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Biomedical subjects

K Radsak

Publications and source records attributed to K Radsak.

At least 55 records · Page 3Linked to original sources
PubMed1985

Sodium butyrate selectively inhibits host cell glycoprotein synthesis in human fibroblasts infected with cytomegalovirus.

Host cell as well as viral DNA synthesis in human fibroblasts infected with human cytomegalovirus was found to be largely resistant even to high concentrations of sodium butyrate. Likewise, production of viral progeny was reduced by 1-2 orders of magnitude but not abolished. On the other hand, the drug allowed (modified) glycosylation only of viral polypeptides whereas that of host proteins was suppressed. Immunofluorescence studies on living cells suggested that butyrate may interfere with processing and intracellular transport of virus-specific surface membrane antigens.

Antigens, Surface↗
PubMed1985

Distinction of viral and host-derived glycopolypeptides induced by "early" functions of human cytomegalovirus.

Human cytomegalovirus is shown to induce in phosphonoacetic acid-treated human fibroblasts glycosylation of five polypeptides with approximate molecular weights of 200-250, 150, 135, 130 and 100 kilodaltons (kd). Except for the 130 kd product, these glycopolypeptides (gp) separate with the cytoplasmic fraction, only one (200-250 kd) with the chromatin fraction as well. The gp of 135 and 100 kd were found to be virus-specified as determined by immunoblotting and immunoprecipitation. The gp of 200-250 kd exhibited an immunological relatedness to fibronectin and are therefore considered host-specific products. Both subsets of gp participate in virus-induced surface membrane alterations as documented by living cell immunofluorescence.

Antigens, Surface↗
PubMed1984

Glycosphingolipid synthesis in human fibroblasts infected by cytomegalovirus.

Infection of serum-deprived human foreskin fibroblasts (HFF-cells) by cytomegalovirus (HCMV) resulted in enhanced precursor incorporation into glycosphingolipids (GSL). Analysis of the component patterns revealed a unique biphasic effect on the rate labeling of neutral GSL. Early during infection or in the presence of phosphonoacetic acid, radiolabel was found predominantly in ceramide tri- and tetrahexoside, whereas late after infection label in ceramide monohexoside exceeded that in the other components. Determination of the chemical amounts of neutral GSL components from infected cultures supported the view of increased biosynthesis of ceramide tri- and tetrahexoside early, and of ceramide monohexoside late postinfection. Changes, comparable to those observed under the influence of "early" viral functions were observed also during S-phase of serum-stimulated HFF cells. With respect to acidic GSL a decrease of metabolic labeling occurred late during infection. Relatively little alteration was found in the component pattern.

Cell Differentiation↗
PubMed1983

Microtubular reaction in human fibroblasts infected by cytomegalovirus. Brief report.

By the use of indirect immunofluorescence it is shown that "early" functions of human cytomegalovirus induce a loss of microtubuli in human foreskin fibroblasts within 12 hours postinfection (p.i.) which persists until about 60 hours p.i. At later times p.i. microtubular structures are eventually reestablished. Following depression during the initial 48 hours p.i. tubulin synthesis in infected cells is significantly enhanced during the initial 48 hours p.i. tubulin synthesis in infected cells is significantly enhanced during the late phase of the infectious cycle suggesting that the mechanisms regulating tubulin synthesis are not impaired.

Cytomegalovirus↗
PubMed1982

Actin distribution and synthesis in human fibroblasts infected by cytomegalovirus.

"Early functions" of human cytomegalovirus were found to induce a loss of microfilaments as revealed by indirect immunofluorescence and by the use of fluorescent phalloidin. Actin synthesis in infected cultures, on the other hand, appeared to be largely unchanged as estimated from the specific radioactivity of cytoplasmic actin.

Actins↗
PubMed1982

Studies on the cell association of exogenously added sialo-glycolipids.

We studied the mode of uptake of exogenous sialoglycolipids with a permanent mouse cell line (Clone-1D) and compared the cell association of ganglioside II3 NeuAc-Gg4 Cer with that of a synthetic one-C18-hydrocarbon-chain ganglioside analogue (desphingo-G1-stearamide). In contrast to monolayer cultures, Clone-1D cells in suspension bind both sialo-glycolipids rapidly and independently of time and temperature (4 degrees/37 degrees C) of incubation. Three modes of cell association were distinguished: 1) a serum-and serum albumin-sensitive association; 2) a trypsin-sensitive association and 3) a serum- and trypsin-insensitive association. Inhibition of pinocytosis by deoxyglucose/sodium azide did not significantly influence cellular uptake or release of exogenous ganglioside. In monolayer culture, Clone 1D cells in M-phase associate more ganglioside than randomly growing cells. This may explain in part the inhomogeneous cellular distribution of ganglioside binding. In contrast, uptake of desphingo-G1 -stearamide by cells in mitosis equalled that bound by control cells.

Animals↗
PubMed1980

DNA synthesis in chromatin preparations from human fibroblasts infected by cytomegalovirus.

