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Helping HAND from Buprenorphine

Helping HAND from Buprenorphine—Thanks to antiretroviral drugs, the neurological symptoms experienced by HIV-infected people have shifted from dementia to milder, lifelong, HIV-associated neurocognitive disorders (HAND). The National Institute on Drug Abuse has awarded Joan W. Berman, Ph.D., a five-year, $3.6 million grant to study whether buprenorphine--an opiate addiction medication that works by binding to the brain’s opioid receptors--can prevent HAND by binding to the opioid receptors of monocytes in the blood. Using a mouse model of HIV-induced HAND, Dr. Berman’s group, and Matias Jaureguiberry-Bravo, a Ph.D. student in her lab, with her collaborator Dr. David Volsky (Mount Sinai Icahn School of Medicine), will study whether buprenorphine can prevent HIV-infected monocytes from crossing the blood-brain barrier, a key event in causing HAND. This strategy may help both opioid abusers (who are at increased risk for HIV infection) and non-drug using HIV-infected people. Dr. Berman is professor of pathology and of microbiology & immunology. (1R01DA041931-01A1)

Wednesday, May 24, 2017
 
Studying Lupus Cell by Cell

Studying Lupus Cell by Cell—Systemiclupus erythematosus (SLE) occurs when a hyperactive immune system attacks the body’s own tissues, resulting in chronic inflammation and organ damage. Inflammation of the kidneys, or lupus nephritis (LN), affects nearly half of SLE patients, leading to potentially fatal kidney failure. Medications now used to treat LN are not always effective. To gain better insight into disease pathways in LN and to develop novel treatment strategies, lead author Evan Der, a Ph.D. student in Einstein’s department of microbiology & immunology, together with senior author Chaim Putterman, M.D., and colleagues at Einstein, Montefiore, NYU, and Rockefeller University, have developed a novel approach to analyze the RNA sequences of individual cells from kidney and skin biopsies of patients by using single-cell RNA-sequencing. The study was published online on May 4 in JCI Insight. Dr. Putterman is professor of medicine and of microbiology & immunology at Einstein and chief of rheumatology at Einstein and Montefiore. 

Friday, May 12, 2017
 
Clocking in for Embryonic Development

Clocking in for Embryonic Development—Early in the course of vertebrate development, the primitive backbone (consisting of a clump of cells) must be sliced into vertebral percursors called somites. This segmentation of somites is controlled by oscillator-mechanism (“clock”) genes belonging to the Hes/Her family of genes. The periodic rises and falls in expression of these genes must be precisely regulated: The smallest errors, due to gene mutations or other causes, can result in birth defects. The National Cancer Institute has awarded Ertugrul Ozbudak, Ph.D., a four-year, $1.3 million grant to study the Hes/Her gene family. This work should shed light on the genetic basis of vertebral defects and possible strategies for preventing them. In addition, aberrant oscillations in the levels of Hes/Her proteins (which control the switch from proliferation to differentiation in various tissues) have been detected in certain cancers. So the research may also lead to anti-cancer therapies. Dr. Ozbudak is associate professor of genetics. (1R01GM122956-01)

Wednesday, May 10, 2017
 
Selectively Targeting Leukemia

Selectively Targeting Leukemia—The National Cancer Institute has awarded Ulrich Steidl, M.D., Ph.D., a five-year, $1.9 million grant to study pre-leukemic stem cells and how they are induced to form leukemia cells. The research could lead to better treatment options against acute myeloid leukemia (AML) and myelodysplastic syndrome (MDS), a preleukemic disease. Cure rates over the past 45 years for both conditions have been no better than 20 percent. Dr. Steidl’s group previously showed that PU.1, a transcription factor that regulates the expression of leukemia-related genes, is frequently inactivated in pre-leukemic stem cells and in patients with AML. Using genetic models and novel inhibitors of PU.1, Dr. Steidl hopes to uncover critical pathways that induce pre-leukemic stem cells to produce leukemia cells. These PU.1 inhibitors could potentially be developed into a drug, since they appear to selectively kill leukemia cells. Dr. Steidl is professor of cell biology and of medicine and is the Diane and Arthur B. Belfer Faculty Scholar in Cancer Research. (1R01CA217092-01)

Monday, May 08, 2017
 
Purging Persister Bacteria in TB Treatment

Purging Persister Bacteria in TB Treatment—Tuberculosis treatment is hampered by patients’ need to undergo six months of drug treatment—necessary because of the presence of “persister” bacteria that don’t immediately succumb to treatment and may become resistant to it. In a paper published online on April 10 in the Proceedings of the National Academy of Sciences, a team of researchers led by William Jacobs, Jr., Ph.D., looked at whether adding chemicals to current drug regimens could decrease the length of treatment time by targeting persisters. Dr. Jacobs and colleagues found they could prevent persisters from developing by augmenting treatment with N-acetylcysteine, an amino acid derivative previously approved for treating acetaminophen overdose. Dr. Jacobs is a Howard Hughes Medical Institute Investigator and the Leo and Julia Forchheimer Chair in Microbiology & Immunology. 

