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Biomedical subjects

C Gerhard

Publications and source records attributed to C Gerhard.

7 recordsLinked to original sources
PubMed2004

[Reduction of technology fears in psychosomatic rehabilitation--concepts and results based on a computer training for older employees].

A computer training program was developed specifically oriented toward middle-aged employees, their learning needs and their computer-related fears. This program was based on a pilot study showing a high degree of stresses associated with the introduction of computer technology at the workplace in this age group (50-59 years). A survey of 623 patients confirmed that these persons experienced technological change predominantly as disadvantageous or threatening. Based on 114 patients, concepts and results of the computer training are presented. Participation reduced avoidance behaviors, fears and increased interest and initiative based both on the patients' and their trainers' perspectives.

Attitude to Health↗
PubMed2001

Modification of a choledochoscope for extraction of difficult biliary stones.

Cholelithiasis is a common problem in the United States, affecting 10 to 15 per cent of the population. Although only one per cent of these patients have intrahepatic gallstones their discovery intraoperatively may present a technical challenge for the surgeon. This paper describes a simple method for dislodging difficult intrahepatic biliary stones: modification of a rigid choledochoscope to permit use of a biliary Fogarty catheter and Segura basket under direct visualization.

Adult↗
PubMed1998

Thrombospondin-1 is elevated with both intimal hyperplasia and hypercholesterolemia.

BACKGROUND: Thrombospondin-1 (TSP-1) is important in platelet adhesion and aggregation, inflammation, cell to cell interaction, angiogenesis, and smooth muscle cell (SMC) proliferation. TSP-1 expression increases rapidly with injury. Therefore, we hypothesize that TSP-1 may play a role in the development of intimal hyperplasia (IH). The purpose of this study is to examine the interaction between cholesterol and TSP-1 on SMC proliferation and to quantitatively assess TSP-1 expression in an established model of IH, with and without underlying cholesterol-induced atherosclerosis. MATERIALS AND METHODS: In vitro, rabbit aortic SMC culture studies were performed to see the effect of TSP-1 antibodies on PDGF and, separately, cholesterol-induced SMC proliferation. In vivo, 23 rabbits were fed either a regular or a high-cholesterol diet. Hypercholesterolemia was confirmed by measurement of serum levels. Subsets underwent intraluminal aortic injury. Aortas were harvested 8-10 weeks later. Arterial wall TSP-1 was evaluated immunohistochemically and quantified by computer image analysis. RESULTS: In vitro, TSP-1 antibodies were able to inhibit PDGF and cholesterol-induced SMC proliferation (P < 0.05). In vivo, TSP-1 was found predominantly in the extracellular matrix in the rabbit aorta. IH was uniformly seen status-post angioplasty. Hyperplasia was more prominent in samples from hypercholesterolemic animals. ANOVA and Student's t test analyses demonstrated significantly more TSP-1 in the high-cholesterol/angioplasty group than in all other groups (P = 0.0006 vs regular diet/no angioplasty group). CONCLUSIONS: These data are consistent with the hypothesis that TSP-1 contributes to the development of IH. This study suggests that injured arteries in hypercholesterolemic atherosclerotic rabbits overexpress TSP-1.

Animals↗
PubMed1994

[14C]Methylamine accumulation in cultured human skin fibroblasts--a biochemical test for lysosomal storage and lysosomal diseases.

Incorporation of the lysosomotropic amine [14C]methylamine by fibroblasts cultured from patients with lysosomal storage diseases and from controls was used to estimate the size of the lysosomal compartment. All cell lines from patients with infantile and juvenile forms of mucopolysaccharidoses, mucolipidoses and oligosacharidoses showed markedly increased radioactivity compared with the normal range of controls. In cells from patients with sphingolipidoses and adult forms of storage diseases, however, methylamine accumulation was not significantly increased. Experimentally induced lysosomal storage by enzyme inhibitors (leupeptin, suramin) also caused increased methylamine accumulation. When the lysosomal pH was determined with fluorescein isothiocyanate-dextran, it was in the range of normal controls (pH 4.7-5.0) in patients cells. Thus, [14C]methylamine accumulation should depend on the volume rather than differences in acidity of the lysosomal compartment and be a measure of its eventual pathological enlargement. We conclude that the determination of [14C]methylamine accumulation in fibroblasts provides a valuable tool in the screening for a variety of lysosomal storage disorders.

Cells, Cultured↗
PubMed1985

Morphological aspects of aetiology and the course of infantile spasms (West-syndrome).

The present study using the results of the postmortem examination of twenty-four children, who had infantile spasms (West-Syndrome), gives a view of the aetiology and course of the West-Syndrome. According to the time of occurrence of the lesions three groups could be established: one group of six cases with only embryofetal lesions, one group of ten cases with combined embryofetal and peri/postnatal lesions and one group of eight cases with only peri/postnatal lesions. It is significant, that the time of onset of infantile spasms depends on time of manifestation of lesions. In the groups with combined embryofetal and peri/postnatal lesions the seizures were manifested at the same time as in the cases with isolated embryofetal lesions. Even in the group with combined lesions, microdysgenesis was interpreted as being embryofetal. These embryofetal lesions, as opposed to the peri/postnatal lesions thus appear to dominate and thereby to be pathoplastic. From this correlation two thirds of the cases of infantile spasms can be regarded as fetal epilepsies. The question is open if the infantile spasms which are manifested later on and develop mostly a Lennox-Syndrome indeed should be classified as a separate group together with the isolated peri/postnatal lesions.

Adolescent↗
PubMed1981

Histopathological findings in adrenoleukodystrophy autopsy report of a boy aged 11 years and 11 months.

Clinical and pathohistological findings of a boy who died of adrenoleukodystrophy at the age of 11 years and 11 months are reported. Special features are the advanced diffuse demyelination of cerebral and cerebellar white matter as well as the "burnt-out" stage of myelin breakdown with fibrous gliosis. The leukodystrophic process is accompanied by secondary loss of axons with marked atrophy of grey matter in the whole of the brain stem, dentates and cerebellar cortex of the Purkinje cell type. The degeneration of nerve fibres is considered as a complex mechanism, which is not restricted to the Wallerian type. -- Only free cholesterol was shown by histochemical tests in the preserved myelin sheaths. Free and esterified cholesterol was found in the adrenal cortical cells. The lack of detectable cholesteryl esters in the sparse sudanophilic macrophages was unexpected. This finding may be attributed to the sensitivity of the histochemical method or to interference by achromogenic 7-ketocholesterol.

Adrenal Insufficiency↗