Objective To observe the effects of electroacupuncture on the motor function and mitochondrial dynamics of skeletal muscle of SAMP8 mice;To explore the mechanism of electroacupuncture in improving the motor dysfunction of Alzheimer disease(AD)from the perspective of mitochondrial dynamics.Methods Totally 18 SAMP8 mice were divided into model group and electroacupuncture group,with 9 mice in each group,and the SAMR1 mice with the same age were set as control group."Baihui","Dazhui"and"Shenshu"were selected in the electroacupuncture group,and electroacupuncture was performed daily for 20 min,8 d as a course of treatment.Each course of treatment was separated by 2 d,for a total of 3 courses of treatment.The model group and the control group were not intervened.The motor function of mice was tested by grip strength test,suspension test,hind limb extension test and Morris water maze experiment.The morphology and structure of gastrocnemius were observed by HE staining,ATP content in gastrocnemius was determined by colorimetry,the mRNA expression of optic atrophy 1(OPA1),mitofusin 2(MFN2)and dynamin-related protein 1(DRP1)in gastrocnemius were detected by real-time quantitative PCR,the expressions of OPA1,MFN2 and DRP1 in gastrocnemius were detected by Western blot.Results Compared with the control group,the grip strength,the score in suspension test,and the average speed and maximum speed of Morris water maze experiment of mice in model group significantly decreased(P<0.01);the arrangement of fibers in the gastrocnemius muscle tissue was disordered,the gaps become wider,and the distribution of nuclei was uneven;the ATP content in the gastrocnemius muscle tissue was significantly decreased(P<0.01),the mRNA and protein expressions of OPA1 and MFN2 were significantly decreased(P<0.01),and the expression of DRP1 mRNA and protein significantly increased(P<0.01).Compared with the model group,the grip strength,the score in suspension test,and the average speed and maximum speed of Morris water maze experiment in electroacupuncture group significantly increased(P<0.01);the arrangement of gastrocnemius muscle tissue was relatively neat,the gaps become narrower,and the distribution of nuclei was more uniform;the ATP content in gastrocnemius muscle tissue significantly increased(P<0.01),while the mRNA and protein expressions of OPA1 and MFN2 significantly increased(P<0.05,P<0.01),the expression of DRP1 mRNA and protein significantly decreased(P<0.01).Conclusion Electroacupuncture can improve the skeletal muscle morphological structure and motor dysfunction of SAMP8 mice,and the mechanism may be related to the correction of skeletal muscle mitochondrial dynamic imbalance and the increase of skeletal muscle ATP content.

Objective To observe the effects of electroacupuncture on the motor function and expressions of Irisin,Decorin and Myostatin in skeletal muscle of SAMP8 mice;To explore the mechanism of electroacupuncture in the treatment of the motor dysfunction of Alzheimer disease(AD).Methods Totally 247-month-old male SAMP8 mice were randomly divided into model group and electroacupuncture group,with 12 mice in each group,and the 12 male SAMR1 mice with the same age were set as the control group."Baihui","Dazhui"and"Shenshu"were selected in the electroacupuncture group,once a day,8 days as one course of treatment,with an interval of 2 days,for a total of 3 courses.The control group and the model group were not intervened.The motor function of mice was tested by grip strength test,pole climbing test and open field test,the mRNA expressions of Irisin,Decorin and Myostatin in quadriceps muscle were detected by RT-qPCR,and the protein expressions of Irisin,Decorin and Myostatin in quadriceps muscle were detected by immunohistochemistry and Western blot.Results Compared with the control group,the grip peak and duration of the mice in the model group decreased,head turning time and pole climbing time were prolonged(P<0.01),the mRNA and protein expressions of Irisin and Decorin decreased(P<0.05,P<0.01),and the expressions of Myostatin mRNA and protein increased(P<0.05).Compared with the model group,the grip peak and duration of the mice in the electroacupuncture group increased,head turning time and pole climbing time were decreased(P<0.05),the mRNA and protein expressions of Irisin and Decorin increased(P<0.05),and the expressions of Myostatin mRNA and protein decreased(P<0.05).Conclusion Electroacupuncture can improve the motor dysfunction of SAMP8 mice,and its mechanism may be related to regulating the expressions of Irisin,Decorin and Myostatin in skeletal muscle.

