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Biomedical subjects

J W Harris

Publications and source records attributed to J W Harris.

At least 127 records · Page 7Linked to original sources
PubMed1975

DIP and DIP+2 as glutathione oxidants and radiation sensitizers in cultured Chinese hamster cells.

Two diamide analogues, diazene dicarboxylic acid bis (n'-methylpiperazide) or DIP, and its bis-N'-methyl iodide salt, or DIP + 2, were tested for their ability to penetrate cultured Chinese hamster cells and oxidize intracellular glutathione. DIP penetrated the cells at a reasonable rate at 18 degrees C, 160 nmoles being required to oxidize the endogenous glutathione of 2 X 10(6) cells, but it penetrated very slowly at 0 degrees C. DIP +2 did not effectively oxidize glutathione in Chinese hamster cells, possibly because it did not enter the cells. DIP became toxic after about 10 min of exposure, but its toxicity could be moderated by using anoxic conditions. DIP, but not DIP +2, sensitized anoxic Chinese hamster cells to X-radiation by a factor of 1-5, an effect that was due entirely to removal of the shoulder from the survival curve.

Azo Compounds↗
PubMed1975

Demonstration of lag phase in the sol-gel transformation of deoxygenated S hemoglobin without temperature alteration.

1). During the sol to gel transformation of deoxygenated sickle hemoglobin, a time-dependent process preceding gel formation (lag phase) was demonstrated that was inversely proportional to a function of the hemoglobin concentration and that occurred without alteration in temperature, pH, or oxygen tension. 2). As determined by the Schachman modification of the capillary viscometer, preparations of oxyhemoglobin S and A and deoxyhemoglobin A were indistinguishable when compared over a wide range of concentrations. Up to the concentration at which gelling occurred, deoxyhemoglobin S exhibited the same viscosity behavior. The viscosity of deoxygenated hemoglobin S within the lower gelling concentration range was normal during the lag phase and became abnormally high only at the time of gelation.

Anemia, Sickle Cell↗
PubMed1975

The kinetics of the sol-gel transformation of deoxyhemoglobin S by continuous monitoring of viscosity.

By continuous monitoring of viscosity during the sol-gel transformation of deoxygenated sickle hemoglobin a time: viscosity profile has been demonstrated that can be subdivided into: (1) initial lag phase, (2) gradual and minor increase in viscosity, (3) rapid and major (180 times initial value) increase in viscosity, (4) moderately rapid decrease in viscosity, and (5) achievement of equilibrium at approximately 50 per cent of maximum viscosity increase. The duration of the lag phase, rate of increase in viscosity, and maximum change are greatly influenced by hemoglobin concentration and markedly altered by temperature. Admixtures of hemoglobins A and F lengthen the lag phase and attenuate the rate of increase and magnitude of viscosity change according to proportions added and capacity to interact with deoxyhemoglobin S, but the general configuration of the curve is maintained. A different time: viscosity profile is obtained for mixtures of S and C hemoglobin that is lacking the phase with decreasing viscosity. Relevance to the pathophysiology of the sickling phenomenon is evidence because the quantitative and qualitative changes induced by variations in concentration of deoxygenated hemoglobin S, temperature, amount and type of admixed hemoglobin (A, C, and F), ionic strength, and 2, 3-DPG are in agreement with their known effects upon the sickling of intact cells and upon the minimum gelling point of deoxyhemoglobin S. No final conclusions can be drawn concerning the extent or form of hemoglobin aggregation present in the various phases of the time: viscosity profile; however, the technique lends itself readily to obtaining samples at various points along the curve for additional studies such as electron microscopy and light scattering.

Blood Viscosity↗
PubMed1975

The role of adenosine triphosphate, chalones, and specific proteins in controlling tumor growth fraction.

During growth of Ehrlich ascites tumor cells in vivo, the proportion of cells in the S phase of the proliferative cell cycle decreases in a manner analogous to the decreasing growth fraction often associated with the growth of solid tumors. An examination of biochemical parameters that might regulate the growth fraction of Ehrlich ascites tumors by causing accumulation of cells in G1-G0 shows that (a) the tumor progresses from an aerobic to an anerobic state as it approaches the plateau phase of growth, as indicated by lactate dehydrogenase content, but cellular adenosine triphosphate content remains constant; (b) tumor-specific growth inhibitors (chalones) are not detectable in cell-free ascites fluid from plateau-phase tumors; (c) electrophoretically identifiable soluble proteins isolated from tumor cells that have been exposed to labeled amino acids in vivo are qualitatively identical during early and late tumor growth; and (d) ornithine decarboxylase activity increases in a bimodal fashion in the first 10 hr after transplantation of 10(7) cells and then declines rapidly during the first few days of growth. The second (and larger) of the two ornithine decarboxylase increases coincides with the surge of cells from G1-G0 into S phase, suggesting that this enzyme, or the polyamines that it synthesizes, may play a role in controlling the growth fraction of this cell population.

Adenosine Triphosphate↗