[Social work in geriatric clinics--between autonomy and functional organization]. / Sozialarbeit in geriatrischen Kliniken--zwischen Autonomie und Funktionalisierung.

Geriatric therapy is defined through interdisciplinarity, teamwork, and multiprofessionality. Besides questions of medical therapy, psychosocial dimensions of elderly are highly relevant. Social work is mostly described as an important profession in the process of geriatric therapy. This work refers to the presentation and discussion of the results of an interdisciplinary study to the role of social work in German geriatric hospitals. It shows that the role of social work is determined by the various perceptions of the professions. Another influence on it is by the structures of the hospital. Social workers defines their activities through the relationship to the client; the other professions recognize the tasks of social work in a very diffusely way, mostly reduced in connection with the management of dismission of the patient from hospital. The professional education of social workers is not well known by the nurses and doctors. The fact that social workers are mostly acting under the responsibility of doctors, leads to a definition of problems and aims from a medical point of view. In many of the hospitals there are distinct problems of communication and cooperation between the professions. If the profession of social workers wants to contribute to the reduction of these impediments of communication and cooperation, they must actively and constructively communicate with the other professions and become more clear about their own professional way of acting.

Cyproterone acetate induces DNA damage in cultured rat hepatocytes and preferentially stimulates DNA synthesis in gamma-glutamyltranspeptidase-positive cells.

The synthetic anti-androgen and progestin cyproterone acetate (CPA) is known to increase the liver tumor rate in rats. The tumorigenicity of CPA has been attributed to a tumor-promoting activity of the steroid. In order to discover whether CPA acts directly on preneoplastic liver cells or via indirect effects, we investigated whether CPA stimulates replicative DNA synthesis in vitro in hepatocytes isolated from carcinogen-treated rats (two-thirds hepatectomy, 1 x 30 mg diethylnitrosamine per kg and 0.1% phenobarbital in the drinking water) and whether the degree of stimulation differs in gamma-glutamyltranspeptidase (GGT)-positive, putatively preneoplastic and GGT-negative, 'normal' hepatocytes. The possibility that CPA might also have initiating potential was investigated by studying its effects on DNA repair synthesis. Stimulation of [3H]thymidine incorporation into the DNA by CPA was only observed in the presence of epidermal growth factor (EGF) (10 ng/ml) and insulin (10 mU/ml). Maximal effects were obtained between 2 and 10 microM. DNA synthesis in the presence of EGF/insulin was reduced by the 'pure' anti-androgen flutamide, but stimulated by the 'pure' progestin promegestone. In the presence of CPA, EGF and insulin, the labelling index was twice as high in GGT-positive as in GGT-negative liver cells, regardless of whether mitogens were added at 48 or 72 h. The labelling index did not differ in the GGT-positive and negative hepatocytes when CPA was omitted. These findings are consistent with the idea that CPA has tumor-promoting activity. CPA significantly induced repair synthesis in the isolated hepatocytes from both untreated and carcinogen-treated rats. This increase was detected at a concentration as low as 2 microM and maximal effects were obtained at 20 microM. These results indicate that CPA is not only a tumor-promoting, but also a genotoxic chemical, i.e. that it might also have an initiating potential.

Biotransformation in carcinogen-induced diploid and polyploid hepatocytes separated by centrifugal elutriation.

Biotransformation in carcinogen-induced diploid and polyploid hepatocytes was studied using isozyme-selective substrates for several enzyme pathways. Diploid hepatocytes were induced by partial hepatectomy, a single injection of diethylnitrosamine, and 4 weeks of 2-acetylaminofluorene (2-AAF) feeding. Then, after an additional 3-5 weeks on the control diet, diploid and polyploid hepatocytes were separated from freshly isolated hepatocytes by centrifugal elutriation. Benzo(a)pyrene hydroxylase, ethoxyresorufin O-deethylase, and methoxycoumarin O-demethylase activities were approximately 15-40% lower in the diploid hepatocyte fraction than in the polyploid cell fraction. Activities of 1-chloro-2,4-dinitrobenzene, glutathione S-transferase, 3-hydroxy-benzo(a)pyrene or 4-hydroxybiphenyl UDP-glucuronosyltransferase, and DT-diaphorase were not different in the two cell fractions. Determination of activity during the 2-AAF treatment indicated that 2-AAF increased 7-ethoxyresorufin O-deethylase and 3-hydroxybenzo(a)pyrene glucuronosyltransferase activities by 300 and 200%, respectively, in both the diploid and polyploid hepatocyte fractions. Administration of phenobarbital for 4 days at the end of the control diet period increased ethoxyresorufin and methoxycoumarin dealkylations by 2- and 4-fold, and 3-hydroxybenzo(a)pyrene glucuronidation and 1-chloro-2,4-dinitrobenzene conjugation with glutathione by 1.5- to 2-fold in both hepatocyte fractions. Slight increases in benzo(a)pyrene hydroxylation and 4-hydroxybiphenyl glucuronidation were also evident in diploid cells. Although there is a slight decrease in cytochrome P-450-dependent monooxygenase activities, these data indicate that carcinogen-induced diploid hepatocytes do not show the typical toxicant-resistant phenotype observed in preneoplastic hepatocytes of altered liver foci, which are characterized by large decreases in monooxygenase biotransformations as well as increased activities of several phase II enzymes. This finding is compatible with the hypothesis that 2-AAF-induced nonploidizing growth of diploid hepatocytes is caused by nontoxic mechanisms in the present experimental paradigm. In addition, carcinogen-induced diploid cells respond to phenobarbital in a manner similar to that of polyploid hepatocytes.

Stimulation of DNA synthesis in carcinogen-induced diploid hepatocytes in vitro.

Diploid hepatocytes induced by a combination of diethylnitrosamine and 2-acetylaminofluorene were isolated and separated from polyploid hepatocytes by centrifugal elutriation. The diploid and polyploid cell fractions were approximately 90% pure and contained between 1 and 1.5 x 10(7) cells. When kept in monolayer cultures both cell populations responded to the mitogenic effect of EGF and insulin. However, the percentage of labelled nuclei was higher in predominantly diploid compared to predominantly tetraploid hepatocyte cultures at all epidermal growth factor (EGF) concentrations used in this study. At 10 ng EGF/ml and 10 mU insulin/ml the labelling index was twice as high in the diploid liver cells. Further work is required to show the relevance of the stronger response of the diploid cell fraction to mitogens in the process of carcinogenesis.

Centrifugal elutriation of hepatocytes from 2-acetylaminofluorene-treated rats and their characterization by flow cytometry.

Treatment of male Wistar rats with 2-acetylaminofluorene (2-AAF) markedly altered the ploidy distribution of liver cells. Small diploid hepatocytes first appeared after 4-5 weeks feeding of a diet containing 0.02% 2-AAF; after 9 weeks 65-70% of the hepatocytes were diploid. Approximately two-thirds of this new liver cell population persisted after termination of the treatment. The hepatocytes from 2-AAF treated animals were separated according to size and ploidy by centrifugal elutriation and stained for gamma-glutamyltranspeptidase (gamma-GTase). The percentage of gamma-GTase-positive hepatocytes did not significantly differ between the various elutriated cell fractions. Thus gamma-GTase-positive liver cells obtained by feeding of 2-AAF do not represent a distinct size class of hepatocytes. The significance of carcinogen-induced diploid hepatocytes in hepatocarcinogenesis is discussed.