Purpose: Isocitrate dehydrogenase 1 (IDH1) mutations are the most common genetic abnormalities in low-grade gliomas and secondary glioblastomas. Glioma patients with these mutations had better clinical outcomes. However, the effect of IDH1 mutation on drug sensitivity is still under debate. Materials and Methods: IDH1-R132H mutant cells were established by lentivirus. IDH1-R132H protein expression was confirmed by western blot. The expression of ataxia telangiectasia mutated (ATM) signaling pathway and apoptosis-related proteins were detected by immunofluorescence and western blot. Temozolomide (TMZ) induced cell apoptosis was detected by flow cytometry. Tumor cell proliferation was detected by Cell Counting Kit-8. In vivo nude mice were used to confirm the in vitro roles of IDH1 mutation. Results: We established glioma cell lines that expressed IDH1-R132H mutation stably. We found that TMZ inhibited glioma cells proliferation more significantly in IDH1 mutant cells compared to wild type. The IC50 of TMZ in IDH1-R132H mutant group was less than half that of wild-type group (p < 0.01). TMZ significantly induced more DNA damage (quantification of γH2AX expression in IDH1 mutation vs. wild type, p < 0.05) and apoptosis (quantification of AnnexinV+propidium iodide–cells in IDH1 mutation versus wild type, p < 0.01) in IDH1 mutant gliomas compared to wild-type gliomas. The ATM-associated DNA repair signal was impaired in IDH1 mutant cells. Inhibiting the ATM/checkpoint kinase 2DNA repair pathway further sensitized IDH1 mutant glioma cells to chemotherapy. We found that IDH1 mutation significantly inhibited tumor growth in vivo (the tumor size was analyzed statistically, p < 0.05). Moreover, we confirmed that gliomas with IDH1 mutation were more sensitive to TMZ in vivo compared to wild type significantly and the results were consistent with the in vitro experiment. Conclusion These results provide evidence that combination of TMZ and ATM inhibitor enhances the antitumor effect in IDH1 mutant gliomas.

Purpose: Isocitrate dehydrogenase 1 (IDH1) mutations are the most common genetic abnormalities in low-grade gliomas and secondary glioblastomas. Glioma patients with these mutations had better clinical outcomes. However, the effect of IDH1 mutation on drug sensitivity is still under debate. Materials and Methods: IDH1-R132H mutant cells were established by lentivirus. IDH1-R132H protein expression was confirmed by western blot. The expression of ataxia telangiectasia mutated (ATM) signaling pathway and apoptosis-related proteins were detected by immunofluorescence and western blot. Temozolomide (TMZ) induced cell apoptosis was detected by flow cytometry. Tumor cell proliferation was detected by Cell Counting Kit-8. In vivo nude mice were used to confirm the in vitro roles of IDH1 mutation. Results: We established glioma cell lines that expressed IDH1-R132H mutation stably. We found that TMZ inhibited glioma cells proliferation more significantly in IDH1 mutant cells compared to wild type. The IC50 of TMZ in IDH1-R132H mutant group was less than half that of wild-type group (p < 0.01). TMZ significantly induced more DNA damage (quantification of γH2AX expression in IDH1 mutation vs. wild type, p < 0.05) and apoptosis (quantification of AnnexinV+propidium iodide–cells in IDH1 mutation versus wild type, p < 0.01) in IDH1 mutant gliomas compared to wild-type gliomas. The ATM-associated DNA repair signal was impaired in IDH1 mutant cells. Inhibiting the ATM/checkpoint kinase 2DNA repair pathway further sensitized IDH1 mutant glioma cells to chemotherapy. We found that IDH1 mutation significantly inhibited tumor growth in vivo (the tumor size was analyzed statistically, p < 0.05). Moreover, we confirmed that gliomas with IDH1 mutation were more sensitive to TMZ in vivo compared to wild type significantly and the results were consistent with the in vitro experiment. Conclusion These results provide evidence that combination of TMZ and ATM inhibitor enhances the antitumor effect in IDH1 mutant gliomas.

