An apparatus for concurrent measurement of thermoelectric material parameters.

We describe an apparatus which concurrently and independently measures the parameters determining thermoelectric material conversion efficiency: the Seebeck coefficient, thermal conductivity, and electrical resistivity. The apparatus is designed to characterize thermoelectric materials which are technologically relevant for waste heat energy conversion, and may operate from room temperature to 400 °C. It is configured so the heat flux is axially confined along two boron nitride rods of known thermal conductance. The Seebeck coefficient and thermal conductivity are obtained in steady-state using a differential technique, while the electrical resistivity is obtained using a four-point lock-in amplification method. Measurements on the newly developed NIST Seebeck standard reference material are presented in the temperature range from 50 °C to 250 °C.

Ischemic loss of sarcolemmal dystrophin and spectrin: correlation with myocardial injury.

Sarcolemmal blebbing and rupture are prominent features of irreversible ischemic myocardial injury. Dystrophin and spectrin are sarcolemmal structural proteins. Dystrophin links the transmembrane dystroglycan complex and extracellular laminin receptors to intracellular F-actin. Spectrin forms the backbone of the membrane skeleton conferring an elastic modulus to the sarcolemmal membrane. An ischemic loss of membrane dystrophin and spectrin, in ischemically pelleted rabbit cardiomyocytes or in vivo 30--45 min permanently ischemic, LAD-ligated hearts, was detected by immunofluorescence with monoclonal antibodies. Western blots of light and heavy microsomal vesicles and Triton-extracted membrane fractions from ischemic myocytes demonstrated a rapid loss of dystrophin coincident with sub-sarcolemmal bleb formation, subsequent to a hypotonic challenge. The loss of spectrin from purified sarcolemma of autolysed rabbit heart, and both isolated membrane vesicles and Triton solubilized membrane fractions of ischemic cardiomyocytes correlated linearly with the onset of osmotic fragility as assessed by membrane rupture, subsequent to a hypotonic challenge. In contrast to the ischemic loss of dystrophin and spectrin from the membrane, the dystrophin-associated proteins, alpha-sarcoglycan and beta-dystroglycan and the integral membrane protein, sodium-calcium exchanger, were maintained in the membrane fraction of ischemic cells as compared to oxygenated cells. Preconditioning protected cells, but did not significantly alter ischemic dystrophin or spectrin translocation. This previously unrecognized loss of sarcolemmal dystrophin and spectrin may be the molecular basis for sub-sarcolemmal bleb formation and membrane fragility during the transition from reversible to irreversible ischemic myocardial injury.

Deficient motor synchrony in schizophrenic disorders: clinical correlates.

A laboratory measure of synchronization was used to assess the differential ability of schizophrenics, affectives, and normal controls to take advantage of stimulus predictability. It was hypothesized that (1) schizophrenics will perform on this task in a way that distinguishes them from other groups, (2) clinically observed motor anomalies will be associated with deficient motor synchrony, and (3) deficient motor synchrony will be associated with more severe clinical ratings of thought disorder. Twenty-one schizophrenic, 8 affective, and 16 normal controls were studied. The results were consistent with the hypotheses; schizophrenic subjects had distinctive performance patterns, especially at 40 bpm, which was associated with both motor and thinking disturbance. The authors discuss additional analyses that suggest that deficient motor synchrony is associated with negative symptoms, certain ward behaviors, and not with demographic variables, and that among unmedicated schizophrenic subjects, the performance patterns are worse.