Kidney Cancer Progression—Clear cell renal cell carcinoma (CCRCC) is the most common type of kidney cancer. In a study published online on January 31 in the Journal of Clinical Investigation, Niraj Shenoy, MD., M.S., Amit K. Verma, M.B.B.S., and colleagues describe a new prognostic biomarker for this type of cancer called 5-hydroxymethylcytosine (5hmC). As kidney cancer advances, tumor levels of 5hmc progressively decrease. The researchers found that loss of 5hmC occurs because an aberrant metabolic intermediate inhibits enzymes called TET (Ten-eleven Translocation). Furthermore, the presence of ascorbic acid (Vitamin C) prevents the aberrant intermediate from affecting TET and restores 5hmC levels. High-dose intravenous ascorbic acid inhibited kidney cancer growth in a mouse model and increased 5hmc within the tumors. These findings have led to an ongoing multicenter randomized phase 2 clinical trial of vitamin C as an adjunct to standard of care treatment for metastatic and unresectable CCRCC. Dr. Verma is professor of medicine and of developmental and molecular biology at Einstein and attending physician in oncology at Montefiore Einstein Center for Cancer Care. Dr. Shenoy is an assistant professor of medicine at Einstein and attending physician in oncology at Montefiore Einstein Center for Cancer Care.

Thursday, March 21, 2019
 
A Recipe for Making Therapeutic Liver Cells

A Recipe for Making Therapeutic Liver Cells—So-called pluripotent stem cells can develop into any type of cell in the body—cells that could especially help in treating human diseases in which tissue loss has occurred. However, the signals that direct pluripotent stem cells to develop into desired cell types aren’t well understood. In a new study published online on January 28 in Differentiation, Sanjeev Gupta, M.D., and colleagues showed that human pluripotent stem cells differentiate into hepatocytes (liver cells) when cultured in a medium in which fetal hepatocytes had been grown. Surprisingly, the signals triggering differentiation were identified as small metabolomics products rather than proteins made by fetal hepatocytes. When the hepatocytes resulting from stem cells were transplanted into mice with acute liver failure, they promoted tissue repair and liver regeneration in the mice, indicating that hepatocytes derived in this way possess therapeutic potential. The U.S. Patent and Trademark Office has allowed claims for a patent to Einstein for Dr. Gupta’s differentiation method. Dr. Gupta is professor of medicine and of pathology and is the Eleazar and Feige Reicher Chair in Translational Medicine at Einstein and is an attending physician and hepatologist at Montefiore.

Wednesday, March 13, 2019
 
New Triple-Negative Breast Cancer Target

New Triple-Negative Breast Cancer Target—Up to 20 percent of breast cancers aretriple negative breast cancer (TNBC), an aggressive form of the disease with few treatment options. In looking for genes that promote TNBC metastasis and might be knocked out as a treatment strategy, Harry Ostrer, M.D., and colleagues from Einstein and Montefiore identified Otoconin 90 (OC90)—a gene normally expressed in the ear’s cochlea to form the little calcium stones that help to control equilibrium. But the gene has been repurposed and over-expressed in TNBC as well as prostate and lung cancers to serve a novel and pernicious function. In a cohort of TNBC patients, the researchers found that the altered expression of three genes associated with OC90 overexpression —HMGA2, POLE2 and TRIB3—predicts a greater likelihood that the patients will die from the disease. The findings were published online on February 14 in PLOS ONE. Dr. Ostrer is professor of pathology and of pediatrics at Einstein.

Wednesday, February 27, 2019
 
Investigating the Obesity-asthma Connection

Investigating the Obesity-asthma Connection—Obesity ranks as an important cause of asthma in children. Compared with their lean asthmatic counterparts, children with obese non-allergic asthma tend to have worse asthma control and don’t respond well to treatment. In investigating why obese children face an increased risk for asthma, Deepa Rastogi, M.D., M.B.B.S., found that obese asthmatic children have abnormally active genes in a signaling pathway involving CDC42, a protein that helps activate T cells.  Now the National Heart, Lung, and Blood Institute has awarded Dr. Rastogi a five-year $2.2 million grant to further investigate the CDC42 pathway’s role in non-allergic obesity-related asthma. Using cell samples from obese asthmatics and normal-weight control asthmatics, she and her colleagues will determine the cell types in which the CDC42 pathway is activated and whether it could be targeted for treating obesity-related asthma. Dr. Rastogi is associate professor of pediatrics and the Joseph S. Blume Faculty Scholar in Pediatric Development at Einstein and attending physician at Montefiore. (1R01HL141849-01A1)

