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Ventricle Wall (ventricle + wall)
Selected AbstractsElectrophysiological Basis and Genetics of Brugada SyndromeJOURNAL OF CARDIOVASCULAR ELECTROPHYSIOLOGY, Issue 2005AUGUSTUS O. GRANT M.B.Ch.B., Ph.D. Brugada syndrome is a primary arrhythmic syndrome arising in the structurally normal heart. Any proposed mechanism should account for the major features of the syndrome: localization of the ST segment and T-wave changes to the right precordial leads, association of conduction slowing at several levels, precipitation or aggravation of the major ECG changes by sodium channel-blocking drugs and the occurrence of ventricular fibrillation. Heterogeneity of repolarization across the ventricle wall plays a major role. Any agency that shifts the net current gradient during phase I outward would exaggerate the normal heterogeneity of repolarization and result in the ST segment and T-wave changes characteristic of the syndrome. When the outward current shift is marked, premature repolarization may occur in epicardial zone and the resulting gradient may precipitate reentry. The syndrome is inherited as an autosomal dominant. However, 75% of clinically affected individuals are males. In 20% of cases, the syndrome is associated with mutations of the cardiac sodium channel gene SCN5A. The mutations result in a loss-of-function as a result of the synthesis of a non-functional protein, altered protein trafficking, or change in gating. Agencies that reduce the sodium current may precipitate the characteristic ECG changes, for example, sodium channel blockers and membrane depolarization by hyperkalemia. Sympathetic stimulation may reverse the ECG changes and reduce arrhythmia recurrence. By its nonspecific potassium channel blocking action, quinidine may also reduce arrhythmia recurrence. We still do not know the basis for defect in the majority of patients with Brugada syndrome. [source] Estimation of Pump Flow Rate and Abnormal Condition of Implantable Rotary Blood Pumps During Long-Term In Vivo StudyARTIFICIAL ORGANS, Issue 4 2000K. Nakata Abstract: The control system for an implantable rotary blood pump is not clearly defined. A detection system is considered to be necessary for pump flow monitoring and abnormal conditions such as back flow or a sucking phenomenon where the septum or left ventricle wall is sucked into the cannula, etc. The ultrasound flowmeter is durable and reliable but the control system should not be totally dependent on the flowmeter. If the flowmeter breaks, the rotary blood pumps have no control mechanism. Therefore, the authors suggest controlling the pumps by an intrinsic parameter. One left ventricular assist device (LVAD) calf model was studied where the flow rate and waveform of the pump flow proved to identify the sucking phenomenon. Thus, the pump flow rate was calculated from the required power, motor speed, and heart rate. The value of the coefficient of determination (R2) between the measured and estimated pump flow rate was 0.796. To estimate this abnormal phenomenon, 2 methods were evaluated. One method was the total pressure head in which the pump flow rate and motor speed were estimated. During normal conditions the total pressure head is 79.5 ± 7.0 mm Hg whereas in the abnormal condition, it is 180.0 ± 2.8 mm Hg. There was a statistical difference (p < 0.01). Another method is using a current waveform. There is an association between the current and pump flow waves. The current was differentiated and squared to calculate the power of the differentiated current. The normal range of this value was 0.025 ± 0.029; the abnormal condition was 11.25 ± 15.13. There was a statistical difference (p < 0.01). The predicted flow estimation method and a sucking detection method were available from intrinsic parameters of the pump and need no sensors. These 2 methods are simple, yet effective and reliable control methods for a rotary blood pump. [source] Direct Stimulation of Adult Neural Stem Cells In Vitro and Neurogenesis In Vivo by Vascular Endothelial Growth FactorBRAIN PATHOLOGY, Issue 3 2004Anne Schänzer Hypoxia as well as global and focal ischemia are strong activators of neurogenesis in the adult mammalian central nervous system. Here we show that the hypoxia-inducible vascular endothelial growth factor (VEGF) and its receptor VEGFR-2/Flk-1 are expressed in clonally-derived adult rat neural stem cells in vitro. VEGF stimulated the expansion of neural stem cells whereas blockade of VEGFR-2/Flk-1-kinase activity reduced neural stem cell expansion. VEGF was also infused into the lateral ventricle to study changes in neurogenesis in the ventricle wall, olfactory bulb and hippocampus. Using a low dose (2.4 ng/d) to avoid endothelial proliferation and changes in vascular permeability, VEGF stimulated adult neurogenesis in vivo. After VEGF infusion, we observed reduced apoptosis but unaltered proliferation suggesting a survival promoting effect of VEGF in neural progenitor cells. Strong expression of VEGFR-2/Flk-1 was detected in the ventricle wall adjacent to the choroid plexus, a site of significant VEGF production, which suggests a paracrine function of endogenous VEGF on neural stem cells in vivo. We propose that VEGF acts as a trophic factor for neural stem cells in vitro and for sustained neurogenesis in the adult nervous system. These findings may have implications for the pathogenesis and therapy of neurodegenerative diseases. [source] Neurogenesis in explants from the walls of the lateral ventricle of adult bovine brain: role of endogenous IGF-1 as a survival factorEUROPEAN JOURNAL OF NEUROSCIENCE, Issue 2 2003M. Pérez-Martín Abstract Previous studies have shown the existence of proliferating cells in explants from bovine (Bos Taurus) lateral ventricle walls that were maintained for several days in vitro in the absence of serum and growth factors. In this study we have characterized the nature of new cells and have assessed whether the insulin-like growth factor-1 (IGF-1) receptor regulates their survival and/or proliferation. The explants were composed of the ependymal layer and attached subependymal cells. Ependymal cells in culture were labelled with glial markers (S-100, vimentin, GFAP, BLBP, 3A7 and 3CB2) and did not incorporate bromodeoxiuridine when this molecule was added to the culture media. Most subependymal cells were immunoreactive for ,III-tubulin, a neuronal marker, and did incorporate bromodeoxiuridine. Subependymal neurons displayed immunoreactivity for IGF-1 and its receptor and expressed IGF-1 mRNA, indicating that IGF-1 is produced in the explants and may act on new neurons. Addition to the culture media of an IGF-1 receptor antagonist, the peptide JB1, did not affect the incorporation of bromodeoxiuridine to proliferating subependymal cells. However, JB1 significantly increased the number of TUNEL positive cells in the subependymal zone, suggesting that IGF-1 receptor is involved in the survival of subependymal neurons. In conclusion, these findings indicate that neurogenesis is maintained in explants from the lateral cerebral ventricle of adult bovine brains and that IGF-1 is locally produced in the explants and may regulate the survival of the proliferating neurons. [source] | ||||||||||