Institution
University of Medicine and Dentistry of New Jersey
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About: University of Medicine and Dentistry of New Jersey is a based out in . It is known for research contribution in the topics: Population & Poison control. The organization has 14634 authors who have published 19610 publications receiving 1041794 citations.
Topics: Population, Poison control, Pregnancy, Health care, Gene
Papers published on a yearly basis
Papers
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TL;DR: Interactions between α-syn and tau can promote their fibrillization and drive the formation of pathological inclusions in human neurodegenerative diseases.
Abstract: Alpha-synuclein (alpha-syn) and tau polymerize into amyloid fibrils and form intraneuronal filamentous inclusions characteristic of neurodegenerative diseases. We demonstrate that alpha-syn induces fibrillization of tau and that coincubation of tau and alpha-syn synergistically promotes fibrillization of both proteins. The in vivo relevance of these findings is grounded in the co-occurrence of alpha-syn and tau filamentous amyloid inclusions in humans, in single transgenic mice that express A53T human alpha-syn in neurons, and in oligodendrocytes of bigenic mice that express wild-type human alpha-syn plus P301L mutant tau. This suggests that interactions between alpha-syn and tau can promote their fibrillization and drive the formation of pathological inclusions in human neurodegenerative diseases.
818 citations
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TL;DR: Treatment of NP-C2 fibroblasts with exogenous recombinant HE1 protein ameliorated lysosomal accumulation of low density lipoprotein-derived cholesterol.
Abstract: Niemann-Pick type C2 disease (NP-C2) is a fatal hereditary disorder of unknown etiology characterized by defective egress of cholesterol from lysosomes. Here we show that the disease is caused by a deficiency in HE1, a ubiquitously expressed lysosomal protein identified previously as a cholesterol-binding protein. HE1 was undetectable in fibroblasts from NP-C2 patients but present in fibroblasts from unaffected controls and NP-C1 patients. Mutations in the HE1 gene, which maps to chromosome 14q24.3, were found in NP-C2 patients but not in controls. Treatment of NP-C2 fibroblasts with exogenous recombinant HE1 protein ameliorated lysosomal accumulation of low density lipoprotein-derived cholesterol.
817 citations
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TL;DR: It is suggested that the long-range connections linking dorsal anterior cingulates to posterior cingulate and precuneus should be considered as a candidate locus of dysfunction in ADHD.
814 citations
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TL;DR: It is shown that human bone marrow-derived mesenchymal stem cells exposed to tumor-conditioned medium (TCM) over a prolonged period of time assume a CAF-like myofibroblastic phenotype, which suggests that hMSCs are a source of CAFs and can be used in the modeling of tumor-stroma interactions.
Abstract: Carcinoma-associated fibroblasts (CAF) have recently been implicated in important aspects of epithelial solid tumor biology, such as neoplastic progression, tumor growth, angiogenesis, and metastasis. However, neither the source of CAFs nor the differences between CAFs and fibroblasts from nonneoplastic tissue have been well defined. In this study, we show that human bone marrow–derived mesenchymal stem cells (hMSCs) exposed to tumor-conditioned medium (TCM) over a prolonged period of time assume a CAF-like myofibroblastic phenotype. More importantly, these cells exhibit functional properties of CAFs, including sustained expression of stromal-derived factor-1 (SDF-1) and the ability to promote tumor cell growth both in vitro and in an in vivo coimplantation model, and expression of myofibroblast markers, including α-smooth muscle actin and fibroblast surface protein. hMSCs induced to differentiate to a myofibroblast-like phenotype using 5-azacytidine do not promote tumor cell growth as efficiently as hMSCs cultured in TCM nor do they show increased SDF-1 expression. Furthermore, gene expression profiling revealed similarities between TCM-exposed hMSCs and CAFs. Taken together, these data suggest that hMSCs are a source of CAFs and can be used in the modeling of tumor-stroma interactions. To our knowledge, this is the first report showing that hMSCs become activated and resemble carcinoma-associated myofibroblasts on prolonged exposure to conditioned medium from MDAMB231 human breast cancer cells. [Cancer Res 2008;68(11):4331–9]
807 citations
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TL;DR: It is shown that, under conditions of dysregulated IL15 expression in vivo in patients with celiac disease and in vitro in healthy individuals, multiple steps of the NKG2D/DAP10 signaling pathway leading to ERK and JNK activation are coordinately primed to activate direct cytolytic function independent of TCR specificity in effector CD8 T cells.
800 citations
Authors
Showing all 14639 results
Name | H-index | Papers | Citations |
---|---|---|---|
John Q. Trojanowski | 226 | 1467 | 213948 |
Virginia M.-Y. Lee | 194 | 993 | 148820 |
Danny Reinberg | 145 | 342 | 68201 |
Michael F. Holick | 145 | 767 | 107937 |
Tasuku Honjo | 141 | 712 | 88428 |
Arnold J. Levine | 139 | 485 | 116005 |
Aaron T. Beck | 139 | 536 | 170816 |
Charles J. Yeo | 136 | 672 | 76424 |
Jerry W. Shay | 133 | 639 | 74774 |
Chung S. Yang | 128 | 560 | 56265 |
Paul G. Falkowski | 127 | 378 | 64898 |
Csaba Szabó | 123 | 958 | 61791 |
William C. Roberts | 122 | 1117 | 55285 |
Bryan R. Cullen | 121 | 371 | 50901 |
John R. Perfect | 119 | 573 | 52325 |