Objective To explore metformin improves hyperinsulinemia in obese children, glucose metabolism, serum lipid derived hormone levels. Methods 40 cases of healthy children were selected and included in the control group, 40 cases of mild, moderate and severe obese children in the obese group, moderately obese group, obese group given category; metformin in obese children orally for 3 months, then in each group of body mass index (BMI), the learning situation of adipose derived hormones, blood glucose levels were detected and compared. Results Compared the condition of blood glucose metabolism and body weight obviously, obesity group and control group before treatment there are very significant differences after treatment, the obese group appeared to be improved, indicates that the difference is obvious(P<0.05). Compare the hormone levels of serum leptin and adiponectin are visible in before the treatment and health examination Significant differences after the treatment showed some improvement, but the resistin in the treatment had no obvious improvement. Conclusion The application of metformin improves hyperinsulinemia in obese children with sugar metabolism, visible analysis of serum adipose derived hormones, the patients with improvement of glucose metabolism has a positive effect, while improving the serum hormone level, reduce patient weight (BMI), so it is worthy of clinical use.

AIM:MicroRNAs ( miRNAs) were recognized to play significant roles in cardiac hypertrophy .But, it remains unknown whether cyclin/Rb pathway is modulated by miRNAs during cardiac hypertrophy .This study investigates the potential roles of microRNA-1 (miR-1) and microRNA-16 (miR-16) in modulating cyclin/Rb pathway during cardiomyocyte hypertrophy .METHODS:An animal model of hypertrophy was established in a rat with abdominal aortic constriction (AAC).In addition, a cell model of hypertrophy was also achieved based on PE-promoted neonatal rat ventricular cardiomyocyte .RESULTS:miR-1 and-16 expression were markedly de-creased in hypertrophic myocardium and hypertrophic cardiomyocytes in rats .Overexpression of miR-1 and -16 suppressed rat cardiac hypertrophy and hypertrophic phenotype of cultured cardiomyocytes .Expression of cyclins D1, D2 and E1, CDK6 and phosphorylated pRb was increased in hypertrophic myocardium and hypertrophic cardiomyocytes , but could be reversed by enforced expression of miR-1 and -16.CDK6 was validated to be modulated post-transcriptionally by miR-1, and cyclins D1, D2 and E1 were further validated to be modulated post-transcriptionally by miR-16.CONCLUSION: Attenuations of miR-1 and -16 provoke cardiomyocyte hypertrophy via derepressing the cyclins D1, D2, E1 and CDK6, and activating cyclin/Rb pathway.

AIM:To investigate the effect of miR-214 on cardiomyocyte hypertrophy and the expression of the potential target genes . METHODS:A cell model of hypertrophy was established based on angiotensin-Ⅱ( Ang-Ⅱ)-induced neonatal mouse ventricular car-diomyocytes (NMVCs).Dual luciferase reporter assay was performed to verify the interaction between miR-214 and the 3’ UTR of MEF2C.The expression of MEF2C and hypertrophy-related genes at mRNA and protein levels was determined by RT-qPCR and Wes-tern blotting, respectively.RESULTS:The expression of ANP, ACTA1,β-MHC and miR-214 was markedly increased in Ang-Ⅱ-in-duced hypertrophic cardiomyocytes .Dual luciferase reporter assay revealed that miR-214 interacted with the 3’ UTR of MEF2C, and miR-214 was verified to inhibit MEF2C expression at the transcriptional level .The protein expression of MEF2C was markedly in-creased in the hypertrophic cardiomyocytes .Moreover, miR-214 mimic, in parallel to MEF2C siRNA, inhibited the expression of hy-pertrophy-related genes in Ang-Ⅱ-induced NMVCs.CONCLUSION:MEF2C is a target gene of miR-214, which mediates the effect of miR-214 on attenuating cardiomyocyte hypertrophy .

