Institution
Tulane University
Education•New Orleans, Louisiana, United States•
About: Tulane University is a education organization based out in New Orleans, Louisiana, United States. It is known for research contribution in the topics: Population & Blood pressure. The organization has 24478 authors who have published 47205 publications receiving 1944993 citations. The organization is also known as: University of Louisiana.
Topics: Population, Blood pressure, Poison control, Receptor, Angiotensin II
Papers published on a yearly basis
Papers
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TL;DR: This article found that stocks subject to high differences of opinion and more binding short-sales constraints have a price run-up just prior to earnings announcements that is followed by an even larger decline after the announcements.
287 citations
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TL;DR: The 2017 American College of Cardiology (ACC)/American Heart Association (AHA) Guideline for the Prevention, Detection, Evaluation, and Management of High Blood Pressure in Adults provides an evidence-based approach to reduction of CVD risk through lowering of blood pressure (BP).
Abstract: In November 2017, the American College of Cardiology (ACC) and the American Heart Association (AHA) released the guideline for the prevention, detection, evaluation, and treatment of high blood pre...
287 citations
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TL;DR: The hypothesis that glucocorticoid-induced fast feedback inhibition of the HPA axis is mediated by a nongenomic signaling mechanism that involves endocannabinoid signaling at the level of the PVN is supported.
Abstract: Glucocorticoid hormones are secreted in response to stimuli that activate the hypothalamo-pituitary-adrenocortical (HPA) axis and self-regulate through negative feedback. Negative feedback that occurs on a rapid time scale is thought to act through nongenomic mechanisms. In these studies, we investigated fast feedback inhibition of HPA axis stress responses by direct glucocorticoid action at the paraventricular nucleus of the hypothalamus (PVN). Local infusion of dexamethasone or a membrane-impermeant dexamethasone-BSA conjugate into the PVN rapidly inhibits restraint-induced ACTH and corticosterone release in a manner consistent with feedback actions at the cell membrane. The dexamethasone fast feedback response is blocked by the cannabinoid CB1 receptor antagonist AM-251, suggesting that fast feedback requires local release of endocannabinoids. Hypothalamic tissue content of the endocannabinoid 2-arachidonoyl glycerol is elevated by restraint stress, consistent with endocannabinoid action on feedback processes. These data support the hypothesis that glucocorticoid-induced fast feedback inhibition of the HPA axis is mediated by a nongenomic signaling mechanism that involves endocannabinoid signaling at the level of the PVN.
287 citations
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TL;DR: It is proposed that evolutionary adaptation to both preserve immune function with fewer mucosal CD4+ T cells and attenuate the immune activation that follows acute viral infection protect these animals from progressing to AIDS.
Abstract: HIV-infected humans and SIV-infected rhesus macaques experience a rapid and dramatic loss of mucosal CD4+ T cells that is considered to be a key determinant of AIDS pathogenesis. In this study, we show that nonpathogenic SIV infection of sooty mangabeys (SMs), a natural host species for SIV, is also associated with an early, severe, and persistent depletion of memory CD4+ T cells from the intestinal and respiratory mucosa. Importantly, the kinetics of the loss of mucosal CD4+ T cells in SMs is similar to that of SIVmac239-infected rhesus macaques. Although the nonpathogenic SIV infection of SMs induces the same pattern of mucosal target cell depletion observed during pathogenic HIV/SIV infections, the depletion in SMs occurs in the context of limited local and systemic immune activation and can be reverted if virus replication is suppressed by antiretroviral treatment. These results indicate that a profound depletion of mucosal CD4+ T cells is not sufficient per se to induce loss of mucosal immunity and disease progression during a primate lentiviral infection. We propose that, in the disease-resistant SIV-infected SMs, evolutionary adaptation to both preserve immune function with fewer mucosal CD4+ T cells and attenuate the immune activation that follows acute viral infection protect these animals from progressing to AIDS.
287 citations
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TL;DR: Treatment of many cancers remains a major challenge, but new therapeutic modalities are being developed based on antagonists of GH-RH and bombesin, which inhibit growth factors or their receptors, and somatostatin, which can be targeted to receptors for these peptides in various cancers and their metastases.
287 citations
Authors
Showing all 24722 results
Name | H-index | Papers | Citations |
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Walter C. Willett | 334 | 2399 | 413322 |
JoAnn E. Manson | 270 | 1819 | 258509 |
Frank B. Hu | 250 | 1675 | 253464 |
Eric B. Rimm | 196 | 988 | 147119 |
Krzysztof Matyjaszewski | 169 | 1431 | 128585 |
Nicholas J. White | 161 | 1352 | 104539 |
Tien Yin Wong | 160 | 1880 | 131830 |
Tomas Hökfelt | 158 | 1033 | 95979 |
Thomas E. Starzl | 150 | 1625 | 91704 |
Geoffrey Burnstock | 141 | 1488 | 99525 |
Joseph Sodroski | 138 | 542 | 77070 |
Glenn M. Chertow | 128 | 764 | 82401 |
Darwin J. Prockop | 128 | 576 | 87066 |
Kenneth J. Pienta | 127 | 671 | 64531 |
Charles Taylor | 126 | 741 | 77626 |