Institution
Rappaport Faculty of Medicine
About: Rappaport Faculty of Medicine is a based out in . It is known for research contribution in the topics: Population & Heparanase. The organization has 3205 authors who have published 3915 publications receiving 114533 citations.
Topics: Population, Heparanase, Medicine, Cancer, Pregnancy
Papers published on a yearly basis
Papers
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TL;DR: Results hint that at least in mammary gland CIS3 is likely the main physiological negative regulator of the PRLR‐mediated JAK2/STAT5 pathway.
80 citations
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TL;DR: It is claimed that some tumor cells may become resistant to macrophage-induced death by increasing their expression of microRNA- 146a (miR-146a), which leads to inhibition of iNOS translation, which implies that some cooperation between tumor cells and macrophages is required to induce tumor cell death, and that tumor cells might control their fate.
Abstract: Tumor cell-macrophage interactions change as the tumor progresses, and the generation of nitric oxide (NO) by the inducible nitric oxide synthase (iNOS) plays a major role in this interplay. In early stages, macrophages employ their killing mechanisms, particularly the generation of high concentrations of NO and its derivative reactive nitrogen species (RNS) to initiate tumor cell apoptosis and destroy emerging transformed cells. If the tumor escapes the immune system and grows, macrophages that infiltrate it are reprogramed in situ by the tumor microenvironment. Low oxygen tensions (hypoxia) and immunosuppressive cytokines inhibit iNOS activity and lead to production of low amounts of NO/RNS, which are pro-angiogenic and support tumor growth and metastasis by inducing growth factors (e.g., VEGF) and matrix metalloproteinases (MMPs). We review here the different roles of NO/RNS in tumor progression and inhibition, and the mechanisms that regulate iNOS expression and NO production, highlighting the role of different subtypes of macrophages and the microenvironment. We finally claim that some tumor cells may become resistant to macrophage-induced death by increasing their expression of microRNA-146a (miR-146a), which leads to inhibition of iNOS translation. This implies that some cooperation between tumor cells and macrophages is required to induce tumor cell death, and that tumor cells may control their fate. Thus, in order to induce susceptibility of tumors cells to macrophage-induced death, we suggest a new therapeutic approach that couples manipulation of miR-146a levels in tumors with macrophage therapy, which relies on ex vivo stimulation of macrophages and their re-introduction to tumors.
80 citations
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TL;DR: Computer simulations are provided showing that a twofold difference in the rate of uptake of the haptoglobin-hemoglobin complex by macrophages significantly affects nitric oxide bioavailability thereby providing a plausible explanation for why there is more vasospasm after subarachnoid hemorrhage in individuals and transgenic mice homozygous for the Hp 2 allele.
80 citations
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TL;DR: The detection of a statistically significant association between glatiramer acetate response and a single nucleotide polymorphism in a T-cell receptor &bgr; (TRB@) variant replicated in the two independent cohorts provides additional progress toward development of pharmacogenetics-based personalized treatment for multiple sclerosis.
Abstract: Genetic-based optimization of treatment prescription is becoming a central research focus in the management of chronic diseases, such as multiple sclerosis, which incur a prolonged drug-regimen adjustment This study was aimed to identify genetic markers that can predict response to glatiramer aceta
80 citations
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TL;DR: Findings indicate that baseline levels of activation symptoms, emotional distress, task oriented coping, self-esteem and friend support together explain 41% of the variability in the general QOL index 16 months later.
Abstract: This study aimed to identify factors that influence changes in satisfaction with quality of life (QOL) of schizophrenia patients. Baseline and follow up data for 148 schizophrenia patients were obtained at hospital admission and 16 months later. Relationships between changes over time in the general QOL index, and various factors were investigated using factor, multiple regression, and partial correlation analyses. Findings indicate that baseline levels of activation symptoms, emotional distress, task oriented coping, self-esteem and friend support together explain 41% of the variability in the general QOL index 16 months later. Changes in the general QOL of schizophrenia patients over time is associated with anergia, and paranoid symptoms, emotional distress, side effects, self-esteem, emotion and avoidance related coping styles, expressed emotion, and other social support. Determinants of change in QOL of patients were different being in hospital or out of hospital in the real world. No significant association of age, education, and follow up duration, with general QOL. Based on obtained data three types of overlapping factors were defined: (1) distressing, and protective; (2) primary and secondary; and (3) factors that remained constant or changed over time. Presented data are discussed within the framework of the Distress/Protection model of QOL. The conceptualization of three types of factors influencing QOL outcomes in this model demonstrates their predictive value, and may assist investigators and mental health workers in the interpretation of QOL data that may be used to improve patients' QOL outcomes.
79 citations
Authors
Showing all 3205 results
Name | H-index | Papers | Citations |
---|---|---|---|
Barry M. Brenner | 121 | 540 | 65006 |
Robert R. Edelman | 119 | 605 | 49475 |
David M. Goldenberg | 108 | 1238 | 48224 |
Moussa B.H. Youdim | 107 | 574 | 42538 |
Aaron Ciechanover | 105 | 315 | 58698 |
Israel Vlodavsky | 98 | 494 | 34150 |
Basil S. Lewis | 96 | 651 | 60124 |
Michael Aviram | 94 | 479 | 31141 |
Abraham Weizman | 81 | 1011 | 31083 |
Thomas N. Robinson | 81 | 309 | 26121 |
Peretz Lavie | 81 | 320 | 21532 |
Jacob M. Rowe | 75 | 328 | 20043 |
Hossam Haick | 72 | 279 | 15646 |
Walid Saliba | 70 | 359 | 19254 |
Gad Rennert | 67 | 350 | 17349 |