Objective To investigate the changes of myosin heavy chain ( MyHC) isoforms in rat masseter muscle fibers caused by chronic sleep deprivation ( CSD) and a possible link with the pathogenesis of temporomandibular joint disorders ( TMD ) .Methods Total 180 male rats were randomly divided into three groups( n=60 per group): chronic sleep deprivation group ( CSD),cage control group ( CC),and large-platform control group ( TC ) .Each group was further divided into three subgroups ( n=20 in each group)according to the observation time point(7,14,and 21 days).The expression of MyHC isoforms in mas-seter muscle fibers was investigated by real-time quantitative PCR,Western blotting and immunohistochemi-cal staining.Results The expression of MyHC-Ⅰ,MyHC-ⅡA and MyHC-ⅡB deep and shallow masseter muscle in CSD7d group had differention with the control group(MyHC-Ⅰ:(0.314±0.005,0.134±0.005, P<0.05;MyHC-ⅡA (7.960±0.465,7.090±0.564, P<0.05;MyHC-ⅡB:(2.840±0.054,2.580±0.054, P<0.05) .The expression of MyHC-Ⅰdeep and shallow masseter muscle in CSD 14 d group had differention with the control group(0.284±0.005,0.106±0.015, P<0.05),the same appearance as MyHC-ⅡA deep and shallow masseter muscle(7.030±1.045,6.050±0.976, P<0.05) and MyHC-ⅡB deep and shallow masseter muscle((3.680±0.548,3.850±0.457, P<0.05).CSD groups exhibited increased MyHC-Ⅰexpression in both the deep and shallow muscle fiber layers at 7 days compared with CC and TC groups(P<0.05) ,whereas CSD significantly decreased MyHC-ⅡA and MyHC-ⅡB expression(P<0.05) .The expression of MyHC-Ⅱwas sig-nificantly decreased in CSD 7 d group,while the expression of MyHC-Ⅰwas increased.As the CSD time ex-tended,the MyHC-Ⅱexpression was increased and MyHC-Ⅰexpression was descreased.CSD 21d group ex-hibited significant different from MyHC-Ⅱand MyHC-Ⅰexpression in the deep muscle fiber layer compared with those in CC and TC groups (P<0.05) ,while there was no difference of MyHC-Ⅰor MyHC-Ⅱexpression in the shallow muscle fiber layer between CSD group and CC group (P>0.05) ,and there were no differences between the CC and TC groups at any time point.Conclusion These findings suggest that CSD alters the ex-pression of MyHC isoforms,which may contribute to TMD pathogenesis.

The implantation of biventricular assist device (BiVAD) is more challenging than that of left ventricular assist device for the interaction in the process of multiple input and output. Besides, ventricular assist device (VAD) often runs in constant speed (CS) mode in clinical use and thus BiVAD also faces the problems of low pulsation and imbalance of blood volume between systemic circulation and pulmonary circulation. In this paper, a delay assist mode for a VAD by shortening the support time of VAD was put forward. Then, the effect of the delay mode on cardiac output, pulsation and the function of the aortic valve was observed by numerical method and the rules of hemodynamics were revealed. The research showed that compared with VAD supported in CS mode, the VAD using delay mode in systolic and diastolic period proposed in this paper could meet the demand of cardiac output perfusion and restore the function of the arterial valves. The open ratio of aortic valve (AV) and pulmonary valve (PV) increased with the time set in delay mode, and the blood through the AV/PV helped to balance the left and the right cardiac volume. Besides, delay mode also improved the pulsation index of arterial blood flow, which is conducive to the recovery of the ventricular pulse function of patients.
Cardiovascular System ; Diastole ; Heart Failure ; Heart Rate ; Heart-Assist Devices ; Hemodynamics ; Humans ; Models, Cardiovascular