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Biomedical subjects

O Sperling

Publications and source records attributed to O Sperling.

At least 181 records · Page 10Linked to original sources
PubMed1970

[Xanthinuria].

Explore the source record for details and available documents.

Humans↗
PubMed1968

Metabolic and calcium kinetic studies in idiopathic hypercalciuria.

Calcium balances and calcium kinetic studies using (47)Ca were performed in nine male patients with idiopathic hypercalciuria and in three normal male subjects. A sharp reduction in calcium intake in eight patients with idiopathic hypercalciuria caused a decrease in urinary calcium excretion, the latter remaining elevated above that reported for normal subjects on a low calcium diet. The hypercalciuric patients had an enlarged miscible calcium pool size, an increased calcium turnover rate, increased bone formation and bone resorption rates, and an elevated true intestinal calcium absorption rate, the increase of the latter three parameters being proportional to the increase of the turnover rate. The fraction of the calcium turnover rate excreted in the urine was elevated whereas that constituted by the endogenous fecal calcium excretion was decreased. Arguments are presented for the concept that the primary abnormality in idiopathic hypercalciuria is neither renal calcium hyperexcretion nor intestinal calcium hyperreabsorption, but a more fundamental disturbance in calcium metabolism of as yet unknown cause, leading to a high calcium turnover.

Journal Article↗
PubMedDate not supplied

The adenosine-induced mechanism for the acquisition of ischemic tolerance in primary rat neuronal cultures.

Neurons can be preconditioned by various procedures to resist ischemic insult. The preconditioning mechanism induced by adenosine ("the adenosine mechanism") was characterized in primary rat neuronal cultures, employing a model of chemical ischemia. The protective mechanism, initiated by activation of adenosine receptors, consists of a signal transduction pathway, involving activation of protein kinase C (PKC) and opening of ATP-sensitive potassium (K(ATP)) channels. Direct activation (and inhibition) of PKC, as well as opening of K(ATP) channels, also confers protection. The opening of the K(ATP) channels mediates the signal activated by the adenosine receptors, and probably also that activated by PKC. The acquired ischemic resistance lasts up to 5 days, depending on the activating substance. The adenosine-activated cascade of events leading to ischemic tolerance in neurons is similar to that operating in cardiomyocytes.

Adenosine↗
PubMedDate not supplied

Elevated UTP and CTP content in cultured neurons from HPRT-deficient transgenic mice.

Hypoxanthine-guanine phosphoribosyltransferase (EC 2.4.2.8.; HPRT) catalyzes the salvage synthesis of inosine-5'-monophosphate (IMP) and guanosine-5'-monophosphate (GMP) from the purine bases hypoxanthine and guanine, respectively. Complete deficiency of HPRT activity is associated with the Lesch-Nyhan syndrome (LNS), characterized by excessive purine production and severe neurological manifestations. The etiology of the metabolic consequences of HPRT deficiency is clarified, but that of the neurological manifestations is not yet understood. HPRT-deficient mice represent an experimental animal model of LNS. In search for a possible metabolic abnormality in LNS brains, connecting the neurological deficit to HPRT deficiency, the purine and pyrimidine nucleotide content of cultured neurons, prepared from HPRT-deficient transgenic mice, was now determined. The HPRT-deficient neuronal cultures exhibited a significantly elevated content of the pyrimidine nucleotides UTP (1.33-fold the normal level, p = 0.0002) and CTP (1.28-fold the normal level, p = 0.02), but normal content of the purine nucleotides ATP and GTP. This abnormality in neuronal pyrimidine nucleotide content may be associated with the pathophysiology of the neurological deficit in LNS.

Animals↗
PubMedDate not supplied

The metabolism of adenosine and distribution of adenosine receptor lymphocytes in two human circulating T cell subsets.

Human circulating E rosette forming cells (ERFC), rerosetted with sheep erythrocytes in the presence of adenosine, yielded two T-lymphocyte subpopulations: a major fraction forming E-rosettes (E resistant = ER) and a minor non-rosetting fraction (E sensitive - ES). Both T cell subpopulations converted adenosine mainly into inosine. However, ES cells metabolized adenosine more extensively than ER cells. Adenosine deaminase (ADA) activity was significantly higher in ES cells. Purine nucleoside phosphorylase (PNP) activity, as well as hypoxanthine guanosine phosphoribosyl transferase (HGPRT) activity were similar in both T cell subsets. The ratio of ADA/PNP in ES cells relative to ER cells was 1.8 suggesting that ES cells are at an earlier stage of differentiation. Enrichment of lymphocytes bearing a receptor for adenosine was demonstrated in ES cells.

Adenosine↗