Chronic schizophrenia, lymphocyte growth, and nailfold plexus visualization score.
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Biomedical subjects
Publications and source records attributed to L F Jarvik.
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A newly developed technique for quantitating the locomotion of polymorphonuclear leukocyte (PMN) populations in temperature gradients has revealed that PMNs accumulate toward higher temperatures. The experiments yield measurements of the numbers of cells that adhere to glass and migrate from a cell suspension through a liquid/gel meniscus into a glass/agarose interface, and of their spatial distribution at subsequent time intervals. Cell locomotion was investigated as a function of the magnitude, sign, and temporal variation of the temperature gradient, the cell concentration in the source suspension, and the presence or absence of chemoattractant gradients. It was found (1) that a temperature gradient stimulates crossing of the meniscus toward higher temperatures, (2) that only a portion of the cells reverses direction of locomotion in response to reversal of the temperature gradient after the cells have traversed the meniscus, and (3) that the distribution of cells in the migration space depends on cell concentration, suggesting that the dynamics of PMN locomotion depend on cell-cell interactions.
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The role of microtubules in the philothermal response of polymorphonuclear leukocytes (PMNs) was examined using colchicine, a known microtubule disrupting agent. Colchicine inhibited PMN migration in a dose dependent fashion. Spatial distribution analysis of the responding cell population revealed a preferential inhibition of distal cell migration, a pattern similar to that found for PMNs obtained from patients with dementia of the Alzheimer type (DAT). The result is consistent with the known role of microtubules in directed cell migration and the hypothesized microtubular defect in DAT. Further investigations of microtubules may provide insight into the etiology and pathogenesis of DAT.
This comprehensive review of the literature on Aging and the Neurobiology of Depression points to what may be the most important lesson we have to learn these days. It shows us how after expending scientific efforts, funds and other resources for over two decades on premier quality research by highly qualified investigators we can still remain ignorant of the Neurobiology of Depression, to say nothing of the effects of Aging either superimposed or interactive.
Potassium (K+) channel dysfunction in fibroblasts was recently proposed as a potential diagnostic marker for Alzheimer disease (AD). We utilized a microspectrofluorometric method with Fura-2AM to measure intracellular free calcium ([Ca2+]i) following depolarization with the K+ channel blocker tetraethylammonium (TEA) in seven AD and seven control fibroblast cultures. Contrary to our expectation, 43% of the AD and 36% of the control fibroblast plated coverglasses responded with an increase in [Ca2+]i on addition of 100 mM TEA. The data suggest that the TEA-elicited [Ca2+]i response is not a useful AD screening test.