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Biomedical subjects

C Schuster

Publications and source records attributed to C Schuster.

At least 73 records · Page 4Linked to original sources
PubMed1989

[Microcomputer systems in urology: hardware--mole's hole or useful equipment?].

The basic concepts and elements of micro- and minicomputer hardware components frequently used in urology are described. For advanced users, the details and trends are discussed in more detail. The interdependence of hardware and operating systems is emphasized. In addition, a method for the evaluation of personal computer performance is presented. Finally, proposals are made concerning purchasing procedures and selection criteria.

Humans↗
PubMed1988

Antagonistic action of RU38486 on the activity of transforming growth factor-beta in fibroblasts and lymphoma cells.

Transforming growth factor-beta (TGF-beta) is a multifunctional protein involved in the control of proliferation, differentiation and other functions in many cell types. The anchorage-independent growth of some established lines of untransformed fibroblasts in soft agar is induced by TGF-beta and requires in addition exogenous EGF for certain target cells, notably rat NRK-49 cells. The formation of colonies of NRK-49F cells is completely inhibited by the synthetic 11-beta substituted nor-steroid RU38486 added at a final concentration of 1.3 X 10(-5) M. We also explored the effect of TGF-beta on Daudi and Raji lymphoma cells by measuring the production of Epstein-Barr Virus (EBV) early antigens (EA). In Daudi cells an induction capacity giving rise to 10-16% positive EA-cells was observed; in Raji cells the induction only reached between 6 and 8%. The induction was partially inhibited by the anti-steroid RU38486 in both systems. Thus, RU38486 not only antagonizes the glucocorticoid hormone action but also interferes with the effects of TGF-beta in fibroblasts and in lymphoma cells. The molecular basis of the interactions observed was investigated by considering (1) the binding to specific receptors, (2) transfection experiments, in order to examine if the interference of the anti-steroid with TGF-beta activities occurs at the transcriptional level as in the case of glucocorticoid induction. The results suggest that the blocking by antiglucocorticoids of the effects of TGF-beta and glucocorticoids, in fibroblasts and lymphoma cells, occurs by different mechanisms.

Animals↗
PubMed1988

[Use of electronic data processing in the urologic clinic and practice--possibilities and perspectives].

The development, present status and future trends in the use of computers in urology in the Federal Republic of Germany are reviewed. The hardware, software required for hospital and private practice and the staff needed are discussed. Proposals are given for the installation and stepwise upgrading of computer systems, from simple text processing units to complex hospital communication systems. Finally new technologies that might considerably change the use of computers in urology are presented.

Computers↗
PubMed1987

The influence of socioeconomic factors on the occurrence of fetal alcohol syndrome.

This study was designed to compare manifestations of FAS in the offspring of lower and upper middle class chronic alcoholic mothers, and to compare these offspring with those of nonalcoholic controls. There was highly significant difference in the incidence of FAS offspring between upper middle and lower class alcoholic mothers, 4.5% versus 70.9% respectively. Mean weight, length, and head circumference at birth in children of upper middle class alcoholic women was -ISD, those of lower class alcoholic women fell into -2SD. All other parameters, congenital malformation rate, failure to thrive, mental retardation were also significantly greater in children of lower class alcoholic women (p less than or equal to .01). Attention deficit disorder was found in 21% of upper middle class offspring of alcoholic women as compared to 71% in the children of the lower socioeconomic group (p less than or equal to .01).

Attention Deficit Disorder with Hyperactivity↗
PubMed1986

Cell cycle-dependent initiation of adenosine triphosphatase-deficient populations in adult rat liver by a single dose of N-methyl-N-nitrosourea.

