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Cardiac Ventricle (cardiac + ventricle)
Selected AbstractsPromoter analysis of ventricular myosin heavy chain (vmhc) in zebrafish embryosDEVELOPMENTAL DYNAMICS, Issue 7 2009Daqing Jin Abstract In zebrafish, ventricular myosin heavy chain (vmhc) gene is initially expressed at the anterior lateral mesoderm and thereafter its expression is restricted to the cardiac ventricle. The transcriptional control mechanisms in regulating chamber-specific expression of myosin heavy chains are not well defined. We isolated and analyzed zebrafish vmhc upstream region to examine the spatial and temporal regulation of vmhc using transgenic and transient expression techniques. Promoter deletion analyses defined a basal promoter region sufficient to drive vmhc expression in the ventricle and an upstream fragment necessary for repressing ectopic vmhc expression in the atrium. The transcriptional mechanism that prevents vmhc expression in the atrium is mediated through Nkx2.5 binding elements (NKE). We have further discovered that paired-related homeobox transcriptional factor 2 (Prx2/S8)-like binding elements are required for promoting vmhc expression, and Prrx1b, a Prx-related homeobox protein, participates in the regulation of vmhc expression with other transcriptional factors. Developmental Dynamics 238:1760,1767, 2009. © 2009 Wiley-Liss, Inc. [source] Zebrafish IRX1b in the embryonic cardiac ventricle,DEVELOPMENTAL DYNAMICS, Issue 4 2004Elaine M. Joseph Abstract The synchronous contraction of the vertebrate heart requires a conduction system. While coordinated contraction of the cardiac chambers is observed in zebrafish larvae, no histological evidence yet has been found for the existence of a cardiac conduction system in this tractable teleost. The homeodomain transcription factor gene IRX1 has been shown in the mouse embryo to be a marker of cells that give rise to the distinctive cardiac ventricular conduction system. Here, I demonstrate that zebrafish IRX1b is expressed in a restricted subset of ventricular myocytes within the embryonic zebrafish heart. IRX1b expression occurs as the electrical maturation of the heart is taking place, in a location analogous to the initial expression domain of mouse IRX1. The gene expression pattern of IRX1b is altered in silent heart genetic mutant embryos and in embryos treated with the endothelin receptor antagonist bosentan. Furthermore, injection of a morpholino oligonucleotide targeted to block IRX1b translation slows the heart rate. Developmental Dynamics 231:720,726, 2004. © 2004 Wiley-Liss, Inc. [source] Histochemical evidence of osteoclastic degradation of extracellular matrix in osteolytic metastasis originating from human lung small carcinoma (SBC-5) cellsMICROSCOPY RESEARCH AND TECHNIQUE, Issue 2 2006Minqi Li Abstract The aim of this study was to assess the dynamics of osteoclast migration and the degradation of unmineralized extracellular matrix in an osteolytic metastasis by examining a well-standardized lung cancer metastasis model of nude mice. SBC-5 human lung small carcinoma cells were injected into the left cardiac ventricle of 6-week-old BALB/c nu/nu mice under anesthesia. At 25,30 days after injection, the animals were sacrificed and their femora and/or tibiae were removed for histochemical analyses. Metastatic lesions were shown to occupy a considerable area extending from the metaphyses to the bone marrow region. Tartrate resistant acid phosphatase (TRAPase)-positive osteoclasts were found in association with an alkaline phosphatase (ALPase)-positive osteoblastic layer lining the bone surface, but could also be localized in the ALPase-negative stromal tissues that border the tumor nodules. These stromal tissues were markedly positive for osteopontin, and contained a significant number of TRAPase-positive osteoclasts expressing immunoreactivity for CD44. We thus speculated that, mediating its affinity for CD44, osteopontin may serve to facilitate osteoclastic migration after their formation associated with ALPase-positive osteoblasts. We next examined the localization of cathepsin K and matrix metallo-proteinase-9 (MMP-9) in osteoclasts. Osteoclasts adjacent to the bone surfaces were positive for both proteins, whereas those in the stromal tissues in the tumor nests showed only MMP-9 immunoreactivity. Immunoelectron microscopy disclosed the presence of MMP-9 in the Golgi apparatus and in vesicular structures at the baso-lateral cytoplasmic region of the osteoclasts found in the stromal tissue. MMP-9-positive vesicular structures also contained fragmented extracellular materials. Thus, osteoclasts appear to either select an optimized function, namely secreting proteolytic enzymes from ruffled borders during bone resorption, or recognize the surrounding extracellular matrix by mediating osteopontin/CD44 interaction, and internalize the extracellular matrices. Microsc. Res. Tech. 69:73,83, 2006. © 2006 Wiley-Liss, Inc. [source] Direct evidence of nitric oxide release from neuronal nitric oxide synthase activation in the left ventricle as a result of cervical vagus nerve stimulationTHE JOURNAL OF PHYSIOLOGY, Issue 12 2009Kieran E. Brack Information regarding vagal innervation in the cardiac ventricle is limited and the direct effect of vagal stimulation on ventricular myocardial function is controversial. We have recently provided indirect evidence that the anti-fibrillatory effect of vagus nerve stimulation on the ventricle is mediated by nitric oxide (NO). The aim of this study was to provide direct evidence for the release of nitric oxide in the cardiac ventricle during stimulation of the efferent parasympathetic fibres of the cervical vagus nerve. The isolated innervated rabbit heart was employed with the use of the NO fluorescent indicator 4,5-diaminofluorescein diacetate (DAF-2 DA) during stimulation of the cervical vagus nerves and acetylcholine perfusion in the absence and presence of the non-specific NO synthase inhibitor NG -nito- l- arginine (l- NNA) and the neuronal NO synthase selective inhibitor 1-(2-trifluormethylphenyl)imidazole (TRIM). Using the novel fluorescence method in the beating heart, we have shown that NO-dependent fluorescence is increased by 0.92 ± 0.26, 1.20 ± 0.30 and 1.91 ± 0.27% (during low, medium and high frequency, respectively) in the ventricle in a stimulation frequency-dependent manner during vagus nerve stimulation, with comparable increases seen during separate stimulation of the left and right cervical vagus nerves. Background fluorescence is reduced during perfusion with l- NNA and the increase in fluorescence during high frequency vagal stimulation is inhibited during perfusion with both l- NNA (1.97 ± 0.35% increase before l- NNA, 0.00 ± 0.02% during l- NNA) and TRIM (1.78 ± 0.18% increase before TRIM, ,0.11 ± 0.08% during TRIM). Perfusion with 0.1 ,m acetylcholine increased NO fluorescence by 0.76 ± 0.09% which was blocked by l- NNA (change of 0.00 ± 0.03%) but not TRIM (increase of 0.82 ± 0.21%). Activation of cardiac parasympathetic efferent nerve fibres by stimulation of the cervical vagus is associated with NO production and release in the ventricle of the rabbit, via the neuronal isoform of nitric oxide synthase. [source] B-type natriuretic peptide as an indicator of right ventricular dysfunction in acute pulmonary embolism,INTERNATIONAL JOURNAL OF CLINICAL PRACTICE, Issue 8 2008T. Yardan Summary Objective:, B-type natriuretic peptide (BNP) is a neurohormone secreted from cardiac ventricles in response to ventricular strain. The aim of present study was to evaluate the role of BNP in the diagnosis of the right ventricular (RV) dysfunction in acute pulmonary embolism (PE). Methods:, BNP levels were measured in patients with acute PE as diagnosed by high probability lung scan or positive spiral computed tomography. All patients underwent standard echocardiography and blood tests during the second hour of the diagnosis. Results:, Forty patients diagnosed as acute PE (mean age, 60.4 ± 13.2 years; 62.5% women) were enrolled in this study. Patients with RV dysfunction had significantly higher BNP levels than patients without RV dysfunction (426 ± 299.42 pg/ml vs. 39.09 ± 25.22 pg/ml, p < 0.001). BNP-discriminated patients with or without RV dysfunction (area under the receiver operating