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M Reiter

Publications and source records attributed to M Reiter.

At least 127 records · Page 7Linked to original sources
PubMed1970

[Homocystinuria].

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Adolescent↗
PubMedDate not supplied

Voltage-dependent calcium release in guinea-pig cardiac ventricular muscle as antagonized by magnesium and calcium.

An increase in extracellular potassium concentration from 4 to 16 mmol/l caused a decrease in membrane potential from -92 to -59 mV and selectively diminished the earlier of two contraction components of guinea-pig papillary muscles at 0.2 Hz stimulation frequency in the presence of noradrenaline. The influence on the early contraction component had a threshold of 8 mmol/l K+, corresponding to a membrane potential of -77 mV. However, test contractions elicited 800 ms after the 5 s stimulation interval exhibited an unimpaired early component. Since the activator calcium responsible for the early contraction component is derived, in mammalian ventricular muscle, from the junctional sarcoplasmic reticulum, it is assumed that the release site of the reticulum was filled with calcium shortly (800 ms) after a regular contraction, and lost its calcium at 16 mmol/l extracellular K+, during the 5 s stimulation interval. The potassium-induced depolarization determined the rate of calcium leakage during rest from the intracellular store. The depolarization-induced decline of the early contraction component was equally well antagonized by Mg2+ or Ca2+ without influencing the measured transmembrane potential. Both divalent cations shifted the relation between potassium concentration or membrane potential and the strength of the early contraction component to less negative membrane potentials. In order to reduce the early contraction component by 25% in the presence of 9.6 instead of 1.2 mmol/l Mg2+, the potassium concentration had to be increased from 9.6 to 22.0 mmol/l, with a respective decrease in resting membrane potential from -72.6 to -51.1 mV. The antagonistic effect of both divalent cations is though to result from the neutralization of negative charges outside the sarcolemma with a respective decrease in the outside surface potential.

Animals↗
PubMedDate not supplied

Where is the origin of the activator calcium in cardiac ventricular contraction?

Under normal experimental conditions, the force of rested-state contractions (i.e., contractions after a rest period of 15 min or longer) of mammalian ventricular myocardium is insignificant. In Mg2+-free solution, in low sodium solution or in the presence of a cardioactive steroid, a strong "early" rested-state contraction develops without delay after stimulation, indicating the accumulation during rest of intracellularly stored activator calcium. By contrast, catecholamines cause a "late" rested-state contraction with a characteristic latent period of about 100 ms between stimulation and onset of contraction. Inhibition of the slow inward current by nifedipine has no influence on the contraction velocity of the "early" rested-state contraction, indicating that Ca2+ of the slow inward current is not involved in the calcium release mechanism of prefilled stores during excitation-contraction coupling. Nifedipine suppresses the "late" rested-state contraction in the presence of noradrenaline. In view of the constancy of the latent period, it is proposed that the activator calcium for the "late" rested-state contraction enters the cell with the slow inward current, is sequestered at first by uptake sites of the sarcoplasmic reticulum and subsequently released from its release sites as long as the cell is depolarized. The model of the different origin of activator calcium is discussed in its implication for high-frequency contractions.

Action Potentials↗
PubMedDate not supplied

Pilot scale production of a human monoclonal antibody against human immunodeficiency virus HIV-1.

Human monoclonal antibodies against the transmembrane protein gp41 of HIV-1 were isolated and purified on a pilot scale. A purification scheme was established for the production of human monoclonal antibodies on the gram scale. 50 1 of culture supernatant can be treated in one purification cycle. The hybridomas were mass cultured in an airlift fermenter. The culture broth was clarified by microfiltration and chromatographed on CM-Sepharose fast flow and protein A Superose. Scale up of the high performance affinity chromatography from 1 ml protein A Superose up to 40 ml is described. All desalting steps were performed by gel filtration on Sephadex G-25 coarse. The yield of the whole purification procedure is in the range of 50-60%. The purity is higher than 99.9%. DNA and reverse transcriptase could not be detected. The whole method is designed as a basis for scale up to industrial scale. Results from quality control assays have proven the validity of this approach.

Antibodies, Monoclonal↗
PubMedDate not supplied

Development of a mammalian cell (Vero) derived candidate influenza virus vaccine.

Influenza vaccine production is dependent on the availability of embryonated hen eggs for virus growth. This is an extremely cumbersome system with many disadvantages with respect to selection of virus variants and presence of adventitious viruses. We have developed an alternative cell culture system which allows rapid production of large volumes of vaccine. The World Health Organisation (WHO) approved Vero cell line was used in serum-free culture to grow a multitude of influenza strains to high titre. This system could be scaled-up to allow vaccine production with a 1200 litre fermenter volume. A purification scheme was developed which resulted in a high purity whole virus vaccine. This was demonstrated to be at least as immunogenic as a conventional egg-derived preparation in a mouse model.

Animals↗