Objective To assess the protective effect of the normobaric oxygen (NBO)and hyperbaric oxygen (HBO)on the acute ischemic stroke of rat using MR diffusion weighted imaging (DWI).Methods 30 adult male SD rats were subjected to right middle cerebral artery occlusion (MCAO)model using the suture method and transferred into a MRI scanner at 30 minutes after the onset of MCAO,then 30 rats were randomly divided into 3 groups (n=10 in each group),control,NBO and HBO group.NBO group rats were exposed to 100% oxygen for 2 hours,HBO group rats were administrated with hyperbaric oxygen for 2 hours respectively at 45 minutes after the onset of MCAO.Brain MRI scanner was performed at 12 h after the onset of MCAO,then pathological change of brain tissue was observed with hematoxylin-eosin (HE)staining and compared with DWI-infarct lesion.The relative cerebral infarction area and relative apparent diffusion coefficient (rADC)values of every group were measured on ADC maps.Results High signal intensity on MRI was found in the right cerebral ischemic region on DWI in three groups.The increased rates of the infraction lesion area in both NBO and HBO group were lower than that in control group (P<0.01),however,there was no significant difference between NBO and HBO group (P>0.05).The reduction rates of rADC in NBO and HBO group were significantly less than that in the control group (P<0.01),however,there was no significant difference between NBO and HBO group (P>0.05).HE staining confirmed that the cerebral infraction occured in three groups.There were significant positive correlations of the relative infarction lesion area between HE staining and DWI at 12 h after MCAO in three groups (P<0.01).Conclusion MRI shows that NBO and HBO could reduce the growth rates of cerebral infarction lesion area and the reduction rates of rADC,which proves that NBO and HBO have the neuroprotective effect on acute ischemic stroke of rats.

Objective To investigate the protective effect of ligustrazine on the transporting function of hepatocellular mitochondria membrane in the rats with sepsis-induced acute liver injury (SALI). Methods The Sprague-Dawley (SD) rats were randomly divided into sham operation group, SALI group [established by cecal ligation and puncture (CLP)], ligustrazine treatment group (injection of ligustrazine 60 mg/kg through tail vein after CLP) and ligustrazine preventive group (7 days before CLP, ligustrazine was injected daily through tail vein for 60 mg/kg), and there were 12 rats in each group. Abdominal aorta blood and liver were harvested at 10 hours after operation. The content of serum alanine aminotransferase (ALT), aspartate aminotransferase (AST) and mitochondrial aspartate aminotransferase (m-AST) were determined by enzyme coupling rate method. The content of ATP was detected by colorimetric and chemical fluorescein method. The activity of mitochondrial ATPase was detected by phosphorus quantification. The expressions of mitochondrial membrane aquaporin 8 (AQP8) and carnitine palmitoyl transferase (CPT) were detected by Western Blot. Results Compared with sham operation group, the levels of serum ALT, AST and m-AST were significantly increased in SALI group, ligustrazine treatment group and ligustrazine preventive group, and the content of ATP was reduced, the activity of mitochondrial membrane ATPase, the expressions of AQP8 and CPT-1A were significantly decreased. Compared with SALI group, the levels of serum ALT, AST and m-AST were significantly decreased in ligustrazine treatment and ligustrazine preventive groups [ALT (U/L): 123.8±32.8, 105.0±44.5 vs. 233.0±110.1; AST (U/L):427.0±117.9, 303.9±110.3 vs. 742.6±441.4; m-AST (U/L): 239.6±64.9, 168.2±60.0 vs. 412.8±252.6; all P <0.01], the content of ATP were significantly increased (nmol/mg: 29.5±10.3, 34.6±11.2 vs. 19.3±8.8, both P < 0.01), the activity of ATPase in hepatocellular mitochondrial membrane were significantly increased [Na+-K+-ATPase (U/mg):3.91±0.30, 3.97±0.35 vs. 2.87±0.82; Mg2+-ATPase (U/mg): 3.75±0.38, 3.88±0.35 vs. 2.64±1.06; Ca2+-ATPase (U/mg): 3.15±0.58, 2.98±0.31 vs. 1.75±1.25; Ca2+-Mg2+-ATPase (U/mg): 3.82±0.31, 3.91±0.42 vs. 2.57±1.01, all P < 0.01], the expressions of AQP8 and CPT-1A were significantly increased [percentage increase from sham operation group (100%), AQP8/COX-Ⅳ: (79.12±7.79)%, (88.40±9.22)% vs. (62.08±11.91)%; CPT-1A/COX-Ⅳ:(87.92±10.06)%, (84.91±17.48)% vs. (72.11±7.82)%, all P < 0.01]. The levels of serum AST and m-AST in ligustrazine preventive group were significant lower than those in ligustrazine treatment group [AST (U/L): 303.9± 110.3 vs. 427.0±117.9; m-AST (U/L): 168.2±60.0 vs. 239.6±64.9, both P < 0.05]. There was no significant difference in the expression of CPT-2 in mitochondrial membrane between the four groups. Conclusions Ligustrazine could play a protective role on the mitochondrial membrane function of transporting water, ion and fat in the rats with SALI. The preventive function of ligustrazine is better than the treatment effect of the rats with sepsis.