Chromatin prepared from (14C)-thymidine pulse labelled cytomegalovirus-infected human fibroblasts 72 hours postinfection exhibited under appropriate conditions endogenous activity of (3H)-thymidine triphosphate incorporation which was relatively salt-resistant and phosphonoacetic acid-sensitive. Isopycnic centrifugation of the doubly labelled DNA in CsCl revealed that cell-free incoporation occurred into viral as well as into host cell DNA. Density labelling experiments with bromodeoxyuridine triphosphate suggested the incoporation into viral DNA to be due to replicative DNA synthesis. Chromatin from infected cells contained, in addition to cellular, viral DNA polymerase activity.

Cell Line↗
PubMed1980

Unimpaired histone synthesis in human fibroblasts infected by human cytomegalovirus.

Serum-starved human foreskin fibroblasts were infected by human cytomegalovirus (Towne strain) that is thought to induce DNA replication in host cells during lytic infection. At various times postinfection, the cultures were pulse labeled with either 3H-thymidine or 14C-thymidine and 3H-lysine to examine DNA synthesis and histone synthesis, respectively. Isopycnic centrifugation of labeled DNA in CsCl revealed that precursor incorporation into host-cell DNA was enhanced over the control around 24 h postinfection and decreased after onset of viral DNA synthesis which reached a peak around 72 h postinfection. For analysis of histones 3H-lysine-labeled proteins of lysates of unfractionated cells and of chromatin preparations were subjected to polyacrylamide gel electrophoresis in presence of sodium dodecyl sulfate and subsequent fluorography. Comparison of the fluorograms from the various pulses postinfection suggested that 3H-lysine incorporation into histones exhibited no major variations concurrent with the changes of host-cell DNA synthesis. In contrast, herpes simplex virus type 1 was found progressively to extinguish histone synthesis in the course of the cellular infection. Furthermore, histone synthesis in phosphonoacetic acid-treated cytomegalovirus-infected cultures was not enhanced over that in mock-infected controls. These observations do not support the view that human cytomegalovirus induces host-cell DNA replication under the conditions used.

Cell Line↗
PubMed1978

Changes of mitochondrial DNA polymerase-gamma activity in synchronized mouse cell cultures.

Following synchronization by a double hydroxyurea block, mouse cell cultures exhibited a period of accelerated precursor incorporation into mitochondrial DNA during the late nuclear S phase. Peak activity of mitochondrial DNA polymerase-gamma occurred concurrent to the interval of accelerated organelle DNA synthesis. Mixing experiments suggested that the variations in mitochondrial DNA polymerase activity during the cell cycle were not due to free inhibitors in the enzyme preparations examined.

Cell Cycle↗
PubMed1978

Effect of herpes simplex virus type 1 infection on the cellular DNA polymerase activities of mouse cell cultures.

Thymidine kinase-deficient mouse cell cultures infected with herpes simplex virus type 1 exhibited a maximum of virus DNA synthesis around 8 h post-infection as determined by pulse labelling with 3H-thymidine. Cellular DNA synthesis was progressively inhibited, but still appreciable until 8 h post-infection and not completely abolished at any time during the infectious cycle. Phosphonoacetic acid was found to be a potent and selective inhibitor of virus DNA synthesis only when added to infected cultures before the onset of virus DNA synthesis. During the interval of increasing virus DNA synthesis the activity of cellular alpha polymerase decreased rapidly, whereas the beta polymerase activity increased significantly; a slight increase was observed for the gamma polymerase activity. When infected cells were kept in the presence of phosphonoacetic acid following virus adsorption the effect on cellular DNA polymerases was less pronounced.

Animals↗
PubMed1976

Mechanism of fever induction in rabbits.

Three exogenous pyrogens (Escherichia coli lipopolysaccharide, synthetic double-stranded ribonucleic acid. Newcastle disease virus) were compared with respect to their mechanisms of fever induction in rabbits. All inducers stimulated the production of an endogenous pyrogen demonstrated in the blood as well as prostaglandins of the E group, and of cyclic adenosine 3',5'-monophosphate in the cerebrospinal fluid. The concentrations of these compounds were elevated approximately twofold as compared to the controls. Independently of the mode of induction, the fever reaction could be prevented by pretreatment with 5 mg of cycloheximide per kg, although the three fever mediators were induced as in febrile animals. Consequently, at least one additional fever mediator that is sensitive to a 30 to 50% inhibition of protein synthesis by cycloheximide has to be postulated. The comparable reactions of the rabbits after administration of different pyrogens argues for a similar fever mechanism. In contrast to fever induction there was no stimulation of endogenous pyrogen, prostaglandins of the E group, and cyclic adenosine 3',5'-monophosphate in hyperthermia as a consequence of exposure of the animals to exogenous overheating. Furthermore, hyperthermia could not be prevented by cycloheximide.

Animals↗
PubMed1976

Chloramphenicol-induced loss of mitochondrial DNA polymerase activity in HeLa cells.

HeLa cells exposed to chloramphenicol for approximately one cell generation were found to contain a mitochondria-associated DNA polymerase with a significantly lower specific activity than that of control cells. This observation was not due to the presence of inhibitors in mitochondrial DNA polymerase preparations of chloramphenicol-treated cell cultures. In addition, there was no accumulation of a typical mitochondrial DNA polymerase in the post-mitochondrial supernatant of drug-treated cells.

Chloramphenicol↗