AIM： To summarize the operative experiences for giant leiomyoma of esophagus.METHODS： Eight cases of giant esophageal leiomyoma （GEL） whose tumors were bigger than 10 cm were treated surgically in our department f...AIM： To summarize the operative experiences for giant leiomyoma of esophagus.METHODS： Eight cases of giant esophageal leiomyoma （GEL） whose tumors were bigger than 10 cm were treated surgically in our department from June 1980 to March 2004.All of these cases received barium swallow roentgenography and esophagoscopy. Leiomyoma located in upper thirds of the esophagus in one case, middle thirds of the esophagus in five cases, lower thirds of the esophagus in two cases. Resection of tumors was performed successfully in all of these cases. Operative methods included transthoracic extramucosal enucleation and buttressing the muscular defect with pedicled great omental flap （one case）, esophagectomy and esophagogastrostomy above the arch of aorta （three cases）, total esophagectomy and esophageal replacement with colon （four cases）. Histological examination confirmed that all of these cases were leiomyoma.RESULTS： All of the eight patients recovered approvingly with no mortality and resumed normal diet after operation. Vomiting during meals occurred in one patient with esophagogastrostomy, and remained 1 mo. Reflux esophagitis occurred in one patient with esophagogastrostomy and was alleviated with medication. Thoracic colon syndrome （TCS） occurred in one patient with colon replacement at 15 mo postoperatively. No recurrence occurred in follow-up from 6 mo to 8 years.CONCLUSION： Surgical treatment for GEL is both safe and effective. The choices of operative methods mainly depend on the location and range of lesions. We prefer to treat GEL via esophagectomy combined with esophagogastrostomy or esophagus replacement with colon. The long-time quality of life is better in the latter.展开更多
Background Studies have shown that staged percutaneous coronary intervention （PCI） for non-culprit lesions is beneficial for prog- nosis of ST-segment elevation myocardial infarction （STEMI） patients with multives...Background Studies have shown that staged percutaneous coronary intervention （PCI） for non-culprit lesions is beneficial for prog- nosis of ST-segment elevation myocardial infarction （STEMI） patients with multivessel disease. However, the optimal timing of staged re- vascularization is still controversial. This study aimed to find the optimal timing of staged revascularization. Methods A total of 428 STEMI patients with multivessel disease who underwent primary PCI and staged PCI were included. According to the time interval between primary and staged PCI, patients were divided into three groups （〈 1 week, 1- weeks, and 2-12 weeks after primary PCI）. The primary endpoint was major adverse cardiovascular events （MACE）, a composite of all-cause death, non-fatal re-infarction, repeat revascularization, and stroke. Cox regression model was used to assess the association between staged PCI timing and risk of MACE. Results During the follow-up, 119 participants had MACEs. There was statistical difference in MACE incidence among the three groups （〈 1 week： 23.0%; 1-2 weeks： 33.0%; 2-12 weeks： 40.0%; P = 0.001）. In the multivariable adjustment model, the timing interval of staged PCI ≤ 1 week and l-2 weeks were both significantly associated with a lower risk of MACE [hazard ratio （HR）： 0.40, 95% confidence intervals （CI）： 0.24-4）.65; HR： 0.54, 95% CI： 0.3 lq3.93, respectively], mainly attributed to a lower risk of repeat revascularization （HR： 0.41, 95% CI： 0.24-0.70; HR： 0.36, 95% CI： 0.18-0.7）, compared with a strategy of 2-12 weeks later of primary PCI. Conclusions The optimal timing of staged PCI for non-culprit vessels should be within two weeks after primary PCI for STEMI patients.展开更多
Objective. The purpose of the study was to build up an animal model of mitochondrial myopathy in order to analyse the pathogenesis of the disease. Methods. The skeletal muscles from Wistar rats treated with germanium ...Objective. The purpose of the study was to build up an animal model of mitochondrial myopathy in order to analyse the pathogenesis of the disease. Methods. The skeletal muscles from Wistar rats treated with germanium dioxide for 24 weeks were analysed by histopathologic and electron- microscopic studies. A quantitative analysis was carried out in mitochondrial DNAs of these samples. The biological function of the model was determined. Results. An animal model of mitochondrial myopathy was built up, in which oxygen free radicals were increased and mitochondrial DNA copies were decreased contrasted with controls. Conclusion. It suggested that environmental toxin may play a role in the pathogenesis of mitochondrial myopathy. The increase of oxygen free radicals is an important link causing the disease.展开更多
