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1.
Chinese Journal of Rehabilitation Theory and Practice ; (12): 1297-1304, 2020.
Article in Chinese | WPRIM | ID: wpr-905369

ABSTRACT

Objective:To investigate the effects and mechanism of Tuina on denervation-induced atrophy. Methods:A total of 42 Sprague-Dawley rats were randomly divided into sham group (n = 6), model group (n = 18) and Tuina group (n = 18). The model group and Tuina group freed and excised right tibia nerve about one centimeter, while the sham group freed the right tibia nerve only. From the second day after operation, Tuina group accepted Tuina on the injured area, while the sham group and the model group were only fixed without any intervention. Six rats were sacrificed on the 14th, 21st and 28th day after operation in the model and Tuina groups, and the sham group was sacrificed on the 28th day after operation. The gastrocnemius muscles were measured wet weight ratio. The diameter and area of muscle cells were measured under HE staining. The expression of Pax7, MyoD, MyoG, microRNA-1, microRNA-133a and microRNA-206 in the gastrocnemius muscles were detected with reverse transcription real-time quantitative polymerase chain reaction. Results:Compared with the sham group, the wet weight ratio, the area of muscle cells (except the 14-day-Tuina group) and the diameter of muscle cells decreased at each time point in the model group and Tuina group (P < 0.05); compared with the model group, the wet weight ratio, muscle cell diameter and muscle cell area increased at each time point in Tuina group (P < 0.05). Compared with the sham group, the expression of Pax7 increased in the 14-day-model group (P < 0.05) and decreased in the 28-day-model group (P < 0.05), and it increased at each time point (except 28-day) in Tuina group (P < 0.05); compared with the model group, the expression of Pax7 increased at each time point in Tuina group (P < 0.05). Compared with the sham group, the expression of MyoD and MyoG increased at each time point in the model group and Tuina group (P < 0.05); compared with the model group, the expression of MyoD and MyoG increased at each time point (except 14-day) in Tuina group (P < 0.05). Compared with the sham group, the expression of microRNA-1 and microRNA-133a decreased, and microRNA-206 increased in the model group and Tuina group at 21-day (P < 0.05); compared with the model group, the expression of microRNA-1, microRNA-133a and microRNA-206 increased in Tuina group (P < 0.05). Conclusion:Tuina may activate the Pax7/MyoD/MyoG pathway by increasing the expression of muscle-specific microRNA, to promote the proliferation and differentiation of muscle satellite cells, and delay denervation-induced atrophy.

2.
Chinese Journal of Rehabilitation Theory and Practice ; (12): 434-438, 2019.
Article in Chinese | WPRIM | ID: wpr-905546

ABSTRACT

Muscle loses normal function after skeletal muscle atrophy that will greatly reduce the quality of personal life. There is no effective way to treat muscle atrophy currently. microRNA (miRNA) as a small molecule of non-coding RNA brings new hope for the treatment of muscular atrophy. The mechanism of miRNA regulating muscle atrophy mainly includes: regulating abnormal muscle protein metabolism by ubiquitin-proteasome system (UPS) and mammalian target of rapamycin pathway (IGF/PI3K/Akt/mTOR), inhibiting abnormal apoptosis of muscle cells by inhibiting the expression of apoptotic factors, promoting muscle regeneration by regulating myogenic factor expression, and promoting angiogenesis by promoting the expression of angiogenic factors, and so on.

3.
Journal of Kunming Medical University ; (12): 34-38, 2018.
Article in Chinese | WPRIM | ID: wpr-694527

ABSTRACT

Objective Through the screening of candidate pathogenic gene among family members of a family with familial hypertrophic cardiomyopathy in Yuxi, Yunnan Province, the study is designed to analyze the relationship between genotype and phenotype and to provide an important theoretical basis for the research of molecular genetic mechanism, early screening and early intervention of familial hypertrophic cardiomyopathy. Methods A detailed medical history was collected and physical examination and routine twelve lead electrocardiogram and cardiac ultrasonography examination were performed among the family members. The peripheral venous blood samples were collected for genetic testing. The genetic map was drawn and the genetic characteristics, genotype and clinical phenotype were analyzed. Results In this family, the dominant inheritance mode of hypertrophic cardiomyopathy is X- linked dominant inheritance. Candidate genes screening showed that a missense mutation was found in the GLA, ZFPM2, SCN5A genes and the translated amino acids were changed. Conclusion X- linked dominant inheritance is the main genetic mode of HCM in this family. GLA c.167G>A (p. Cys56Tyr) heterozygous or hemizygous missense mutation may be the major pathogenic mutation in this family with non-obstructive hypertrophic cardiomyopathy. The clinical significance of ZFPM2 c.1332G> C (p.Lys444Asn) heterozygous missense mutation and SCN5A c.5216G>A (p.Arg1739Gln) heterozygous missense mutation in this family is undetermined.

