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Biomedical subjects

M Olbrich

Publications and source records attributed to M Olbrich.

At least 19 recordsLinked to original sources
PubMed2005

Transcriptome analysis of ozone-responsive genes in leaves of European beech (Fagus sylvatica L.).

Suppression subtractive hybridization (SSH) was performed to isolate cDNAs representing genes that are differentially expressed in leaves of Fagus sylvatica upon ozone exposure. 1248 expressed sequence tags (ESTs) were obtained from 2 subtractive libraries containing early and late ozone-responsive genes. Sequences of 1139 clones (91 %) matched the EBI/NCBI database entries. For 578 clones, no putative function could be assigned. Most abundant transcripts were O-methyltransferases, representing 7 % of all sequenced clones. ESTs were organized into 12 functional categories according to the MIPS database. Among them, 12 % (early)/15 % (late) were associated with disease and defence, 19/11 % with cell structure, 4/10 % with signal transduction, and 9/6 % with transcription. The expression pattern of selected ESTs (ribulose-1,5-bisphosphate carboxylase/oxygenase small subunit [rbcS], WRKY-type transcription factor, ultraviolet-B-repressible protein, aquaporine, glutathione S-transferase, catalase, caffeic acid O-methyltransferase, and pathogenesis-related protein 1 [PR1]) was analysed by quantitative real-time RT-PCR (qRT-PCR) which confirmed changed transcript levels upon ozone treatment of European beech saplings. The ESTs characterized will contribute to a better understanding of forest tree genomics and also to a comparison of ozone-responsive genes in woody and herbaceous plants.

Europe↗
PubMed2000

The STAR/GSG family protein rSLM-2 regulates the selection of alternative splice sites.

We identified the rat Sam68-like mammalian protein (rSLM-2), a member of the STAR (signal transduction and activation of RNA) protein family as a novel splicing regulatory protein. Using the yeast two-hybrid system, coimmunoprecipitations, and pull-down assays, we demonstrate that rSLM-2 interacts with various proteins involved in the regulation of alternative splicing, among them the serine/arginine-rich protein SRp30c, the splicing-associated factor YT521-B and the scaffold attachment factor B. rSLM-2 can influence the splicing pattern of the CD44v5, human transformer-2beta and tau minigenes in cotransfection experiments. This effect can be reversed by rSLM-2-interacting proteins. Employing rSLM-2 deletion variants, gel mobility shift assays, and linker scan mutations of the CD44 minigene, we show that the rSLM-2-dependent inclusion of exon v5 of the CD44 pre-mRNA is dependent on a short purine-rich sequence. Because the related protein of rSLM-2, Sam68, is believed to play a role as an adapter protein during signal transduction, we postulate that rSLM-2 is a link between signal transduction pathways and pre-mRNA processing.

Alternative Splicing↗
PubMed1994

Obesity and hypertestosteronaemia are independently and synergistically associated with elevated insulin concentrations and dyslipidaemia in pre-menopausal women.

The association of obesity and hypertestosteronaemia with elevated insulin concentration and dyslipidaemia was studied in 15 non-obese and 15 obese, hypertestosteronaemia patients; 14 non-obese and 10 obese, normotestosteronaemic subjects served as controls. Data were subjected to multivariate analysis. Enhanced body mass index (BMI kg/m2) resulted in a significant elevation of basal insulin (b-Ins), glucose-stimulated (delta) insulin (del-Ins), triglycerides (TG), very low density lipoprotein (VLDL), low density lipoprotein (LDL), and LDL/high density lipoprotein (HDL) ratio, and in a significant reduction of HDL. Furthermore, it was shown that BMI was positively correlated with TG, VLDL, LDL and LDH/HLD ratio, and negatively correlated with HDL in the normotestosteronaemic groups. Hypertestosteronaemia was associated with a significant increase of del-Ins, VLDL and LDL/HDL ratio, and with a significant decrease of HDL concentration. Testosterone was directly associated with del-Ins and LDL/HDL ratio, and inversely related to HDL in the non-obese groups. Summation effects of obesity and hypertestosteronaemia were found for del-Ins and VLDL. The data suggest that obesity and hypertestosteronaemia are independently and jointly associated with insulin resistance and dyslipidaemia, indicating an increased risk for coronary heart disease. The highest risk rate was found in obese hypertestosteronaemic patients. Serum testosterone may be a useful marker in detecting metabolic disorders connected with cardiovascular risk.