Thursday, February 21, 2019
 
Learning How Neural Networks Form

Learning How Neural Networks Form—In two recent papers involving the roundworm C. elegans, Hannes E. Buelow, Ph.D., and colleagues shed light on how neural networks are assembled during development. Dendrites are string-like extensions of neurons that sample the environment or connect with other neurons at junctions called synapses. Electrical impulses from a neuron’s dendrites are conveyed by the neuron’s other long projection—its axon—to the next neuron in the network. Sensory nerves often form elaborately branched dendritic trees, or “arbors,” so that they can collect information or sample the environment appropriately. Researchers have long known that an axon’s neuronal activity can shape the dendrites of neurons with which they are connected. In a study published on January 17 in Developmental Cell, Dr. Buelow and his team report that axons can also shape dendrites of certain C. elegans sensory neurons, known as PVD neurons, by acting as scaffolds; the researchers identified several conserved genes involved in this process. The second paper, which published January 29 in eLife, uncovers an additional mechanism involved in forming dendritic arbors. Dr. Buelow and colleagues describe how three different proteins interact within the extracellular matrix to help form the PVD dendrites and regulate the growth of dendritic branches. Psychiatric conditions such as autism spectrum disorders and schizophrenia may result from incorrectly interconnected neural networks. So defects in any one or more of these conserved genes, or in genes coding for the interacting proteins, may be a cause of those disorders. Dr. Buelow is professor of genetics and in the Dominick P. Purpura Department of Neuroscience at Einstein.

Wednesday, February 13, 2019
 
Recognizing Early-Stage TB

Recognizing Early-Stage TB—Tuberculosis is a leading cause of global mortality, responsible for around 1.6 million deaths each year. Some people who test negative based on sputum testing still have active pulmonary tuberculosis (PTB); diagnosing and treating them is vital for preventing the development of disease that can spread. Moreover, sputum culture-negative PTB is an early stage of the disease that can be treated with fewer drugs for a shorter time than sputum-culture positive PTB. To gauge the frequency of culture-negative PTB among adult PTB patients, Jacqueline Achkar, M.D., M.Sc., and colleagues analyzed data reported to the New York City Department of Health from 2011 through 2013 on 796 patients with active PTB. A significant number of patients—116, or 15 percent—were culture-negative. Compared with people with culture-positive PTB, culture-negative individuals tended to have fewer symptoms such as coughing and weight loss and had fewer abnormalities on radiographic imaging. Awareness of these findings could improve the detection and treatment of this early-disease state and reduce PTB transmission. Dr. Achkar is associate professor of medicine and of microbiology & immunology. The first author of the study, which published online on February 8 in JAMA Network Open, is Minh-Vu H. Nguyen, M.D., M.Sc., who was an Einstein medical student and a scholar of Einstein’s Master of Science Clinical Research Training Program (CRTP).

Friday, February 08, 2019
 
Inhibiting a Cell-Execution Protein

Inhibiting a Cell-Execution Protein—Apoptosis is a normal cellular process that enables damaged or defective cells to self-destruct—but uncontrolled apoptosis can be harmful.  For example, the death of heart-muscle tissue following heart attacks is largely due to apoptotic cell death. In a study published online on February 4 in Nature Chemical Biology, Evripidis Gavathiotis, Ph.D., describes previously unknown, small molecules that bind to and inhibit BAX, the protein that plays a key role in causing apoptosis. Dr. Gavathiotis and colleagues also identified a pocket within the BAX protein to which these novel inhibitors bind, thereby stabilizing BAX and preventing it from triggering apoptosis. In in vitro experiments, Dr. Gavathiotis and colleagues showed that the inhibitors protected mouse fibroblasts from apoptotic stimulation. Such BAX inhibitors could potentially be used as drugs to prevent cell death during heart attacks, strokes, neurodegenerative diseases, and chemotherapy or radiation treatment. Dr. Gavathiotis is an associate professor of biochemistry and of medicine at Einstein.

Thursday, February 07, 2019
 
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