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Biomedical subjects

W Frisch

Publications and source records attributed to W Frisch.

9 recordsLinked to original sources
PubMed1999

LPS and TNFalpha induce SOCS3 mRNA and inhibit IL-6-induced activation of STAT3 in macrophages.

Recent findings indicate that cytokine signaling can be modulated by other mediators of simultaneously activated signal transduction pathways. In this study we show that LPS and TNFalpha are potent inhibitors of IL-6-mediated STAT3 activation in human monocyte derived macrophages, rat liver macrophages and RAW 264.7 mouse macrophages but not in human hepatoma cells (HepG2) or in rat hepatocytes. Accordingly, LPS and TNFalpha were found to induce the expression of SOCS3 mRNA in each of the investigated type of macrophages but not in HepG2 cells. Using a specific inhibitor, evidence is presented that the p38 MAP kinase might be involved, especially for the inhibitory effect of TNFalpha.

Animals↗
PubMed1996

Oncostatin M differentially regulates tissue inhibitors of metalloproteinases TIMP-1 and TIMP-3 gene expression in human synovial lining cells.

Tissue inhibitor of metalloproteinases (TIMP) 1, 2 and 3 are related proteins that can form complexes with all known matrix metalloproteinases (MMPs). They inhibit the action of MMPs on extracellular matrix components. The balance of MMPs and TIMPs is important for tissue remodeling and its disturbance is believed to play a crucial role in pathophysiological processes such as tumor metastasis, destruction of cartilage and fibrosis. Cytokines and growth factors were found to regulate TIMPs and MMPs in a complex manner. In order to better understand the role of TIMPs in inflammatory joint diseases we have studied in vitro the regulation of TIMP-1 and TIMP-3 by inflammatory cytokines in cultured human synovial lining cells. We found that transforming growth factor beta 1 as well as interleukin-1 beta induce gene expression of both TIMP-1 and TIMP-3. In contrast, oncostatin M, an interleukin-6-type cytokine produced by activated T-lymphocytes and monocytes, had a differential effect on TIMP mRNA levels. After oncostatin M treatment, TIMP-1 expression was up-regulated but basal, as well as interleukin-1 beta-induced, TIMP-3 expression was inhibited. Interleukin-6 itself had no effect on synovial lining cells but a complex of interleukin-6 and the soluble interleukin-6 receptor induced activation of signal transducer and activator of transcription (STAT) factors in these cells and regulated TIMP-1 and TIMP-3 expression in a similar fashion as oncostatin M. Since TIMP-3 is matrix-associated whereas TIMP-1 is found in many body fluids, the role of oncostatin M during inflammatory processes might be to promote ECM degradation in the local environment but to prevent it systemically.

Blotting, Northern↗
PubMed1990

[Increased expression of the OKM5 antigen in blood monocytes in vitiligo].

In 25 patients suffering from vitiligo, we determined the T-cell profile (OKT3, 4 and 8; anti-Leu7) as well as the peripheral monocytes (OKM5) by means of monoclonal antibodies. Comparing the patients with a control group (n = 8), we found no differences regarding the T-cell count, whereas the expression of OKM5 antigens on peripheral monocytes was significantly elevated in patients with vitiligo.

Adolescent↗
PubMed1986

Metallic dust collectors for low velocity impacts.

Experiments simulating the non-destructive collection of cosmic dust are conducted at the laboratory of the Lehrstuhl fur Raumfahrttechnik (LRT) of the Technische Universitat Munchen (TUM). The electromagnetic accelerator setup is described, which is capable of obtaining an impact velocity between 10 and 400 m/s with particle masses up to 1 g. The evaluation method of the ratio of collected to impacting particles is given. Various metallic surface structures were tested with respect to their collection efficiency using different types of particles from 1 to 500 micrometers in size for simulation of cosmic dust. The simulation results are presented with emphasis on collection mechanisms. Particular influences on the collection mechanisms are discussed.

Aluminum↗
PubMed1981

The kinetics of the formation of rotational isomers in the hydrophobic tail region of phospholipid bilayers.

Very fast structural changes in dipalmitoyl phosphatidylcholine molecules forming a vesicular bilayer were investigated by means of a laser temperature-jump technique. After temperature increases of about 1 K within 1 ns, the solution turbidity increases with a time constant of about 4 ns. This time constant exhibited no appreciable temperature dependence and represents a noncooperative process. It is interpreted as a local increase in density in the bilayer which results from a shortening of the individual lipid molecule due to formation of rotational isomers (e.g., kinks) without an appropriate expansion of the molecular environment. The final membrane expansion is achieved in consecutive steps with a decrease in turbidity and time constants between 100 mus and several seconds which are maximal in the midpoint of the phospholipid phase transition. These steps represent cooperative processes, namely the molecular interaction leading to the membrane expansion. The rate of kink formation implies that kinks migrate through the membrane by energetic transitions forwarded from lipid to lipid, rather than by hopping of individual lipids thereby carrying a kink.

Chemical Phenomena↗
PubMed1980

Effects of several lipidosis-including drugs upon the area postrema and adjacent medullary nuclei of adult rats. I. Alterations is perikarya and dendrites.

The present study is concerned with the question of whether or not amphiphilic drugs (chloroquine, quinacrine, perhexiline) that fail to induce general lipidosis in the central nervous system (CNS) of adult rats can produce lipidosis in a circumventricular organ (area postrema) not furnished with a blood-brain barrier. Chlorphentermine known to induce general lipidosis in CNS of adult rats served as reference compound. All drugs, when chronically applied in high oral doses, induced significant perikaryal lipidosis in the area postrema. In the adjacent nuclei (nucleus tractus solitarii, nucleus dorsalis nervi vagi, nucleus nervi hypoglossi, nucleus gracilis), only chlorphentermine caused generalized lipidosis, whereas the other drugs had either limited or no effects. The present findings strongly suggest that the exemption, of most regions of the CNS of adult rats, from lipidosis induced by chloroquine and others is due to hindered drug distribution across the blood-brain barrier, rather than being due to non-susceptibility of central neurons toward the lipidosis-inducing action of the drugs.

Animals↗
PubMed1979

Differential effects of chloroquine and of several other amphiphilic cationic drugs upon rat choroid plexus.

Several cationic amphiphilic drugs, each of which is known to induce generalized lipidosis in rats, were compared with respect to their cytological effects on rat choroid plexus epithelium. Chloroquine induced large cytoplasmic vacuoles, whereas the other drugs (quinacrine, 4,4'-diethylaminoethoxyhexestrol, chlorphentermine, iprindole, 1-chloro-amitriptyline, clomipramine) caused formation of lamellated or crystalloid inclusions as usually seen in drug-induced lipidosis. The ultrastructure of the chloroquine-induced vacuoles suggested storage of water-soluble materials (polar lipids and/or non-lipid materials) in addition to non-water-soluble polar lipids.

Amitriptyline↗