[Protein metabolism in the salivary glands of rats treated with cortisone].
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Biomedical subjects
Publications and source records attributed to I Boros.
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The promoters of the rrnB gene of Escherichia coli have been cloned on a multicopy, pBR322-derived plasmid by deleting most of the structural part of rrnB and fusing the terminators of the gene immediately to the promoters. Several further deletions were constructed to vary the promoter-terminator distance, destroy or damage selectively any of the promoters or terminators, and vary the distance between the two pairs of P1 P2 and P3 P4 promoters. All these transcription signals were shown to function on the plasmids in vitro and in vivo. The truncated in vivo transcription products initiated at the P1 and P2 promoters of the recombinant plasmids were found to be stable, and the accumulated transcripts could be easily distinguished from the chromosome-coded rRNA. This provides a convenient experimental system to study the regulation of rRNA biosynthesis.
Heat shock proteins (HSPs) are cytoprotective proteins that are expressed constitutively and/or at elevated levels upon the exposure of cells to stress. The aim of this study was to investigate the potential effects of HSP preinduction by cold- (CWI) or hot-water immersion (HWI) on pro-inflammatory cytokine production (IL-1, IL-6, TNF-alpha) in cholecystokinin-octapeptide(CCK)-induced acute pancreatitis. Rats were injected with 3 x 75 microg/kg CCK subcutaneously at intervals of 2 h at the peak level of HSP synthesis, as determined by Western blot analysis. The animals were killed by exsanguination through the abdominal aorta 2 h after the last CCK injection. The serum IL-1, IL-6, TNF-alpha, and amylase levels, the pancreatic weight/body weight ratio, and the pancreatic contents of DNA, protein, amylase, lipase and trypsinogen were measured; biopsy for histology was taken. HWI significantly elevated the HSP72 expression, while CWI significantly increased the HSP60 expression. HWI pretreatment decreased all of the measured serum cytokine levels in this acute pancreatitis model. CWI and HWI pretreatment ameliorated most of the examined laboratory and morphological parameters of CCK-induced pancreatitis. The findings suggest the possible roles of HSP60 and HSP72 in the protection against CCK-induced pancreatitis. HSP72 might also participate in the reduction of pro-inflammatory cytokine synthesis.
Following a fluoride depletion period 6 subjects repeatedly rinsed with 30-ml volumes of milk with or without added fluoride (5 ppm). Rinsing time was timed according to the measurements on how long it took to drink 200 or 500 ml milk. Rinsing with fluoridated milk for a total interval of 20 and 60 s, respectively, did not influence significantly the fluoride concentration of unstimulated centrifuged whole saliva 45 min later. Neither the urinary fluoride concentration nor the fluoride excretion were significantly affected by rinsing with fluoridated milk during the first hour. However, intake of 1 or 2.5 mg of fluoride with 200 and 500 ml milk, respectively, resulted in significant elevations in whole saliva fluoride levels 45 min later. In addition, the fluoride excretions into urine produced during 60 min after the fluoride intakes were significantly elevated and those reflected the ingested dose of fluoride. The intake of either 1 or 2.5mg fluoride with milk did not significantly influence the fluoride level of unstimulated labial gland saliva collected simultaneously with whole saliva.
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