Objective To search for A3243G point mutations in mitochondrial DNA (mtDNA) from 10 cases of mitochondrial encephalomyopathy, lactic acidosis and strokelike episodes (MELAS) Methods Using PCR restriction analysis,...Objective To search for A3243G point mutations in mitochondrial DNA (mtDNA) from 10 cases of mitochondrial encephalomyopathy, lactic acidosis and strokelike episodes (MELAS) Methods Using PCR restriction analysis, we investigated A3243G point mutations in mtDNA of muscle and/or blood cells from 10 patients and their 8 maternal relatives We also quantitated the A3243G mtDNA in samples harboring the mutation Results A3243G point mutations were identified in all muscle and/or blood samples from 10 MELAS patients The proportion of mutant mtDNA was 10 8%-47 8% in blood (7 cases), and 39 4%-67 7% in muscle (5 cases) This ratio was invariably higher in muscle than in blood from two patients whose blood and muscle samples were both available Younger patients usually carried higher proportions of A3243G mutant mtDNA in blood Eight maternal relatives from 6 families were also examined Maternal transmission of the disease could be identified in one family No A3243G point mutations were found in mothers' blood from 3 families and siblings' blood from 2 families Conclusions All 10 MELAS patients were found to have the mtDNA A3243G mutation in their muscle and/or blood The A3243G mutation seems to be sporadic in 5 of the families examined, suggesting the mechanism of de novo mutation for the pathogenesis of their MELAS syndrome展开更多
Objective To study the relation between point mutations at nt3243 and nt8344 of muscle mitochondrial DNA from patients with mitochondrial encephalomyopathies and phenotypes. Methods DNA was extracted from muscle speci...Objective To study the relation between point mutations at nt3243 and nt8344 of muscle mitochondrial DNA from patients with mitochondrial encephalomyopathies and phenotypes. Methods DNA was extracted from muscle specimens from 5 patients with mitochondrial encephalomyopathies and amplified by PCR method, using corresponding oligonucleotide primers. DNA fragments were digested with restriction enzymes BglⅠ and ApaⅠ, then the digested DNA fragments were analyzed with an electrophoresis method.Results The point mutation at nt3243 of mtDNA was found in 2 patients, one with mitochondrial encephalomyopathy, lactic acidosis and stroke-like episodes (MELAS) and another with myoclonic epilepsy with ragged red fibers (MERRF). The point mutation at nt8344 was found in 2 patients with MERRF, including the one with point mutation at nt3243.Conclusion The point mutation of DNA at nt3243 correlated with MELAS and nt8344 correlated with MERRF. In addition, the detection of point mutations at both nt3243 and nt8344 in a patient with MERRF shows the association of mutation with diversity in clinical manifestations of mitochondrial encephalomyopathies.展开更多
基金Supported by the Science and Technology Foundation of Hubei Province, No. 992P1203
文摘AIM： To summarize the operative experiences for giant leiomyoma of esophagus.METHODS： Eight cases of giant esophageal leiomyoma （GEL） whose tumors were bigger than 10 cm were treated surgically in our department from June 1980 to March 2004.All of these cases received barium swallow roentgenography and esophagoscopy. Leiomyoma located in upper thirds of the esophagus in one case, middle thirds of the esophagus in five cases, lower thirds of the esophagus in two cases. Resection of tumors was performed successfully in all of these cases. Operative methods included transthoracic extramucosal enucleation and buttressing the muscular defect with pedicled great omental flap （one case）, esophagectomy and esophagogastrostomy above the arch of aorta （three cases）, total esophagectomy and esophageal replacement with colon （four cases）. Histological examination confirmed that all of these cases were leiomyoma.RESULTS： All of the eight patients recovered approvingly with no mortality and resumed normal diet after operation. Vomiting during meals occurred in one patient with esophagogastrostomy, and remained 1 mo. Reflux esophagitis occurred in one patient with esophagogastrostomy and was alleviated with medication. Thoracic colon syndrome （TCS） occurred in one patient with colon replacement at 15 mo postoperatively. No recurrence occurred in follow-up from 6 mo to 8 years.CONCLUSION： Surgical treatment for GEL is both safe and effective. The choices of operative methods mainly depend on the location and range of lesions. We prefer to treat GEL via esophagectomy combined with esophagogastrostomy or esophagus replacement with colon. The long-time quality of life is better in the latter.
