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Objective:To explore the effect of individualized aerobic training combined with resistance training on heart rate recovery and exercise capacity among patients with obstructive sleep apnea syndrome (OSAS) and explore possible mechanisms.Methods:Forty middle-aged patients with moderate to severe OSAS were randomly assigned to an observation group (OG, n=20) or a control group (CG, n=20). Both groups were given routine health guidance and motor training, while the OG additionally underwent individualized aerobic exercise training at 60%~75% of their peak power and resistance training loaded at 60%~80% of their ten-times maximum repetition figure. The training was three times a week for 3 months. Both groups underwent cardiopulmonary exercise testing and polysomnography before and after the 12-week intervention. The changes in their sleep apnea hypopnea index (AHI), oxygen desaturation index (ODI) and lowest oxygen saturation (L-SAO 2) were collected. Exercise capacity indicators such as peak oxygen uptake (VO 2peak), peak power, anaerobic threshold and sitting heart rate recovery (HRR) 1, 2 and 3 minutes after the test were recorded (denoted as HRR-1, HRR-2 and HRR-3). Results:There were no significant differences between the two groups in any of the measurements before the intervention. Afterward the average AHI, ODI and L-SAO 2 values of the observation group had all improved significantly compared with those before the training and compared with the control group′s values after the training. After the training, the VO 2peak and peak power of the observation group had also improved significantly compared with before the training and compared with the control group. HRR-1, HRR-2 and HRR-3 were all significantly higher in the observation group than before the training and higher than the control group′s values after the training. Conclusion:Combining aerobic and resistance training can improve the exercise ability and heart rate of middle-aged patients with moderate to severe OSAS, and also reduce the severity of their OSAS to some extent.
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Objective To observe the role of programmed cell death 5(PDCD5) gene combined with cisplatin for inducing the ap-optosis of human lung adenocarcinoma A549 cells and to investigate its possible mechanism .Methods The PDCD5 recombinant plas-mid was transiently transfected into A549 cells by lipofectamine .Its transfection efficiency was detected by RT-PCR .The expressions of trasfected PDCD5 protein ,Bcl-2 and Survivin protein were examined by Western bolt .The apoptosis of A549 cells by single PDCD5 and its combination with cisplatin was measured by the MTT method and the flow cytometry .Results PDCD5 recombinant plasmid was transfect into A549 cells successfully .The Western blot results showed that the expression of PDCD5 protein in the transfection recombinant plasmid group was higher than that in the blank control group and the transfection empty plasmid group ,while the expres-sion of Bcl-2 and Survivin protein was lower than that in the other two groups ,the difference was statistically significant (P<0 .05) . The MTT and flow cytometry results demonstrated that the cell apoptosis rate in the transfection recombinant plasmid group was higher than that in the blank control group and the transfection empty plasmid group (P<0 .05) .Conclusion PDCD5 gene may pro-mote cisplatin induced A549 cells apoptosis .
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The abdominal visceral fat content in obese SD rats induced by high fat diet for 10 weeks was significantly higher than that in control group [(26±6 vs 13±3)g,P<0.01] ,along with increased CRP mRNA expression in abdominal visceral fat (0.901±0.085 vs O. 402±0.036, P<0.01). As compared with normal control group, in the high fat group the concentrations of CRP in portal vein [(743.8±95.8 vs 558.3 ±118.3) mg/L, P<0.01] and peripheral vein[(596.3±38.9 vs 485.8±30.2) mg/L,P<0. 05] were higher. The concentration of CRP in portal vein was significantly higher than that in peripheral vein in high fat diet group(P<0.01) ,but this was not evident in control group. These results suggest that the increased CRP expression in visceral adipose tissue may partially account for the elevation of serum CRP in obesity.