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The aim of the study was to investigate the whole-body protein turnover, either before or after continuous, moderate ethanol-induced oxidative stress by red wine consumption over a relatively short period in healthy volunteers. Ten healthy adults received an individual regular diet over 20 days. After 10 days, the subjects consumed 0.4 ml ethanol kg(-1) day(-1) as red wine together with dinner over a 10-day period. After 8 and 18 days, respectively, a (15)N-labelled yeast protein was administered in a dosage of 4.2 mg kg(-1) body weight. Urine and faeces were collected over 48 h, respectively. The (15)N-enrichment was measured by isotope ratio mass spectrometry, whereas the protein flux rates were calculated by a three-compartment model. The whole-body protein turnover without/with red wine consumption amounted to 3.73±0.6 and 3.49±0.6 g kg(-1) day(-1) (not significant), respectively. Moderate alcohol consumption does not induce significant short-term changes in the whole-body protein turnover of healthy adults.

Wilms' tumor is a childhood nephroblastoma that is postulated to arise through the inactivation of a tumor suppressor gene by a two-hit mechanism. A candidate 11p13 Wilms' tumor gene, WT1, has been cloned and shown to encode a zinc finger protein. Patients with the WAGR syndrome (Wilm's tumor, aniridia, genitourinary abnormalities, and mental retardation) have a high risk of developing Wilms' tumor and they carry constitutional deletions of one chromosome 11 allele encompassing the WT1 gene. Analysis of the remaining WT1 allele in a Wilms' tumor from a WAGR patient revealed the deletion of a single nucleotide in exon 7. This mutation likely played a key role in tumor formation, as it prevents translation of the DNA-binding zinc finger domain that is essential for the function of the WT1 polypeptide as a transcriptional regulator.

Using somatic cell genetics and Southern blot hybridization, we have mapped five structural genes in the owl monkey, coding for catalase (CAT), the β-globin gene cluster (HBBC), c-Ha-ras 1 (HRAS1), insulin (INS), and parathyroid hormone (PTH). All five loci are mapped to chromosome 19 of karyotype VI (2n = 49,50) of the owl monkey; CAT, HBBC, INS, and PTH can be assigned to chromosome 4 of karyotype V (2n = 46), while CAT and HBBC can be assigned to chromosome 2 of karyotype III (2n = 53). Using in situ hybridization, the CAT gene was precisely mapped on the mid-region and the β-globin gene cluster on the telomeric end of chromosome 2q(K-ΠI). Our results provide significant insight into the evolutionary history of these gene loci. While these loci are separated into at least two major segments in rodents such as the mouse, our results suggest conservation of a single chromosome arm among higher primates.

The author describes a psychoanalytical liaison service conducted over a period of two years on behalf of a psychiatric ward for acutely demented patients. About one-sixth of the psychiatric patients admitted during this time were subjected to psychoanalytical examination. Psychiatric inpatient treatment was suggested for about one-tenth of them, i.e. two per cent of all referrals to the ward. Due to the introduction of a psychodynamic mode of viewing the cases, together with a patient-centered interpretation of interaction patterns, the general atmosphere in the ward changed gradually. The article concludes with general considerations as to the use of the psychoanalytical approach in psychiatry.

In the recent century research in cancer metastasis has greatly improved; nowadays it is a superior topic in cancer literature. Most of its problems result from alternate assumptions: The functional seed and soil and the hemomechanic hypothesis, after all putting two questions on account of metastasis being either a permanent likewise passive or a cascade phenomenon. In regard of metastasizing bronchial-, breast- and prostate carcinomas or multifocal tumors and most of rodent neoplasms a passive tumor cell transport might be a single effect, but the characteristic feature rather a step by step metastasizing cascade, implicating special organ localizations, and the fact, that metastasis distribution correlates with tumor biology, localization of the first metastasis and in manifold metastasizing tumors with typical organ patterns. From introduction of recent in vitro and cloning-techniques the metastasizing potency of tumors now becoming able to be defined by function of its genetic heterogeneity, developing metastasizing phenotypes respective neoplastic evolution by mutation, gene amplification, and epigenetic factors. On the other side having an unique xenobiotic metabolism metastasizing tumor cells are in accordance with the conception of their inherent "commonality".

This essay on prognosis in tumor diagnosis pathology resp. tumor etiology, cancerogenesis and molecular oncology is the authors personal opinion. Generally tumor diagnosis improves with progress in histo- and cytological methods for example in tumors of the APUD-system and precancerous lesions especially of the breast. Fundamental principle of developed tumor diagnosis is the knowledge of malignant transformation. Its profits favours the etiology in cancerogenesis and e.g. non Hodgkin lymphomas (Burkitt lymphoma, adult T-cell lymphoma) and to result from new methods in molecular biology and viral genetics (DNS-hybridizing, -recombination and gene technology). With the beginning century a stepwise fitted diagnosis of malignant lymphomas is evident up to monoclonal dedifferentiated lymphoid cells and their multifarious phenotypical markers. This concept may be of general significance in tumor diagnosis already indicated in prelymphomas. Finally the present prognosis of tumor diagnosis is evaluated by contents, tasks and strategies of its corresponding research lines in clinical and experimental tumor pathology resp. its organization.

In human fibroblast cultures derived from adults, clones of cells with a common chromosome rearrangement have been widely reported. Cells derived from one of these clones have been used in hybridization experiments using mouse cells to localize the genes for β-glucuronidase and mitochondrial malate dehydrogenase on human chromosome 7. The results of this study indicate that the genes for these isozymes are located on the region pter→q22 of human chromosome 7.