Friday, April 28, 2017
 
Sugar Modification Essential for Notch Signaling

Sugar Modification Essential for Notch Signaling—Normal development of mammals and other multicellular organisms depend on Notch—a large cell-surface receptor that enables cells to communicate with each other. In a paper published online on April 11 in eLife, researchers led by Pamela Stanley, Ph.D., and Tetsuya Okajima, M.D., Ph.D., of Nagoya University, looked at how glycan modifications of Notch affect its cell-signaling ability. The researchers showed that, in the development of the retina, Notch-regulated signaling depends on the presence of the sugar O-GlcNAc on certain epidermal growth factor-like (EGF) repeats of the extracellular domain of Notch1. Cell-based assays showed that Delta Notch ligands (molecules that bind to and activate receptors) recognize O-GlcNAc on Notch1. The deletion of O-GlcNAc leads to a decrease in signaling that causes defects in perinatal retinal development. Dr. Stanley is professor of cell biology and the Horace W. Goldsmith Foundation Chair.

Wednesday, April 26, 2017
 
Tracing the Origin of Breast Tissue

Tracing the Origin of Breast Tissue—Researchers had long assumed that two of the main types of human mammary tissue--estrogen-receptor positive and estrogen-receptor negative cells—develop from a single type of stem cell. Now, Wenjun Guo, Ph.D., and his group have collaborated with Maja Oktay, M.D., Ph.D., to show that these two cell types are derived from and maintained by two distinct stem cell populations. Their study published online on March 21 in Cell Reports, used genetic techniques to monitor cells over multiple generations in a mouse model of mammary development. These findings have important clinical applications, since breast cancers are classified and treated based on whether they are estrogen-receptor positive or negative. Dr. Guo is assistant professor of cell biology. Dr. Oktay is associate professor of pathology and of anatomy and structural biology.

Monday, April 10, 2017
 
Suppressing Leukemia Progression

Suppressing Leukemia Progression—Myeloproliferative neoplasms (MPNs) are poorly understood malignant diseases caused by overproduction of white cells, red cells or platelets. Some types of MPN can develop into acute leukemia. In a paper published online on February 23 in the Journal of Experimental Medicine involving a newly developed mouse model of MPN, Ulrich Steidl, M.D., Ph.D., and colleagues describe a novel tumor suppressor role for the gene NOL3 in MPN. NOL3 had previously been shown to be an oncogene in other tissue types. The researchers also found that the NOL3 gene is deleted and its levels are lower in a subset of patients with MPNs. This major finding regarding the biology of MPNs means that NOL3 should be considered important for preventing disease progression in a subset of patients, as opposed to being a driver of disease. This insight may help researchers develop new approaches for targeted therapies for MPNs and leukemia. Dr. Steidl is professor of cell biology and of medicine, and is the Diane and Arthur B. Belfer Faculty Scholar in Cancer Research.

Friday, April 07, 2017
 
Studying How Nerve Cells Connect

Studying How Nerve Cells Connect—The National Institute of Mental Health has awarded Scott W. Emmons, Ph.D., a five-year, $2 million grant to investigate the synaptic connections that allow signals to travel from neuron to neuron throughout the brain. The researchers will conduct their studies on the nematode worm Caenorhabditis elegans, which depends on genes similar to those that lay down the neuronal architecture in human brains. Through a combination of genetic, molecular and biochemical studies, the research should shed light on the function of these genes and the factors that make accurate nerve connectivity possible. Dr. Emmons is professor of genetics and of neuroscience and holds the Siegfried Ullmann Chair in Molecular Genetics. (1R01MH112689-01)

Thursday, March 23, 2017
 
New Target For Dystonia Therapy

New Target For Dystonia Therapy—Dystonia—when someone’s muscles contract uncontrollably—is the third most common movement disorder (after Parkinson’s and essential tremor), affecting about 250,000 Americans. Research and treatment for the most common inherited form of dystonia, called DYT1, has focused mainly on the basal ganglia region of the brain. But new animal research by Einstein scientists implicates a different part of the brainthe cerebellumas the site of the problem. The study, published in the February 15 online issue of eLife, was led by Kamran Khodakhah, Ph.D., professor and chair of the Dominick P. Purpura Department of Neuroscience and the Harold and Muriel Block Chair in Neuroscience. He and his colleagues made their discovery after generating the first mouse model of DYT1 to exhibit the overt symptoms of dystonia seen in patients. Previous research in Dr. Khodakhah’s lab has shown that severing the link between the cerebellum and the basal ganglia might be an effective way to treat cerebellar-induced dystonias.

Monday, March 20, 2017
 
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