It is not certain whether the myocyte contractile function in the heartfailure is normal according to recent some studies,therefore the contractile functionof the myocytes with the heart failure should be studied. The...It is not certain whether the myocyte contractile function in the heartfailure is normal according to recent some studies,therefore the contractile functionof the myocytes with the heart failure should be studied. The myocyte heart failuremodel was set up by the method of stretching the cultured myocytes,and the myocytes with and without the heart failure were measured the contractile mechanicscharacteristic,the parameters being the maximal contractive velocity of the myocyte(Vmax), the maximal shortening length of myocyte contraction (ΔLmax) and themaximal decrease of the myocyte size during contraction (ΔSmax), by the videoedgedetector system. And then the protein genes (including α-MHC and β-MHC)expression of these myocytes were quantitatively measured by the dot blotting. Thecorrelative and regressive analysis were used to analyze the relationship between themyocyte contractile mechanics characteristic and the contractile protein genes expression level. The results showed that the contractile mechanics parameters,Vmax=41．5±6．0(μm/sec), △Lmax= 10．6±1．9 (% ) and △Smax= 14．3± 2．3 (% ), in themyocytes with the heart failure are statistically significant lower than the normalmyocytes (P<0．01), whose parameters are Vmax=67．9±6．7 (μm/sec), △Lmax=17．7±1．6 (% ) and △Smax=21．5±2．4 (%). The myocyte contractile protein gene (αMHC) expression level in the heart failure myocytes is statistically significant lowerthan that in the normal myocytes,but β-MHC gene expression level is statisticallysignificant higher than the normal myocytes. The α-MllC gene expression level is apositive correlation coefficient with the myocyte contractile mechanics parametersseparately,covering Vmax,△Lmax and △max; but the β- MHC gene expression levelis a negative correlation coefficietn with the myocyte contractile mechanics parameters separately.展开更多
AIM: To investigate the effects of taurolithocholate (TLC)on the canalicular motility in isolated rat hepatocyte cou-plets (IRHC).METHODS: TLC was added to IRHC at concentrationsof 10 and 50 μmol/L, respectively. In ...AIM: To investigate the effects of taurolithocholate (TLC)on the canalicular motility in isolated rat hepatocyte cou-plets (IRHC).METHODS: TLC was added to IRHC at concentrationsof 10 and 50 μmol/L, respectively. In each group, fi vetime-lapse movies containing 3 representative bile cana-liculi were taken under phase-contrast microscopy for12 h. The number of bile canalicular contractions andthe intervals between consecutive canalicular contrac-tions were calculated. Furthermore, the effects of TLC onIRHC were examined by transmission electron micros-copy.RESULTS: The bile canalicular contractions were spon-taneous and forceful in the controls. Active vesicularmovement was observed in the pericanalicular region.Immediately after the addition of TLC, the bile canaliculiwere deformed, and canalicular bile was incorporatedinto the vacuoles. The canaliculi were gradually dilated,and canalicular contractions were markedly inhibited byTLC. The vesicular movements became extremely slowin the pericanalicular region. The number of canalicularcontractions significantly decreased in the TLC-treatedgroups, as compared with that in the controls. The timeintervals were prolonged, as the TLC dosage increased,indicating that bile secretion into the canaliculi wasimpaired with TLC. Transmission electron microscopyrevealed the lamellar transformation of the canalicularmembranes in IRHC treated with TLC.CONCLUSION: TLC impairs both the bile canalicularcontractions and the canalicular bile secretion, possiblyby acting directly on the canalicular membranes in TLC-induced cholestasis.展开更多
Based on the results of our observation, the delayed alteration of contractile structures resulted from the delayed predominant degradation of contractile proteins of skeletal muscle constitute the background of the c...Based on the results of our observation, the delayed alteration of contractile structures resulted from the delayed predominant degradation of contractile proteins of skeletal muscle constitute the background of the chronic or acute skeletal muscle injury. There fore,the arrangement of workload should be considered as the most important factor in preventing skeletal muscle injury.展开更多
The number of patients suffering from symptoms associated with gastrointestinal(GI) motility disorders is on the rise. GI motility disorders are accompanied by alteration of gastrointestinal smooth muscle functions. C...The number of patients suffering from symptoms associated with gastrointestinal(GI) motility disorders is on the rise. GI motility disorders are accompanied by alteration of gastrointestinal smooth muscle functions. Currently available drugs,which can directly affect gastrointestinal smooth muscle and restore altered smooth muscle contractility to normal,are not satisfactory for treating patients with GI motility disorders. We have recently shown that ERK1/2 and p38MAPK signaling pathways play an important role in the contractile response not only of normal intestinal smooth muscle but also of inflamed intestinal smooth muscle. Here we discuss the possibility that ERK1/2 and p38MAPK signaling pathways represent ideal targets for generation of novel therapeutics for patients with GI motility disorders.展开更多
