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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
 
Modeling an Immune Response

Modeling an Immune Response—Tumor necrosis factor (TNF) binds to TNF receptors on cell surfaces, triggering signaling pathways that bolster the immune response. TNF acts to promote inflammation, which can sometimes lead to autoimmune disorders such as rheumatoid arthritis. Most previous studies have looked at the TNF binding process in the lab, which limits the usefulness of their findings. Yinghao Wu, Ph.D., was recently awarded a four-year, $1.3 million grant from the National Institutes of Health to simulate TNF binding to cell-surface receptors in vivo using computational modeling methods. Since drugs for some autoimmune diseases work by blocking TNF, the findings could potentially aid in developing more effective therapies. Dr. Wu is an assistant professor of systems & computational biology at Einstein. (1R01GM122804-01)

Friday, January 12, 2018
 
CAR T Therapy for Lymphoma Available at Montefiore/Einstein

CAR T Therapy for Lymphoma Available at Montefiore/Einstein—In results published online on December 10 in The New England Journal of Medicine, a type of immunotherapy called CAR-T cell therapy achieved impressive results in a phase 2 clinical trial involving 101 patients with large B-cell lymphomas that had not responded to other forms of treatment. Symptoms disappeared completely in 54 percent of patients, 82 percent had measurable improvement and more than half of patients survived 18 months after treatment. In CAR-T therapy, T cells are separated from a patient’s blood and are genetically engineered to produce receptors on their surfaces called chimeric antigen receptors, or CARs. These synthetic receptors allow the T cells to recognize and attach to a specific antigen on tumor cells—in this case, the CD19 antigen on B cells from which this type of lymphoma arises. After the modified T cells multiply in the laboratory, they are infused back into the patient to seek out and kill cancer cells bearing the CD19 antigen. Ira Braunschweig, M.D., associate professor of medicine at Einstein and director of the Stem Cell Transplant Program and clinical director of Hematologic Malignancies at Montefiore co-authored the NEJM paper and treated six of the patients in the CAR-T therapy trial. Montefiore is now an approved center of excellence for CART therapy and is one of the few such centers in the US to offer this treatment to patients with lymphoma and leukemia.

Tuesday, January 09, 2018
 
Following mRNA from Birth to Death

Following mRNA from Birth to Death—Messenger RNA (mRNA) is crucial for converting genetic information into proteins and for regulating gene expression. The life of an mRNA molecule in cells—including its transcription in the nucleus and translation of its message into a protein—can be followed using the MS2 imaging system, developed by Robert Singer, Ph.D., Evelina Tutucci Ph.D., and Maria Vera Ph.D., at Einstein. In a paper published online on November 13 in Nature Methods, Dr. Singer and colleagues describe re-engineering the MS2 system so that it can now follow mRNAs all the way from birth to degradation. Emerging evidence indicates that this final stage in the life of mRNA molecules is highly regulated: The need for rapid activation and de-activation of specific genes requires that mRNA production and degradation be coordinated so that protein levels can be tightly controlled. Dr. Singer is professor and co-chair of anatomy & structural biology, as well as co-director of the Gruss-Lipper Biophotonics Center and of the Integrated Imaging Program. He also is professor in the Dominick P. Purpura Department of Neuroscience and of cell biology and the Harold and Muriel Block Chair in anatomy & structural biology.

Tuesday, January 02, 2018
 
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