Objective To investigate the impact of enterovirus 71(EV71)on skeletal muscle injury and explore its mechanism in relation to the caspase-1/interleukin(IL)-1 β signaling pathway in EV71-induced skeletal muscle damage.Methods One-day-old BALB/c suckling mice were divided randomly into three groups:normal control(NC)(n=60),EV71 infection model(n=60),and caspase-1 inhibitor(EV71+VX765)(n=15)groups.The NC and EV71 model groups were further subdivided into four subgroups(5,7,10,and 14 days)(n=5 mice per group).An EV71-infected model was established by intraperitoneal injection of 25 × 103 μL/kg EV71 viral solution for 3 consecutive days.Mice in the caspase-1 inhibitor group received VX765(20 mg/kg)intraperitoneally 6 hours post-viral inoculation,continued daily for 10 days until sample collection.Mice in the NC group received an equivalent volume of saline containing 5％dimethylsulfoxide and 10％PEG300,followed by 2％cell maintenance solution after 6 hours.Post-modeling body weight and clinical disease scores were recorded.Pathological skeletal muscle damage was observed by hematoxylin-eosin(HE)staining,and expression levels of EV71 VP-1(viral capsid protein),pro-caspase-1,cleaved-caspase-1,IL-1 β,α-smooth muscle actin(SMA),and Collagen Ⅰ were detected by Western blot and immunofluorescence.Results Compared with the NC group at the same time points,mice in the EV71 model group exhibited reduced body weight,elevated disease scores,and skeletal muscle pathology characterized by inflammatory cell infiltration,myofiber dissolution,and decreased cross-sectional area(HE staining).Western blot showed significantly increased levels of EV71 VP-1,IL-1β,α-SMA,and Collagen Ⅰ in skeletal muscle homogenate from EV71 mice at 5,7,and 10 days post-infection(P＜0.001).In contrast,mice in the VX765 group showed improved body weight,reduced clinical scores(P＜0.01),and significant downregulation of EV71 VP-1(P＜0.01),pro-caspase-1,cleaved-caspase-1,IL-1β,and Collagen Ⅰ compared with the EV71 model group(P＜0.01).These findings were confirmed by immunofluorescence,indicating that inhibition of caspase-1 alleviated EV71-induced skeletal muscle injury.Conclusions EV71 may induce skeletal muscle injury by activating the caspase-1/IL-1β signaling pathway.

Objective To investigate the impact of enterovirus 71(EV71)on skeletal muscle injury and explore its mechanism in relation to the caspase-1/interleukin(IL)-1 β signaling pathway in EV71-induced skeletal muscle damage.Methods One-day-old BALB/c suckling mice were divided randomly into three groups:normal control(NC)(n=60),EV71 infection model(n=60),and caspase-1 inhibitor(EV71+VX765)(n=15)groups.The NC and EV71 model groups were further subdivided into four subgroups(5,7,10,and 14 days)(n=5 mice per group).An EV71-infected model was established by intraperitoneal injection of 25 × 103 μL/kg EV71 viral solution for 3 consecutive days.Mice in the caspase-1 inhibitor group received VX765(20 mg/kg)intraperitoneally 6 hours post-viral inoculation,continued daily for 10 days until sample collection.Mice in the NC group received an equivalent volume of saline containing 5％dimethylsulfoxide and 10％PEG300,followed by 2％cell maintenance solution after 6 hours.Post-modeling body weight and clinical disease scores were recorded.Pathological skeletal muscle damage was observed by hematoxylin-eosin(HE)staining,and expression levels of EV71 VP-1(viral capsid protein),pro-caspase-1,cleaved-caspase-1,IL-1 β,α-smooth muscle actin(SMA),and Collagen Ⅰ were detected by Western blot and immunofluorescence.Results Compared with the NC group at the same time points,mice in the EV71 model group exhibited reduced body weight,elevated disease scores,and skeletal muscle pathology characterized by inflammatory cell infiltration,myofiber dissolution,and decreased cross-sectional area(HE staining).Western blot showed significantly increased levels of EV71 VP-1,IL-1β,α-SMA,and Collagen Ⅰ in skeletal muscle homogenate from EV71 mice at 5,7,and 10 days post-infection(P＜0.001).In contrast,mice in the VX765 group showed improved body weight,reduced clinical scores(P＜0.01),and significant downregulation of EV71 VP-1(P＜0.01),pro-caspase-1,cleaved-caspase-1,IL-1β,and Collagen Ⅰ compared with the EV71 model group(P＜0.01).These findings were confirmed by immunofluorescence,indicating that inhibition of caspase-1 alleviated EV71-induced skeletal muscle injury.Conclusions EV71 may induce skeletal muscle injury by activating the caspase-1/IL-1β signaling pathway.

