Institution
Southern Illinois University School of Medicine
Education•Springfield, Illinois, United States•
About: Southern Illinois University School of Medicine is a education organization based out in Springfield, Illinois, United States. It is known for research contribution in the topics: Population & Cancer. The organization has 3747 authors who have published 5977 publications receiving 209115 citations. The organization is also known as: SIU School of Medicine.
Topics: Population, Cancer, Ototoxicity, Receptor, Health care
Papers published on a yearly basis
Papers
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TL;DR: Evidence for chronic plastic neuropathic changes in the central auditory system of animals with psychophysically-defined tinnitus is examined, suggesting that long-term neuroplastic changes responsible for chronic tinnitis are likely to be responsible for its persistence.
129 citations
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TL;DR: Clinical, biochemical and radiologic evaluations and linkage analysis indicate a unique locus in this family with autosomal dominant limb-girdle muscular dystrophy and Paget disease of bone is an unusual disorder.
128 citations
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TL;DR: It is found that health literacy is lower in the rural population although this difference is explained by known confounders.
Abstract: Objective To determine whether health literacy is lower in rural populations. Method We analyzed health, prose, document, and quantitative literacy from the National Assessment of Adult Literacy study. Metropolitan Statistical Area designated participants as rural or urban. Results Rural populations had lower literacy levels for all literacy types (P 0.05). However, rural populations had higher document (P=0.04) and quantitative (P=0.01) literacy. Conclusion Health literacy is lower in the rural population although this difference is explained by known confounders.
128 citations
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TL;DR: Investigation of growth hormone signaling in mice found that decreased GH signaling associates with increased metabolism per body weight and may beneficially affect mitochondrial flexibility by increasing the capacity for fat oxidation; generally, GH excess produces opposite metabolic effects.
Abstract: Growth hormone (GH) signaling influences longevity in mice, with decreased GH signaling associated with longer life span and increased GH signaling with shortened life span. A proposed mechanism through which GH signaling influences life span postulates that decreased GH signaling lowers metabolic rate, thus slowing aging by decreasing production of damaging free radicals. The influence of altered GH signaling on metabolism was tested by monitoring oxygen consumption (VO2), respiratory quotient (RQ), and heat production in long-lived GH receptor knockout (GHRKO) and Ames dwarf mice, and short-lived bovine GH-overexpressing transgenic (bGH TG) mice. Intriguingly, both GHRKO and Ames dwarf mice have increased VO2 and heat per gram body weight, and decreased RQ, whereas bGH TG mice have decreased VO2 and heat per gram body weight and increased RQ. In conclusion, decreased GH signaling associates with increased metabolism per body weight and may beneficially affect mitochondrial flexibility by increasing the capacity for fat oxidation; generally, GH excess produces opposite metabolic effects.
128 citations
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TL;DR: It is demonstrated that the expression of the tumor suppressor gene PTEN has a significant inverse correlation with FAS expression in the case of prostate cancer in the clinical setting, and inhibition of the PTEN gene leads to the overexpression of FAS in vitro.
Abstract: Fatty acid synthase (FAS), a key enzyme of the fatty acid biosynthetic pathway, has been shown to be overexpressed in various types of human cancer and is, therefore, considered to be an attractive target for anticancer therapy. However, the exact mechanism of overexpression of the FAS gene in tumor cells is not well understood. In this report, we demonstrate that the expression of the tumor suppressor gene PTEN has a significant inverse correlation with FAS expression in the case of prostate cancer in the clinical setting, and inhibition of the PTEN gene leads to the overexpression of FAS in vitro. We also found that the combination of the expression status of these two genes is a better prognostic marker than either gene alone. Furthermore, our results indicate that the specific inhibition of FAS gene by siRNA leads to apoptosis of prostate tumor cells, and inhibition of PI 3-kinase pathway synergizes with FAS siRNA to enhance tumor cell death. These results provide a strong rationale for exploring the therapeutic use of an inhibitor of the PTEN signaling pathway in conjunction with the FAS siRNA to inhibit prostate tumor growth.
128 citations
Authors
Showing all 3778 results
Name | H-index | Papers | Citations |
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Jatin P. Shah | 119 | 725 | 45680 |
Harold G. Koenig | 99 | 678 | 46742 |
Chawnshang Chang | 97 | 534 | 35629 |
Richard J. K. Taylor | 91 | 1543 | 43893 |
Martin R. Farlow | 82 | 381 | 26820 |
David A. D'Alessio | 80 | 272 | 22955 |
Dirk R. Larson | 79 | 271 | 24067 |
Andrzej Bartke | 78 | 516 | 22865 |
Michael Brenner | 76 | 564 | 22010 |
Arnulf Stenzl | 73 | 791 | 23285 |
Wolfgang H. Dillmann | 72 | 200 | 17595 |
Michael Bonkowski | 66 | 279 | 13851 |
Jacob E. Friedman | 65 | 191 | 12485 |
Richard Salvi | 65 | 447 | 16289 |
Russell Noyes | 63 | 229 | 12790 |