AIM:To investigate the effect of microRNA-214 ( miR-214) on cardiomyocyte hypertrophy and the expression of the potential target genes .METHODS:A cell model of hypertrophy was established based on angiotensin-Ⅱ( Ang-Ⅱ)-induced neonatal mouse ventricular cardiomyocytes ( NMVCs) .Dual luciferase reporter assay was performed to verify the interaction between miR-214 and the 3’ UTR of MEF2C.The expression of MEF2C and hypertrophy-related genes at mRNA and protein levels was determined by RT-qPCR and Western blot , respectively .RESULTS:The expression of ANP, ACTA1,β-MHC and miR-214 was markedly increased in Ang-Ⅱ-induced hypertrophic cardiomyocytes .Dual lu-ciferase reporter assay revealed that miR-214 interacted with the 3’ UTR of MEF2C, and miR-214 was verified to inhibit MEF2C expression at the transcriptional level .The protein expression of MEF2C was markedly increased in the hypertro-phic cardiomyocytes .Moreover, miR-214 mimic, in parallel to MEF2C siRNA, inhibited the expression of hypertrophy-re-lated genes in Ang-Ⅱ-induced NMVCs.CONCLUSION:MEF2C is a target gene of miR-214, which mediates the effect of miR-214 on attenuating cardiomyocyte hypertrophy .

OBJECTIVETo investigate the association of desmoplakin with the distribution and function of Nav1.5 by RNA silencing technology in HL-1 cells.

METHODSHL-1 cells with desmoplakin expression suppression by RNA silencing were examined for desmoplakin and Nav1.5 protein expressions by Western blotting, and the distribution and co-location of desmoplakin and Nav1.5 protein were detected by immunofluorescence staining. Patch-clamp recording was applied to analyze the changes in whole-cell sodium current after desmoplakin silencing.

RESULTSCompared with the untreated group and negative control group, the cells with desmoplakin silencing showed obviously reduced expressions of desmoplakin and Nav1.5 proteins. Co-localization of desmoplakin and Nav1.5 was detected at cell-cell contact in untreated and control conditions, and desmoplakin expression silencing induced a drastic redistribution of Nav1.5 with decreased peak current density (156.3∓6.2 vs 41.8∓3.1, n=6, P<0.05), a shift in voltage dependence of steady-state inactivation (-42 mV vs -61 mV, n=5, P<0.05), and prolonged time of recovery from inactivation.

CONCLUSIONDesmoplakin silencing caused redistribution of Nav1.5 protein and also changes in its electrophysiological properties in HL-1 cells.

Animals ; Cell Line ; Desmoplakins ; genetics ; metabolism ; Gene Silencing ; Mice ; Mutation ; Myocytes, Cardiac ; metabolism ; NAV1.5 Voltage-Gated Sodium Channel ; metabolism

BACKGROUND:Most balance disorders after total hip arthroplasty require a variety of rehabilitation methods to improve.Body weight support Tai Chi footwork can be used as a safe and effective balance training method. OBJECTIVE:To observe the effect of body weight support Tai Chi footwork on the balance function of patients after total hip arthroplasty. METHODS:Totally 74 subjects undergoing total hip arthroplasty were recruited and randomly divided into a control group(n=37)and a trial group(n=37).The control group received 30 minutes of body weight support walking training and 60 minutes of routine rehabilitation training;the trial group received 30 minutes of body weight support Tai Chi footwork training and 60 minutes of routine rehabilitation training,once a day,5 times a week,for 12 consecutive weeks.Before the intervention,4,8,and 12 weeks after intervention,the Berg balance scale and the dynamic balance ability test were used to evaluate the balance function.Harris score was used to evaluate the hip joint function,and the fall risk index was used to evaluate the fall risk. RESULTS AND CONCLUSION:(1)The four observation indicators all showed significant time effects(P<0.001).(2)Berg balance scale,Harris score and fall risk index all had an interaction effect(P<0.001),and there was a significant inter-group difference after 12 weeks of intervention(P<0.001),and the effect of the trial group was better than that of the control group.(3)After 12 weeks of intervention,there was an interaction and group effect in the scores of the front and left directions of the dynamic balance test(P<0.001),and there were significant group differences in the scores of the overall,front,left and right directions(P<0.001).(4)The results showed that after 12 weeks of intervention,the balance functions of the trial group and the control group were improved,and the improvement effect of body weight support Tai Chi footwork training was better than body weight support walking training on patients after total hip arthroplasty.

