PubMed Health⌕ Search

Biomedical subjects

C Szabo

Publications and source records attributed to C Szabo.

44 records · Page 3Linked to original sources
PubMed1989

Mechanism of hemoglobin-induced spasm in the isolated middle cerebral artery of the cat.

a./Great regional differences were observed in the vasospastic effect of hemoglobin. Namely, hemoglobin was far more potent in the middle cerebral artery than in the mesenteric artery. b./The role of potassium ions as well as activation of calcium mobilizing adrenergic, serotoninergic and PGF2 alpha smooth muscle receptors were excluded in the mechanism of cerebral vasospasm induced by hemoglobin. c./First in the literature we showed that atropine significantly attenuates the vasospastic effect of hemoglobin, and hemoglobin releases peptidergic neurotransmitters and modulators from nerve terminals that are located in the adventitia of the middle cerebral artery.

Acetylcholine↗
PubMed1989

Regional differences in the regulation of contraction-relaxation machinery of vascular smooth muscle.

In the present study we revealed substantial differences in the regulation of the contraction-relaxation machinery of the middle cerebral and mesenteric arteries. a. Although K+-Krebs solution resulted in similar contractile responses in both vascular beds, norepinephrine, serotonin and PGF2 alpha were more potent in inducing contraction in the mesenteric artery than in the middle cerebral artery. Contrary, extremely high concentrations of acetylcholine produced negligible contractions in the mesenteric artery as compared to the middle cerebral artery. b. In more than 50% of the cases a considerable spontaneous tone developed in the middle cerebral artery, which was not due to the activation of adrenergic alpha receptors or some arachidonic acid metabolite. A similar phenomenon never occurred in the mesenteric artery. c. Acetylcholine, adenosine triphosphate and adenosine brought about similar dilatory concentration-response curves in the middle cerebral artery, but greatly different ones in the mesenteric artery where acetylcholine was the most, adenosine triphosphate the least potent dilator.

Acetylcholine↗
PubMed1976

Inhibition of infectious Rous sarcoma virus production by rifamycin derivative.

A new rifamycin derivative, rifazone-82 (R-82), an inhibitor of viral RNA-dependent DNA polymerase, is selectively toxic to transformed chicken cells in culture. R-82 has now been shown to possess antiviral activity as well. The relatively nontoxic properties of R-82 to nontransformed cells have permitted the execution of experiments examining the effect of a rifamycin derivative on virus reproduction. Addition of low concentrations of R-82 (15 mug/ml) to cultures soon after Rous sarcoma virus infection prevents the spread of infection thoroughout the culture. This inhibition is not dependent on concomitant cellular transformation as identical results were obtained with cells infected with a transformation-defective Rous sarcoma virus. Addition of R-82 to cultures in which all the cells are infected does not substantially affect the yield of physical particles as measured by RNA-dependent DNA polymerase activity and by (3H) uridine incorporation into viral RNA. However, the infectivity of the progeny virus, as measured by focus-forming ability, is decrreased 95 to 99% by R-82 treatment.

Animals↗
PubMed1975

The regulation of transcription in bacteriophage T5-infected Escherichia coli.

The expression of bacteriophage T5-specific RNA and protein in infected cells is temporally separated into three classes: class I (preearly), class II (early), and class III (late). By immunoprecipitation techniques we have shown that T5 infection of cells leads to the synthesis of one class I polypeptide (11,000 daltons) and two class II polypeptides (90,000 and 15,000 daltons) capable of binding to the RNA polymerase of the host Escherichia coli cell. One of the class II polypeptides (90,000 daltons) is the product of gene C2, which is an essential gene product required for the initiation of class III RNA synthesis. The colicinogenic factor, ColIb, is a plasmid which prevents the normal synthesis of class II and the III bacteriophage T5-specific RNA in infected colicinogenic (ColIb+) cells. In T5-infected colicinogenic cells, only the T5 class I polypeptide is found associated with the RNA polymerase. Mutants of T5, designated T5h minus, are capable of growth on both noncolicinogenic and ColIb+ hosts. Extracts of T5h minus infected ColIb+ cells were shown to lack a small class I polypeptide (12,000 daltons) as compared to T5-infected cells. The h minus mutation, however, has no effect on the levels of the class I T5 polypeptide of similar molecular weight which is bound to the RNA polymerase. One effect of the h minus mutation is to enhance the quantities of the two class II polypeptides bound to the enzyme.

Bacterial Proteins↗
PubMed1975

Purification and properties of a bacteriophage T5-modified form of Escherichia coli RNA polymerase.

A modified form of Escherichia coli RNA polymerase that contains one of the three T5-specific polypeptides known to interact with the host enzyme was purified from bacteriophage T5-infected cells. The properties of this T5-modified enzyme appeared identical to those of the RNA polymerase derived from uninfected non-colicinogenic cells and to a fully active enzyme isolated from T5-infected ColIb+ cells after the limited in vivo transcription of T5 genes allowed by the plasmid had ceased.

Coliphages↗
PubMed1972

Regulation of bacteriophage T5 development by ColI factors.

The I-type colicinogenic factor ColIb transforms Escherichia coli from a permissive to a nonpermissive host for bacteriophage T5 reproduction by preventing complete expression of the phage genome. T5-infected ColIb(+) cells synthesize only class I (early) phage protein and ribonucleic acid (RNA). Neither phage-specific class II proteins [associated with viral deoxyribonucleic acid (DNA) replication] nor class III proteins (phage structural components) are formed due to the failure of the infected ColIb(+) cells to synthesize class II or class III phage-specific messenger RNA. Comparable studies with T5-infected cells colicinogenic for the related ColIa factor revealed no decrease in the yield of progeny phage although the presence of the ColIa factor leads to a significant reduction in the amount of phage-directed class III protein synthesis.

Adenine↗