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Treating Both MDR-TB and HIV Improves Survival and Cure Rates

Treating Both MDR-TB and HIV Improves Survival and Cure Rates—Survival odds are stacked against people co-infected with multidrug-resistant tuberculosis (MDR-TB) and HIV. HIV weakens the immune system, and co-infected patients have high mortality. To help guide treatment for these individuals, James Brust, M.D., with colleagues from Emory, the Centers for Disease Control and Prevention, and the University of KwaZulu-Natal, prospectively measured survival and treatment outcomes in MDR-TB/HIV co-infected patients on antiretroviral therapy (ART) compared to outcomes in patients with MDR-TB alone. Read full story.

Friday, February 16, 2018
Imaging the Effects of Hydrocephalus Shunts

Imaging the Effects of Hydrocephalus Shunts—Hydrocephalus, a chronic condition in which excess fluid builds up in the brain, is treated with a fluid-draining tube called a shunt. Although shunts do save lives, their long-term effects on the brain are unknown. Mark E. Wagshul, Ph.D., and colleagues at Montefiore used an advanced MRI method called diffusion tensor imaging (DTI) to scan the brain’s white matter tracts (important structures that send electrical signals between parts of the brain)and determine the possible impacts of shunting on 21 hydrocephalus patients and 21 healthy controls. The study, published online on January 19 in Journal of Neurosurgery, found marked impairment of the major white matter tracts even in patients whose hydrocephalus was well-controlled with shunts. The results suggest DTI could be a valuable tool for tailoring treatments or developing new therapies for hydrocephalus. Dr. Wagshul is associate professor of radiology and is an assistant professor of physiology & biophysics at Einstein.

Friday, February 16, 2018
Uncovering Herpes Simplex Infection Tactic

Uncovering Herpes Simplex Infection Tactic—Understanding how the herpes simplex virus (HSV) invades cells could lead to new strategies for preventing or treating infections. In a study published online on January 2 in PloS Pathogens, Natalia Cheshenko, Ph.D., and Betsy Herold, M.D. showed that HSV activates a membrane enzyme called scramblase, which then “flips” certain lipids from the inner layer of the cell membrane to the outer layer—making it easier for HSV to interact with membrane proteins such as Akt, which are normally found only on the inside. Interactions between HSV and these proteins promote viral entry. Normally, moving those lipids to the membrane’s outer layer would trigger cell death, known as apoptosis. But the infecting viruses prevent apoptosis by causing the lipids to flip back within two hours of infection. The finding suggests that drugs that inhibit scramblase or Akt could prevent or treat HSV infection. Dr. Herold is professor of pediatrics, of microbiology & immunology, and of obstetrics & gynecology and women’s health. Dr. Herold also holds the Harold and Muriel Block Chair in Pediatrics at Einstein. Dr. Cheskenko is an assistant professor of pediatrics at Einstein.

Wednesday, February 14, 2018
Studying the Biology of Embryonic Stem Cells

Studying the Biology of Embryonic Stem Cells—Embryonic and induced pluripotent stem cells hold great promise for regenerative medicine. Gene expression in stem cells is influenced by epigenetic marks including methyl groups that are added to or removed from DNA. A class of proteins called Tet enzymes aid in removing methyl groups from DNA, thereby activating specific genes in stem cells. Aberrant Tet-mediated regulation of gene activity can lead to abnormal stem cell function and development and lead to diseases such as cancer. Meelad Dawlaty, Ph.D., has received a 5-year, $1.75 million grant from the National Institutes of Health to investigate how Tet proteins regulate embryonic stem cells. Findings from these studies will improve basic understanding of stem cell biology and could help identify new targets for treating diseases. Dr. Dawlaty is an assistant professor of genetics and member of the Ruth L. and David S. Gottesman Institute for Stem Cell and Regenerative Medicine Research at Einstein. (1R01GM122839)

Monday, February 12, 2018
Mutation Protects Certain Cells

Mutation Protects Certain Cells—Cell competition can occur when tissues contain both normal and abnormal cells. It may contribute to the early growth or elimination of tumors, for example, and to how many genetic errors accumulate during aging. Nicholas E. Baker, Ph.D., is using fruit flies to study cell competition. In a paper published online on January 8 in Developmental Cell, he and his colleagues looked at competition involving cells with mutated ribosomal proteins. Such proteins are also mutated in human diseases (ribosomopathies) and in cancer. They found that the ribosomal protein S12 was unusual because cells heterozygous for this mutation resisted competition from wild-type cells. The researchers concluded that in the competition between wild-type cells and cells containing mutated ribosomal proteins, the S12 ribosomal protein sends a signal promoting cell competition. Dr. Baker is professor of genetics, of developmental and molecular biology and of ophthalmology and visual sciences and the paper’s corresponding author. Dr. Baker also holds the Harold and Muriel Block Chair in Genetics. The paper’s first author, Abhijit Kale, Ph.D., was a doctoral student in Dr. Baker’s lab.

