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Biomedical subjects

G Wolf

Publications and source records attributed to G Wolf.

At least 541 records · Page 30Linked to original sources
PubMed1987

[Changes in nasal volume flow following local administration of neuropeptide substance P and capsaicin].

In a recently published paper, the author discovered the neuropeptide Substance-P (SP) in human nasal mucosa. SP is the transmitter substance of sensory neurons in the central and peripheral nervous system. The influence of SP and CAPSAICIN on the vascular system of human nasal mucosa is investigated. The application of these substances on the nasal mucosa of volunteers leads to a significant decrease of nasal air flow which can be registered by anterior rhinomanometry. The pathogenetic importance of vascular protein leakage and vasodilatation caused by the neuropeptide SP is discussed.

Capsaicin↗
PubMed1987

[Modern aspects of epilepsy research and its application].

At present most authors agree with the hypothesis that epilepsy is primarily caused by an imbalance of inhibitory and excitatory transmitter systems of CNS in favour of the latter. Epilepsy research focuses more and more on disorders in structures using amino acids as transmitters. There is a world-wide searching for new antiepileptic strategies with an emphasis on a causally guided therapy. Besides possibilities of pharmacological enhancement of GABA-mediated inhibition, e.g. by recently tested GABA prodrugs, highly potent antagonists of transmitter glutamate, acting as anticonvulsant drugs, are expected to gain in significance for clinical practice.

Anticonvulsants↗
PubMed1987

The action of calcium antagonists in the human natural killer cell-mediated cytotoxicity.

The Ca2+-channel blocker Nifedipine and the Calmodulin inhibitor Prothazin suppressed the human NK-mediated cytolysis. Both drugs exerted the same dose-dependent effect. The inhibition was partially reversible after withdrawing of the Ca2+-antagonists. There exists evidence that neither effector-target cell binding, nor effector cell function, but the initiation of the target cell lysis was affected by these inhibitors. Hence, the Ca2+-requirement of the NK cytotoxic reaction seems to be due to an essential Ca2+-influx into the target cell.

Cell Line↗
PubMed1987

[The stability of hydrochlorothiazide and cyclopenthiazide in various dosage forms. 4. Stability of hydrochlorothiazide injection solutions II].

The hydrolytic decomposition of hydrochlorothiazide (1) in an optimized dispensing with polyethyleneglycol 400/ethanol as solvent led to an equilibrium in the isothermic short-term test as well as in the long-term stability test. Corresponding equilibrium concentrations were obtained for forward and back reaction. When comparing the precalculated equilibrium values with the long-term results the evaluation after Van't Hoff proved superior compared with an evaluation after the Arrhenius plot which is only applicable when the equilibrium concentrations are taken into consideration. By adding the decomposition product aminodisulfamide (2) the hydrolysis of 1 can be inhibited completely.

Cyclopenthiazide↗
PubMed1986

Histochemical demonstration of sodium-dependent glutamate uptake in brain tissues by glutamate dehydrogenase reaction.

Using a special tetrazolium salt technique, a striking correlation was observed between Na+ concentration of the incubation medium and the formation of formazan catalyzed by glutamate dehydrogenase (GDH) in glutamatergic neuropil areas of the hippocampal formation, cerebellum, and other brain regions. Na+ concentrations of 130-150 mmol/l caused maximal formazan production. The GDH catalyzed sodium-dependent increase in formazan production is suggested to be a consequence of the sodium dependence of glutamate uptake in glutamatergic brain structures supplying the enzyme with substrate.

Animals↗
PubMed1986

Histophotometric evaluation of glutamate dehydrogenase activity of the rat hippocampal formation during postnatal development, with special reference to the glutamate transmitter metabolism.

Transmitter glutamate/aspartate synthesis is known to proceed along different metabolic pathways. In this light, the functional relevance of glutamate dehydrogenase in postnatally maturing glutamatergic/aspartatergic structures was studied by means of quantitative enzyme histochemistry. The basic requirements concerning the kinetics and calibration of the histochemical glutamate dehydrogenase reaction used were proved to be met in order to obtain valid quantitative data. The histochemically demonstrable activity of glutamate dehydrogenase (EC 1.4.1.3) in the hippocampal formation of the rat increased markedly during postnatal development. On day 30, the distribution pattern observed was similar to that in adult animals. While the enzyme activity rose within cell body layers from day 0 to day 30 by 240-285%, the increase in neuropil layers was found to be up to 830%. Maximum values were seen in the stratum lacunosum-moleculare of CA1 and CA3 and the stratum moleculare of the dentate fascia on day 30. Since the hippocampal neuropil is supposed to be copiously provided with glutamatergic (and aspartatergic?) structures which become functional in rats during the first weeks of postnatal life, the increase in enzyme activity is discussed to be primarily a consequence of maturing synaptic systems using glutamate and/or aspartate as transmitters.

Animals↗
PubMed1986

[Aspartate aminotransferase activity high affinity (3H) glutamate/(3H) aspartate uptake in rat nervous tissue in postnatal development].

The regional distribution and cellular localization of aspartate aminotransferase (AspAT) as a glutamate and aspartate metabolizing enzyme was studied in the hippocampal formation, in dorsal root ganglia, and in superior cervical ganglia during the postnatal development of the rat. At birth, in all neuronal tissues studied the enzyme activity was rather low. Whereas in the dendritic layers of the hippocampal formation enzyme levels rose strikingly during the first weeks of postnatal life, those of peripheral ganglia remained remarkably stable. The high affinity uptake of [3H]labelled L-glutamate and D-aspartate were studied in surface autoradiograms of incubated slices of hippocampal formation during postnatal development of the rat. Our data indicate that the postnatal development of high affinity uptake capacity is parallel to the increase of histochemically demonstrable AspAT activity in the hippocampal formation suggesting that the enzyme may be involved in glutamate/aspartate neurotransmitter metabolism.

Aging↗
PubMed1986

[Enzyme histochemical demonstration of sodium-dependent glutamate uptake in glutamatergic brain structures in the rat].

Using a special tetrazolium salt technique, a striking correlation was observed between Na+ concentration of the incubation medium and the activity of glutamate dehydrogenase (GDH) in glutamatergic neuropil areas of the hippocampal formation, cerebellum, and other brain regions. Na+ concentration of 130 to 150 mmol/l caused maximal formazan production. The histochemical enzyme reaction in neuronal perikarya as well as biochemically estimated GDH activity were found to be rather inhibited by such Na+ concentrations. The GDH catalyzed sodium dependent increase in formazan production is discussed to be a consequence of the sodium dependence of glutamate uptake in glutamatergic brain structures supplying the enzyme with substrate.

Animals↗