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Institution

Saint Louis University

EducationSt 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 & Health care. The organization has 18927 authors who have published 34895 publications receiving 1267475 citations. The organization is also known as: SLU & St. Louis University.


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Journal ArticleDOI
TL;DR: Most studies using generic HRQOL tools are of groups with specific impairments rather than heterogeneous groups of people with disability, so more specific testing of these problems is needed.

218 citations

Journal ArticleDOI
Abstract: [1] Impact of climate change on streamflow in the Upper Mississippi River Basin is evaluated by use of a regional climate model (RCM) coupled with a hydrologic model, Soil and Water Assessment Tool (SWAT). The RCM we used resolves, at least partially, some fine-scale dynamical processes that are important contributors to precipitation in this region and that are not well simulated by global models. The SWAT model was calibrated and validated against measured streamflow data using observed weather data and inputs from the U.S. Environmental Protection Agency Better Assessment Science Integrating Point and Nonpoint Sources (BASINS) geographic information systems/ database system. Combined performance of SWAT and RCM was examined using observed weather data as lateral boundary conditions in the RCM. The SWAT and RCM performed well, especially on an annual basis. Potential impacts of climate change on water yield and other hydrologic budget components were then quantified by driving SWAT with current and future scenario climates. Twenty-one percent increase in future precipitation simulated by the RCM produced 18% increase in snowfall, 51% increase in surface runoff, and 43% increase in groundwater recharge, resulting in 50% net increase in total water yield in the Upper Mississippi River Basin on an annual basis. Uncertainty analysis showed that the simulated change in streamflow substantially exceeded model biases of the combined modeling system (with largest bias of 18%). While this does not necessarily give us high confidence in the actual climate change that will occur, it does demonstrate that the climate change ‘‘signal’’stands out from the climate modeling (global plus regional) and impact assessment modeling (SWAT) ‘‘noise.’’ INDEX TERMS: 1655 Global Change: Water cycles (1836); 1860 Hydrology: Runoff and streamflow; 1866 Hydrology: Soil moisture; KEYWORDS: climate change, streamflow, SWAT Citation: Jha, M., Z. Pan, E. S. Takle, and R. Gu (2004), Impacts of climate change on streamflow in the Upper Mississippi River Basin: A regional climate model perspective, J. Geophys. Res., 109, D09105, doi:10.1029/2003JD003686.

218 citations

Journal ArticleDOI
28 Jul 2016
TL;DR: Treatment of A1ATD-associated lung disease includes standard therapies that are also used for the treatment of COPD, in addition to the use of augmentation therapy (that is, infusions of human plasma-derived, purified α1-antitrypsin).
Abstract: α1-Antitrypsin deficiency (A1ATD) is an inherited disorder caused by mutations in SERPINA1, leading to liver and lung disease. It is not a rare disorder but frequently goes underdiagnosed or misdiagnosed as asthma, chronic obstructive pulmonary disease (COPD) or cryptogenic liver disease. The most frequent disease-associated mutations include the S allele and the Z allele of SERPINA1, which lead to the accumulation of misfolded α1-antitrypsin in hepatocytes, endoplasmic reticulum stress, low circulating levels of α1-antitrypsin and liver disease. Currently, there is no cure for severe liver disease and the only management option is liver transplantation when liver failure is life-threatening. A1ATD-associated lung disease predominately occurs in adults and is caused principally by inadequate protease inhibition. Treatment of A1ATD-associated lung disease includes standard therapies that are also used for the treatment of COPD, in addition to the use of augmentation therapy (that is, infusions of human plasma-derived, purified α1-antitrypsin). New therapies that target the misfolded α1-antitrypsin or attempt to correct the underlying genetic mutation are currently under development.

