Institution
Texas Medical Center
Healthcare•Houston, Texas, United States•
About: Texas Medical Center is a healthcare organization based out in Houston, Texas, United States. It is known for research contribution in the topics: Population & Cancer. The organization has 2845 authors who have published 2394 publications receiving 79426 citations.
Topics: Population, Cancer, Stroke, Gene, Health care
Papers published on a yearly basis
Papers
More filters
••
TL;DR: There was no anamnestic response to Norwalk virus following the SRSV UK3/Hawaii outbreak although those affected had preexisting antibodies to Norwalker virus.
Abstract: Two successive outbreaks of gastroenteritis in South Africa were investigated to identify the aetiological agents. Some patients were involved in both outbreaks. Enteropathogenic bacteria or parasites were not evident in either outbreak. Small round structured viruses (SRSVs) were demonstrated in both outbreaks by direct electron microscopy. SRSV UK3/Hawaii virus was identified by immune electron microscopy as the causative agent in the first outbreak. Using new recombinant Norwalk virus (rNV) immunoassays for antibodies and antigen, Norwalk virus was implicated in the second outbreak. Preexisting antibodies to Norwalk virus were not protective and there was no cross protection between Hawaii and Norwalk viruses. There was no anamnestic response to Norwalk virus following the SRSV UK3/Hawaii outbreak although those affected had preexisting antibodies to Norwalk virus. To our knowledge, this is the first definitive diagnosis of SRSV-associated gastroenteritis in South Africa.
52 citations
••
51 citations
••
TL;DR: The utility of the guinea pig as an animal model of retinoid-induced epiphyseal closure is demonstrated and RAR activation is suggested to be necessary and sufficient for this activity.
51 citations
••
TL;DR: A strategy to compare and isolate mRNAs that are expressed differentially in cell lines derived from primary versus metastatic mouse prostate cancer using differential display-PCR proved to be successful and Caveolin-1, a metastasis-related gene and a candidate gene for hormone-resistant prostate cancer in man, is found to be overexpressed.
Abstract: Prostate cancer continues to be a significant cause of death in U.S. men despite screening of asymptomatic men and extensive treatment with potentially curative therapies, predominantly radical prostatectomy and irradiation therapy. The reason for the persistent mortality resides in part in the presence of occult metastases at the time of treatment. Currently there are no curative therapies for metastatic prostate cancer. To better understand the metastatic phenotype in prostate cancer, we developed a strategy to compare and isolate mRNAs that are expressed differentially in cell lines derived from primary versus metastatic mouse prostate cancer using differential display-PCR. This strategy has proven to be successful and multiple gene sequences associated with metastasis in this model are being investigated. One of the genes isolated by this method was caveolin-1. Caveolin-1 was found to be overexpressed not only in metastatic mouse prostate cancer, but also human metastatic disease. Recent studies have indicated that suppression of caveolin expression induces androgen sensitivity in high-caveolin, androgen-insensitive mouse prostate cancer cells derived from metastases. Overexpression of caveolin leads to androgen insensitivity in low-caveolin, androgen-sensitive mouse prostate cancer cells. Caveolin-1, therefore, is a metastasis-related gene and a candidate gene for hormone-resistant prostate cancer in man.
51 citations
•
TL;DR: The present data reveal a higher inflammatory status in the important tissues in SHR and indicate that inflammation might play a potential role in pathogenesis of hypertension and secondary organ complications.
Abstract: The hypertension is one of chronic vascular diseases, which often implicates multiple tissues causing stroke, cardiac hypertrophy, and renal failure. A growing body of evidence suggests that inflammatory mechanisms are important participants in the pathophysiology of hypertension. In this study, the inflammatory status of these tissues (kidney, liver, heart, and brain) in spontaneously hypertensive rats (SHR) was analyzed and its molecular mechanism was explored. The tissues were dissected from SHR and age-matched control Wistar-Kyoto (WKY) rats to investigate the abundance of inflammation-related mediators (IL-1beta, TNFalpha, ICAM-1, iNOS, C/EBPdelta and PPARgamma). mRNA levels were determined by reverse transcription-polymerase chain reaction and protein expression was evaluated by Western blot. To evaluate the oxidative stress of tissues, carbonyl protein content and total antioxidant capacity of tissues were detected by spectrophotometry and ferric reduction ability power (FRAP) method. The results suggest that: (1) Expressions of inflammation-related mediators (IL-1beta, TNFalpha, ICAM-1, iNOS, C/EBPdelta and PPARgamma) in SHR were higher compared with those in WKY rats except no evident increase of IL-1beta mRNA in liver and brain in SHR. (2) Tissues in SHR contained obviously increased carbonyl protein (nmol/mg protein) compared to that in WKY rats (8.93+/-1.08 vs 2.27+/-0.43 for kidney, 2.23+/-0.23 vs 0.17+/-0.02 for heart, 13.42+/-1.10 vs 5.72+/-1.01 for brain, respectively, P<0.05). However, no evident difference in the amount of carbonyl protein in liver was detected between SHR and WKY rats. (3) Total antioxidant capacities of kidney, liver, heart and brain were markedly lower in SHR than that in WKY rats (P<0.05). Thus, the present data reveal a higher inflammatory status in the important tissues in SHR and indicate that inflammation might play a potential role in pathogenesis of hypertension and secondary organ complications.
51 citations
Authors
Showing all 2878 results
Name | H-index | Papers | Citations |
---|---|---|---|
Eric N. Olson | 206 | 814 | 144586 |
Scott M. Grundy | 187 | 841 | 231821 |
Joseph Jankovic | 153 | 1146 | 93840 |
Geoffrey Burnstock | 141 | 1488 | 99525 |
George Perry | 139 | 923 | 77721 |
David Y. Graham | 138 | 1047 | 80886 |
James R. Lupski | 136 | 844 | 74256 |
Savio L. C. Woo | 135 | 785 | 62270 |
Henry T. Lynch | 133 | 925 | 86270 |
Joseph P. Broderick | 130 | 504 | 72779 |
Huda Y. Zoghbi | 127 | 463 | 65169 |
Paul M. Vanhoutte | 127 | 868 | 62177 |
Meletios A. Dimopoulos | 122 | 1371 | 71871 |
John B. Holcomb | 120 | 733 | 53760 |
John S. Mattick | 116 | 367 | 64315 |