Identification of cytochrome b2 in oxygen-adapted yeast cells.
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Biomedical subjects
Publications and source records attributed to R Lorenc.
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In 16 children with malabsorption syndrome, out of which 5 had impaired lipid absorption or diarrhoea, and in 14 children in the control group the concentrations of vitamin D and 25 OH D3 were determined after oral administration of vitamin D in dose of 1200 U/kg.b.wt. or 12000 U/kg.b.wt. No decrease in initial 25 OH D3 concentrations was noted in children with malabsorption syndrome (40,5 +/- 0,7 ng/ml) in comparison with the control group (40,0 +/- 0,4 ng/ml). In children with impaired lipid absorption and diarrhoea the 25 OH D3 concentration was 33,6 +/- 2,4 ng/ml. After oral administration of vitamin D in small doses no differences were noted in the increase in vitamin D and 25 OH D3 concentrations in children with malabsorption syndrome or the control group. After administration of vitamin D in the dose 10 times higher no difference in the increase in vitamin D concentration was noted in children with malabsorption syndrome and the control group. However the increase in 25 OH D3 concentration in children with malabsorption syndrome was 49,8 +/- 1,2 ng/ml and 145,0 +/- 3,5 ng/ml in the control group. In the children with impaired lipid absorption and diarrhoea decreased vitamin D and 25 OH D3 concentrations were noted. This means that physiological doses of vitamin D in children with malabsorption syndrome are sufficient to supply vitamin D. Diarrhoea and impaired lipid absorption however, are indications for stimulation of skin synthesis of vitamin D.
The effects of vitamin D3 on rat kideney metabolism under conditions of experimental hypercalcemia. Acta Physiol. Pol., 1978, 29 (2) 153--159. The effect of vitamin D3 on renal gluconeogenesis processes was studied in the rat. The performed estimations of gluconeogenesis rate from malate and lactate demonstrated significant increases of glucose formation rate when kidney cortex slices of the vitamin D3 treated animals were analyzed. Further studies on the mechanism of the observed phenomenon were performed using kidney cell fractionation procedure and fluorometric estimation of the concentration of selected gluconeogenetic metabolites. Significant increases of phosphoenolpyruvate concentration in the cytosol fraction and citrate concentration in the mitochondrial fraction were observed. Comparison of the described action of vitamin D3 on gluconeogenesis and the effect of parathyriod hormone, as known from the literature suggests similar mechanism of both factor actions. A possibility of vitamin D3 action through the increase in intracellular calcium has been discussed.
It was stated that in patients with chronic gastrointestinal disorders (CGD) and decreased supply of Vit. D (25/OH/D = 6.8 +/- 3.0 ng/ml) during UVB stimulated skin synthesis of Vit.D the increment of Vit.D and 25-hydroxycholecalciferol (25/OH/D) depends on the starting values of Vit.D and 25/OH/D and is accompanied by significant increment of calciuria (delta mean UCa). Before the irradiation with UVB, mean 1,25/OH/2D in age paired healthy controls (50.66 +/- 12.35 pg/ml) when compared with CGD (47.62 +/- 12.08 pg/ml) and F.1,25/OH/2D in controls (2.02 +/- 0.80) and CGD (2.03 +/- 0.46) did not differ when mean PTH in CGD (135.3 +/- 61.6 pg/ml) was significantly higher in CGD (44.6 +/- 18.54 pg/ml, p less than 0.01) than in control group. During and after UVB irradiation completion of CGD mean 1,25/OH/2D levels (129.0 +/- +31.9 pg/ml) as well as F. 1,25/OH/2D index (5.54 +/- +1.54) were rising with the maximum reached on the 14-th day which was paralleled with a subsequent drop in mean PTH (72.3 +/- 24.42 pg/ml) concentration. The data indicated that UVB stimulated calciuria in CGD patients was correlated with increased synthesis of 1,25/OH/2D and increased F. 1,25/OH/2D index which was accompanied with suppression of mean PTH.
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The effects of vitamin D3, 1-alpha-OH D3 and calcitonin treatment on the rate of glucose synthesis in rat renal cortex slices were studied. The rate of glucose synthesis was significantly increased in animals treated with vitamin D3 and 1-alpha-OH D3 as compared to the control. The increase in the rat of glucose synthesis observed after vitamin D3 and 1-alpha-OH D3 treatment was abolished after administration of calcitonin in doses normalizing the serum calcium level. The obtained data point to a correlation between the serum calcium level observed in vivo and the ability to synthesize glucose measured in vitro in renal cortex slices.
UVB irradiation of the skin of patients with chronic gastrointestinal disorder (CGD) and decreased serum concentrations of 25-OHD (6.8 +/- 3.0 ng/ml, n = 15) result in a subsequent increase in circulating vitamin D and 25-hydroxyvitamin D (25-OHD) levels and is associated with a marked increase in calcuria (mean increase: 82 mg/d). Before UVB irradiation the mean total 1,25-(OH)2D concentration (48 +/- 12 pg/ml) and free 1,25-(OH)2D index (2.0 +/- 0.5) in CGD was not different from the values obtained in age-matched healthy controls (51 +/- 12 pg/ml and 2.0 +/- 0.8, respectively), but the mean PTH levels were significantly higher in CGD (135 +/- 62 pg/ml) than those in controls (45 +/- 19 pg/ml, p < 0.01). During and after UVB irradiation of CGD, mean 1,25-(OH)2D levels (129 +/- 32 pg/ml) as well as free 1,25-(OH)2D index (5.5 +/- 1.5) were on the rise with a maximum reached on the 14th day and were paralleled with a drop in PTH (72 +/- 24 pg/ml) concentration. These data indicate that UVB stimulated calciuria in CGD is due to increased synthesis of 1,25-(OH)2D and suppression of PTH.
The intestinal calcium and phosphate transport under conditions of experimental hypercalcemia. Acta Physiol. Pol., 1977, 28 (2): 127--134. Intestinal calcium and phosphate transport was examined in various segments of small intestine under two differently processed hypercalcemic conditions. The analysis of the serum calcium and phosphate level changes, showed the increasing serum calcium values without any concomitant change in the serum phosphate concentration during the course of the experiment. The observed discrepancy of the intestinal phosphate transport when compared the in vitro and in vivo studies, suggests the presence of phosphate transport regulatory mechanism acting on the intestinal level.