4.
Chinese Journal of Hepatobiliary Surgery ; (12): 203-207, 2011.
Article in Chinese | WPRIM | ID: wpr-413966

ABSTRACT

Objective To systematically evaluate the efficacy and safety of combined hepatectomy and splenectomy in hepatocellular carcinoma complicated with hepatic cirrhosis and hypersplenism.Methods Medline (1966-August 2009), Embase (1974-August 2009), Cochrane Library, CBMdisc (1978-August 2009), and Wanfang Database were searched without language limitation. All relevant studies were screened and the data were extracted by two independent reviewers, and the methodological qualities of the included studies were evaluated by the Minors scale. The data were analyzed with the RevMan5 software. Results Five non-randomized comparative studies (NRCs) involving 476 patients (232 in HS group, 244 in control group) were enrolled into the analysis. There was no significant difference in the operative mortalities (OR=0. 57, 95%CI 0. 12-2. 66, P=0. 47) and postoperative morbidities (OR= 0. 93, 95 % CI 0.59- 1.46, P = 0.75) between the two groups. Compared with hepatectomy only, CD4+ T cell (WMD=7.90, 95%CI 7.01-8.79, P<0.01), CD4+ T cell/CD8+ T cell ratio (WMD=0. 75, 95%CI 0. 70-0.80, P<0.01), white blood cell count (WMD=5.47, 95%CI 5.13-5.82, P<0.01) and platelet count (WMD=174.89, 95%CI 116.61-233.18,P<0.01) were significantly higher, but CD8+ T cell (WMD = - 7.66, 95%CI - 8. 53~ - 6. 79,P<0. 01) was lower compared with combined hepatectomy and splenectomy. There was no significant difference in the 5-year survival rates (OR= 1.37, 95%CI 0.86-2.18, P=0. 18). Conclusion Combined hepatectomy and splenectomy did not increase the operative mortalities and postoperative morbidities in hepatocellular carcinoma complicated with hepatic cirrhosis and hypersplenism. The white blood cell and platelet counts markedly increased after surgery. There was no evidence to show any improvement in the 5-year survival.

5.
International Journal of Surgery ; (12): 769-773, 2009.
Article in Chinese | WPRIM | ID: wpr-392267

ABSTRACT

Cancer of digestive system is one of the most common worldwidely cancers and seriously threats to human health. However its etiology and pathogenesis are still not clear. Toll-like receptor (TLR), a newly discovered transmembrane receptor, plays an important role in innate immunity. Recent researches suggested that TLRs had extensive relationship with inflammation, autoimmune diseases and cancer. A large number of researches indicated that TLRs not only participated in the occurrence, development and immune escape of cancer, but also acted in immunotherapy in digestive system. Further investigation of TLRs may re-veal the effects of TLRs in the development of malignant tumors of digestive system, moreover may find new therputic target for the treatment of cancers. We reviewed the relationship between TLRs and cancers of di-gestive system.

6.
Journal of Experimental Hematology ; (6): 712-716, 2008.
Article in Chinese | WPRIM | ID: wpr-267905

ABSTRACT

Mitochondria is the main place of biological oxidation and energy transform. Mitochondrial DNA encodes the complex of respiratory chain in mitochondria and its mutation can cause a series of human disease. Mitochondrial DNA mutation which observed in myelodysplastic syndrome (MDS) patients cause the MDS by the mechanism of iron metabolism disorder, gene instability and hemopoietic progenitor cell apoptosis. In this review the characteristics of mitochondrial DNA structure, the mitochondrial DNA mutation and the possible mechanism of mitochondrial DNA mutation in pathogenesis of MDS were summarized.


Subject(s)
Humans , Anemia, Sideroblastic , Genetics , DNA, Mitochondrial , Genetics , Myelodysplastic Syndromes , Genetics , Point Mutation
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