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Biomedical subjects

P Kling

Publications and source records attributed to P Kling.

10 recordsLinked to original sources
PubMed1991

A 7-year old white-male boy with progressive neurological deterioration.

A 9-month-old boy presented with rapid deterioration of psychomotor development. He developed seizures at 2 months, and shortly thereafter lost motor skills and developed feeding difficulties, increased startle response, red maculas, and decreased vision. His measurements, including head circumference, were greater than the 95th centile. No organomegaly was found. Serum determination of the hemoxsaminidases confirmed the diagnosis of Sandhoff disease.

Brain↗
PubMed1991

Increased amino acid transport into brain tumors measured by PET of L-(2-18F)fluorotyrosine.

The uptake of L-(2-18F)fluorotyrosine (F-Tyr), a newly synthetized amino acid tracer, was studied in 15 patients with various brain tumors by dynamic PET. The higher F-Tyr accumulation in tumors (mean 27% above contralateral tissue) was associated with two-fold transport rates into tumors, while the rate constants describing irreversible incorporation were decreased. The increased F-Tyr transport was not correlated to 68Ga-EDTA accumulation and cannot be explained by disruption of the blood-brain barrier. Kinetic analysis of 2-(18F)-fluoro-deoxy-glucose accumulation in the same patients demonstrated that increased metabolic rates in tumors are mainly caused by altered phosphorylation rates while transport of glucose is less affected. Since F-Tyr transport rates clearly separated tumors from normal tissue and since F-Tyr accumulation was related to tumor grade, PET studies of F-Tyr uptake are of clinical value for diagnosis and classification of brain tumors.

Adult↗
PubMed1990

SPECT studies of brain tumors with L-3-[123I] iodo-alpha-methyl tyrosine: comparison with PET, 124IMT and first clinical results.

L-3-[123I]iodo-alpha-methyltyrosine (123IMT) like tyrosine has been reported previously to have a high affinity for a transport system in the blood-brain-barrier (BBB). We examined the kinetic behavior of 124IMT in brain and plasma in two patients with glioblastoma using dynamic positron emission tomography (PET). 124IMT accumulated in brain and tumor tissue, reaching a maximum after 15 min, with a washout of 20% to 35% at 60 min postinjection. Animal experiments confirmed the accumulation of the intact tracer in murine brain, but there was no incorporation into proteins. SPECT studies with 123IMT in patients with different types of brain tumors showed increased uptake in 26 of 32 tumors. Although nonspecific uptake in tumors must be considered, the accumulation of IMT in normal brain and in some tumors with intact BBB suggests a specific uptake of IMT. As transport is the main determinant of initial amino acid uptake, 123IMT appears to be a suitable SPECT tracer of amino acid uptake although it is not incorporated into protein.

Animals↗
PubMed1989

Cerebral metabolism of L-[2-18F]fluorotyrosine, a new PET tracer of protein synthesis.

L-[2-18F]fluorotyrosine (2-18FTyr) was evaluated as a tracer of cerebral protein synthesis for positron emission tomography (PET). Its metabolism in murine cerebrum was studied. The uptake in brain reaches a value of approximately 2% of the injected dose per gram tissue after 60 min. The incorporation of the tracer into tissue proteins was proven by discontinuous SDS gel electrophoresis. The protein bound fraction of tissue activity increased to 84% and 89% after 60 and 120 min p.i., respectively. High performance liquid chromatography analysis showed a concomitant decrease of free 2-18FTyr in tissue with time. The sum of free 2-18FTyr, tRNA-and protein-bound 2-18FTyr in cerebral tissue gave an almost quantitative activity balance of 96 +/- 4% at all times examined. A significant formation of fluorodopa or fluorodopamine must therefore be excluded. This shows that L-[2-18F]fluorotyrosine is a promising tracer for quantitation of protein synthesis rates with PET based on a three-compartment model.

Animals↗
PubMed1979

A new platelet aggregation inhibitor which possesses hypolipemic and uricosuric properties, 2-[3-(2-thiazolylthio)phenyl]propionic acid (TPA).

In vitro, 2-[3-(2-thiazolylthio)phenyl]propionic acid (TPA) at plasma concentrations ranging from 0.02 to 1.0 microgram/ml prevents aggregation of human platelets induced by various aggregating agents. Oral administration of TPA to guinea pigs inhibits platelet aggregation; the estimated dose to reduce aggregation by 50% is 0.3 mg/kg. TPA protects rabbits against arachidonate-induced thromboembolic death (50% protection at 0.79 mg/kg i.p.). TPA is a potent hypotriglyceridemic agent in rats when present in the diet in concentrations as low as 0.003%. In chimpanzees, TPA is uricosuric at oral doses of 0.625 and 2.5 mg/kg. This rare combination of pharmacological properties suggests that TPA is a potentially useful antithrombotic agent.

Adenosine Diphosphate↗
PubMed1976

The effect of halofenate or halofenate free acid on human, rat and guinea pig platelet aggregation.

Halofenate free acid (HFA), the major metabolite of the hypolipemic agent halofenate, blocked the secondary phase of human platelet aggregation induced by ADP, epinephrine, or thrombin; higher concentrations of clofibrate free acid (CFA) were required to produce similar inhibitory effects on platelet aggregation. HFA and CFA inhibited collagen-induced aggregation of human, rat, or guinea pig platelets. Halofenate orally administered to rats caused inhibition of collagen-induced aggregation when plasma levels of HFA exceeded 300 mug/ml, a clinically achievable human plasma concentration. The platelet inhibitory effects of clofibrate administration were less than those observed with halofenate administration.

Animals↗
PubMedDate not supplied

Nursing interventions to decrease the risk of periventricular-intraventricular hemorrhage.

Periventricular-intraventricular hemorrhage (PIVH) is a serious neurologic insult that can have lifelong consequences for the preterm infant and the infant's family. A review is presented of research on postnatal factors associated with the development of PIVH that can be influenced by nursing care. Recommendations are presented for nursing interventions that may lead to a decrease in the incidence or severity of this lesion.

Cerebral Hemorrhage↗