Institution
Saint Louis University
Education•St Louis, Missouri, United States•
About: Saint Louis University is a education organization based out in St Louis, Missouri, United States. It is known for research contribution in the topics: Population & Poison control. The organization has 18927 authors who have published 34895 publications receiving 1267475 citations. The organization is also known as: SLU & St. Louis University.
Topics: Population, Poison control, Health care, Transplantation, Virus
Papers published on a yearly basis
Papers
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TL;DR: Recent advances in biofuel cell technology have addressed deficiencies and include methods to increase lifetime and environmental stability, but remain limited by short lifetimes, low power densities and inefficient oxidation of fuels.
477 citations
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TL;DR: It is intended that from the considerations recorded here a conceptual framework will begin to emerge that is amenable to further experimental substantiation as regards how multiple basal forebrain systems and the cortices to which they are related by connections work together to fashion a unitary object--the adaptive response.
476 citations
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TL;DR: BBB transport of insulin provides a mechanism for peripheral insulin to act within the CNS as a regulatory peptide, with the transport rate of insulin being altered during development and by fasting, obesity, hibernation, diabetes mellitus and Alzheimer's disease.
474 citations
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University of California, Los Angeles1, University of Münster2, Martin Luther University of Halle-Wittenberg3, Tulane University4, VU University Amsterdam5, Ghent University6, University of Liège7, Bar-Ilan University8, Queen's University9, Saint Louis University10, Université libre de Bruxelles11, University of Manchester12
TL;DR: This research presents a meta-analysis of 129 cases of meningitis in mice over a 12-month period and shows clear trends in progeria and in particular in cases of high prolapse preoperatively and during the course of pregnancy.
Abstract: Demographic data clearly demonstrate that the percentage of the population in the older age group is increasing. Androgen deficiency in the aging male has become a topic of increasing interest and debate throughout the world. Cross-sectional and longitudinal data indicate that the testosterone falls progressively with age and that a significant percentage of men over the age of 60 years have serum testosterone levels that are below the lower limits of young adult (age 20–30 years) men (1–4). The principal questions raised by these observations are whether older hypogonadal men will benefit from testosterone treatment and what will be the risks associated with such intervention.
The past decade has brought evidence of benefit of androgen treatment of hypogonadal men on multiple target organs and the recent studies show short-term beneficial effects of testosterone in older men that are similar to those in younger men. This has been comprehensively reviewed and summarized by the Institute of Medicine in ‘Testosterone and Aging: Clinical Research Directions’ (5). Long-term data on the effects of testosterone treatment in the older population are limited mainly to effects on body composition and bone mass (6–11). Key questions of the effects of testosterone on patient reported outcomes and functional benefits that may retard physical or mental frailty of the elderly or improve the quality of life are not yet available. Specific risk data on the prostate and cardiovascular systems are needed.
473 citations
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TL;DR: The authors' data indicate that SMC3 and SMC1A mutations contribute to approximately 5% of cases of CdLS, result in a consistently mild phenotype with absence of major structural anomalies typically associated with Cd LS, and in some instances, result with a phenotype that approaches that of apparently nonsyndromic mental retardation.
Abstract: Mutations in the cohesin regulators NIPBL and ESCO2 are causative of the Cornelia de Lange syndrome (CdLS) and Roberts or SC phocomelia syndrome, respectively. Recently, mutations in the cohesin complex structural component SMC1A have been identified in two probands with features of CdLS. Here, we report the identification of a mutation in the gene encoding the complementary subunit of the cohesin heterodimer, SMC3, and 14 additional SMC1A mutations. All mutations are predicted to retain an open reading frame, and no truncating mutations were identified. Structural analysis of the mutant SMC3 and SMC1A proteins indicate that all are likely to produce functional cohesin complexes, but we posit that they may alter their chromosome binding dynamics. Our data indicate that SMC3 and SMC1A mutations (1) contribute to ∼5% of cases of CdLS, (2) result in a consistently mild phenotype with absence of major structural anomalies typically associated with CdLS, and (3) in some instances, result in a phenotype that approaches that of apparently nonsyndromic mental retardation.
473 citations
Authors
Showing all 19076 results
Name | H-index | Papers | Citations |
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Douglas G. Altman | 253 | 1001 | 680344 |
John E. Morley | 154 | 1377 | 97021 |
Roberto Romero | 151 | 1516 | 108321 |
Daniel S. Berman | 141 | 1363 | 86136 |
Gregory J. Gores | 141 | 686 | 66269 |
Thomas J. Smith | 140 | 1775 | 113919 |
Richard T. Lee | 131 | 810 | 62164 |
George K. Aghajanian | 121 | 277 | 48203 |
Reza Malekzadeh | 118 | 900 | 139272 |
Robert N. Weinreb | 117 | 1124 | 59101 |
Leslee J. Shaw | 116 | 808 | 61598 |
Thomas J. Ryan | 116 | 675 | 67462 |
Josep M. Llovet | 116 | 399 | 83871 |
Robert V. Farese | 115 | 473 | 48754 |
Michael Horowitz | 112 | 982 | 46952 |