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Biomedical subjects

E Windler

Publications and source records attributed to E Windler.

72 records · Page 4Linked to original sources
PubMed1988

[The clinical picture of a giant elongated basilar artery].

Lack of volition and immobilizing dizziness were the cardinal presenting symptoms of a 67-year-old man. On account of nonspecific inflammatory signs and weight loss of 18 kg, broad diagnostic tests were undertaken to exclude inflammatory or malignant disease. All were negative, but discrete neurological deficits pointed to cranial nerve or cerebral lesions which had brought about dizziness and dysphagia with vomiting and recurrent aspirations. The cause was found to be a giant aneurysmic dilation and lengthening of the basilar artery. Anticoagulant treatment may be used to reduce the risk of embolism, but complications caused by pressure on cerebral structures or by rupture cannot be avoided.

Aged↗
PubMed1985

Inhibitory effects of C apolipoproteins from rats and humans on the uptake of triglyceride-rich lipoproteins and their remnants by the perfused rat liver.

Like rat C apolipoproteins, each of the C apolipoproteins from human blood plasma (C-I, C-II, C-III-1, and C-III-2) bound to small chylomicrons from mesenteric lymph of estradiol-treated rats and inhibited their uptake by the isolated perfused rat liver. This inhibitory effect of the C apolipoproteins was independent of apolipoprotein E, which is present only in trace amounts in these chylomicrons. Addition of rat apolipoprotein E to small chylomicrons from mesenteric lymph of normal rats did not displace C apolipoproteins and had no effect on the uptake of these particles by the perfused liver, indicating that an increased ratio of E apolipoproteins to C apolipoproteins on chylomicron particles, unaccompanied by depletion of the latter, may not promote recognition by the chylomicron remnant receptor. The hepatic uptake of remnants of rat hepatic very low density lipoproteins (VLDL) and small chylomicrons, which had been produced in functionally eviscerated rats, was also inhibited by addition of C apolipoproteins. These observations are consistent with the hypothesis that the addition of all of the C apolipoproteins to newly secreted chylomicrons and VLDL inhibits premature uptake of these particles by the liver and that depletion of all of these apolipoproteins from remnant particles facilitates their hepatic uptake. Remnants of chylomicrons and VLDL incubated with rat C apolipoproteins efficiently took up C-III apolipoproteins, but not apolipoprotein C-II (the activator protein for lipoprotein lipase). Preferential loss of apolipoprotein C-II during remnant formation may regulate the termination of triglyceride hydrolysis prior to complete removal of triglycerides from chylomicrons and VLDL.

Animals↗
PubMed1983

[Poisoning caused by the organophosphate parathion (E-605)].

In a 41-year-old patient administration of 5 g parathion led to respiratory failure and unconsciousness. Ventilatory support and antidote therapy were initiated early. However, only extensive gastric lavage and lowering of the plasma concentration by hemoperfusion with activated carbon resulted in the crucial elimination of the poison. Antidote and supportive measures may overcome the hazards of cholinesterase-inhibition, but not the direct toxic effect on the cardiovascular system which is currently regarded as the predominant cause of death.

Adult↗
PubMed1983

[Hepatosplenic granulomatosis with portal hypertension].

A 40-year-old female patient was admitted with bleeding from esophageal varices. The histology of liver and spleen showed granulomatous infiltrations that had developed without symptoms so far. The portal hypertension and a thrombopenic bleeding diathesis gave rise to the establishment of a splenorenal shunt with exstirpation of the spleen. By this the patient could be cured symptomatically, as three years after the acute episode liver functions are still normal. In the light of this case, pathogenesis, the variety of etiologies and the clinical courses of granulomatous liver diseases are discussed in detail with regard to the differential diagnosis.

Adult↗
PubMed1982

[Fasciitis with eosinophilia and hypergammaglobulinaemia (author's transl)].

A case of fasciitis with eosinophilia and hypergammaglobulinaemia (Shulman's syndrome) in a 33-year-old patient is described. Both the lower arms and the lower legs were affected. The diagnosis was established by biopsy which revealed cellular infiltration of the deep fascia with thickening. In addition to typical symptoms there was hepatosplenomegaly. Gastrointestinal or haematological disease was excluded. Under systemic corticosteroid administration all symptoms of fasciitis quickly disappeared.

Adult↗
PubMed1980

Determinants of hepatic uptake of triglyceride-rich lipoproteins and their remnants in the rat.

The uptake and metabolism of lymphatic large chylomicrons from fat-fed rats, lymphatic small chylomicrons from glucose-fed rats, and hepatic very low density lipoproteins from perfusates of isolated livers, and of remnants produced from these lipoproteins in functionally eviscerated rats were studied in the isolated perfused rat liver. All lipoproteins were labeled isotopically in their cholesteryl ester and triglyceride moieties. Uptake of the labeled lipids or large chylomicrons was slow and limited, but these lipids in small chylomicrons and hepatic very low density lipoproteins were taken up and metabolized progressively and at equal rates. Incubation with very low density lipoprotein-free plasma increased the content of C apolipoproteins in small chylomicrons and hepatic very low density lipoproteins and greatly retarded the hepatic uptake of their labeled lipids. In remnants from all sources, which are depleted of C apolipoproteins but not of apolipoprotein E, the labeled lipids were rapidly taken up and metabolized. Neither extensive hydrolysis of core triglycerides nor the production of monoglycerides was required for this rapid hepatic uptake. These results are consistent with the hypothesis that one or more of the C apolipoproteins opposes and apolipoprotein E promotes recognition of triglyceride-rich lipoproteins by a hepatic receptor.

Animals↗