文摘It is not certain whether the myocyte contractile function in the heartfailure is normal according to recent some studies,therefore the contractile functionof the myocytes with the heart failure should be studied. The myocyte heart failuremodel was set up by the method of stretching the cultured myocytes,and the myocytes with and without the heart failure were measured the contractile mechanicscharacteristic,the parameters being the maximal contractive velocity of the myocyte(Vmax), the maximal shortening length of myocyte contraction (ΔLmax) and themaximal decrease of the myocyte size during contraction (ΔSmax), by the videoedgedetector system. And then the protein genes (including α-MHC and β-MHC)expression of these myocytes were quantitatively measured by the dot blotting. Thecorrelative and regressive analysis were used to analyze the relationship between themyocyte contractile mechanics characteristic and the contractile protein genes expression level. The results showed that the contractile mechanics parameters,Vmax=41．5±6．0(μm/sec), △Lmax= 10．6±1．9 (% ) and △Smax= 14．3± 2．3 (% ), in themyocytes with the heart failure are statistically significant lower than the normalmyocytes (P<0．01), whose parameters are Vmax=67．9±6．7 (μm/sec), △Lmax=17．7±1．6 (% ) and △Smax=21．5±2．4 (%). The myocyte contractile protein gene (αMHC) expression level in the heart failure myocytes is statistically significant lowerthan that in the normal myocytes,but β-MHC gene expression level is statisticallysignificant higher than the normal myocytes. The α-MllC gene expression level is apositive correlation coefficient with the myocyte contractile mechanics parametersseparately,covering Vmax,△Lmax and △max; but the β- MHC gene expression levelis a negative correlation coefficietn with the myocyte contractile mechanics parameters separately.
文摘AIM: To investigate the effects of taurolithocholate (TLC)on the canalicular motility in isolated rat hepatocyte cou-plets (IRHC).METHODS: TLC was added to IRHC at concentrationsof 10 and 50 μmol/L, respectively. In each group, fi vetime-lapse movies containing 3 representative bile cana-liculi were taken under phase-contrast microscopy for12 h. The number of bile canalicular contractions andthe intervals between consecutive canalicular contrac-tions were calculated. Furthermore, the effects of TLC onIRHC were examined by transmission electron micros-copy.RESULTS: The bile canalicular contractions were spon-taneous and forceful in the controls. Active vesicularmovement was observed in the pericanalicular region.Immediately after the addition of TLC, the bile canaliculiwere deformed, and canalicular bile was incorporatedinto the vacuoles. The canaliculi were gradually dilated,and canalicular contractions were markedly inhibited byTLC. The vesicular movements became extremely slowin the pericanalicular region. The number of canalicularcontractions significantly decreased in the TLC-treatedgroups, as compared with that in the controls. The timeintervals were prolonged, as the TLC dosage increased,indicating that bile secretion into the canaliculi wasimpaired with TLC. Transmission electron microscopyrevealed the lamellar transformation of the canalicularmembranes in IRHC treated with TLC.CONCLUSION: TLC impairs both the bile canalicularcontractions and the canalicular bile secretion, possiblyby acting directly on the canalicular membranes in TLC-induced cholestasis.
文摘Based on the results of our observation, the delayed alteration of contractile structures resulted from the delayed predominant degradation of contractile proteins of skeletal muscle constitute the background of the chronic or acute skeletal muscle injury. There fore,the arrangement of workload should be considered as the most important factor in preventing skeletal muscle injury.
基金Supported by the Research Grant from the Canadian Institutes for Health Research,and Partly by an Alberta Innovates-Health Solutions Senior Scholar Award and Canada Research Chair in Smooth Muscle Pathophysiology
文摘The number of patients suffering from symptoms associated with gastrointestinal(GI) motility disorders is on the rise. GI motility disorders are accompanied by alteration of gastrointestinal smooth muscle functions. Currently available drugs,which can directly affect gastrointestinal smooth muscle and restore altered smooth muscle contractility to normal,are not satisfactory for treating patients with GI motility disorders. We have recently shown that ERK1/2 and p38MAPK signaling pathways play an important role in the contractile response not only of normal intestinal smooth muscle but also of inflamed intestinal smooth muscle. Here we discuss the possibility that ERK1/2 and p38MAPK signaling pathways represent ideal targets for generation of novel therapeutics for patients with GI motility disorders.