文摘Background Studies have shown that staged percutaneous coronary intervention （PCI） for non-culprit lesions is beneficial for prog- nosis of ST-segment elevation myocardial infarction （STEMI） patients with multivessel disease. However, the optimal timing of staged re- vascularization is still controversial. This study aimed to find the optimal timing of staged revascularization. Methods A total of 428 STEMI patients with multivessel disease who underwent primary PCI and staged PCI were included. According to the time interval between primary and staged PCI, patients were divided into three groups （〈 1 week, 1- weeks, and 2-12 weeks after primary PCI）. The primary endpoint was major adverse cardiovascular events （MACE）, a composite of all-cause death, non-fatal re-infarction, repeat revascularization, and stroke. Cox regression model was used to assess the association between staged PCI timing and risk of MACE. Results During the follow-up, 119 participants had MACEs. There was statistical difference in MACE incidence among the three groups （〈 1 week： 23.0%; 1-2 weeks： 33.0%; 2-12 weeks： 40.0%; P = 0.001）. In the multivariable adjustment model, the timing interval of staged PCI ≤ 1 week and l-2 weeks were both significantly associated with a lower risk of MACE [hazard ratio （HR）： 0.40, 95% confidence intervals （CI）： 0.24-4）.65; HR： 0.54, 95% CI： 0.3 lq3.93, respectively], mainly attributed to a lower risk of repeat revascularization （HR： 0.41, 95% CI： 0.24-0.70; HR： 0.36, 95% CI： 0.18-0.7）, compared with a strategy of 2-12 weeks later of primary PCI. Conclusions The optimal timing of staged PCI for non-culprit vessels should be within two weeks after primary PCI for STEMI patients.
基金This study was supported by the National Natural Sciences Foundation of China (No. 39470260)
文摘Objective. The purpose of the study was to build up an animal model of mitochondrial myopathy in order to analyse the pathogenesis of the disease. Methods. The skeletal muscles from Wistar rats treated with germanium dioxide for 24 weeks were analysed by histopathologic and electron- microscopic studies. A quantitative analysis was carried out in mitochondrial DNAs of these samples. The biological function of the model was determined. Results. An animal model of mitochondrial myopathy was built up, in which oxygen free radicals were increased and mitochondrial DNA copies were decreased contrasted with controls. Conclusion. It suggested that environmental toxin may play a role in the pathogenesis of mitochondrial myopathy. The increase of oxygen free radicals is an important link causing the disease.
文摘Objective To search for A3243G point mutations in mitochondrial DNA (mtDNA) from 10 cases of mitochondrial encephalomyopathy, lactic acidosis and strokelike episodes (MELAS) Methods Using PCR restriction analysis, we investigated A3243G point mutations in mtDNA of muscle and/or blood cells from 10 patients and their 8 maternal relatives We also quantitated the A3243G mtDNA in samples harboring the mutation Results A3243G point mutations were identified in all muscle and/or blood samples from 10 MELAS patients The proportion of mutant mtDNA was 10 8%-47 8% in blood (7 cases), and 39 4%-67 7% in muscle (5 cases) This ratio was invariably higher in muscle than in blood from two patients whose blood and muscle samples were both available Younger patients usually carried higher proportions of A3243G mutant mtDNA in blood Eight maternal relatives from 6 families were also examined Maternal transmission of the disease could be identified in one family No A3243G point mutations were found in mothers' blood from 3 families and siblings' blood from 2 families Conclusions All 10 MELAS patients were found to have the mtDNA A3243G mutation in their muscle and/or blood The A3243G mutation seems to be sporadic in 5 of the families examined, suggesting the mechanism of de novo mutation for the pathogenesis of their MELAS syndrome
文摘Objective To study the relation between point mutations at nt3243 and nt8344 of muscle mitochondrial DNA from patients with mitochondrial encephalomyopathies and phenotypes. Methods DNA was extracted from muscle specimens from 5 patients with mitochondrial encephalomyopathies and amplified by PCR method, using corresponding oligonucleotide primers. DNA fragments were digested with restriction enzymes BglⅠ and ApaⅠ, then the digested DNA fragments were analyzed with an electrophoresis method.Results The point mutation at nt3243 of mtDNA was found in 2 patients, one with mitochondrial encephalomyopathy, lactic acidosis and stroke-like episodes (MELAS) and another with myoclonic epilepsy with ragged red fibers (MERRF). The point mutation at nt8344 was found in 2 patients with MERRF, including the one with point mutation at nt3243.Conclusion The point mutation of DNA at nt3243 correlated with MELAS and nt8344 correlated with MERRF. In addition, the detection of point mutations at both nt3243 and nt8344 in a patient with MERRF shows the association of mutation with diversity in clinical manifestations of mitochondrial encephalomyopathies.
