Boston, MA, United States

Beth Israel Deaconess Medical Center

www.bidmc.org/
Boston, MA, United States

Beth Israel Deaconess Medical Center in Boston, Massachusetts is a teaching hospital of Harvard Medical School. It was formed out of the 1996 merger of Beth Israel Hospital and New England Deaconess Hospital . Among independent teaching hospitals, Beth Israel Deaconess Medical Center consistently ranks in the top three recipients of biomedical research funding from the National Institutes of Health. Research funding totals nearly $200 million annually. BIDMC researchers run more than 850 active sponsored projects and 200 clinical trials. The Harvard-Thorndike General Clinical Research Center, the oldest clinical research laboratory in the United States, has been located on this site since 1973. Wikipedia.

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Patent
Brigham, Women's Hospital, Stanford University and Beth Israel Deaconess Medical Center | Date: 2017-01-04

Magnetic cell levitation and cell monitoring systems and methods are disclosed. A method for separating a heterogeneous population of cells is performed by placing a microcapillary channel containing the heterogeneous population of cells in a magnetically-responsive medium in the disclosed levitation system and separating the cells by balancing magnetic and corrected gravitational forces on the individual cells. A levitation system is also disclosed, having a microscope on which the microcapillary channel is placed and a set of two magnets between which the microcapillary channel is placed. Additionally, a method for monitoring cellular processes in real-time using the levitation system is disclosed.


Patent
Childrens Medical Center Corporation and Beth Israel Deaconess Medical Center | Date: 2017-07-19

Disclosed herein is a formulation that can take the form of an emulsion which contains total enteral or parenteral nutrition for a recipient subject. The formulation includes as the sole fat components: (i) medium chain triglycerides; and (ii) very long chain fatty acids selected from (a) very long chain omega-3 polyunsaturated fatty acids; and (b) docosahexaenoic acid and arachidonic acid in a ratio of about 10:1 (v/v or w/w) to about 2000:1 (v/v or w/w). The sole fat components provide about 10% to about 90% total calories of the formulation, and the medium chain triglycerides provide about 25%-95% total fat calories of the formulation. Methods and kits for utilizing the formulation and for treating various disorders and diseases that involve an inflammatory response are also disclosed.


Patent
Beth Israel Deaconess Medical Center and Janssen Vaccines & Prevention B.V. | Date: 2017-08-02

Compositions, vaccines and methods for inducing protective immunity against Human Immunodeficiency Virus (HIV) infection are described. Heterologous vaccine combinations of one or more viral expression vectors and an isolated antigenic polypeptide induced strong protective immunity against infections by one or multiple clades of HIV.


Patent
Janssen Vaccines & Prevention B.V. and Beth Israel Deaconess Medical Center | Date: 2017-01-04

Replicating recombinant adenovirus vectors derived from human adenovirus serotype 26 or human adenovirus serotype 35 are described. The replicating recombinant adenovirus vectors have attenuated replicative capacity as compared to that of the corresponding wild-type adenovirus. They can be used for stable expression of heterologous genes in vivo. Also described are compositions and methods of using these recombinant adenovirus vectors to induce an immune response in a subject, and vaccinate a subject against an immunogenic human immunodeficiency virus (HIV) infection.


Patent
Childrens Medical Center Corporation and Beth Israel Deaconess Medical Center | Date: 2017-04-19

Filtration apparatuses, kits, and methods for rapid isolation of intact, viable mitochondria from tissues are described with mitochondria isolated by differential filtration through nylon mesh filters. Mitochondria can be isolated in less than 30 minutes using the filtration apparatuses, kits, and methods described.


Patent
Los Alamos National Security LLC, Beth Israel Deaconess Medical Center, Duke University and University of Alabama at Birmingham | Date: 2017-06-14

The present invention relates, in general, to an immunogenic composition (e.g., a vaccine) and, in particular, to a polyvalent immunogenic composition, such as a polyvalent HIV vaccine, and to methods of using same. The invention further relates to methods that use a genetic algorithm to create sets of polyvalent antigens suitable for use, for example, in vaccination strategies.


Patent
Beth Israel Deaconess Medical Center | Date: 2017-04-26

The invention relates to the treatment and prevention of cancer by administering agents that inhibit the activity of microRNAs that modulate tumor suppressor genes, which can include PTEN, p53, and INPP4B, among others. Inhibitors can include oligonucleotides that are at least partially complementary to these miRNAs. In some embodiments, these inhibitors are chemically modified oliognucleotides, including locked nucleic acids (LNAs).


Background: N-methyl-D-aspartate receptor (NMDA-R) hypofunction plays an important role in cognitive impairment in schizophrenia. NMDA-R antagonists elicit psychotic symptoms in humans and schizophrenia-relevant signs in rodents, including a strong increase in cortical gamma activity. NMDA-Rs are composed of different subunits, and accumulating evidence indicates that neuronal damage due to NMDA-R antagonists depends on their action on a specific type of the receptor containing the NR2A subunit. In human schizophrenics, NR2A is selectively reduced in fast-firing interneurons. These neurons are critical for gamma oscillations, indicating that pathological changes in gamma activity may depend on subunit-specific NMDA-R deficit. The present study tested this hypothesis. Methods: Cortical electroencephalograms were recorded in freely moving rats and the changes in gamma power were measured after administration of NMDA-R antagonists with different subunit selectivity, including NR2A-preferring (PEAQX, n = 5; NVP-AAM077, n = 18), NR2B-selective (ifenprodil, n = 6; threo-ifenprodil, n = 4; Ro25-6985, n = 13), and NR2C/D-selective (n = 8) antagonists, along with vehicle and nonselective NMDA-R antagonists (ketamine, n = 10; MK801, n = 12). Changes in prepulse inhibition of startle was tested after MK-801 (n = 6), NVP-AAM077, and Ro-6891 (n = 5) injection. Results: Strong increase in gamma power was induced by nonselective NMDA-R antagonists and by blockade of NMDA-Rs containing the NR2A subunit, with co-occurring gating deficits and diminished low-frequency modulation of gamma oscillations. In contrast, selective blockade of NR2B, C, or D subunit-containing receptors had minor effects. Conclusions: Major subtype-specific differences in the role of NMDA-Rs in cortical gamma oscillation may have implications for the pathomechanism and treatment of cognitive impairment in schizophrenia. © 2012 Society of Biological Psychiatry.


Stickgold R.,Beth Israel Deaconess Medical Center
Current Opinion in Neurobiology | Year: 2013

It would be nice if we could talk about sleep and memory as if there were only one type of memory and one type of sleep. But this is far from the case. Sleep and memory each comes in many forms, and furthermore, memories can go through multiple forms of post-encoding processing that must be individually addressed. Finally, sleep stages per se do not affect memories. Rather, the neuromodulatory and electrophysiological events that characterize these sleep stages must mediate sleep-dependent memory processing. In this review, we attempt to parse out the relative contributions and interactions of these often frustratingly complex systems. © 2013 Elsevier Ltd.


Tsokos G.C.,Beth Israel Deaconess Medical Center
New England Journal of Medicine | Year: 2011

SLE is an autoimmune disease that predominantly affects women and typically has manifestations in multiple organs. Immune-system aberrations, as well as heritable, hormonal, and environmental factors, contribute to the expression of organ damage. Immune complexes, autoantibodies, autoreactive lymphocytes, dendritic cells, and local factors are all involved in clinical manifestations of SLE. Biologic therapies and small-molecule drugs that can correct the aberrant immune-cell function are being developed in the hope that they will be more effective and less toxic than current treatments. Copyright © 2011 Massachusetts Medical Society.

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