218 citations

Journal ArticleDOI
TL;DR: In this paper, the authors provide evidence-based rationale for using exercise and physical activity (PA) for health promotion and disease prevention and treatment in older adults, and discuss the specific modalities and doses that have been studied in randomised controlled trials for their effectiveness in attenuating physiological changes of ageing, disease prevention, and/or improvement of older adults with chronic disease and disability.
Abstract: The human ageing process is universal, ubiquitous and inevitable. Every physiological function is being continuously diminished. There is a range between two distinct phenotypes of ageing, shaped by patterns of living - experiences and behaviours, and in particular by the presence or absence of physical activity (PA) and structured exercise (i.e., a sedentary lifestyle). Ageing and a sedentary lifestyle are associated with declines in muscle function and cardiorespiratory fitness, resulting in an impaired capacity to perform daily activities and maintain independent functioning. However, in the presence of adequate exercise/PA these changes in muscular and aerobic capacity with age are substantially attenuated. Additionally, both structured exercise and overall PA play important roles as preventive strategies for many chronic diseases, including cardiovascular disease, stroke, diabetes, osteoporosis, and obesity; improvement of mobility, mental health, and quality of life; and reduction in mortality, among other benefits. Notably, exercise intervention programmes improve the hallmarks of frailty (low body mass, strength, mobility, PA level, energy) and cognition, thus optimising functional capacity during ageing. In these pathological conditions exercise is used as a therapeutic agent and follows the precepts of identifying the cause of a disease and then using an agent in an evidence-based dose to eliminate or moderate the disease. Prescription of PA/structured exercise should therefore be based on the intended outcome (e.g., primary prevention, improvement in fitness or functional status or disease treatment), and individualised, adjusted and controlled like any other medical treatment. In addition, in line with other therapeutic agents, exercise shows a dose-response effect and can be individualised using different modalities, volumes and/or intensities as appropriate to the health state or medical condition. Importantly, exercise therapy is often directed at several physiological systems simultaneously, rather than targeted to a single outcome as is generally the case with pharmacological approaches to disease management. There are diseases for which exercise is an alternative to pharmacological treatment (such as depression), thus contributing to the goal of deprescribing of potentially inappropriate medications (PIMS). There are other conditions where no effective drug therapy is currently available (such as sarcopenia or dementia), where it may serve a primary role in prevention and treatment. Therefore, this consensus statement provides an evidence-based rationale for using exercise and PA for health promotion and disease prevention and treatment in older adults. Exercise prescription is discussed in terms of the specific modalities and doses that have been studied in randomised controlled trials for their effectiveness in attenuating physiological changes of ageing, disease prevention, and/or improvement of older adults with chronic disease and disability. Recommendations are proposed to bridge gaps in the current literature and to optimise the use of exercise/PA both as a preventative medicine and as a therapeutic agent.

218 citations

Journal ArticleDOI
TL;DR: These newly isolated glutamine transporter genes provide the long awaited tools necessary to study their molecular regulation during the catabolic states in which glutamine is considered to be "conditionally essential."
Abstract: Much has been learned about plasma membrane glutamine transporter activities in health and disease over the past 30 years, including their potential regulatory role in metabolism. Since the 1960s, discrimination among individual glutamine transporters was based on functional characteristics such as substrate specificity, ion dependence, and kinetic and regulatory properties. Within the past two years, several genes encoding for proteins with these defined activities (termed "systems") have been isolated from human and rodent cDNA libraries and found to be distributed among four distinct gene families. The Na(+)-dependent glutamine transporter genes isolated thus far are System N (SN1), System A (ATA1, ATA2), System ASC/B(0) (ASCT2 or ATB(0)), System B(0,+) (ATB(0,+)) and System y(+)L (y(+)LAT1, y(+)LAT2). Na(+)-independent glutamine transporter genes encoding for System L (LAT1, LAT2) and System b(0,+) (b(0,+)AT) have also been recently isolated, and similar to y(+)L, have been shown to function as disulfide-linked heterodimers with the 4F2 heavy chain (CD98) or rBAT (related to b(0,+) amino acid transporter). In this review, the molecular features, catalytic mechanisms and tissue distributions of each are addressed. Although most of these transporters mediate the transmembrane movement of several other amino acids, their potential roles in regulating interorgan glutamine flux are discussed. Most importantly, these newly isolated transporter genes provide the long awaited tools necessary to study their molecular regulation during the catabolic states in which glutamine is considered to be "conditionally essential."

217 citations


Authors

Showing all 19076 results

NameH-indexPapersCitations
Douglas G. Altman2531001680344
John E. Morley154137797021
Roberto Romero1511516108321
Daniel S. Berman141136386136
Gregory J. Gores14168666269
Thomas J. Smith1401775113919
Richard T. Lee13181062164
George K. Aghajanian12127748203
Reza Malekzadeh118900139272
Robert N. Weinreb117112459101
Leslee J. Shaw11680861598
Thomas J. Ryan11667567462
Josep M. Llovet11639983871
Robert V. Farese11547348754
Michael Horowitz11298246952
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Performance
Metrics
No. of papers from the Institution in previous years
YearPapers
202344
2022233
20211,619
20201,600
20191,457
20181,375