PubMed Health⌕ Search

Biomedical subjects

P Boer

Publications and source records attributed to P Boer.

At least 163 records · Page 9Linked to original sources

The excretion of metabolites of cortisol and aldosterone in male patients on haemodialysis treatment.

A single intravenous infection of 14C-cortisol and 3H-aldosterone was given to four male uraemic patients on haemodialysis (HD) treatment. The excretion of radioactivity was measured during two weeks in urine, HD fluid and faeces, In two patients, who were injected just before dialysis, large amounts of radioactivity were eliminated in the HD fluid (38% and 56% for 3H, 45% and 57% for 14C) and minor amounts were found 3 in the urine ( less than 5%); in the faeces respectively 32% and 30% of 3H and 18% and 26% of 14C were excreted. Two patients who were injected immediately after dialysis (and who also had a somewhat better kidney function) excreted larger amounts of radioactivity in th urine (10% and 24% for 3H, 13% and 41% for 14C) and in the faeces (44% and 62% for 3H, 29%, and 37% for 14C), while in the HD fluid respectively 18% and 4% of 3H and 30% and 12% of 14C was eliminated. The plasma radioactivity just before and just after dialysis showed a very good correlation (r=0.96 to 0.99, p less than 0.001) with the radioactivity eliminated in the first and last hour of HD treatment. Between HD treatments, the radioactivity in plasma did not change or decreased only very little. This finding suggests that metabolities of cortisol and aldosterone to be excreted in the faeces, are very quickly removed from the circulation.

Adult↗

Localization of acid phosphatase in Saccharomyces cerevisiae: a clue to cell wall formation.

Acid phosphatase is present in two layers of the cell envelope of Saccharomyces cerevisiae. These are separated by another layer, which is free of acid phosphatase. We have evidence that the cell wall is built up in two stages, which are independent. In the first stage, the cell wall is built up during the formation of the bud. Glucanase vesicles are involved in this process. In the second stage, a thick layer is deposited at the inside against the new cell wall. This results in the thick, rigid wall of the mature yeast cell. This latter layer is probably assembled on the outer surface of the plasmalemma.

Acid Phosphatase↗

"Upright hyperkalemia" in selective hypoaldosteronism.

A new phenomenon, increase of serum potassium in response to the upright posture in patients with selective hypoaldosteronism is described in the present preliminary report. Further studies are in progress concerning its possible clinical and pathophysiological significance.

Adult↗

Postural plasma aldosterone response in "upright hyperkalemia" associated with selective hypoaldosteronism.

Upright posture induced a consistent increase in serum K with a blunted plasma aldosterone response in four male renal patients with selective hypoaldosteronism. Dietary Na restriction induced a dramatic increase in the suppressed plasma aldosterone without returning the elevated serum K levels to normal and abolishing the postural serum K change. Therefore it is concluded that "upright hyperkalemia" may not be caused exclusively by suppression or/and inadequate postural response of aldosterone. Cellular disturbance in the regulation of K distribution might be an additional explantation for the aldosterone unresponsive postural K change.

Adult↗

Glycosylation in vitro of an asparagine sequon catalysed by preparations of yeast cell membranes.

Preparations of yeast cell membranes can catalyse in vitro the N-acetyl-beta-D-glucosaminylation of the asparagine sequon at residues 34--36 of bovine pancreatic ribonuclease A. The relevant glycopeptides were isolated from tryptic hydrolysates of the glycosylated ribonuclease and analysed. The donor used was UDP-N-acetyl-D-glucosamine, although the mechanism of the transfer is unknown. Mn2+ ions at concentrations of 25 mM double the activity of the enzymic transfer.

Acetylglucosamine↗

Renin dependency of blood-pressure. Analysis by angiotensin II antagonist P113 in hypertensive patients treated with salt depletion and propranolol.

The effect of infusion of the angiotensin II antagonist P113 on blood-pressure (B.P.) has been studied in 10 patients with various forms of hypertension under four different conditions: before and after salt depletion and with or without propranolol treatment. The fall in B.P. after P113 infusion significantly correlated with log P.R.A. (plasma-renin activity), irrespective of diagnosis or treatment. P113 infusion caused a consistent fall in B.P. only after sodium depletion. The changes in B.P. after P113 infusion and those induced by propranolol correlated only during sodium depletion, when P.R.A. values rose. It is concluded that sodium depletion induced "renin dependency" of B.P. in all patients. The decrease in B.P. renin dependency after propranolol therapy suggests that suppression of P.R.A. is one of the antihypertensive mechanisms underlying the action of this drug.

Adolescent↗

The effect of ribose 5-phosphate and 5-phosphoribosyl-1-pyrophosphate availability on de novo synthesis of purine nucleotides in rat liver slices.