Changes in the sensitivity of hepatocytes to initiation during the cell cycle were investigated in partially resected hydroxyurea-synchronized regenerating rat liver. At defined periods of the cell cycle the animals were given injections of a single dose of N-methyl-N-nitrosourea (MNU) (25 mg/kg) and were subsequently exposed to diethylnitrosamine for 30 days (2 mg/kg/day) or to phenobarbital (0.05% in the diet) for 80 days. Adenosine triphosphatase-deficient cell populations in the liver, determined 90 days after MNU treatment, served as a marker for the initiating action of the carcinogen. Few foci were observed when MNU treatment was performed during early G1. Their frequency increased steeply after MNU injection at G1-S boundary and reached a maximum after carcinogen exposure in early S phase, when the number of adenosine triphosphatase-deficient foci was higher by a factor of 5 (after diethylnitrosamine feeding) or 10 (after phenobarbital feeding) than after MNU exposure in early G1 phase. A rapid decline was observed in middle S phase. The frequency of altered foci after MNU in late S phase and during G2-M was in the same range as in early G1. Their size distribution was similar in all groups. The results confirm and extend earlier observations of an increased initiating effect of a carcinogen during liver regeneration. Under in vivo conditions, hepatocytes are, after HU synchronization, at the highest risk of being initiated by a carcinogen when they traverse the early S phase of the cell cycle.

Adenosine Triphosphatases↗
PubMed1985

Hallucinogenic amphetamine selectively destroys brain serotonin nerve terminals.

(+/-)-3,4-Methylenedioxyamphetamine (MDA), an amphetamine analog with hallucinogenic activity, produced selective long-lasting reductions in the level of serotonin, the number of serotonin uptake sites, and the concentration of 5-hydroxyindoleacetic acid in rat brain. Morphological studies suggested that these neurochemical deficits were due to serotonin nerve terminal degeneration. These results show that MDA has toxic activity for serotonin neurons in rats and raise the question of whether exposure to MDA and related hallucinogenic amphetamines can produce serotonin neurotoxicity in the human brain.

3,4-Methylenedioxyamphetamine↗
PubMed1985

O6-Methylguanine repair of methylated DNA in vitro: cell cycle-dependence of rat liver methyltransferase activity.

O6-Methylguanine DNA transferase activity was investigated in liver proteins obtained at various intervals after partial hepatectomy and/or after hydroxyurea-induced synchronization of the liver cell cycle. Liver proteins were incubated with 3H-methylated calf thymus DNA as previously described by Pegg et al. (1981). The loss of O6-methylguanine was measured by radiochromatography of DNA hydrolysates. The extent of O6-methylguanine repair differed during the cell cycle: the activity increased in late G1, reached a maximum in early S phase and declined in late S phase and G2M. These results indicate that hepatocytes are endowed with an increased DNA repair capacity for this promutagenic lesion during the period of highest transformation sensitivity in the cell cycle. Though increased, however, this repair potential does not, because of its exhaustibility, appear to be sufficient to prevent initiation of transformation after high doses of alkylating carcinogens.

Animals↗
PubMed1985

Cell proliferation and DNA repair in the liver during early stages of chemical carcinogenesis.

X-chromosomal phosphoglycerate kinase mocaicisms in organ samples of female heterozygous mice provided a means to prove, because of a selective expression of one of the two allozymes, the clonal origin of carcinogen-induced preneoplastic hepatocellular populations (see also ref. 61). The occurrence of these clonal preneoplastic foci was used in rats to determine cell cycle dependent differences of transformation sensitivity and DNA repair. The highest transformation rate was found after carcinogen exposure in late G1/early S phase of the cell cycle. Experimental disturbance of DNA precursor pools by continuous thymidine infusion during carcinogen exposure results in an increased formation of preneoplastic clones. This is a further argument in favor of an essential role of base-mispairing during initiation. Cell cycle dependent fluctuations of O6-methylguanine DNA transferase with an increasing enzyme activity in late G1 and a maximum in early S phase indicate that cells possess an increased potential for eliminating promutagenic O6-methylguanine during the most transformation sensitive parts of the cell cycle to prevent base-mispairing during DNA replication or transcription. However, this putatively protective effect is limited because the enzyme is rapidly expended in the reaction and drops again in later stages of the cell cycle.

2-Acetylaminofluorene↗
PubMed1984

O6-methylguanine repair in liver cells in vivo: comparison between G1- and S-phase of the cell cycle.

