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Biomedical subjects

W Winkelmann

Publications and source records attributed to W Winkelmann.

At least 199 records · Page 11Linked to original sources
PubMed1978

[Concentration in bone and haematoma of the aminoglycoside antibiotic tobramycin (author's transl)].

Tobramycin concentrations were assayed in the rabbit in serum during surgery and in serum, haematoma and bone tissue of the condyle of the femur in the absence of surgery. After a single i. m. injection serum levels were found to be 30% higher initially than in humans, but then dropped at a faster rate to zero. The hardening haematoma appeared to slow penetration of the antibiotic. The concentration in bone tissue was dependent on vascular supply. Surgery did not show any influence on the level of the concentrations.

Animals↗
PubMed1977

[Osteomyelitis of the os calcis (author's transl)].

The treatment of osteomyelitis in the os calcis causes problems in most cases. The os calcis as a cancellous bone offers ideal conditions for the spreading of infection. Specially in posttraumatic osteomyelitis the infection is supported by disturbed blood circulation. Hind foot deformity, trophical disturbance, excessive scars and ulceration cause therapeutical problems. According to literature and to our own experiences none of the different operative procedures received extraordinary importance. The procedure has to be evaluated according to the special circumstances.

Adolescent↗
PubMed1977

[Spondylitis caused by Salmonella typhimurium (author's transl)].

Described is a case of spondylitis caused by Salmonella typhimurium. According to literature osteomyelitis and spondylitis are rare as local manifestation of a salmonella infection. Spondylitis caused by Salmonella typhimurium, the most common species, is almost unknown. The problems in diagnosis and therapy are discussed.

Adult↗
PubMed1975

[131I-cholesterol scanning of the adrenals: results in various adrenal diseases, especially unilateral adrenal turmours (author's transl)].

133I-cholesterol scanning of five patients with primary hyperaldosteronism due to adrenocortical adenoma, gave correct lateralization and localization in three, while in two cases lateralization was not definitively determined. In two patients with phaeochromocytoma unilateral localization was clear-cut in the scan. In two patients with hormone-producing adrenal carcinoma the adrenals were localized poorly or not at all on both sides, because of the size of the tumours and suppression of the healthy contralateral adrenal by the autonomous hormone production. In case of retroperitoneal tumour with destruction of the adrenal the scan demonstrated a hyperplastic but healthy adrenal on the other side. Because 133I-cholesterol scanning exposes the steroid-producing gonads to high radioactivity, the method should only be used for diagnosing which side a unilateral adrenal tumour is on. It should not be used to complement a diagnosis of bilateral adrenal disease achieved by other means.

Adenoma↗
PubMed1975

Investigations on pituitary and Leydig cell function in chronic hemodialysis and after renal transplantation.

The hypothalamus-pituitary-Leydig cell axis was investigated in 20 male patients undergoing intermittent hemodialysis and in 21 male patients following renal transplantation compared to normal controls. Plasma testosterone as well as luteinizing hormone and follicle stimulating hormone were determined by radioimmunoassay under basal conditions and after stimulation with choriongonadotropic hormone and hypothalamus releasing hormone respectively. Suppressed Leydig cell function has been demonstrated in dialysed patients as well as in patients after renal transplantation. The Leydig cell insufficiency is more pronounced in the hemodialysed patients. None of these showed testosterone levels in the normal range. They are different in various dialysis schedules. In contrast Leydig cell function is much better in patients after renal transplantation compared to those undergoing intermittent hemodialysis. But even after renal transplantation a diminished Leydig cell function takes place. The degree of Leydig cell insufficiency however varies individually. In a few cases Leydig cell function is restored completely after transplantation. It remains uncertain whether the duration of the posttransplantation period or the function of the graft effects Leydig cell function. Anterior lobe insufficiency has been excluded since plasma concentrations of gonadotropins were slightly elevated before and after LH-RH stimulation as compared to normals.

Adult↗
PubMed1975

[Long-term treatment with L-DOPA in a case of torsion dystonia (authors transl)].

A 36-year old woman had been able to move from place to place only by crawling until 1971 after she had been treated with L-DOPA, the dose of which was increased to a maximum of 2.5 g daily. Within 4 weeks there was a diminution of her increased muscle tone and she experienced a dramatic improvement in her daily living activities, being able to walk without assistance for the first time in 20 years. This improvement has continued with a daily maintenance dose of 1.25 g. For patients with torsion dystonia, where the so-called myostatic component preponderates, cautious application of L-DOPA seems to be justified and further clinical studies are suggested.

Adult↗
PubMed1975

Investigations on Leydig cell function and regulation after renal transplantation.

The hypothalamic-hypophyseal-Leydig cell axis was investigated in 17 male patients following renal transplantation. Plasma levels of testosterone, luteinizing hormone (LH) and follicle stimulating hormone (FSH) were determined by radioimmunoassay under basal conditions and after stimulation with chorionic gonadotrophin (HCG) and hypothalamic releasing hormone (LH/FSH-RH) respectively. The investigations were carried out one to five years after renal transplantation. It was demonstrated, that primary dysfunction of Leydig cells may occur after renal transplantation. In some cases however normal Leydig cell function with adequate testosterone secretion may return. It remains uncertain, whether the Leydig cell dysfunction is a result of preexisting toxic uremic damage or whether it is due to immunosuppressive therapy with prednisone and azathioprine.

Adult↗