Intravenous hydroxyzine HCl and meperidine HCl in periodontal surgery: clinical judgments and patient impressions.
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Biomedical subjects
Publications and source records attributed to J W Clark.
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Neurons of the mammalian medullary respiratory center have complex patterns of electrophysiological behavior. Three typical phenomena associated with these patterns are spike frequency adaptation (SFA), delayed excitation (DE), and postinhibitory rebound (PIR). Although several nuclei are associated with the medullary-pontine respiratory center, we focused on neurons from two nuclei: (1) the ventral subnucleus of the nucleus tractus solitarius (vNTS) of the dorsal respiratory group and (2) the nucleus ambiguus (NA) of the ventral respiratory group. We developed a Hodgkin-Huxley (HH) type model of the typical medullary neuron that is capable of mimicking the discharge pattern of real neurons to a very high degree. Closer examination of typical data revealed, however, that there was not one type of medullary respiratory neuron, but at least three (types A, B1, and B2). We classified these neurons based on the electrophysiologic phenomena that they exhibited (type A exhibits DE but not PIR; types B1 and B2 exhibit PIR but not DE; all types are adapting). Our objective was to relate each of these well-known phenomena to specific ionic current mechanisms. In the model, three currents directly affect the phenomena investigated: the Ca2+-activated K+ current, I(K,Ca), controls peak and steady-state firing rates and the time constant of adaptation; the transient outward K+ current, I(A), is responsible for all aspects of DE, including the dependence of delay on the magnitude and duration of conditioning hyperpolarization; and the hyperpolarization-activated current, Ih, elicits PIR and dictates its dependencies. We consider that our HH model represents a unifying structure, whereby different electrophysiological phenomena or discharge patterns can be emulated using different strengths of the component ionic membrane currents (particularly I(K,Ca), I(A), and Ih). Moreover, its predictions suggest that the electrophysiological characteristics of medullary respiratory neurons, from different areas of the brainstem and even from different species, can be modeled using the same structural framework, wherein the specific properties of individual neurons are emulated by adjusting the strengths of key ionic membrane currents in the model.
We have developed a mathematical model of the human atria myocyte based on averaged voltage-clamp data recorded from isolated single myocytes. Our model consists of a Hodgkin-Huxley-type equivalent circuit for the sarcolemma, coupled with a fluid compartment model, which accounts for changes in ionic concentrations in the cytoplasm as well as in the sarcoplasmic reticulum. This formulation can reconstruct action potential data that are representative of recordings from a majority of human atrial cells in our laboratory and therefore provides a biophysically based account of the underlying ionic currents. This work is based in part on a previous model of the rabbit atrial myocyte published by our group and was motivated by differences in some of the repolarizing currents between human and rabbit atrium. We have therefore given particular attention to the sustained outward K+ current (I[sus]), which putatively has a prominent role in determining the duration of the human atrial action potential. Our results demonstrate that the action potential shape during the peak and plateau phases is determined primarily by transient outward K+ current, I(sus) and L-type Ca2+ current (I[Ca,L]) and that the role of I(sus) in the human atrial action potential can be modulated by the baseline sizes of I(Ca,L), I(sus) and the rapid delayed rectifier K+ current. As a result, our simulations suggest that the functional role of I(sus) can depend on the physiological/disease state of the cell.
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This case describes a young, healthy, white female who demonstrated anterior alveolar bone loss along with premature loss of her primary incisors. The alveolar bone loss remains unexplained. The root surfaces of most of the primary anterior teeth exhibited one or more eroded areas devoid of cementum with some evidence in two teeth of cellular resorptive activity. These findings suggest that premature root resorption was occurring concurrently with unexplained extensive alveolar bone loss. The child will be examined periodically to determine whether this process of bone loss with subsequent tooth loss will involve additional primary or permanent teeth.
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