Biomedical subjects
Publications and source records attributed to H Binder.
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The use of guanidine hydrochloride is reported in the treatment of 4 cases of Werdnig-Hoffmann disease. Improvement was achieved in two cases. Amelioration was initially observed in the third patient, but a relapse occurred during temporary discontinuation of therapy and the disease progressed, albeit at a slower rate, after resumption of therapy. The final case was a terminal one in which, however, slight temporary improvement occurred in response to therapy. A maximum dosage of 0.4 g (based on the assumption of an average body weight of 15 kg in these children) was reached by gradual increments. Side effects like shortlasting vomiting were observed only in case 1. The pharmacological action of guanidine hydrochloride is discussed. According to Otsuka and Endon the mechanism of action may be based on an increase in the end-plate potential amplitude. However, an augmented supply of spinal transmitters may also play a role in the mediation to the pharmacological action.
A progressive form of myoclonus-epilepsy was described in an 21 year old girl. Electrophysiological and neuropharmacological studies were carried out. The typical EEG-pattern, the close association of cortical discharges and myoclonic jerks, the form of myoclonus indicated a "pyramidal" myoclonus. Pharmacological data suggested that two possible mechanisms--a partial deafferentation of cortical neurones and a failure of thalamic, extrapyramidal and brain stem reticular formations--might be responsible for the EEG-abnormalities and concomitant myoclonus. Results from neuropharmacological studies demonstrated a suppressive effect (on EEG-discharges and myoclonic jerks) of clonazepam, diazepam, phenobarbital, taurine, levodopa and budipin. Taurine, levodopa and budipin might induce a new aspect in therapy of progressive myoclonus epilepsy and of myoclonus caused by other etiologic factors.
The chemical compounds which are discharged from the site at which old tires are incinerated in the open air roughly corresponded to those of waste water. In the smoke "mushroom" above the site of incineration, at a height of 31 to 40 metres, many types and large quantities of polycyclic aromatic and also cancerogenic hydrocarbons were found adsorbed on soot particles.
The case histories of four patients with severe cerebral manifestations as a result of CO poisoning are reported. All patients displayed an acute mesencephalic syndrome in the initial stage. One case developed a fatal bulbar syndrome following a transitional phase. Autopsy showed cerebral oedema, in addition to necrotic areas in the basal ganglia and cerebellar haemorrhage. The other 3 patients developed an apallic syndrome with all the typical features and symptoms. Two of these patients died without showing any improvement, displaying not only necroses in the basal ganglia, but also diffuse destruction of the white matter and, in one case, even of the cortex. The third patient recovered. His recovery took a similar course to that of a case of traumatic apallic syndrome and he was subsequently able to take up normal activities. It is concluded from these four cases that secondary brain oedema precedes the development of the most serious form of CO poisoning and is of grave prognostic significance.
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On the basis of reports in the literature and of our own clinical experience it appears that melanocyte inhibiting factor (MIF) is a very promising therapeutic agent in the management of Parkinson's disease. Besides theoretical considerations relating to biochemical and pathophysiological spheres, the question of the current dosage for clinical usage seems to be of the utmost importance. We are of the opinion that the currently-employed dosage of 400 mg daily is still too low. Hence, the present investigation will be continued with a view to establishing the optimum dosage for maximal therapeutic effect.
The diffusion and permeability of large organic molecules through polymeric films were investigated, specifically the passage of estrogen through films of polyethylene, silicone, or a composite of these two films. Such systems are of interest because of the possibility of constructing a biocompatible implant that releases a hormone at a controlled and desired rate. Diffusion and permeability coefficients through implants of a desirable size-successfully tested in rats-were measured by the "time lag" method of diffusion, and solubility coefficients were determined by the method of sorption kinetics. Independently derived values were in good agreement. An interesting observation was made with implications for the controlled release from membrane-based drug delivery systems. Permeability coefficients of estrogen are orders of magnitude higher when estrogen is present as a solid rather than in a dilute solution, while diffusion coefficients are equal. This finding is explained by the considerably higher partial vapor pressure of estrogen in the former case. In fact, control of the partial vapor pressure of the encapsulated drug is a powerful method for controlling its release rate.
Urinary catecholamine excretion and thyroid hormone blood level were studied in 16 patients following severe cerebral trauma. Increased excretion rates of epinephrine and norepinephrine were found. There was no significant difference in the catecholamine excretion when compared with generally traumatized patients. The relationships between catecholamine excretion, increased metabolic rates, and negative nitrogen balance indicate that in patients with a midbrain syndrome there exists an additional diencephalic metabolic factor, which leads to a rise in fat oxidation and perpetuation of catabolism. Early high caloric parenteral nutrition seems to inhibit the initial increase of catecholamine excretion and thus protects the body from an unnecessary breakdown of its own reserves. If the course is classified according to neurological stages, it can be shown that patients with a traumatic apallic syndrome in poor condition have a high increase of catecholamine excretion. Secretion of thyroid hormones is not influenced significantly by cerebral trauma.
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Explore the source record for details and available documents.
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