28 research outputs found

    Regulation of Coronary Blood Flow

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    The heart is uniquely responsible for providing its own blood supply through the coronary circulation. Regulation of coronary blood flow is quite complex and, after over 100 years of dedicated research, is understood to be dictated through multiple mechanisms that include extravascular compressive forces (tissue pressure), coronary perfusion pressure, myogenic, local metabolic, endothelial as well as neural and hormonal influences. While each of these determinants can have profound influence over myocardial perfusion, largely through effects on end-effector ion channels, these mechanisms collectively modulate coronary vascular resistance and act to ensure that the myocardial requirements for oxygen and substrates are adequately provided by the coronary circulation. The purpose of this series of Comprehensive Physiology is to highlight current knowledge regarding the physiologic regulation of coronary blood flow, with emphasis on functional anatomy and the interplay between the physical and biological determinants of myocardial oxygen delivery. Ā© 2017 American Physiological Society. Compr Physiol 7:321-382, 2017

    The Truman Presidency

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    Truman and the broadcaster

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    Using Environmental Modification and Teacher Mediation to Increase Literacy Behaviors in Inclusive Preschool Settings

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    It is considered a recommended practice to integrate literacy concepts into child-initiated choice center time long before formal reading instruction begins. The purpose of this study was to determine whether environmental modification and a teacher-mediated literacy intervention would increase child engagement of literacy behaviors during free choice time in the classroom. Data were collected on the literacy behaviors of 9 children across 3 inclusive preschool classrooms in a suburban public school system. A multiple baseline design was used to determine the effects of an environmental modification using the Early Language and Literacy Classroom Observation and a teacher-mediated intervention on children\u27s literacy behaviors. Results included an average increase of 43 percentage points (range = 39ā€“45 percentage points) in observed literacy behaviors in each of the 3 classrooms. Individual children in each classroom demonstrated an increase in literacy behaviors from baseline to intervention. These results are consistent with previous research, which indicated that the modification of the environment and teacher mediation increase literacy behaviors

    Platelet receptor polymorphisms do not influence Staphylococcus aureusā€“platelet interactions or infective endocarditis

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    Cardiac vegetations result from bacteriumā€“platelet adherence, activation and aggregation, and are associated with increased morbidity and mortality in infective endocarditis. The GPIIb/IIIa and FcĪ³RIIa platelet receptors play a central role in platelet adhesion, activation and aggregation induced by endocarditis pathogens such as Staphylococcus aureus, but the influence of known polymorphisms of these receptors on the pathogenesis of infective endocarditis is unknown. We determined the GPIIIa platelet antigen PlA1/A2 and FcĪ³RIIa H131R genotype of healthy volunteers (nĀ =Ā 160) and patients with infective endocarditis (nĀ =Ā 40), and investigated the influence of these polymorphisms on clinical outcome in infective endocarditis and S. aureusā€“platelet interactions in vitro. Platelet receptor genotype did not correlate with development of infective endocarditis, vegetation characteristics on echocardiogram or the composite clinical end-point of embolism, heart failure, need for surgery or mortality (PĀ >Ā 0.05 for all), even though patients with the GPIIIa PlA1/A1 genotype had increased in vivo platelet activation (PĀ =Ā 0.001). Furthermore, neither GPIIIa PlA1/A2 nor FcĪ³RIIa H131R genotype influenced S. aureus-induced platelet adhesion, activation or aggregation in vitro (PĀ >Ā 0.05). Taken together, our data suggest that the GPIIIa and FcĪ³RIIa platelet receptor polymorphisms do not influence S. aureusā€“platelet interactions in vitro or the clinical course of infective endocarditis
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