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AB - Evidence accumulating from other cell systems suggests that fibronectin, if present in the heart, might modulate patterns of cell organization during myocardial development. Accordingly, we examined hearts of fetal, neonatal and adult rats for the presence and distribution of fibronectin, and quantitatively measured fibronectin synthesis by cultured cardiac myocytes and mesenchymal cells to assess the relative importance of these potential intracardiac sources of this glycoprotein. Fibronectin was present in the hearts from all age groups and was distributed in a reticular pattern suggesting a pericellular or interstitial location. In fetal hearts, specific immuno-fluorescence was particularly prominent at the crest of the developing interventricular septum. In post-confluent cardiac mesenchymal cultures, a dense fibrillar network of fibronectin formed over the surface of the cells. The content of fibronectin in the culture medium assessed by enzyme-linked immunosorbent assay increased substantially at confluence from 2 to 17 mg/dish, stabilizing at 11 mg in post-confluent mesenchymal cultures. In myocytic cultures, fibronectin formed a fine reticular pattern over cell surfaces and the fibronectin content of the medium ranged from 0.8 to 2.1 mg. Thus, fibronectin is present in the heart, may be synthesized in the neonate predominantly by cardiac mesenchymal cells, and may contribute by mechanisms still to be characterized in vivo to normal development of the critical septal region during embryogenesis.

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T1 - Hypertension, aging, and myocardial synthesis of heat-shock protein 72

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Many but not all SRs on the comparative effectiveness of health interventions include a quantitative synthesis (meta-analysis) of the findings of RCTs. Whether or not a quantitative or qualitative synthesis is planned, the assessment of what is known about an intervention’s effectiveness should begin with a clear and systematic description of the included studies (CRD, 2009; Deeks et al., 2008). This requires extracting both qualitative and quantitative data from each study, then summarizing the details on each study’s methods, participants, setting, context, interventions, outcomes, results, publications, and investigators. Data extraction refers to the process that researchers use to collect and transcribe the data from each individual study. Which data are extracted depends on the research question, types of data that are available, and whether meta-analysis is appropriate. lists the types of data that are often collected.

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Goldsmith, M. R., C. R. Bankhead, and J. Austoker. 2007. Synthesising quantitative and qualitative research in evidence-based patient information. Journal of Epidemiology & Community Health 61(3):262–270.

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These date show that in the intact heart the unidirectional rate of ATP synthesis exceeds the net rate of ATP synthesis and consumption by approximately a factor of 2.

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N2 - The effects of ischemia on mitochondrial function and the unidirectional rate of ATP synthesis (P(i) → ATP rate) were studied using a Langendorff-perfused heart preparation and 31P NMR spectroscopy. There was significant postischemic depression of mechanical function assessed as the heart rate pressure product, and the myocardial oxygen consumption rate at a given rate pressure product was elevated. Experiments performed on glucose- and pyruvate-perfused hearts demonstrated the presence of a large contribution to the unidirectional P(i) → ATP rate catalyzed by glyceraldehyde-3-phosphate dehydrogenase and phosphoglycerate kinase. This rate was much greater than the maximal glucose utilization rate in the myocardium, demonstrating that the glyceraldehyde-3-phosphate dehydrogenase/phosphoglycerate kinase reactions are near equilibrium both before and after ischemia. In the pyruvate-perfused postischemic hearts, the glycolytic contribution was eliminated and the net rate of ATP synthesis by oxidative phosphorylation was measurable. Despite the reduced mechanical function and increased myocardial oxygen consumption rate, the ratio of the net rate of ATP synthesis by oxidative phosphorylation to oxygen consumption rate (the P:O ratio) was not altered subsequent to ischemia (2.34 ± 0.12 and 2.36 ± 0.09 in normal and postischemic hearts, respectively). Therefore, mitochondrial uncoupling cannot be the cause of postischemic depression in mechanical function; instead, the data suggest the existence of ischemia-induced inefficiency in ATP utilization.

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The effects of ischemia on mitochondrial function and the unidirectional rate of ATP synthesis (P(i) → ATP rate) were studied using a Langendorff-perfused heart preparation and 31P NMR spectroscopy. There was significant postischemic depression of mechanical function assessed as the heart rate pressure product, and the myocardial oxygen consumption rate at a given rate pressure product was elevated. Experiments performed on glucose- and pyruvate-perfused hearts demonstrated the presence of a large contribution to the unidirectional P(i) → ATP rate catalyzed by glyceraldehyde-3-phosphate dehydrogenase and phosphoglycerate kinase. This rate was much greater than the maximal glucose utilization rate in the myocardium, demonstrating that the glyceraldehyde-3-phosphate dehydrogenase/phosphoglycerate kinase reactions are near equilibrium both before and after ischemia. In the pyruvate-perfused postischemic hearts, the glycolytic contribution was eliminated and the net rate of ATP synthesis by oxidative phosphorylation was measurable. Despite the reduced mechanical function and increased myocardial oxygen consumption rate, the ratio of the net rate of ATP synthesis by oxidative phosphorylation to oxygen consumption rate (the P:O ratio) was not altered subsequent to ischemia (2.34 ± 0.12 and 2.36 ± 0.09 in normal and postischemic hearts, respectively). Therefore, mitochondrial uncoupling cannot be the cause of postischemic depression in mechanical function; instead, the data suggest the existence of ischemia-induced inefficiency in ATP utilization.