Acetylcholine-induced conductance fluctuations in cultured human myotubes.
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Biomedical subjects
Publications and source records attributed to J Rice.
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Nine cultures of fibroblast cell types and 13 epithelial-like cell types were maintained for 1 week in media supplemented with L-asborbic acid (50 microgram per ml). All fibroblast-like cultures produced extracellular fibers that stained positively by a silver-impregnation reticulin stain. Nine of the 13 epithelial-like cultures produced fibers that stained positively for reticulin. Nearly all cultures not supplemented with ascorbic acid showed no fiber staining. Those few lines that stained positively for reticulin in the absence of ascorbic-acid supplementation demonstrated only slight reticulin formation. Reticulin from one fibroblast culture and one epithelial culture was examined by electron microscopy, and the silver-impregnated fibrils were morphologically identical to collagen. The reticulin was digestible with collagenase, providing further evidence that the silver-impregnation reticulin stain identifies collagen in culture. The demonstartion of collagen can be performed easily in histology laboratories using Formalin-fixed cells, and provides a means of assaying a functional property of cells in culture which is characteristic of connective tissue fibroblasts in general as well as certain specialized epithelia.
General expression for the distribution of identity by descent (IBD) scores at a marker locus have been derived given neither, one or both sibs affected with a disorder determined by a linked trait locus with arbitrary gene frequency and penetrance vector. It is shown that the distirbution of IBD scores depends only on the additive and dominance variances and the population prevalence of the disorder. A one-sided test is suggested as an appropriate means of statistically testing the hypothesis that the recombination fraction is significantly less than 1/2. This sib pair approach is designed primarily to detect the presence of a critical disease susceptibility locus but when the assumptions of the incompletely penetrant single locus model are correct the methodology proposed here results in consistent estimates of the recombination fraction. The affected sib pair methodology seems especially suited to traits determined by single loci with non-Mendelian transmission.
Two hundred fourteen survivors of single aortic (AVR) or mitral valve replacement (MVR) were evaluated. The present model of the Smeloff-Cutter prosthesis was used in these patients, and the series was started in September, 1966, following the last structural change in the valve. Clinical follow-up ended in September, 1976. Bleeding, thromboembolism, and peristent left ventricular dysfunction were the major complications. Thromboembolism occurred at a rate of 0.13 percent per month of patient follow-up. Late deaths occurred in 19.2 percent of patients, half of these within the first year. Acturarial data indicated a 5 year survival rate of approximately 75 percent after both mitral and aortic replacements. Bleeding and thromboembolism were more frequent causes of death after mitral replacement. Myocardial function was of greatest importance in long-term survival after replacement of either valve. Variations in warfarin dosage significantly affected both bleeding and thromboembolic complications.
A general linear model of familial resemblance is described which allows for cultural transmission from parent to offspring, polygenic inheritance, phenotypic assortative mating, common environment, maternal and paternal effects, and threshold effects. Three special cases are described in detail which are particularly useful when data are only available about a few classes of relatives reared in intact families. The cultural model, the polygenic model, and the pseudopolygenic model share the common feature that all factors which are transmitted from parent to offspring may be represented by one parameter without any loss of information. We introduce a new model, termed the unitary model, which includes these models and is appropriate when combined genetic and cultural transmission is present and when data are available only for individuals reared in intact nuclear families. The basic properties of these models are explored using path analysis and computer simulation, including description of the relationship between parameters under random and assortative mating, rate of approach to equilibrium, and constraints on the magnitude of the parameters. General formulae for familial resemblance in extended pedigrees are given for any ancestor or descendant of either vertical or collateral relatives. Estimation procedures are described and a FORTRAN program TAU, available upon request, is used to provide maximum likelihood estimates of the parameters from reported correlations. A powerful test for detecting the presence of cultural transmission is suggested and applied to simulated data and to data sets reported by others for human stature, for which cultural transmission is suggested. In addition, it is shown that there is no need to postulate dominance to account for available data about height.
Antibody against acetylcholine receptor induces an increase in the rate of degradation of acetylcholine receptors on a mouse cell line (BC(3)H-1) and cultured rat skeletal muscle. The increased rate of degradation results in a lowered density of acetylcholine receptors on muscle membrane and a lowered sensitivity to iontophoretically applied acetylcholine. The modulation of acetylcholine receptor is energy, temperature, and time dependent and may be related to antigenic modulation found in other systems. Acetylcholine noise analysis demonstrates that antibody against acetylcholine receptor reduces the channel mean conductance and mean open time slightly. It is concluded that antibody binds to the acetylcholine receptor, impairs its function, and induces receptor degradation. This results in a lowered density of acetylcholine receptor and a lowered sensitivity to acetylcholine. Patients with myasthenia gravis have antibodies to their acetylcholine receptor in their serum. Antigenic modulation of receptor in the muscle of patients with myasthenia gravis could contribute to the observed decrease in amplitudes of miniature endplate potentials and in muscle acetylcholine sensitivity, and the symptoms of muscular weakness.
Feed medication with monensin caused delays in development of immunity in two floor-pen experiments which simulated commercial broiler production. Development of immunity was retarded with the higher level of monensin (120 p.p.m.) but was progressively less delayed as the monensin level was decreased (100, 60 or 0 p.p.m.). Delay was greatest with Eimeria tenella, but also occured with intestinal species including E. acervulina, E. brunetti, E. maxima, E. mivati, and E. necatrix. Drug withdrawal permitted earlier development of immunity. Plans involving use of monensin on layer replacements which later will be maintained on the floor without medication should consider: 1) prevalence of infective oocyst exposure in the area, 2) the lowest possible level of drug required for protection, and 3) its use for the shortest possible period of time.
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A nuclease-resistant complex of polyriboinosinic-polyribocytidylic acid containing poly-L-lysine and carboxymethylcellulose was used as prophylactic treatment of simian hemorrhagic fever in rhesus monkeys. This infection has proven uniformly fatal to more than 50 monkeys. Treatment 8 hr before infection and repeatedly thereafter completely prevented the development of viremia and death. Untreated animals died before development of antibodies to the virus. None of the treated animals developed antibody to the virus, a fact which suggested that viral growth was essentially completely blocked by the compound.
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A comlex of polyriboinosinic-polyribocytidylic acid (poly I-poly C) with poly-L-lysine and carboxymethylcellulose has been prepared. This complex is five to 10 times as resistant to hydrolysis by primate serum as the parent poly I-poly C. It has a thermal denaturation temperature about 40 C higher than that of poly I-poly C. The complex induces significant levels of serum interferon in monkeys and chimpanzees under conditions in which poly I-poly C itself induces no interferon.
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