Fiber type of skeletal muscle and its multiple and specialized protein isoform are the structure and molecular basis of the skeletal muscle's function and adaptability.Myosin heavy chain(MHC)isoform,as the factor determinating the type of the skeletal muscle to be fast or slow one,has become molecular biomarker of muscle fiber type and adaptability.Exercise may lead to the transform between myosin subtypes.This article reviewed not only the relation between myosin heavy chain and muscle fiber type of skeletal muscle,but also the influences of different motor patterns' on the transform of skeletal muscle fiber MHC isoform.

Objective: To observe the biocompatibility of titanium implant surfaces using laser scanning confocal microscopy (LSCM). Methods; Titanium implant surfaces were prepared by 3 different methods. Osteoblasts were seeded onto the titanium surfaces. The cells were investigated by LSCM. Results: The sand-blasted titanium surfaces showed the best biocompatibility. Conclusion; The biocompatibility of titanium implant surfaces depends on the surface preparation method.

Objective To compare the efficacy of patient-controlled epidural analgesia(PCEA) and routine analgesia on treatment of bleeding in patients prostate pit after prostatectomy.Methods 82 patients underwent prostatectomy were randomly divided into two groups:patient-controlled epidual analgesia(n=40) and routine postoperative analgesia (n=42).Results As compared with control group,the rate and duration of bladder spasm were reduced significantly in PCEA group(P

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BACKGROUND:Heavy load exercises can induce the ultrastructural changes in the skeletal muscle by the depolymerization and/or degradation of tubulin in the skeletal muscle, thereby lessening contraction activities of the skeletal muscle. OBJECTIVE:To observe the effects of heavy load exercise and acupuncture on tubulin levels, and to analyze their roles and mechanisms in skeletal muscle injury and repair. METHODS:138 male Sprague-Dawley rats aged 8 weeks were randomly divided into acute exercise group (n=114) and long-term exercise group (n=24). The acute exercise group included four subgroups:sedentary group (n=6), exercise group (n=36), acupunctured group (n=36) and exercise plus acupuncture group (n=36). In the acute exercise experiment, rats were acupunctured after a medium-large intensity downhil running. Rat’s soleus samples were taken immediately, 6, 12, 24, 48 and 72 hours after exercise and/or acupuncture. In the long-term exercise experiment, rats underwent exercise and acupuncture for 3 weeks, and rat’s soleus samples were col ected at 24 hours after the last training. Expressions ofα-tubulin and microtubule-associated protein 4 (MAP4) in the soleus were detected by western blot assay. RESULTS AND CONCLUSION:After acute exercise, expression ofα-tubulin and MAP4 was up-or down-regulated transiently. After acute exercise combined with acupuncture, the protein expressions ofα-tubulin and MAP4 changed slightly. However, the long-term exercise induced an increase inα-tubulin protein expression, while a significant decrease in MAP4 protein expression. It was worth noting that acupuncture treatment reduced long-term exercise-induced variations of MAP4 expression. These results suggest that the heavy load exercise can induce the depolymerization of tubulins in the skeletal muscle, and acupuncture may relieve this effect.

Alzheimer's disease(AD)and Parkinson's disease(PD)are common neurodegenerative diseases that seriously threaten the health of the elderly, involving various abnormalities in physiology and metabolism including the impairment of mitochondrial function, Ca 2+ homeostasis deregulation, oxidative stress, aggregation of misfolded proteins, autophagy and inflammation.However, mechanisms underlying the pathogenesis of these diseases have not been clearly elucidated, thus impeding advances in their treatment.In recent years, it has been found that mitochondria-associated endoplasmic reticulum membranes(MAM)play an important role in the development of AD and PD and exert their effects by regulating the functions of mitochondria and endoplasmic reticula.This article reviews studies of the past decade related to the effects of MAM on AD and PD, aiming to generate insights for exploring the constituent proteins of MAM and the molecular mechanisms of AD and PD via endoplasmic reticulum-mitochondria Ca 2+ transport and ER stress regulated by MAM.