ObjectiveTo systematically review the efficacy of robot-assisted training on upper limb motor dysfunction in stroke patients. MethodsRelated literatures were searched in PubMed, Medline, Embase, Cochrane Library, Web of Science, CNKI, Wanfang Data, SinoMed, VIP data from July 1, 2019 to July 1, 2022. Two researchers screened the studies and extracted the data independently, and evaluated the methodological quality. Rev Man 5.4 was used for meta-analysis. ResultsA total of 19 randomised controlled trials with 1 258 subjects were finally included. The scores of Fugl-Meyer Assessment-Upper Extremity (SMD = 0.55, 95%CI 0.40 to 0.71, P < 0.001), modified Bathel Index (MD = 7.55, 95%CI 6.55 to 8.54, P < 0.001) and Motor Activity Log (SMD = -0.84, 95%CI -1.38 to -0.31, P = 0.002) were better in the experimental group than in the control group. However, no significant difference was found in the scores of Brunnstrom stages (upper extremity) (SMD = 0.61, 95%CI -0.08 to 1.30, P = 0.08) and modified Ashworth Scale (MD = -0.51, 95%CI -1.18 to 0.17, P = 0.14) between two groups. ConclusionRobot-assisted training could significantly improve the motor function of upper limbs in stroke patients.

Driven by multiple factors such as policy incentives,enhanced economic capacity of residents,aging popula-tion,and medical system reform,China's rehabilitation industry has been in a rapid development stage where opportunities and challenges coexist.Various rehabilitation hospitals urgently need new development thinking on how to seize the new opportunities for the development of rehabilitation medicine,give full play to the benefits of high-quality rehabilitation medical resources,and deal with the development of rehabilitation institutions under the new situation.Taking the tertiary rehabilitation hospital where the authors work as an example,this paper deeply analyzes the practical difficulties and challenges faced by the development of reha-bilitation hospital under the new circumstance,further explores the construction of a new working mode based on people-oriented and medical-rehabilitation integration.It also briefly summarizes the beneficial experiences and practices in the reform of rehabili-tation service models,and elaborates on the periodic achievement,so as to provide a meaningful reference for the majority of re-habilitation hospitals to plan and practice high-quality development and reform.

OBJECTIVETo investigate the role of miR-199a-3p in cardiac fibrosis and the potential target of miR-199a-3p.

METHODSCardiac fibroblasts were isolated from C57BL/6 mice and cultured. The miR-199a-3p mimic and Smad1 siRNA were transiently transfected into the cardiac fibroblasts via liposome. Dual luciferase reporter assay was performed to confirm the interaction between miR-199a-3p and the 3'-UTR of Smad1. The expressions of Smad1 and fibrosis-related genes at the mRNA and protein levels in the cells after miR-199a-3p mimic transfection were determined using RT-qPCR and Western blotting, respectively. The expressions of Smad1, Smad3 and fibrosis-related genes at the protein level in cells transfected with miR-199a-3p mimic and Smad1 siRNA were detected using Western blotting.

RESULTSOver-expression of miR-199a-3p significantly increased the expression of cardiac fibrosis-related genes in cultured mouse cardiac fibroblasts. Dual luciferase reporter assay revealed the interaction of miR-199a-3p with the 3'-UTR of Smad1. The results of RT-qPCR and Western blotting confirmed that miR-199a-3p inhibited Smad1 expression at the post- transcriptional level. Transfection with miR-199a-3p mimic and siRNA-mediated Smad1 silencing consistently activated the Smad3 signaling pathway and enhanced the expressions of cardiac fibrosis-related genes in the cardiac fibroblasts.

CONCLUSIONSAs the target gene of miR-199a-3p, Smad1 mediates the pro-fibrotic effect of miR-199a-3p by activating the Smad3 signaling in cultured mouse cardiac fibroblasts.