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Biomedical subjects

R Klein

Publications and source records attributed to R Klein.

At least 883 records · Page 49Linked to original sources
PubMed1975

The activation of phospholipase C from Clostridium Welchii by quinine: an absolute requirement for calcium ions.

Quinine activates the hydrolysis of phosphatidyl choline suspensions by phospholipase C (E.C. 3.1.4.3) obtained from Clostridium welchii. Low levels of calcium are an absolute requirement for this activation: Mg2+, Ba2+, Sr2+, and Zn2+ are ineffective. The induction period, or lag phase for this enzyme is dependent upon both calcium concentration and substrate interfacial surface area. At low concentrations (less then 50 muM) calcium ions affect the induction period but not the maximal rate of hydrolysis, whereas guinine predominantly affects the rate of hydrolysis by alterations in the surface charge carried by the substrate.

Calcium↗
PubMed1975

Malaria, quinine and red cell lysis.

An hypothesis is presented to explain the red cell lysis which accompanies an acute malarial infection, as well as the mode of action of certain schizonticidal drugs in the quinoline and acridine series. Quinine and a number of other antimalarial drugs have been found to counteract the inhibition by protein of fatty acid-induced lysis, when tested in an in vitro system. It is suggested that these schizonticides exert their chemotherapeutic effect by inducing the premature lysis of the parasitized red cell, as a result of relieving the inhibition by protein of haemolysis.

Binding, Competitive↗
PubMed1975

Kinetics of murine type C virus-specific DNA synthesis newly infected cells.

Replicating transforming functions of Rauscher leukemia virus (RLV) and the RLV pseudotype of Moloney sarcoma virus in mouse embryo fibroblasts were found to be most sensitive to inhibition by cytosine arabinoside (ara-C) 30 to 90 min after infection. The initiation of intracellular RLV DNA synthesis was detected by nucleic acid hybridization within this time interval. Treatment of infected cells with cytosine arabinoside abolished RLV DNA synthesis. Peak synthesis of the DNA complementary to the infecting RLV genome, the (-) strand, occurred 40 to 60 min after infection. During this interval two s two species of DNA were observed with estimated molecular weights of 0.5 X 10(5) to 1.0 X 10(5) and 3 X 10(6). Peak synthesis of the (+) strand viral DNA occurred 50 to 70 min after infection. The initial species detected had a molecular weight of 1.5 X 10(5) to 4.0 X 10(5) which shifted as a function of time to 3 X 10(6). Both (+) strand species were initially detected in the cytoplasm followed by a rapid (10-min interval) appearance of the faster-sedimenting species in the nucleus. The virus-specific (-) and (+) strand DNA species are presumably unintegrated intermediates in provirus formation.

Cell Transformation, Neoplastic↗
PubMed1975

Methylmercury-cholinesterase interactions in rats.

The interaction of methylmercury hydroxide (MMH) and cholinesterases was studied in male and female rats. MMH administered subcutaneously in doses of 10 mg/kg for 2 days reduced the level of plasma cholinesterase (ButChE) by 68% in females and 47% in males while brain acetylcholinesterase (AChE) was unaffected. Normal females had higher but more variable ButChE levels than normal males. In a time-course experiment, a single dose of MMH (10 mg/kg) reduced ButChE levels when mercury levels reached 22 mug/ml in the blood. A 10% reduction in brain AChE was observed at 72 hours; however, mercury reached a concentration of only 2.0 mug/g in brain tissue. The determination of the Michaelis constant Km and maximum velocity value Vmax for butyrylcholine and ButChE in control and MMH-treated (1 mg/kg) animals indicated that MMH reduced Vmax only. Since no loss in ButChE activity occurred when MMH and control plasma were incubated in vitro, MMH is not a direct inhibitor of ButChE. Because only the inactive monomeric form of ButChE contains free sulfhydryl groups, it is postulated that MMH combines covalently with the sulfur, preventing formation of active enzyme. By analogy, it is believed this is also the case with AChE.

Animals↗
PubMed1975

Corneal arcus and cardiovascular disease in Evans County, Georgia.

The population of Evans County, Georgia was surveyed, during a cardiovascular disease study, for the prevalence of corneal arcus. Rates varied with race and sex and increased in prelalence with age in all groups. Arcus was positively correlated with serum cholesterol level. In white males, a significantly higher prevalence rate of coronary heart disease was found in those who had corneal arcues, but arcus was not correlated with subsequent coronary heart disease incidence in any race-sex group.

Adolescent↗
PubMed1975

The growth characteristics of the metastatic Wistar/Furth Wilms' tumor model.

Growth characteristics, metastatic spread, and survival times were evaluated in a transplantable Wistar/Furth rat Wilms' tumor model. Tumor suspensions of various tumor cell dosages were injected in an attempt to find the optimum level of tumor take. Lung metastases were frequent following tumor injection by all routes. However, tumor spread to the lungs was the least frequent following subcutaneous (SC) injection of the tumor. Survival time for the intramuscular (IM) group was statistically longer at all tumor dose levels. For the 1 X 10(5) tumor dosage, survival time ranged from a mean of 27 days for the intrarenal (IR) group to a mean 42 days for the IM group. For the 1 X 10(4) dosage, survival time ranged from a mean of 37 days for the intraperitoneal (IP) group to a mean of 51 days for the IM group. It is concluded that this animal tumor closely resembles the human Wilms' tumor, and that the point at which the transplanted tumor fails to be successfully transplanted is below the dosage level of 1 X 10(3) tumor cells.

Animals↗
PubMed1973

Mutants of nonproducer cell lines transformed by murine sarcoma viruses. I. Induction, isolation, particle production, and tumorigenicity.

A variety of cell mutants were obtained by a single 5'-bromodeoxyuridine (BrdU) treatment of an nonproducer (NP) cell line transformed by the Kirsten strain of murine sarcoma virus (Ki-MSV). Isolation procedures of these cell See PDF for Structure mutants are described. The cell mutants obtained were classified by tumorigenic potential and shedding of Type C virus particles. The cell mutants were classified into four groups: (A) tumorigenic, without particles; (B) tumorigenic, with Type C particles; (C) nontumorigenic, without particles; and (D) nontumorigenic, with Type C particles. The tumorigenic cell lines showed variability in morphology with both flat and typical transformed appearing cell lines showing equal transplantability.

Animals↗
PubMed1973

Mutants of nonproducer cell lines transformed by murine sarcoma virus. II. Relationship of tumorigenicity to presence of viral markers and rescuable sarcoma genome.

Tumorigenic and nontumorigenic mutants induced by a single 5'-bromodeoxyuridine (BrdU) treatment of a nonproducer (NP) tumorigenic cell line were isolated and characterized. Among the cloned derivatives were examples of virus-free and sarcoma virus-producing cell lines. Oncogenicity did not correlate with production of virus or ease of rescue of the sarcoma genome. All lines, including nononcogenic derivatives, retained the sarcoma genome. Phenotypic reversion of some cell mutants was observed after in vivo inoculation or long term in vitro cultivation. The M-50T cell line, obtained from a tumor induced by M-50 cells, had a sarcoma genome rescuable by direct superinfection; this was only achieved with parental M-50 cells by a cell fusion rescue technique. The M-43-2T cell, obtained from a single small static tumor induced by otherwise nononcogenic M-43-2 cells, shed sarcoma virus and became tumorigenic. M-58-4-48 became tumorigenic after passage 48 of the M-58-4 line, which was originally nontumorigenic. These observations of phenotypic reversion demonstrate that the presence of the sarcoma gene in cells is an essential but not sufficient condition of tumorigenesis.

Animals↗