BACKGROUND: High-intensity exercise can induce the depolymerization and/or degradation of tubulin in the skeletal muscle. According to the close relation with the mitochondria, tubulin may influence mitochondrial movement track and molecular motor, thereby varying the movement and distribution of mitochondria. OBJECTIVE: To observe the effect of high-intensity exercise on α-tubulin, MAP4, Miro1 and mitochondrial ultrastructures, analyze their sequential changes and further explore whether tubular depolymerization regulates the movement and distribution of mitochondria via Miro1. METHODS: Fifty-six Sprague-Dawley rats were divided into control (n=8) and exercise (n=48) groups. The rats in the exercise group ran on the treadmill ( -16°, 20 m/minute) for 90 minutes, and the soleus samples were removed immediately, 6, 12, 24, 48 and 72 hours after exercise (n=8 each time point). The expression levels of α-tubulin, MAP4 and Miro1 were detected by western blot assay, and the ultrastructural changes of mitochondria were observed under transmission electron microscope. RESULTS AND CONCLUSION: The expression level of α-tubulin was decreased significantly at 6 and 12 hours after exercise. The expression level of MAP4 was increased significantly at 6, 12, 48 and 72 hours after exercise. The expression level of Miro1 was increased firstly at 6 and 12 hours after exercise, and decreased at 72 hours after exercise. In the control group, the paired mitochondria were arranged on the both sides of Z line, and few appeared in the myolemma. Mitochondria began to accumulate in the myolemma immediately and 6 hours after exercise; the number achieved the peak at 12 hours, reduced at 24 and 48 hours, and returned to normal at 72 hours. These results suggest that high-intensity exercise can induce the depolymerization of microtubules in the skeletal muscle, thus regulating the movement and distribution of mitochondria via Miro1.

Objective To investigate the clinical characteristics of tuberculosis (TB) first presenting as fever of unknown origin (FUO). Methods The clinical data of 100 cases of FUO, diagnosed as TB finally, among in-patients in Peking Union Medical College Hospital were analyzed retrospectively.Results ( 1 ) Sites of TB: there were 39 patients with merely pulmonary TB, 28 patients with merely extrapulmonary TB, and 33 patients with both pulmonary and extrapulmonary TB. (2) Clinical manifestations: depending on the different sites of tuberculous lesion, the clinical symptoms varied accordingly. The common laboratory findings included anemia, hypoalbuminemia, elevation of the level of ESR and C-reactive protein (CRP). (3) Methods for diagnosis: 34 cases were diagnosed by sputum smearor cultivation-positive for acid-fast bacilli; 8 cases by histopathology; 49 cases by clinical diagnosis of TB with an effective anti-TB therapy; and 9 cases by effective diagnostic anti-TB therapy. (4) Responses to treatment: among 73 cases with complete follow-up data, only 2 cases (2. 7% ) died and the other cases were cured or alleviated. Fifty-five cases (77.5%) showed marked efficacy after less than 4 weeks of regular anti-TB therapy, 37 cases ( 52. 1% ) suffered adverse effects of anti-TB agents, and all of them had improved after modifying anti-TB therapy and supporting treatment. Conclusions The diagnosis of TB that presents as FUO is quite difficult, and the median interval time for making diagnosis is 14 weeks (3-77weeks). Investigating clinical manifestations comprehensively, reviewing radiology data carefully, and eliciting microbiological and pathologic evidence of TB, are extremely important for making the correct diagnosis. In some cases, a therapeatic trial of anti-TB therapy is necessary.