Tuesday, February 06, 2018
Exploring Dystonia's Genetic Cause

Exploring Dystonia's Genetic Cause—The neurological disorder dystonia causes muscles to contract involuntarily. It is the third most common movement disorder (after Parkinson’s and essential tremor) and affects about 250,000 Americans. Einstein’s Kamran Khodakhah, Ph.D. and colleagues developed a mouse model of DYT1, the most common inherited form of dystonia that replicates the neurological symptoms of patients. Using this mouse model, they determined that dystonia is caused primarily by dysfunction of the brain’s cerebellum. The National Institute of Neurological Disorders and Stroke has awarded Dr. Khodakhah a five-year, $2.3 million grant to use his mouse model to determine at the cellular and molecular level how mutations associated with DYT1 cause dystonia. Dr. Khodakhah is professor and chair of the Dominick P. Purpura Department of Neuroscience and the Florence and Irving Rubinstein Chair in Neuroscience. (1R01NS105470-01)

Friday, February 02, 2018
Investigating Ebola Infection

Investigating Ebola Infection—Viruses must infect host cells so they can replicate. Ebola virus and other filoviruses, which cause fatal hemorrhagic fever in humans, have evolved a highly complex infection and replication process. Kartik Chandran, Ph.D., has already described the key steps, in which filoviruses bind to the host cell’s outer membrane, are taken up by lysosomes (intracellular bags filled with enzymes) and then multiply by propelling their RNA genetic material through the lysosome and into the cell’s cytoplasm. He was recently awarded a four-year, $1.9 million grant from the National Institute of Allergy and Infectious Diseases to conduct further filovirus research. His group aims to define the molecular mechanism by which filoviruses bind to host cells and to find new host factors that could be targeted to prevent filoviruses from infecting cells and multiplying inside them. Dr. Chandran is professor of microbiology & immunology and the Harold and Muriel Block Faculty Scholar in Virology. (1R01AI134824-01)

Wednesday, January 31, 2018
Rapid HIV Tests Underperform in Children

Rapid HIV Tests Underperform in Children—Rapid diagnostic tests (RDTs) to determine the HIV status of children in the African country of Malawi are not always accurate, according to a paper published online on December 6 in the American Journal of Tropical Medicine and Hygiene. The study involved 341 hospitalized children, aged two months to 16 years old, whose two positive RDTs meant they had tested positive for HIV infection according to hospital guidelines; the children were later retested using standard blood tests for detecting viral loads. A significant percentage of children had false-positive results on the RDTs, meaning the tests incorrectly indicated that they were infected with HIV. Such inaccurate test results put children at risk for lifelong misdiagnosis and unnecessary treatment with antiretroviral therapy. The paper’s lead author was Theresa F. Madaline, M.D., assistant professor of medicine at Einstein and Montefiore.

Monday, January 29, 2018
New Data for TB Research

New Data for TB Research—To develop faster and more cost-effective therapies for tuberculosis, researchers need to better understand the biology of Mycobacterium tuberculosis, the bacterium that causes the disease. William R. Jacobs, Jr., Ph.D., has received a five-year, $2.85 million grant from the National Institute of Allergy and Infectious Diseases to systematically delete the coding regions of each of the nearly 4,000 genes of M. tuberculosis and mark each of those mutant variants with an identifying “barcode” DNA sequence. The complete set of barcoded deletion mutants of the bacillus will then be distributed to researchers around the world. Studying how the mutations affect the bacterium’s function and survival may give researchers insights into better strategies for preventing or treating TB infections. Dr. Jacobs is the Leo and Julia Forchheimer Chair in Microbiology and Immunology, a Howard Hughes Medical Institute investigator and a professor of genetics and microbiology and immunology at Einstein. (1R24AI134650-01

Friday, January 26, 2018
Mapping Bone Marrow Nerves

Mapping Bone Marrow Nerves—Stem cells in the bone marrow multiply and differentiate to form all the cells of the bloodstream—a process regulated by sympathetic nerves that infiltrate the marrow. With a three-year, $1.25 million grant from the National Institute of Diabetes and Digestive and Kidney Diseases, Paul S. Frenette, M.D., will map those nerves to better understand their functions and physiology. In a three-stage experiment, Dr. Frenette and colleagues will define the marrow’s system of nerves, identify how those nerves relay signals and manipulate certain nerves to increase blood cell production (which could help reverse low blood cell counts in patients undergoing marrow-damaging chemotherapy). Dr. Frenette is professor of medicine and of cell biology and director of the Ruth L. and David S. Gottesman Institute for Stem Cell and Regenerative Medicine Research at Einstein. (1U01DK116312-01)

Thursday, January 25, 2018
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