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: Treating Compassion Fatigue and Trauma Treatment Training for Bosnian and Croation Mental Health Workers, Geoffry D. White.
Abstract: Section I: Contemporary Views and Findings Introduction: Treating Compassion Fatigue, Charles Figley 1. Diagnosis and Treatment of Helper Stresses Traumas and Illnesses, Paul Valent 2. The Trauma of Working with Traumatized Children, Tracy Woodard-Myers and Thomas A. Cornille 3. Stress Responses of Mental Health Workers Following Disaster: The Oklahoma City Bombing, David F. Wee and Diane Myers 4. Secondary Traumatic Stress in Case Managers Working in Community Mental Health Services, Lenore Meldrum, Robert King, and Darren Spooner 5. Measuring Compassion Satisfaction As Well As Fatigue: Developmental History of the Compassion Satisfaction and Fatigue Test, B. Hundall Stamm Section II: Treatment and Prevention Innovations 6. The Accelerated Recovery Program for Compassion Fatigue, Eric Gentry, Anna B. Baranowsky and Kathleen Dunning 7. Humor as a Moderator of Compassion Fatigue, Carmen C. Moran 8. The Silencing Response in Clinical Practice: On the Road to Dialogue, Anna B. Baranowsky 9. Trauma Treatment Training for Bosnian and Croation Mental Health Workers, Geoffry D. White 10. Strategies for Managing Disaster Mental Health Worker Stress Diane Myers and David F. Wee Epilogue, Charles R. Figley Index
612 citations
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TL;DR: In this article, the authors present new evidence on the direct costs of bankruptcy and violation of priority of claims, and present a sample of 37 New York and American Stock Exchange firms that filed for bankruptcy between November 1979 and December 1986, showing that direct costs average 3.1% of the book value of debt plus the market value of equity.
610 citations
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TL;DR: Monitoring of newly-diagnosed patients with idiopathic intracranial hypertension over a period of 2 to 39 months found visual loss in patients with IIH is common and is often reversible, and improvement of visual field grade was significantly associated only with weight gain during the year before diagnosis.
Abstract: Management of patients with idiopathic intracranial hypertension (IIH) should be based on the presence and progression of visual loss. To characterize the clinical course of IIH more completely, we monitored the clinical status, especially visual function, in 50 consecutive newly-diagnosed patients over a period of 2 to 39 months (average follow-up 12.4 months). The mean age at onset of symptoms was 31 (range 11-58) yrs; 46 (92%) were women and 47 (94%) were obese (mean weight 90 kg). Common symptoms were headache (92%), transient visual obscurations (72%) and intracranial noises (60%); 13 of the patients (26%) initially had complaints of sustained visual loss. There was visual loss as determined by Goldmann perimetry in 96% and by automated perimetry in 92%. Contrast sensitivity testing was abnormal in 50% and Snellen acuity in 22%. Two patients (4%) became blind in both eyes. The Goldmann visual field grade improved in 60% of patients but visual function deteriorated in 5 (10%). Deterioration of visual field grade was significantly associated only with weight gain during the year before diagnosis. Visual loss in patients with IIH is common and is often reversible. Patients should be evaluated by perimetry using an appropriate strategy and contrast sensitivity testing, along with careful examination of the optic discs.
606 citations
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TL;DR: The existence of MSC subpopulations that co-express neurotrophins and other potent neuro-regulatory molecules, which contribute to MSC-induced effects on neuronal cell survival and nerve regeneration, may represent more potent vectors for treating a variety of neurological disorders.
606 citations
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TL;DR: Experiments addressing the concept of gene imprinting or induction of epigenetic memory by estrogen or other hormones suggest a link to persistent, heritable phenotypic changes seen after developmental estrogenization, independent of mutagenesis.
Abstract: The term "endocrine disrupting chemicals" is commonly used to describe environmental agents that alter the endocrine system. Laboratories working in this emerging field-environmental endocrine research-have looked at chemicals that mimic or block endogenous vertebrate steroid hormones by interacting with the hormone's receptor. Environmental chemicals known to do this do so most often with receptors derived from the steroid/thyroid/retinoid gene family. They include ubiquitous and persistent organochlorines, as well as plasticizers, pharmaceuticals, and natural hormones. These chemicals function as estrogens, antiestrogens, and antiandrogens but have few, if any, structural similarities. Therefore, receptor-based or functional assays have the best chance of detecting putative biological activity of environmental chemicals. Three nuclear estrogen receptor forms-alpha, beta, and gamma-as well as multiple membrane forms and a possible mitochondrial form have been reported, suggesting a previously unknown diversity of signaling pathways available to estrogenic chemicals. Examples of environmental or ambient estrogenization occur in laboratory experiments, zoo animals, domestic animals, wildlife, and humans. Environmentally estrogenized phenotypes may differ depending upon the time of exposure-i.e., whether the exposure occurred at a developmental (organizational and irreversible) or postdevelopmental (activational and reversible) stage. The term "estrogen" must be defined in each case, since steroidal estrogens differ among themselves and from synthetic or plant-derived chemicals. An "estrogen-like function" seems to be an evolutionarily ancient signal that has been retained in a number of chemicals, some of which are vertebrate hormones. Signaling, required for symbiosis between plants and bacteria, may be viewed, therefore, as an early example of hormone cross-talk. Developmental feminization at the structural or functional level is an emerging theme in species exposed, during embryonic or fetal life, to estrogenic compounds. Human experience as well as studies in experimental animals with the potent estrogen diethylstilbestrol provide informative models. Advances in the molecular genetics of sex differentiation in vertebrates facilitate mechanistic understanding. Experiments addressing the concept of gene imprinting or induction of epigenetic memory by estrogen or other hormones suggest a link to persistent, heritable phenotypic changes seen after developmental estrogenization, independent of mutagenesis. Environmental endocrine science provides a new context in which to examine the informational content of ecosystem-wide communication networks. As common features come to light, this research may allow us to predict environmentally induced alterations in internal signaling systems of vertebrates and some invertebrates and eventually to explicate environmental contributions to human reproductive and developmental health.
602 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 |