[Mania--very rarely diagnosed?].
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Biomedical subjects
Publications and source records attributed to W Hartmann.
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In 9 patients with chronic bronchitis and cor puomonale and in one patient with vascularly pulmonary hypertension the efficiency of 0,04 mug and 0,16 mug Sch 1000 (isopropylatropin,), applicated with metered dose inhaler referring to blood gases and hemodynamics was examined. Inhalation of drug was not followed by any variations either referring to hemodynamic parameters (pulmonary pressure, systemic blood pressure, cardiac output, peripheral resistance) nor to the blood gases. After a dosage as high as eigth time as normal side effects were not found.
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In the present paper the mechanism of the adenosine formation by a mixture of nerve ending and transmitter granula fractions was invesitgated. The adenosine formation in vivo is only possible via the whole degradation chain ATP - ADP - AMP - adenosine. The enzymes involved are ATPases, adenylate kinase and 5'-nucleotidase. The ATPase and adenylate kinase effectors Ca++ and Mg++ can be regarded as trigger ions switching on and off the degradation chain. The adenylate kinase represents a key enzyme within the whole chain. In the ion-activated state a non-inhibited adenosine formation was observed, when the initial ATP concentration amounted to less than 0,1 muMol per mg synaptosomal membrane protein. Under these conditions the whole chain velocity is mainly dependent on the 5'-nucleotidase concentration, because ATPases and adenylate kinase remove the nucleotidase inhibitors ATP and ADP spontanously. The conditions for the optimal velocity of the adenosine formation at the synaptic membrane in vivo in all probability are present. A hypothesis for the mechanism of the synaptic adenosine formation in vivo was developed. The importance of this process in respect to the synaptic transmission was discussed.
99 schizophrenic patients from the General Mental Hospital in Göttingen who had received hospital treatment for the first time, where, after their discharge from hospital, studied for a period of 1 1/2 to 4 1/2 years. Information was collected with regard to the further progress of the disease on the one hand, and the response to drugs used in treatment on the other. Less than half the patients who had suffered from the disease from several years without receiving any out-patient treatment could not be helped or cured by the following hospital treatment. Over half of them had to be readmitted to hospital at last once (mostly within one year). A persisting or newly developing illness could be ascertained by catamnestic means in about 2/3 of the patients. The post-hospital treatment was left predominantly to the GP. Psycho-social help was generally lacking. Drugs were used regulary as far as could be ascertained in only 1/5 of the patients. In most cases the after-care was stopped after several months. This data shows that the treatment before, during and after hospitalization was in many cases inadequate. For different reasons the therapeutical possibilities hat not been used to their full extent. Due to the strict separation between the out-patient and hospital therapy the schizophrenic patients received treatment too late, for too short a time, and not suited usually to their individual needs.
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