The effect of increasing cellular ribose 5-phosphate (ribose-5-P) availability by methylene blue-induced acceleration of the oxidative pentose phosphate pathway on the rate of 5-phosphoribosyl-1-pyrophosphate (P-ribose-PP) generation, was studied in slices of rat liver at varying Pi concentration. It was found that at Pi concentration prevailing in the tissue of extracellular physiological Pi concentration, ribose-5-P availability is saturating for P-ribose-PP generation, as gauged by the rate of adenine incorporation into tissue nucleotides. The effect of altering P-ribose-PP availability on the rate of de novo purine production gauged by the rate of formate incorporation into purines, was also studied. It was found that the physiological P-ribose-PP concentration in rat liver tissue is limiting for purine synthesis de novo. Depletion of cellular P-ribose-PP, achieved by increase of P-ribose-PP consumption, decelerated purine synthesis, while increase of P-ribose-PP availability, achieved by activation of P-ribose-PP synthetase occurring at elevated Pi concentration, resulted in acceleration of purine synthesis.

Animals↗

Change in the renin dependency of blood pressure induced by volume depletion and/or propranolol therapy in hypertensive patients.

1. Plasma renin activity (PRA) and renin dependency of the blood pressure was analysed in ten patients with various forms of hypertension before and during treatment with volume depletion and/or propranolol. Renin dependency was tested by infusion of the specific competitive angiotensin II antagonist Sar1-Ala8-angiotensin II (P113). 2. The P113-induced fall of the blood pressure did correlate with the log PRA (r=0-888, P less than 0-001). This correlation was found irrespective of different types of hypertension and treatment schedules. 3. During volume depletion, PRA was stimulated and renin dependency of the blood pressure increased. Propranolol therapy suppressed PRA during normovolaemia as well as during volume depletion, and this was accompanied by a decrease of the renin dependency. 4. No incication was found that a given PRA is of special importance for blood pressure elevation in different patients. 5. Suppression of PRA by propranolol is one of the anti-hypertensive mechanisms of this drug.

Adolescent↗

De novo synthesis of purine nucleotides in human peripheral blood leukocytes. Excessive activity of the pathway in hypoxanthine-guanine phosphoribosyltransferase deficiency.

Human peripheral blood leukocytes were studied for the presence and the regulatory properties of the pathway of de novo synthesis of purine nucleotides. The cells were found to incorporate the labeled precursors formate and glycine into purines. The rate of [14C]-formate incorporation was decreased by several compounds known to inhibit purine synthesis by affecting the activity by glutamine phosphoribosylpyrophosphate (PRPP) amidotransferase, the first committed enzyme in the pathway, either through decreasing the availability of PRPP, a substrate for this enzyme, or through exerting inhibition on this enzyme. PRPP availability in the leukocyte was found to be limiting for purine synthesis. Increased PRPP availability resulting from activation of PRPP synthetase by increasing inorganic phosphate (Pi) concentration caused acceleration of purine synthesis. On the other hand, no clear-cut evidence was obtained for the availability of ribose-5-phosphate in the leukocyte being rate limiting at physiological extracellular Pi concentration for PRPP generation, and thus for purine synthesis. However, the addition of methylene blue, which accelerates the oxidative pentose shunt that produces ribose-5-phosphate, resulted in acceleration of PRPP generation and of purine synthesis only when PRPP synthetase was largely activated at high Pi concentration. These results may be taken to suggest that ribose-5-phosphate availability is indeed not limiting for PRPP generation under physiological conditions. Purine synthesis de novo was accelerated more than 13-fold in the leukocytes of two gouty patients affected with partial deficiency of hypoxanthine-guanine phosphoribosyltransferase, but was normal in the leukocytes of an obligate heterozygote for this enzyme abnormality. The results domonstrate in peripheral human leukocytes the presence of the complete pathway of de novo synthesis of purine nucleotides and the manifestation in these cells of the biochemical consequences of hypoxanthine-guanine phosphoribosyltransferase deficiency, i.e., increased availability of PRPP and acceleration of purine synthesis de novo. The results indicate the usefulness of leukocytes as a model tissue for the study of purine metabolism in man.

Amidophosphoribosyltransferase↗

Comparison of the antihypertensive effect of propranolol and practolol combined with chlorthalidone.

A double blind cross-over trial of fixed doses of propranolol (640 mg/day) and the cardioselective drug practolol (1600 mg/day) was performed in 28 patients with essential hypertension whose blood pressure was not adequately controlled by chlorthalidone (100 mg 3 times weekly) alone. Chlorthalidone alone was given during the first (control) period, and it was continued throughout the propranolol and practolol treatment periods, each of 10 weeks. The systolic and diastolic blood pressures were lowered significantly by both the beta blocking drugs. The changes in blood pressure caused by altering the patient's position were the same after both beta blockers. Propranolol produced slightly lower values than practolol, but the difference was significant only for diastolic blood pressure in the sitting and supine positions. In individual patients the final blood pressure after propranolol was correlated with the final blood pressure after practolol. Only minimal side-effects of either drug were noticed. It is concluded that the doses employed both of propranolol and practolol had a good and approximately equal antihypertensive effect when combined with chlorthalidone treatment. There was no correlation between the final blood pressure and plasma renin activity.

