6,898 research outputs found

    Recovery of the critically endangered river pipefish, Syngnathus watermeyeri, in the Kariega Estuary, Eastern Cape province

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    An intensive ichthyofaunal survey in the permanently open Kariega Estuary along the Eastern Cape coast has identified a breeding population of the critically endangered river pipefish, Syngnathus watermeyeri, within the middle and upper reaches of the system. This is the first recorded capture of this species in the estuary for over four decades. We suggest that the presence of S. watermeyeri is the result of the heavy rainfall within the region, which contributed to the establishment of optimum habitat requirements (mesohaline conditions and increased food availability) of the pipefish

    Newly identified NO-sensor guanylyl cyclase/connexin 43 association is involved in cardiac electrical function

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    Background: Guanylyl cyclase, a heme-containing alpha 1 beta 1 heterodimer (GC1), produces cGMP in response to Nitric oxide (NO) stimulation. The NO-GC1-cGMP pathway negatively regulates cardiomyocyte contractility and protects against cardiac hypertrophy-related remodeling. We recently reported that the beta 1 subunit of GC1 is detected at the intercalated disc with connexin 43 (Cx43). Cx43 forms gap junctions (GJs) at the intercalated disc that are responsible for electrical propagation. We sought to determine whether there is a functional association between GC1 and Cx43 and its role in cardiac homeostasis. Methods and Results: GC1 and Cx43 immunostaining at the intercalated disc and coimmunoprecipitation from membrane fraction indicate that GC1 and Cx43 are associated. Mice lacking the alpha subunit of GC1 (GC alpha 1 knockout mice) displayed a significant decrease in GJ function (dye-spread assay) and Cx43 membrane lateralization. In a cardiac-hypertrophic model, angiotensin II treatment disrupted the GC1-Cx43 association and induced significant Cx43 membrane lateralization, which was exacerbated in GC alpha 1 knockout mice. Cx43 lateralization correlated with decreased Cx43-containing GJs at the intercalated disc, predictors of electrical dysfunction. Accordingly, an ECG revealed that angiotensin II-treated GCa1 knockout mice had impaired ventricular electrical propagation. The phosphorylation level of Cx43 at serine 365, a protein-kinase A upregulated site involved in trafficking/assembly of GJs, was decreased in these models. Conclusions: GC1 modulates ventricular Cx43 location, hence GJ function, and partially protects from electrical dysfunction in an angiotensin II hypertrophy model. Disruption of the NO-cGMP pathway is associated with cardiac electrical disturbance and abnormal Cx43 phosphorylation. This previously unknown NO/Cx43 signaling could be a protective mechanism against stress-induced arrhythmia

    Parameter Identification Methods in a Model of the Cardiovascular System

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    To be clinically relevant, mathematical models have to be patient-specific, meaning that their parameters have to be identified from patient data. To achieve real time monitoring, it is important to select the best parameter identification method, in terms of speed, efficiency and reliability. This work presents a comparison of seven parameter identification methods applied to a lumped-parameter cardiovascular system model. The seven methods are tested using in silico and experimental reference data. To do so, precise formulae for initial parameter values first had to be developed. The test results indicate that the trust-region reflective method seems to be the best method for the present model. This method (and the proportional method) are able to perform parameter identification in two to three minutes, and will thus benefit cardiac and vascular monitoring applications
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