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Institution

Jewish Hospital

HealthcareCincinnati, Ohio, United States
About: Jewish Hospital is a healthcare organization based out in Cincinnati, Ohio, United States. It is known for research contribution in the topics: Antigen & Population. The organization has 3881 authors who have published 3414 publications receiving 123044 citations.


Papers
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Journal ArticleDOI
TL;DR: The R1101K sequence alteration of the DCTN1 gene may predispose subjects to ALS and FTD and the involved genes for copper/zinc superoxide dismutase (SOD1) and tau were excluded.
Abstract: A heterozygous R1101K mutation of the p150 subunit of dynactin (DCTN1) is reported in a family with amyotrophic lateral sclerosis (ALS) and co-occurrence of frontotemporal dementia (FTD). Two members of our kindred were affected with motor neuron disease and two with dementia in an autosomal dominant pattern of inheritance. We excluded the involvement of the ALS and FTD-linked genes for copper/zinc superoxide dismutase (SOD1) and tau. The R1101K sequence alteration of the DCTN1 gene may predispose subjects to ALS and FTD.

182 citations

Journal ArticleDOI
TL;DR: Metformin safely and effectively reduces CHD risk factors (weight, fasting insulin, leptin, LDL cholesterol, centripetal obesity) in morbidly obese, nondiabetic subjects with BMI > 30, probably by virtue of its insulin-sensitizing action.
Abstract: We studied 31 nondiabetic, habitually (> or =5 years) morbidly obese subjects (mean +/- SD body mass index [BMI] 43 +/- 8.7, median 43). Our specific aim was to determine whether metformin (2.55 g/d for 28 weeks) would ameliorate morbid obesity and reduce centripetal obesity; lipid and lipoprotein cholesterol, insulin, and leptin levels; and plasminogen activator inhibitor activity (PAI-Fx), risk factors for coronary heart disease (CHD). The patients were instructed to continue their prestudy dietary and exercise regimens without change. After 2 baseline visits 1 week apart, the 27 women and 4 men began receiving metformin, 2.55 g/d, which was continued for 28 weeks with follow-up visits at study weeks 5, 13, 21, and 29. Daily food intake was recorded by patients for 7 days before visits then reviewed with a dietitian. Kilocalories per day and per week were calculated. At each visit, fasting blood was obtained for measurement of lipid profile, insulin, leptin, and PAI-Fx. The mean +/- SD kilocalories consumed per day, 1,951 +/- 661 at entry, fell by week 29 to 1,719 +/- 493 (P =.014) but did not differ at weeks 5, 13, and 21 from that at week 29 (P >.2). Weight fell from 258 +/- 62 pounds at entry to 245 +/- 54 pounds at week 29 (P =.0001). Girth was reduced from 51.8 +/- 6.2 to 49.2 +/- 4.5 inches (P =.0001). Waist circumference fell from 44.0 +/- 6.4 inches to 41.3 +/- 5.9 (P =.0001). The waist/hip ratio fell from 0.85 +/- 0.09 to 0.84 +/- 0.09 (P =.04). Fasting serum insulin, 28 +/- 15 microU/mL at entry, fell to 21 +/- 11 microU/mL at week 29 (P =.0001), and leptin fell from 79 +/- 33 ng/mL to 55 +/- 27 ng/mL (P =.0001). On metformin, there were linear trends in decrements in weight, girth, waist circumference, waist/hip ratio, insulin, and leptin throughout the study period (P 30, probably by virtue of its insulin-sensitizing action.

179 citations

Journal ArticleDOI
TL;DR: Systemically dissected the relationship among plasma endotoxin elevation, hepatic oxidative stress, and TNF-α production following acute alcohol administration, and the results demonstrate that oxidative stress mediates endotoxin-induced hepatic TNF -α production in acute alcohol intoxication.
Abstract: Tumor necrosis factor-α (TNF-α) production is a critical factor in the pathogenesis of alcoholic liver injury. Both oxidative stress and endotoxin have been implicated in the process of alcohol-induced TNF-α production. However, a cause-and-effect relationship between these factors has not been fully defined. The present study was undertaken to determine the mediators of acute alcohol-induced TNF-α production using a mouse model of acute alcohol hepatotoxicity. Alcohol administration via gavage at a dose of 6 g/kg to 129/Sv mice induced hepatic TNF-α production in Kupffer cells as demonstrated by measuring protein levels, immunohistochemical localization, and mRNA expression. Alcohol intoxication caused liver injury in association with increases in plasma endotoxin and hepatic lipid peroxidation. Treatment with an endotoxin neutralizing protein significantly suppressed alcohol-induced elevation of plasma endotoxin, hepatic lipid peroxidation, and inhibited TNF-α production. Treatment with antioxidants, N-acetyl-l-cysteine, or dimethylsulfoxide, failed to attenuate plasma endotoxin elevation, but significantly inhibited alcohol-induced hepatic lipid peroxidation, TNF-α production and steatosis. All treatments prevented alcohol-induced necrotic cell death in the liver. This study thus systemically dissected the relationship among plasma endotoxin elevation, hepatic oxidative stress, and TNF-α production following acute alcohol administration, and the results demonstrate that oxidative stress mediates endotoxin-induced hepatic TNF-α production in acute alcohol intoxication.

177 citations

Journal ArticleDOI
TL;DR: Mapping of the binding site on laminin suggests that the 67-kDa chondroblast receptor interacts with a hydrophobic elastin-like sequence in domain V of the B1 chain, and chemotaxis studies indicate that cell migration toElastin peptides and lamination involves the same receptor.

177 citations

Journal ArticleDOI
TL;DR: It is suggested that respiration rate alone is an insufficient measure of respiratory reactivity to psychological stimuli and more appropriate functional assessments of respiratory response to stress are discussed.
Abstract: The occurrence of hyperventilation (overbreathing resulting in lowered end-tidal CO2) in conjunction with psychological stress was investigated. Twenty-nine normal subjects were individually placed in a stress condition by being required to make perceptual judgments under threat of electric shock for exceeding a specified number of errors. Feedback of errors was controlled by the experimenter and no subject was ever shocked since manipulated feedback never exceeded shock criterion. Stress induction consisted of four phases: request for participation, subject decision, pre-task instruction, and task. Dependent measures consisted of end-tidal CO2, respiration rate, heart rate, and State Anxiety scores. Stress manipulation was confirmed by significantly increased heart rate and anxiety scores from baseline values. Baseline comparisons indicated significant decreases in end-tidal CO2 (i.e., hyperventilation) for all phases as well as significant increases in respiration rate for all phases but one. Comparisons among several phases revealed significant changes in end-tidal CO2 either unaccompanied by or uncorrelated with changes in respiration rate. These results: 1) support the occurrence of hyperventilation to stress in normals, 2) suggest that respiration rate alone is an insufficient measure of respiratory reactivity to psychological stimuli, and 3) are discussed in terms of more appropriate functional assessments of respiratory response to stress.

177 citations


Authors

Showing all 3894 results

NameH-indexPapersCitations
John C. Morris1831441168413
David L. Kaplan1771944146082
Robert H. Purcell13966670366
Nancy J. Cox135778109195
Jennifer S. Haas12884071315
David A. Cheresh12533762252
John W. Kappler12246457541
Philippa Marrack12041654345
Arthur Weiss11738045703
Thomas J. Kipps11474863240
Michael Pollak11466357793
Peter M. Henson11236954246
Roberto Bolli11152844010
William D. Foulkes10868245013
David A. Lynch10871459678
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Performance
Metrics
No. of papers from the Institution in previous years
YearPapers
20232
202217
202148
202038
201944
201828