Antihypertensive Agents↗

Further studies on the formation of cardiolipin and phosphatidylglycerol in rat liver mitochondria. Effect of divalent cations and the fatty acid composition of CDP-diglyceride.

The divalent cation requirement for mitochondrial cardiolipin biosynthesis has been further investigated. The relative order of divalent cation activity was Co-2+ greater than Mn-2+ greater than Mg-2+. Cardiolipin was not formed in the incubations with Zn-2+, Fe-2+, Cu-2+, Hg-2+, and Ca-2+. Cardiolipin synthesis in the presence of optimal cincentration of Co-2+ was inhibited by Ca-2+. A series of CDP-diglycerides was synthesized having differences in fatty acid chain lenth and degree of unsaturation. These compounds were tested in mitochondrial cardiolipin and phosphatidylglycerol synthesis. Although there were some minor differences between phosphatidylglycerol and cardiolipin synthesis, in general, saturated shorter chain CDP-diglycerides (dilauroyl and dimyristoyl) were better substrates than the longer chain dipalmitoyl and distearoyl homologues. Introduction of double bonds into distearoyl CDP-diglyceride resulted in more rapid rates of synthesis (e.g. dioleoyl and dilinoleoyl CDP-diglyceride). Significance of the results is dicussed with regard to possible mechanisms of linoleic acid incorporation into rat liver cardiolipin.

Animals↗

Biosynthesis of acid phosphatase of baker's yeast. Characterization of a protoplast-bound fraction containing precursors of the exo-enzyme.

1. Yeast protoplasts, secreting acid phosphatase (orthophosphoric-monoester phosphohydrolase (acid optimum) EC 3.1.3.2) contain a small amount of firmly bound enzyme, even after lysis (Van Rijn, H.J.M., Boer, P. and Steyn-Parvé, E.P. (1972) Biochim. Biophys. Acta 268, 431-441). The major part (70%) of this protoplast-bound acid phosphatase can be solubilized by nonionic detergents, such as Triton X-100. 2. The kinetics of radioactive amino acid incorporation in the solubilized and in the secreted enzyme has been estimated by pulse-chase labelling of secreting protoplasts, followed by fractionation and counting radioactivity in the enzyme band in polyacrylamide gels after electrophoresis at pH 5.0. A precursor-product relationship between the Triton X-100-extractable fraction of the protoplast-bound acid phosphatase and the secreted enzyme is apparent. 3. The solubilized acid phosphatase is essentially indistinguishable from the secreted enzyme with regard to a number of enzymatic properties and its stability towards pH and temperature. Both enzymes also behave alike on polyacrylamide-gel electrophoresis, producing a single acid phosphatase band with glycoprotein character and comparable mobility. 4. A striking difference is seen in isopycnic equilibrium sedimentation in CsCl: the secreted acid phosphatase is homogeneous, with a buoyant density of p equals 1.47 g/cm3, while the Triton X-100-extractable part of the protoplast-bound acid phosphatase is heterogeneous; besides heavier material a major component with buoyant density of p equals 1.37 g/cm3 is always visible.

Acid Phosphatase↗

Localization of acid phosphatase in protoplasts from Saccharomyces cerevisiae.

The localization of acid phosphatase (EC 3.1.3.2) in secreting protoplasts prepared from Saccharomyces cerevisiae is reported for the first time. Using a Gomori technique we were able to show acid phosphatase at those organelles in the protoplasts which are generally involved in the processes of biosynthesis and secretion of glycoproteins in eukaryotic cells.

Acid Phosphatase↗

Normal activity of metabolic pathways involved in the formation and utilization of phosphoribosylpyrophosphate in erythrocytes of patients with primary metabolic gout.

The activity of metabolic pathways involved in the formation and utilization of phosphoribosylpyrophosphate (PRPP) was studied in. The erythrocytes of 34 patients with idiopathic metabolic gout. The activities of the oxidative pentose shunt, of the hypoxanthine-guanine and adenine phosphoribosyltransferases (HGPRT, APRT) and of PRPP synthetase, as well as the rates of PRPP generation and of adenine incorporation into nucleotides were found to be normal in the erythrocytes of all these patients. Four patients with metabolic gout due to enzymatic abnormalities, two relatives with partial deficiency of HGPRT and two relatives with mutant feedback-resistant PRPP synthetase, were studied for comparison. The significance of the results is discussed in relation to postulated mechanisms for purine overproduction in metabolic gout.

Adenine Phosphoribosyltransferase↗

Pentose shunt, phosphoribosylpyrophosphate generation and purine-phosphoribosyltransferases in erythrocytes of patients with polycythemia vera.

Erythrocytes of patients with polycythemia vera exhibited increased activity of oxidative pentose shunt, accelerated generation of phosphoribosylpyrophosphate, increased incorporation of 14C-adenine into nucleotides, and increased activity and thermostability of adenine-phosphoribosyltransferase. These abnormalities are attributed to age dependency of the pathways concerned and presence in polycythemia vera of an erythrocyte population younger than normal.

Adenine↗