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.

Objective To study liver function, hepatic energy metabolism, regeneration and apoptosis in obstructive jaundiced or normal liver after 70% partial hepatectomy (PH) with hepatic artery resection (HAR) in rats. Methods In this study, 133 male SD rats were enrolled, 6 rats were in sham operation group, 20 rats underwent choledochoduodenostomy after 70% PH and 20 rats did 70%- PH, choledochoduodenostomy plus HAR. The remaining 87 rats 5 days after common bile duct ligation (CBDL) were randomized into two groups: 70% PH with choledochoduodenostomy, and 70% PH with choledochoduodenustomy plus HAR. Serum TB, ALT, ALB and ALP; tissue of hepatic HGF, bcl-2 mRNA and protein expression; ATP, ADP and AMP in hepatic tissues; hepatocyte proliferation/ apoptosis index were observed postoperatively (24 h, 72 h and 7 d). MortaLity was calculated. Results Rats without obstructive jaundice could tolerate 70% PH plus HAR with good liver regeneration. Compared with other groups, the serum liver function index; ATP content and EC value; HGF,bcl-2 mRNA content of liver tissue and the hepatocyte proliferation/apoptosis index in 70% PH with HAR group significantly aggravated and the mortality signiticanfly increased in obstructive jaundice rats ( P < 0. 05). Conclusions (1) The liver regeneration and apoptosis were not significantly influenced in normal mrs undergoing 70% PH and 70% PH with HAR, moreover hepatoeyte energy metabolism and liver function recovered rapidly in both groups. (2) With the existence of severe bilirubinemia, 70% PH with HAR caused an increased mortality suggesting a rationale for a preoperative bilirubin reducing procedures before a major surgery in malignant obstructive jaundice.