A novel trisialosyl ganglioside, IV3 alpha (NeuAc)3nLcOse4Cer, from hog kidney cortex.
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Studies into the activity of adenosine triphosphatase (ATPase) in homogenates of liver, cerebral cortex, renal cortex, and mucosa of small intestine of swine have shown differentiated activity patterns, with peak activity developing in the liver. This has been related to a particularly high metabolism performance of the liver in fattening pigs. No difference was found to exist between magnesium activation of ATPase of swine tissue homogenates and that in tissue obtained from ruminants. ATPase which could be activated by sodium and potassium ions and inhibited by ouabain was detectable from cerebral and renal cortex. Sodium and potassium ATPases accounts from some 25 per cent of the total activity. ATPase that could be stimulated by calcium ions was recorded only from liver homogenate. The optimum pH values of ATPase were between 7.5 and 8 in the liver, 9 in mucosa of small intestine, and 9.5 in cerebral and renal cortex.
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The development of experimental vitamin D deficiency in rats was accompanied by changes in cyclic nucleotides metabolism in the cortical part of kidneys, namely the increase in cyclic AMP synthesis and the decrease in cyclic GMP. The above changes appear in combination with marked deviations in calcium/phosphorus metabolism.
In 85 patients with ascertained chronic pyelonephritis the relations between the measured values of the combined PAH-inulin-clearance, the index of the adrenal cortex and other radiological findings were investigated. Here the determination of the cortex of the adrenal cortex resulted in a better correlation with the sizes clarification values than the calculation of the size of the kidney. By variance analysis (F-test) significant differences between the individual function groups became clear.
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The Walker 256 (W256) carcinosarcoma did not significantly modify calcium uptake by brush border membrane (BBM) vesicles in the kidney of the host rat, compared with that in membranes isolated from control animals. However, it showed a tendency to increase at near equilibrium in W256 tumor-host rats, associated with a decreased BBM protein content. ATP-dependent calcium influx by basolateral membrane (BLM) vesicles from W256 tumor-bearing rats was also increased compared with that in control BLM. This stimulation was due to a decreased Km for calcium. Passive calcium permeability or the Na+/Ca2+ exchanger were unchanged in BLM from W256 tumor-host rats compared with control BLM. Pre-stimulation of control rat cortical tubules with either 10(-7) M parathyroid hormone-related protein (PTHrP) (1-34) or 10(-4) M N6,2'-O-dibutiryl cyclic AMP before BLM isolation, did not modify the ATP-dependent calcium uptake by BLM vesicles compared with control membranes. However, our results do not rule out that the stimulated ATP-dependent calcium influx in BLM from W256 tumor-host rats could be mediated by the interaction among PTHrP and other humoral factors. Our findings suggest a possible mechanism for the increased renal calcium reabsorption in this animal model for humoral hypercalcemia of malignancy.
It was shown that the level of gamma-carboxyglutamic acid-containing protein is increased in perfused rat kidney after long-term administration (60 and 350 days) of a high-fat diet. No difference was found between the effect of vegetable fat and animal fat. Concomitantly it was shown that the relative molecular weight, N-terminal sequence over four residues, the profile of chymotryptic peptides and the sequence around the two (of the three in total) gamma-carboxyglutamic acid residues (over the span of seven residues) are identical with those found previously in osteocalcin and the gamma-carboxyglutamic acid-containing protein isolated from at least partially calcified connective tissue.
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The influence of hyperfiltration-hypertrophy, proteinuria and glucosuria on the renal cortical uptake of gentamicin was studied in several experimental models. Two groups of remnant kidney rats, one fed a standard protein diet and one a low protein diet, heavy proteinuric rats (adriamycin) and diabetic rats, each with their own control group, were treated with increasing doses of gentamicin, given as a continuous infusion over 6 hr. The relationship between increasing steady-state serum levels (ranged from 1 to 100 micrograms/ml) and the cortical gentamicin concentrations at the end of the infusions was examined by means of Michaelis-Menten kinetics. The uptake curves were compared to their respective control curves. It was demonstrated that gentamicin uptake was reduced in remnant kidney rats fed standard diet (showing hyperfiltration and heavy proteinuria), in adriamycin rats (showing heavy proteinuria in the absence of hyperfiltration) and in diabetic rats. Uptake of gentamicin in remnant kidney rats fed low protein diet (showing hyperfiltration and slight proteinuria) was comparable to controls. It appeared that among the pathophysiological factors examined, proteinuria is the most important in decreasing the cortical uptake of gentamicin. It is suggested that high levels of proteins in the proximal tubular fluid interfere with the adsorptive endocytic process, involved in the uptake of both proteins and gentamicin.
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