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Unlocking Another Key to Aging

Unlocking Another Key to Aging—Transposons, also known as “jumping genes,” are DNA sequences that move from one location in the genome to another. Transposons are thought to contribute to aging, but their actual role remains to be clarified. The National Institute on Aging has awarded Julie Secombe, Ph.D., a five-year, $1.69 million grant to study whether transposons influence aging. So far, research on transposons and aging has been limited by available techniques. Dr. Secombe and her team will use novel methods to analyze the genomes of single cells. They will also focus on the role of Myc, a transcription factor (i.e., a protein regulating gene expression) known to affect aging in model organisms. By determining interconnections among Myc transposons that contribute to aging, the team may develop strategies for suppressing this activity and, ultimately, improve human longevity. Dr. Secombe is associate professor of genetics and is associate professor in the Dominick P. Purpura Department of Neuroscience. (1R01AG053269-01A1)

Wednesday, October 18, 2017
Investigating Chronic Fatigue Syndrome

Investigating Chronic Fatigue Syndrome—The NIH has established four new centers for mylagic encephalomyelitis/chronic fatigue syndrome (ME/CFS), which affects more than one million Americans. There is no treatment and no laboratory test to diagnose the disease, which is characterized by profound fatigue that does not improve with rest and may include cognitive dysfunction and pain. Now, John Greally, M.B., B.Ch., Ph.D., has been awarded a five-year, $2.17 million grant from the National Institute of Allergy and Infectious Diseases to lead a subproject core at the center based at Columbia’s Mailman School for Public Health. The Einstein lab has access to blood samples from newly diagnosed and existing ME/CFS patients and will look for transcriptional changes in peripheral blood mononuclear cells—a type of immune cell shown by previous studies to function abnormally in ME/CFS patients. Dr. Greally is a clinical geneticist at Montefiore and professor of genetics, of medicine and of pediatrics and is director of the Center for Epigenomics at Einstein. (1U54AI138370)

Tuesday, October 10, 2017
Curbing Appetite with Oxytocin

Curbing Appetite with Oxytocin—The rare neurodevelopmental genetic disorder Prader-Willi Syndrome (PWS) is characterized by compulsive eating (hyperphagia). The resulting obesity is the leading cause of deaths for people with PWS. Signaling by the hormone oxytocin—which normally acts on brain receptors to inhibit people from eating—is inadequate in PWS, and giving supplemental oxytocin to mouse models of the disorder is known to reduce food intake and body weight. Eric Hollander, M.D., has received a three-year, $1.49 million grant from the U.S. Food and Drug Administration to study whether oxytocin can be safely and effectively given intranasally PWS patients to reduce hyperphagia. Dr. Hollander is professor of psychiatry and behavioral sciences at Einstein and director of the Autism and Obsessive Compulsive Spectrum Program at Montefiore Health System and Einstein. (1R01FD005106-01A3)

Wednesday, October 04, 2017
New Niemann-Pick Treatment Shows Promise

New Niemann-Pick Treatment Shows Promise—In the genetic disorder Niemann-Pick disease type C1 (NPC1), abnormally high levels of lipids accumulate in cells and damage organs including the liver, spleen and brain. NPC1 is usually diagnosed when children develop neurological symptoms such as clumsiness or learning difficulties. Symptoms progressively worsen and patients usually die 10 to 15 years following diagnosis. No FDA-approved treatment exists. Steven Walkley, D.V.M., Ph.D., has co-authored a study in the August 10 issue of The Lancet showing that the drug 2-hydroxypropyl-β-cyclodextrin (HPβCD) can safely slow NPC1’s progression. Patients received monthly or bi-weekly spinal injections of the drug for 18 months. Following the treatment period, biochemical and neurological tests showed that, compared with historical data for patients the same age, patients treated with the drug experienced significantly less cognitive dysfunction, with minimal side effects. Dr. Walkley is director of the Rose F. Kennedy Intellectual and Developmental Disabilities Research Center and professor in the Dominick P. Purpura Department of Neuroscience, in the department of pathology, and in the Saul R. Korey Department of Neurology at Einstein.

Monday, October 02, 2017
Communicating Through Tunnels

Communicating Through Tunnels—After they become activated, the immune system’s macrophages recruit neighboring macrophages and other immune cells to inflammation sites and tumors. But the mechanisms by which activated macrophages contact distant cells are not well understood. In a paper published online on August 17 in Scientific Reports, Dianne Cox., Ph.D., and colleagues described how macrophages use a network of channels called tunneling nanotubes (TNTs) to communicate with other cells at long distances. Using multiple imaging techniques including super-resolution microscopy and live-cell imaging, the authors identified a group of essential molecules that macrophages use to assemble TNTs. The authors found that depletion of any of these molecules can impair signal transfer between cells and could potentially disturb normal physiological immune responses. The study’s first author is Ph.D. candidate Samer Hanna. Dr. Cox is associate professor of anatomy and structural biology and of developmental and molecular biology.