To compare the formation and persistence of alkylated DNA bases in the G1- and S-phase compartments in liver in vivo, regenerating rat liver was exposed to [14C]dimethylnitrosamine (0.57 mg/kg, IP injection) or N-[methyl14C]-N-nitrosourea (3.3 mg/kg, intraportal injection) during the G1 phase of the cell cycle (12 h after partial hepatectomy), or at 24 h after partial hepatectomy with 30% hepatocytes in DNA synthesis, or at 43 h after partial hepatectomy, 4 h after an hydroxyurea block from 14 to 39 h after operation with 80% hepatocytes in DNA synthesis. At 120 min after dimethylnitrosamine and 90 s, 5, 10, or 60 min after the intraportal pulse of N-methyl-N-nitrosourea the molar fractions of 7-methylguanine (7megua), O6-methylguanine (O6megua), and 3-methyladenine (3mead) and of metabolically labeled guanine were determined from DNA hydrolysates by Sephadex-G10 radiochromatography. After dimethylnitrosamine only minor differences were observed for 7megua formation in the three groups; the 3mead/7megua ratio remained constant irrespective of the number of cells in S phase. In contrast, the O6megua/7megua ratio revealed a loss of O6megua, the extent of which appeared proportional to the fraction of DNA-synthesizing cells in the liver. The rapid loss of O6megua in S-phase cells was confirmed after intraportal administration of N-methyl-N-nitrosourea. During the first 10 min after the methylnitrosourea pulse the O6megua/7megua ratio was constant in G1 cells and dropped from 90 s to 10 min by about 15% in liver containing 30% S-phase cells and by about 40% with 80% cells in DNA synthesis. DNA-synthesizing hepatocytes are apparently endowed with a higher O6megua DNA transferase activity than nonproliferating liver cells. The rapid, though exhaustible elimination of O6megua during S-phase might result in partial protection of DNA-synthesizing cells from base-mispairing and/or from hypomethylation at G-C sites.

Alkylation↗
PubMed1984

Effect of diets containing varying concentrations of essential fatty acids and triglycerides on renal function in uremic rats and NZB/NZW F1 mice.

Influences of essential fatty acids (EFA) and triglycerides as reasons for the progression of chronic renal failure are still in debate. We studied the outcome of four diets containing different concentrations of triglycerides and EFA in 5/6 nephrectomized rats and in NZB/W mice up to 45 weeks. The results showed no significant differences in the outcome of survival rate, proteinuria, urea, and creatinine levels as well as histological findings in the different groups of both animal models. We conclude that diets containing EFA up to C18:2 or being free of EFA or that triglyceride-enriched diets have no influence on the natural course of the renal disease in these both experimental models.

Animals↗
PubMed1981

Central blood pressure effects of substance P and angiotensin II: role of the sympathetic nervous system and vasopressin.

The role of the sympathetic nervous system and of arginine vasopressin (AVP) in the mediation of the central cardiovascular effects of angiotensin II (ANG II) and substance P (SP) was investigated. ANG II and SP caused dose-dependent blood pressure increases when injected into the lateral brain ventricle (i.c.v.) of conscious rats; ANG II was tenfold more potent than SP. Peripheral blockade of alpha-adrenoceptors with prazosin or blockade of the vasopressor action of AVP by the AVP antagonist d(CH2)5VDAVP both partially inhibited the pressor responses to central ANG II. Combined treatment with the two blockers produced almost complete inhibition of the central ANG I responses. Substance P injected i.c.v. produced increases in noradrenaline and adrenaline but not AVP in the plasma. Peripheral alpha-receptor blockade by prazosin reversed the central pressor effects of SP to depressor responses. The AVP antagonist did not alter the cardiovascular responses to SP. It is concluded that in conscious animals, stimulation of the sympathetic nervous system and release of AVP contribute to the central pressor action of ANG II to a similar extent and independently of each other. In contrast, the central pressor responses to SP appear to be exclusively mediated by the sympathetic nervous system without participation of AVP.

Angiotensin II↗