Objective To report the clinical characteristics of prosthetic valve endocarditis (PVE).Methods All 25 cases of definite PVE (Duke criteria) diagnosed at our hospital between January 1992 to December 2008 were retrospectively analyzed. Among them, 7 cases were pathologically confirmed and the others were clinically confirmed with either 2 major criteria or 1 major and ≥3 minor criteria. Their clinical characteristics, underlying heart diseases, previous heart operations, presenting manifestations, causative microbes, echocardiographic findings and prognosis, were studied. Results (1) Although most cases underwent valve transplantations for underlying heart diseases of rheumatic heart diseases and congenital heart diseases, 10 patients were complicated with infectious endocarditis (IE) prior to the operations, 4 of them were PVE. (2) Eleven of them developed PVE within 2 months postoperatively. Fever (100%),major vessel embolism (48%), and anemia (36%) were the most frequently manifestations. Fourteen cases (56%) had positive culture results with 15 causative pathogens, including 5 coagulase-negative Staphylococcus (CNS, 3 were methicillin-resistant coagulase-negative Staphylococcus, MRSCoN), 4 fungi, 2Enterococcus faecalis, 2 Burkholderia cepacia, 1 Stenotrophomonasmal-tophilia, and 1 Streptococcus.(3)Prosthetic valve vegetations, periannular leakage, regurgitation, were the main echocardiographic findings.Transesophageal echocardiography (TEE) revealed 13 PVE who had no positive findings on previous transthoracic echocardiography (TTE). (4) Eighteen PVE (72%) developed peri-annular complications (12 leakage, 3 dehiscence, 2 abscesses, 1 fistula), major vessel embolism, congestive heart failure (16%) were frequently observed, 9 of the 17 patients died in hospital, in spite of intensive managements.Conclusions PVE has a high mortality and is a severe complication for patients who underwent heart surgery. Its causative pathogen spectrum is quite different from that of native valve endocarditis. TTE is not sensitive for some PVE cases.

Objective: To evaluate the role of G protein-coupled receptor 30 (GPR30) in 17β estradiol-induced inhibition of ketamine-caused neuroapoptosis in the hippocampus of newborn rats and the relationship with phosphorylated extracellular signal-regulated kinase 1/2 (p-ERKl/2). Methods: Twenty-four clean-grade healthy male Sprague-Dawley rats, aged 7 days, weighing 11-18 g, were divided into 4 groups (n=6 each) using a random number table method: control group (group C), ketamine group (group K), 17β estradiol plus ketamine group (group EK), and GPR30 inhibitor G15 plus 17β estradiol plus ketamine group (group G15EK). Ketamine 75 mg/kg (diluted to 0.1 ml in normal saline) was intraperitoneally injected every 24 h for 3 consecutive days in group K. In group EK, 17β estradiol 600 μg/kg was subcutaneously injected and ketamine 75 mg/kg was intraperitoneally injected every 24 h for 3 consecutive days.G15 300 μg/kg and 17β estradiol 600 μg/kg were subcutaneously injected and ketamine 75 mg/kg was intraperitoneally injected every 24 h for 3 consecutive days in group G15EK.The equal volume of normal saline 0.1 ml was intraperitoneally injected instead in group C. The animals were sacrificed at 24 h after the last injection for determination of the expression of cleaved caspase-3, ERK1/2 and phosphorylated ERK1/2(p-ERK1/2) (by Western blot). Results: There was no significant difference in the expression of ERK1/2 in hippocampus among the four groups (P>0.05). Compared with group C, the expression of cleaved caspase-3 was significantly up-regulated, and the expression of p-ERK1/2 was down-regulated in K and G15EK groups (P<0.05). Compared with group K, the expression of cleaved caspase-3 was significantly down-regulated, and the expression of p-ERK1/2 was up-regulated in group EK (P<0.05). Compared with group EK, the expression of cleaved caspase-3 was significantly up-regulated, and the expression of p-ERK 1/2 was down-regulated in group G15EK (P<0.05). Conclusion GPR30 is involved in 17β estradiol-induced inhibition of ketamine-caused neuroapoptosis in the hippocampus of newborn rats, which is related to up-regulating the expression of p-ERKl/2.