Adult↗
PubMed1988

Immunological mechanisms giving rise to latency of herpes simplex virus in the spinal ganglia of the mouse.

In the model of genital herpes simplex virus (HSV)-infection of mice, early latency could be induced by passive immunization with HSV-specific antibodies and, to a lesser degree, by adoptive transfer of immune lymphocytes prepared from spleen and draining lymph nodes of genitally infected syngeneic mice. Conversely, spontaneously occurring latency was inhibited by treatment of the animals with cyclophosphamide (Cph) and, to a lesser degree, with cyclosporin A (CyA). Whereas the effect of CyA could be compensated by passively administered HSV-specific antibodies, that of Cph could not. Apparently specific antibodies cooperate with a non-specific proliferating cell type, probably macrophages and/or NK-cells, as could be demonstrated by significantly reduced antibody effect in silica-treated mice. Moreover, F(ab)2 fragments, in contrast to complete antibody molecules, were inactive. HSV-specific antibodies and also immune lymphocytes had little effect on virus production in the mucous membranes, immune lymphocytes being at least as active as antibodies. It is therefore not probable that latency is induced by attenuation of the peripheral disease. It can rather be concluded that the neuron itself is the target for the action of specific antibodies, cooperating in turn with macrophages and/or NK cells.

Animals↗
PubMed1984

Pathogenesis of genital herpes simplex virus infection in mice. III. Comparison of the virulence of wild and mutant strains.

This study was undertaken to establish the role of virulence of various herpes simplex virus (HSV) strains in the course of infection when applying the virus to the non-injured mucous membranes of mice. Wild-type HSV-type 1 (HSV-1) strains with marked differences in their neurovirulence following intracerebral inoculation showed minor differences in virulence after vaginal inoculation, but essentially their neurovirulence in cerebral infection corresponded to their virulence on the mucous membranes. In comparison with the wild-types, however, there were pronounced differences among syn- and TK--mutants of HSV-1 and HSV-2 in the degree of virulence at different sites in the course of virus infection. Whereas syn-mutants proved avirulent on the mucous membranes but not in neural tissues, TK--mutants were avirulent both on mucous membranes and in neural tissues. Ts-mutants of HSV-2 were not found to establish themselves when administered to the non-injured mucous membranes, nor did they induce neutralizing antibodies, but a later challenge with the wild-type virus at the same site lead only to an attenuated course of infection.

Animals↗
PubMed1982

Effects of genetic resistance against Herpes simplex virus in vaginally infected mice.

In order to take the conditions of natural Herpes simplex virus (HSV) infection into consideration, the genetic resistance of C57-Bl mice, which was established by intraperitoneal HSV-1 infection [Lopez, 1975], was investigated in vaginally infected mice. The course of infection in the mucous membranes did not differ in sensitive (NMRI) and resistant (C57-Bl) mice: both number of takes and virus elimination from the vagina were equal, and no difference in viral titer produced in the vagina was detected. Viral titer in the productively infected lumbosacral ganglia, however, was less in the resistant mice. An experiment with foot-pad-infected mice confirmed that the number of productively infected ganglia was reduced in resistant mice, and contralateral ganglia were infected only in the sensitive mouse strain. In spite of this, the number of latently infected animals did not vary significantly in the mouse strains. Higher activity of defense mechanisms in resistant mice, apparently localized in the ganglia, resulted in reduced lethality. As to the mechanisms of the resistance, neither antibody nor interferon response were enhanced in C57-Bl mice, but resistance was abolished by depletion of several cellular functions, i.e., lymphocytes by cyclophosphamide or X-rays, macrophages by silica or macrophage-antiserum, and M-cells by 89Sr.

Animals↗