Biomedical subjects
M F Kelley
Publications and source records attributed to M F Kelley.
Outbreak of histoplasmosis among cavers attending the National Speleological Society Annual Convention, Texas, 1994.
In June 1994, 18 people developed serologically confirmed histoplasmosis following cave exploration associated with the annual National Speleological Society Convention in Bracketville, Texas. Six others had an undiagnosed illness suspected to be histoplasmosis. Two persons were hospitalized. We conducted a survey of convention attendees and a nested case-control study of those entering caves. We also conducted a histoplasmin skin test survey of a subgroup of the society, the Texas Cavers Association, who were attending a reunion in October 1994. Among the national convention attendees, exposure to two caves was identified as responsible for 22 (92%) of the 24 cases; 12 (75%) of 16 people exploring one cave (Cave A) and 10 (77%) of 13 exploring a separate cave (Cave B) developed acute histoplasmosis. Additional risk-factors included fewer years of caving experience, longer time spent in the caves, and entering a confined crawl space in Cave A. Of 113 participants in the separate skin test survey, 68 (60%) were found to be skin test positive, indicating previous exposure to Histoplasma capsulatum. A positive skin test was significantly associated with male sex and more years of caving experience. Those less experienced in caving associations should be taught about histoplasmosis, and health care providers should pursue histories of cave exposure for patients with bronchitis or pneumonia that does not respond to initial antibiotic therapy.
Social interaction among people with dementia.
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Subchronic toxicity studies with the leukotriene D4 antagonist RG 12525.
Preclinical safety studies with the leukotriene D4 antagonist RG 12525 were conducted by the oral route in mice, rats, and monkeys. Oral administration of RG 12525 was repeated daily in studies up to 6 months in duration. RG 12525 was shown to have limited high-dose toxicity after repeated oral administration. The effects of RG 12525 were strongly dependent upon the species considered. High doses of RG 12525 caused significant increases in liver weight in mice, rats, and monkeys that were associated with diffuse hepatocellular hypertrophy in mice and rats but not in monkeys. No related clinical chemistry changes were observed in any of the species and hepatic activities of peroxisomal enzymes or cytochrome P450 were increased only slightly. Proliferation of brown adipose tissue (BAT) was observed in rats and mice but not in monkeys. The BAT reaction was more pronounced in the interscapular area but it was also observed in other subcutaneous locations as well as in mediastinal and bone marrow fat. In all locations, the RG 12525-induced BAT had some morphological similarities with cold-adapted BAT. Repeated administration of RG 12525 at high doses to female rats resulted in a lack of progression to the luteal phase of the estrous cycle that was reversible after discontinuation of treatment. Finally, RG 12525 was nephrotoxic in mice with males being more sensitive than females.
Older women and heart disease: beliefs about preventive behaviors.
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Controlling tuberculosis in minority populations in Texas.
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Hib vaccine is available and soon to be required.
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Transforming growth factor beta 1 regulates production of acute-phase proteins.
We explored the possible role of transforming growth factor beta 1 (TGF-beta), a cytokine that appears to be an important modulator of inflammation and tissue repair, in regulation of human plasma protein synthesis during the acute-phase response. In Hep 3B cells, TGF-beta led to increased secretion of the positive acute-phase proteins alpha 1-protease inhibitor and alpha 1-antichymotrypsin and decreased secretion of the negative acute-phase protein albumin. In Hep G2 cells, after incubation with TGF-beta, the same changes in secretion of alpha 1-protease inhibitor, alpha 1-antichymotrypsin, and albumin were observed, as well as decreased secretion of both the negative acute-phase protein alpha-fetoprotein and the positive acute-phase protein fibrinogen. In addition, TGF-beta modulated the effects of interleukin 6; these cytokines, in combination, were additive in inducing synthesis and secretion of alpha 1-protease inhibitor and alpha 1-antichymotrypsin and in decreasing secretion of albumin and alpha-fetoprotein. TGF-beta inhibited the induction of fibrinogen caused by interleukin 6. The effects on alpha 1-protease inhibitor were confirmed by metabolic labeling in Hep 3B cells and by demonstrating increased accumulation of specific mRNA in Hep G2 cells, and the effects on fibrinogen were confirmed in Hep 3B cells by studies of mRNA for the alpha chain of fibrinogen. TGF-beta had no effect on haptoglobin or alpha 1-acid glycoprotein secretion, either directly or in the presence of interleukin 6, which is capable of inducing these proteins. These studies demonstrate that TGF-beta can affect hepatic synthesis and secretion of a subset of acute-phase proteins, both directly and by modulating the effect of interleukin 6. The affected group of plasma proteins is distinct from those affected by other recognized acute-phase protein-inducing cytokines. These findings support the view that combinations of cytokines mediate the response of the hepatocyte to inflammatory stimuli.
The interleukin 2 gene is expressed in the syncytiotrophoblast of the human placenta.
The lymphokine interleukin 2 is an important immune system regulatory glycopolypeptide. It is produced by antigen- or mitogen-stimulated T lymphocytes and is required for the proliferation or clonal expansion of activated T lymphocytes. In this report, it is demonstrated by RNA transfer blot hybridization that the poly(A)+ RNA population of the human placenta contains a 0.85-kilobase RNA transcript that specifically hybridizes to a human interleukin 2 cDNA probe. By using hybridization histochemistry in situ, it is further shown that interleukin 2 RNA transcripts are localized, primarily, to the syncytial (syncytiotrophoblast) layer of the human placenta. Possible roles for syncytiotrophoblast-produced interleukin 2 are suggested and discussed.
Kinetics of cell death and disintegration in human lymphocyte cultures.
In order to quantitate lymphocyte proliferative responses, we explored the role of cell death in the kinetics of phytohemagglutinin-stimulated cultures. Unless the disintegration time (tDIS) of nonviable lymphocytes in culture is known, the rate of cell death cannot be calculated. To obtain tDIS, we determined the time interval between total and viable cell population decay after various killing events. Two subpopulations of lymphocytes were observed, the major (80%) with a mean (+/-SEM) tDIS of 16+/-2 hr and the minor (20%) with a tDIS of 45+/-7 hr. Kinetic balance sheets were constructed predicting total culture DNA content (cells plus medium), as calculated both from proliferation rates and from observed death and disintegration rates. In an experiment characterized by extensive cell death, the two tallies were well-matched when the above data were utilized. The large discrepancy between predicted and observed DNA contents of the medium indicates that the DNA of disintegrated lymphocytes is extensively degraded. We conclude that cell death explains proliferation deficits in stimulated lymphocyte cultures. Our approach to quantitation of cell death may have general applicability to kinetic studies of cultured cells.
Garre's disease in an Enga adolescent.
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TB transmission in hospitals.
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