Thursday, September 28, 2017
Investigating the Cause of Myelodysplastic Syndrome

Investigating the Cause of Myelodysplastic Syndrome—Within the bone marrow, hematopoietic stem cells (HSCs) occupy niches that include stromal and mesenchymal cells. In myelodysplastic syndromes (MDS), which precede acute myeloid leukemia, HSCs behave abnormally, either because of genetic aberrations or epigenetic alterations to DNA that influence whether genes are expressed or not. In a study published online on July 6 in Cancer Research, collaborators found that novel epigenetic alterations in the bone marrow microenvironment are critically important in causing MDS to progress. More specifically, the presence of an abnormally high number of methyl groups (hypermethylation) in stromal cells activated the Wnt/β-catenin signaling pathway in MDS stem cells, stimulating their progression to leukemia. The findings suggest that drugs that inhibit DNA methyltransferases (DNMTs) that are used to treat MDS can exert their beneficial actions via influencing the surrounding cells of the bone marrow. Senior author, Amit Verma, M.B.B.S., is professor of medicine and of developmental and molecular biology. First author Tushar Bhagat, Ph.D., is a postdoctoral fellow in Dr. Verma’s lab at Einstein.

Tuesday, September 26, 2017
Memories Are Made of This

Memories Are Made of This—Long-term potentiation (LTP) strengthens synapses (specialized junctions where neurons come together to communicate) by repetitively stimulating them. It’s considered a key mechanism underlying learning and memory. In their study of hippocampal mossy cells and granule cells of the brain’s hippocampus, Pablo Castillo, M.D., Ph.D., and colleagues identified a novel form of LTP in which synaptic strengthening depends on the presynaptic neuron (which releases the neurotransmitter into the synapse) rather than on the postsynaptic neuron (which receives the neurotransmitter). This form of LTP may be involved in learning as well as the neuronal excitation that causes temporal lobe epilepsy. The researchers reported their findings online on August 16 in Neuron. Dr. Castillo is professor in the Dominick P. Purpura Department of Neuroscience and of psychiatry and behavioral sciences, as well as the Harold and Muriel Block Chair in Neuroscience.

Wednesday, September 20, 2017
A Key Cervical Cancer Virus in the Crosshairs

A Key Cervical Cancer Virus in the Crosshairs—A dozen human papillomaviruses cause cervical cancer, and one of them—HVP16—accounts for more than half of all cases. In a paper published online on September 7 in Cell, researchers analyzed the HPV16 genomes in 5,570 HPV16-infected cell and tissue samples from cases (women with cervical cancer or pre-cancer) and controls (women with benign HPV16 infections). Compared to the HPV16 genomes in the benign infections, significantly fewer differences were detected in the HPV16 genomes associated with the cancer and precancer cases. This genomic pattern was also clearly observed when researchers focused on the cancer-causing E7 gene, indicating that HPV16’s potent carcinogenicity depends on retaining the E7 gene in a conserved form. The findings suggest that drugs that disable the E7 gene or the protein it expresses could help to treat or even prevent cervical cancer. One of the paper’s co-senior authors was Robert Burk, M.D., professor of pediatrics, of microbiology & immunology, of epidemiology & population health and of obstetrics & gynecology and women’s health at Einstein.

Monday, September 18, 2017
9/11 Firefighters and Early Cancer Detection

9/11 Firefighters and Early Cancer Detection—9/11 firefighters were exposed to known and suspected carcinogens in the dusts and gases at the World Trade Center site. An Einstein study of exposed firefighters found an increased incidence of certain cancers in those firefighters compared with non-exposed firefighters. Now, the Einstein researchers have received a three-year, $1.49 million grant from the Centers for Disease Control and Prevention to conduct an extensive follow-up study of 9/11 firefighters to look for blood cancers, which were among those cancers found to be more common among exposed firefighters. The researchers will check specifically for multiple myeloma, chronic lymphocytic leukemia, myelodysplastic syndromes, and their associated precursor conditions. Early detection of these cancers could prove crucial for successfully treating any cases found. The research team is led by Amit Verma, M.D., professor of medicine and of developmental and molecular biology at Einstein; David Prezant, M.D., professor of medicine at Einstein and attending physician at Montefiore; and Ola Landgren, M.D., Ph.D., of Memorial Sloan Kettering Cancer Center. (1U01OH011475-01)

Friday, September 15, 2017
Insights into Autism Spectrum Disorder

Insights into Autism Spectrum Disorder—Noboru Hiroi, Ph.D., has been awarded a five-year, $1.8 million grant from the National Institute on Deafness and Other Communication Disorders to investigate the interplay among genes, early social communication and neonatal maternal care in determining the severity of autism spectrum disorder (ASD). Working with a genetic mouse model of ASD, Dr. Hiroi’s lab has observed that newborn mice display an unusual vocalization or “call,” to communicate with their mothers and that this abnormal call reduces the level of maternal care that newborns receive. The researchers will study whether abnormal newborn-to-mother vocalization is caused by ASD-related gene variants and whether this early experience of social communication gone awry worsens ASD-like behaviors through the epigenetic modification of these gene variants. Dr. Hiroi is professor in the Dominick P. Purpura Department of Neuroscience and of psychiatry and behavioral sciences. (1R01DC015776-01A1)

Wednesday, September 13, 2017
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