Objective: To determine the association between physical health fitness with Chinese reading ability of schoolaged children, so as to provide evidence for improving children s reading ability. Methods: A questionnaire survey was conducted among 1 923 school aged children in grades 2-6 in a primary school in Wuhan, Hubei Province, China. The questionnaire included basic demographic information and Dyslexia Checklist for Chinese Children and the Pupil Rating Scale Revised Screening. At the same time, participants underwent physical fitness tests which included an assessment of height, weight, and lung capacity, as well as a 50 meter run, sit forward bend, one minute skipping rope task, sit ups, and a 50 × 8 round trip. Results: A total of 59 children were identified with dyslexia. Normal children achieved higher scores than children with dyslexia in the total physical health score, as well as the one minute skipping rope score, one minute sit up score, and sitting forward score ( P <0.05). Multiple linear regression analyses showed that the reading ability of girls was higher than that of boys ( β =-3.04, P <0.01), and the children who regularly participated in more intense physical activity and who had higher fitness scores had a higher reading ability ( β =-1.68, -0.08, P <0.01). Children s reading ability increased significantly with parental educational level( P <0.05). Conclusion Gender, parents education level, physical exercise intensity, and children s physical fitness were identified as influencing factors of school age children s reading ability. A positive correlation was found between children s physical health level and reading ability.

Objective To explore the changes of appendicular skeletal muscle (ASM) in peritoneal dialysis (PD) patients, and to analyze the relationship between ASM changes and dietary intake.Methods One hundred and fourteen PD patients were enrolled in Department of Nephrology, Peking University Third Hospital using convenience sampling.At baseline, and 6 and 12 months after PD, bioelectrical impedance analysis was used to assess the body weight, total muscle mass, and ASM of these patients, and three-day food record was used to assess the dietary intake.Demographics and clinical data were also collected at baseline.Results Compared with baseline, the patients' ASM at 12 months after PD decreased significantly [(19.27 ± 5.59) kg vs.(25.65 ±6.09) kg, P =0.000], the dietary protein intake and energy intake decreased significantly [(0.85 ± 0.21) g/(kg · d) vs.(0.90 ± 0.27) g/(kg · d), P =0.038;(128.37 ± 26.67) kJ/(kg· d)vs.(137.27 ±29.23) kJ/(kg· d), P=0.001].The patients were divided into three groups based on ASM loss, the mean dietary protein intake of the top-loss 1/3 group was statistically lower than that of the bottom-loss 1/3 group [(0.82 ± 0.18) g/(kg · d) vs.(0.91 ± 0.20) g/(kg · d), P =0.021].Conclusions With the continuation of PD, ASM of patients may decrease, which is likely to be mainly related to deficiency in protein and energy intakes.Dietary management should be strengthened in PD patients to alleviate the loss of ASM.

80% activity rate against E.coli included piperacillin/tazobactam(93.4%)、ceftazidime(86%),and amikacin(83.3%);The susceptible rate to piperacillin/tazobactam in K.pneumoniae was 84.6%. The susceptible rate to ceftazidime decreased from 82.3% to 69.9%, which was lower than to cefepime (77.2%). Over 50% of Enterobacter cloacae were resistant to ceftazidime, cefotaxime and ceftriaxone. Susceptible rates to piperacillin/tazobactam in E. cloacae,E. aerogenes,Citrobacter freundii and Serratia marcescens (67.7%-96.4%) were higher than those to cefepime (68.8%-77.5%), cefoperazone/sulbactam (59.7%-87.5%). Susceptibility to amikacin among these 4 species (70%-83.7%) was higher than to ciprofloxacin (48.1%-79.5%). All of Morganella morganii and Proteus vulgaris isolates were susceptible to meropenem and imipenem; Over 90% of the isolates were susceptible to cefepime, cefoperazone/sulbactam and piperacillin/tazobactam.The most active agent against Pseudomonas aeruginosa was meropenem (84%), followed by amikacin, piperacillin/tazobactam, ceftazidime and imipenem (72.5%-76.6%). Mutiple-drug-resistant Acinetobacter baumannii increased from 33% in 2003 to 48% in 2004. Resistance to carbapenems increased to 18% in this species in 2004. The most active agents against Burkholderia cepacia were meropenme (64.9%), cefoperazon/sulbactam (63.2%), ceftazidime (59.6%), piperacillin/tazobactam (56.1%) and cefepime (52.6%).Conclusions Carbapenems remained very high activity against Enterobacteriaceae. Increasing resistance to 10 antimicrobials agents tested among A. baumanni brought great concern. Meropenem was 4-to 16-fold more active against common gram-negative bacilli than imipenem.