characteristic curve, 0.943; 95% CI, 0.863,1.022). BNP > 90 pg/ml was associated with a risk ratio of 165 (95% CI, 13.7,1987.2) for the diagnosis of RV dysfunction. There was a significant correlation between RV end-diastolic diameter and BNP (r = 0.89, p < 0.001). Sixteen patients (40%) were diagnosed as having low-risk PE, 19 patients (47.5%) with submassive PE and five patients (12.5%) with massive PE. The mean BNP was 39.09 ± 25.2, 378.4 ± 288.4 and 609.2 ± 279.2 pg/ml in each group respectively. Conclusion:, Measurement of BNP levels may be a useful approach in diagnosis of RV dysfunction in patients with acute PE. The possibility of RV dysfunction in patients with plasma BNP levels > 90 pg/ml should be strongly considered. [source] The clinical value of rapid assay for plasma B-type natriuretic peptide in differentiating congestive heart failure from pulmonary causes of dyspnoeaINTERNATIONAL JOURNAL OF CLINICAL PRACTICE, Issue 2 2008S.-Q. Zhao Summary Background:, B-type natriuretic peptide (BNP) is a cardiac neurohormone secreted from the cardiac ventricles in response to pressure overload. Objective:, To evaluate the optimal cutoff point of plasma BNP in diagnosing congestive heart failure (CHF). Methods:, We conducted a prospective study of 195 patients who were hospitalised with dyspnoea. Pulmonary capillary wedge pressure (PCWP) was measured with a Swan-Ganz catheterisation and plasma BNP level was obtained by a rapid immunofluorescence assay in all patients. PCWP > 12 mmHg was chosen as the golden standard for left ventricular dysfunction in this study. The subjects were divided into two groups by the criteria, one group with dyspnoea caused by CHF (n = 134) and the other caused by lung diseases (n = 61). Results:, (1) BNP cutoff point of 100 pg/ml had a sensitivity of 94.34%, a specificity of 92.13% and an accuracy of 93.33% for differentiating CHF from pulmonary dyspnoea. (2) By multiple logistic-regression analysis, measurements of BNP added significantly independent predictive power to other clinical variables in models predicting which patients had CHF. Conclusion:, A value of 100 pg/ml or more for a rapid BNP assay may be the most accurate independent predictor of the presence or absence of CHF. [source] Altered T Wave Dynamics in a Contracting Cardiac ModelJOURNAL OF CARDIOVASCULAR ELECTROPHYSIOLOGY, Issue 2003NICOLAS P. SMITH Ph.D. Introduction: The implications of mechanical deformation on calculated body surface potentials are investigated using a coupled biophysically based model. Methods and Results: A cellular model of cardiac excitation-contraction is embedded in an anatomically accurate two-dimensional transverse cross-section of the cardiac ventricles and human torso. Waves of activation and contraction are induced by the application of physiologically realistic boundary conditions and solving the bidomain and finite deformation equations. Body surface potentials are calculated from these activation profiles by solving Laplace's equation in the passive surrounding tissues. The effect of cardiac deformation on electrical activity, induced by contraction, is demonstrated in both single-cell and tissue models. Action potential duration is reduced by 7 msec when the single cell model is subjected to a 10% contraction ramp applied over 400 msec. In the coupled electromechanical tissue model, the T wave of the ECG is shown to occur 18 msec earlier compared to an uncoupled excitation model. To assess the relative effects of myocardial deformation on the ECG, the activation sequence and tissue deformation are separated. The coupled and uncoupled activation sequences are mapped onto the undeforming and deforming meshes, respectively. ECGs are calculated for both mappings. Conclusion: Adding mechanical contraction to a mathematical model of the heart has been shown to shift the T wave on the ECG to the left. Although deformation of the myocardium resulting from contraction reduces the T wave amplitude, cell stretch producing altered cell membrane kinetics is the major component of this temporal shift. (J Cardiovasc Electrophysiol, Vol. 14, pp. S203-S209, October 2003, Suppl.) [source] | |||||||||||||