Virtual Reality Training for Balance Function for Old Adults: A Meta-analysis / 中国康复理论与实践

Objective:To systematically evaluate the effects of virtual reality (VR) training on balance function for old adults. Methods:The randomized controlled trials between VR training and routine rehabilitation for balance function for old adults were retrieved from databases of CNKI, Wangfang data, CBM, VIP, Web of Science, PubMed, Clinical Science, EMBASE, Science Direct, Medline, Cohrane Library and Google Scholar. The literatures were screened, data were extracted and the risk of bias were assessed, and analysed with RevMan. Results:A total of 20 randomized controlled trials were included. Compared with the routine rehabilitation, VR training promoted recovery in score of Berg Balance Scale (BBS) for all the old adults (WMD = 2.33, 95%CI 0.88 to 3.78), those < 75 years old (WMD = 2.59, 95%CI 0.22 to 4.97) and > 75 years old (WMD = 2.69，95%CI 1.82 to 3.57). VR training also promoted recovery in time of Timed "Up & Go" Test (TUGT) for all the old adults (WMD = 　-0.96, 95%CI -1.65 to -0.28) and those < 75 years old (WMD = -1.06, 95%CI -1.98 to -0.15), but those > 75 years old (WMD = -0.81, 95%CI -1.98 to 0.37). Conclusion:VR training may promote the recovery of balance and walking for old adults.

The effect of relgulation of PPAR-α on cardiac hypertrophy and the relationship between the effect of PPAR-α with PI3K/Akt/mTOR pathway / 中国应用生理学杂志

<p><b>OBJECTIVE</b>To investigate the effect of peroxisiome proliferator activated receptor-α (PPAR-α) on the regulation of cardiomyocyte hypertrophy and the relationship between the effect of PPAR-α with PI3K/Akt//mTOR signal pathway.</p><p><b>METHODS</b>Cardiomyocyte hypertrophy was induced by isoproterenol (ISO). The cell surface area was measured by image analysis system (Leica). The expressions of atrial natriuretic peptide (ANP), β-myosin heavy chain (β-MHC) and PPAR-α mRNA were detected by qRT-PCR. The protein expressions of Akt, mTOR and P70S6K were detected by Western blot. The expression of PPAR-α was suppressed by RNAi.</p><p><b>RESULTS</b>(1) The expression of PPAR-α was significantly reduced in cardiomyocyte hypertrophy. PPAR-α activator Fenofibrate (Feno) increased the expression of PPAR-α and suppressed cardiomyocyte hypertrophy. The inhibitory effect of Feno on cardiomyocyte hypertrophy was reversed by PPAR-α RNAi. (2) Feno significantly inhibited the increase of the protein expressions of p-Akt, p-mTOR and p-p70S6K in ISO induced cardiomyocyte hypertrophy, which could be blocked by PPAR-α RNAi. (3) PI3K antagonist LY294002 (LY) or mTOR antagonist rapamycin (RAPA) markedly-inhibited cardiomyocyte hypertrophy. The inhibitory effects of LY or RAPA on cardiomyocyte hypertrophy were reversed by PPAR-α RNAi.</p><p><b>CONCLUSION</b>PPAR-α can negatively regulate cardiomyocyte hypertrophy. The effect might be associated with PPAR-α inhiting PI3K/ Akt/mTOR signal pathway.</p>

MicroRNA-133a attenuates isoproterenol-induced neonatal rat cardiomyocyte hypertrophy by downregulating L-type calcium channel α1C subunit gene expression / 中华心血管病杂志

<p><b>OBJECTIVE</b>To investigate the effects of microRNA-133a on isoproterenol (ISO)-induced neonatal rat cardiomyocyte hypertrophy and related molecular mechanism focusing on the changes of L-type calcium channel α1C subunit.</p><p><b>METHODS</b>Neonatal rat cardiomyocytes were cultured, cardiomyocyte hypertrophy was induced by isoproterenol (ISO, 10 µmol/L). The cell surface area was measured by phase contrast microscope and Leica image analysis system. The mRNA expressions of atrial natriuretic peptide (ANP), β-myosin heavy chain (β-MHC), miR-133a and the α1C were detected by qRT-PCR. The protein expression of α1C was evaluated by Western blot. MiR-133a mimic was transfected into cardiomyocytes to investigate the effects of miR-133a on ISO-induced cardiomyocyte hypertrophy. The targets of miR-133a were predicted by online database Targetscan. The 3' untranslated region sequence of α1C was cloned into luciferase reporter vector and then transiently transfected into HEK293 cells. The luciferase activities of samples were measured to verify the expression of luciferase reporter vector. The expression level of α1C was inhibited by RNAi to determine the effects of α1C on cardiomyocyte hypertrophy. Intracellular Ca(2+) content was measured by confocal laser microscope.</p><p><b>RESULTS</b>(1) The expression of miR-133a was significantly reduced in ISO-induced cardiomyocyte hypertrophy (P < 0.01) . Upregulating miR-133a level could suppress the increase of cell surface area, the mRNA expression of ANP and β-MHC (P < 0.01) . (2) α1C was the one of potential target of miR-133a by prediction using online database Targetscan. The luciferase activities of HEK293 cells with the plasmid containing wide type α1C 3'UTR sequence were significantly decreased compared with control group (P < 0.01) . Upregulation of the miR-133a level by miR-133a mimic transfection could suppress the protein expression of α1C (P < 0.05) . (3) The expression of α1C was significantly increased in ISO treated cardiomyocytes (P < 0.05) . Downregulation of α1C by RNAi could markedly inhibit the increase of cell surface area, the mRNA expression of ANP and β-MHC (P < 0.01, P < 0.05, P < 0.05). (4) Downregulation of α1C expression by RNAi or upregulation of miR-133a level by miR-133a mimic transfection significantly inhibited intracellular Ca(2+) content (P < 0.01) .</p><p><b>CONCLUSIONS</b>Our data confirms that α1C is the target of miR-133a. MiR-133a can negatively regulate the expression of L-type calcium α1C subunit, resulting in the decrease of intracellular Ca(2+) content and the attenuation of ISO-induced cardiomyocyte hypertrophy.</p>