Biomedical subjects
Publications and source records attributed to B Paul.
Fractures of metatarsal bones range from 4 to 5% of all fractures and to less than 1% of all injuries occurring. The usual treatment is non-operative by plaster cast. In case of special physical performance (profession, sports) the indication for operative treatment can be extended. This should be taken into consideration in dislocated multiple fractures as well as in single ones of the first and fifth metatarsal bone.
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To find out the role of pituitary in Mitomycin C (MC) induced reduction of testicular steroidogenesis, MC was administered along with HCG and the testicular steroidogenic activity was assessed on the basis of different parameters which are directly and indirectly related to the rate of testicular steroid biogenesis. The results indicate that MC induced reduction in testicular steroidogenesis is not only due to its direct effect but suppression of pituitary gonadotrophin secretion may be one of the responsible factor.
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Specific damage by selectively absorbed, pulsed lasers can be predicted based on physical models. Thermally mediated alterations can be confined to pigmented targets from the level of subcellular organelles (e.g., melanosomes) to large multicellular tissue structures (e.g., blood vessels) by the appropriate manipulation of wavelength and pulse duration. Highly selective damage to human cutaneous microvessels in vivo is shown to occur after 0.3-microseconds 577-nm dye laser pulses; the epidermis and dermal structures other than vessels are spared. Observations in an animal model suggest that hemorrhage or, at lower doses, selective intravascular coagulation and permanent microvascular hemostasis occur. Highly selective damage to melanized cells and to single melanosomes in situ was shown to occur after single 20-ns 351-nm pulses from a XeF excimer laser. Basal-cell- and melanocyte-specific necrosis is followed by gross hypopigmentation. In this case there is no evidence of vascular damage. The most likely modes of selective alterations include localized thermal denaturation, vaporization, and shock-wave generation. Means of predicting and controlling histologically selective radiant heating effects in skin are suggested.
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Several lines of investigation were pursued to understand mechanisms involved in the in vivo depression of rat hepatic microsomal mixed function oxidase by cyclophosphamide, an important anti-cancer and immunosuppressive agent. Essentially exclusive metabolism-dependent binding to microsomal proteins of 14C from [4-14C]cyclophosphamide, compared with 3H from [chloroethyl-3H]cyclophosphamide, suggests the binding of the metabolite acrolein. Of the various metabolites and analogs of cyclophosphamide tested (which did not contain a peroxy or a hydroperoxy group), only acrolein and 4-hydroxycyclophosphamide (which releases acrolein in solution) caused denaturation of microsomal cytochrome P-450 in vitro; this denaturation was identical with that produced by sulfhydryl reagents. Of the various chemicals tested, only those which contained either a free amino group (except lysine) and/or a free sulfhydryl group (e.g. semicarbazide, cysteine, glycine, glucosamine) effectively blocked (40-80%) the binding of 14C as well as protected against acrolein-induced denaturation of cytochrome P-450. These data further suggested interaction of cyclophosphamide metabolite with free amino and/or free sulfhydryl groups in proteins. However, comparison with [3H]aflatoxin B2a which interacts with free protein amino groups via the formation of Schiff bases, clearly attributed the preferential binding of 14C to cysteine sulfhydryl groups in these proteins. Studies on chemical models derived from reaction between acrolein and cysteine also supported this suggestion. When microsomes isolated from incubations metabolizing [4-14C]cyclophosphamide were subjected to gel electrophoresis, the major radioactive band detected by autoradiography was associated with a cytochrome P-450 band at 55,000 daltons, the major band induced by phenobarbital in the rat. All these results taken together strongly point to the possibility that acrolein is the cyclophosphamide metabolite responsible for the depression of the mixed function oxidase activities. Acrolein most likely produces this effect by alkylation of the sulfhydryl group(s) in the active site of cytochrome P-450.
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Administration of ochratoxin A to pregnant rats from 6 to 12 days of gestation period, resulted in complete resorption of fetuses. On histological examination luteal degeneration was observed along with reduction in the weight of corpus luteum (mg/100 mg ovarian tissue) and pituitary gland. The enzyme delta 5-3 beta-hydroxy steroid dehydrogenase (delta 5-3 beta-OHD) and glucose-6-phosphate dehydrogenase were demonstrated histochemically in the ovary of pregnant rats. The activities of the enzymes were suppressed significantly in ochratoxin A treated rats. The same treatment also resulted in an accumulation of cholesterol and ascorbic acid in the ovary. Based on these results, it is suggested that resorption of fetuses in ochratoxin A treated rats may be related with a diminution in ovarian steroidogenesis possibly due to reduction in pituitary gonadotrophin secretion.
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Several 1-N-substituted derivative [haloacetyl-, glycyl-, (dimethyl)amino-acetyl-, azidoacetyl-, trifluoroacetyl-, and trifluoromethylsulfonyl-] of 2-acetamido-2-deoxy-3,4,6-tri-O-acetyl-beta-D-glucopyranosylamine (1) were synthesized as potential metabolic inhibitors of cellular-membrane glycoconjugates. Several fully acetylated derivatives were found to inhibit growth of mouse mammary adenocarcinoma TA3, leukemia L1210, or leukemia P-288 cells at 1-0.01 mM concentration in vitro. Some of these derivatives were less active after O-deacetylation. Analogs of 1 in which NH2-1 was replaced by OH- or OAc-1 were also active on the same cell systems. The growth-inhibitory activity was correlated with inhibition of the incorporation of 2-amino-deoxy-D-glucose and L-leucine into a macromolecular fraction.
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Treatment with mitomycin C resulted in a decrease in the testicular delta 5-3 beta-hydroxysteroid dehydrogenase level along with a fall of Leydig cell nuclear area. Following the same treatment the significant fall of sex accessory organ weights and testicular accumulation of ascorbic acid and cholesterol were noted. On the basis of above evidence it is suggested that mitomycin C probably suppressed testicular steroidogenesis.
The present experimental design was set up to examine the effect of Ochratoxin A on the onset of reproductive maturity and the ovarian steroidogenic capacity by means of histochemical studies. Ochratoxin A treatment causes a remarkable delay in sexual maturation as evidenced by the age at vaginal opening and appearance of first estrus (cornifid smear). The same treatment also results in a significant diminution of the delta 5-3 beta-hydroxysteroid dehydrogenase and glucose-6-phosphate dehydrogenase activity along with a reduction in the weight of ovary, uterus, and pituitary. On the basis of above data it is assumed that the probable cause of delayed maturation in Ochratoxin A treated rat is due to the suppressed ovarian steroidogenesis.
The enzymes delta 5-3 beta-hydroxy steroid dehydrogenase and glucose-6-phosphate dehydrogenase were demonstrated histochemically in the adrenal cortex of female rats. The activities of these enzymes were increased significantly in ochratoxin A treated rats along with an increase in the weight and reduction in cholesterol and ascorbic acid content of the gland. The observations suggest that after treatment with ochratoxin A, adrenal steroidogenesis was stimulated.
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