OBJECTIVEUsing tooth whitening agents (bleaching clip) in vitro and acidic drinks, we conducted a comparative study of the changes in enamel surface morphology, Ca/P content, and hardness.

METHODSTooth whitening glue pieces, cola, and orange juice were used to soak teeth in artificial saliva in vitro. Physiological saline was used as a control treatment. The morphology of the four groups was observed under a scanning electron microscope (SEM) immediately after the teeth were soaked for 7 and 14 d. The changes in Ca/P content and microhardness were analyzed.

RESULTSThe enamel surfaces of the teeth in the three test groups were demineralized. The Ca/P ratio and the average microhardness were significantly lower than those of the control group immediately after the teeth were soaked (P < 0.05). The Ca/P ratio and microhardness gradually increased after 7 d. No significant difference was observed between the control group and the test groups after 14 d (P > 0.05).

CONCLUSIONBleaching agents caused transient demineralization of human enamel, but these agents could induce re-mineralization and repair of enamel over time. Demineralization caused by bleaching covered a relatively normal range compared with acidic drinks and daily drinking.

Objective To discuss influence factors on prognosis of the patients with capillary leak syndrome (CLS) in ICU.Methods The clinical data of 191 patients with CLS in ICU were reviewed,and the patients were divided into three groups according to prognosis:death group ( n =37),cured group ( n =132) and non-healed group (n =22).The clinical data of death group were compared with those of cured group at admission,during the course of CLS and before discharging from hospital.Results Compared with the cured group,the central venous pressure and serum albumin decreased ( P ＜ 0.01 ) ; anion gap,triglycerides,pressure adjusted heart rate (PAHR) and oxygenation index were lower ( P ＜ 0.01 or P ＜ 0.05) ; serum glucose and SIRS score increased ( P ＜ 0.01 ) in death group.There was higher rate of poor renal function at admission in death group than that in other groups ( P ＜ 0.01 ).There were more many patients treated with intravenous administration of hydroxyethyl starch,ulinastatin and continuous blood filtration therapy in cured group than those in other groups ( P ＜ 0.05).Conclusions The factors influencing the outcomes of the patients with CLS were hypovolemia,severe hypoproteinemia,interior milieu disorder,malnutrition,hypoxemia,renal injury and severe systemic inflammatory response.The outcomes of patients with CLS in ICU could be improved by using hydroxyethyl starch,ulinastatin and continuous blood filtration therapy.

Overall enhancement of the public health system ranks a key task and goal for the ongoing health reform.This paper described the public health development in Shenzhen amid the ongoing health reform.Shenzhen has achieved the following objectives as required in the reform:better public service by public health institutions,availability of major and primary public health services as required by the state and city,overall elevation of public health service capabilities,and significant drop of disease morbidity and mortality.Challenges ahead include room of improvement in public health service network,incentive mechanism of public health service providers,and that of public health service delivery capability.

Objective To investigate the association between morniing blood pressure surge (MBPS) and carotid atherosclerosis in elder patients with essential hypertension. Methods According to the results of24h ambulatory blood pressure monitoring, 106 patients were classified as the morning BP surge group (MBPS group,n = 58) ,and nonsurge group (NMBPS group, n = 48). Patients underwent carotid ultrasound and the intima-medial thickness (CCA-IMT) and plaques were examined. Results The CCA-IMT of the MBPS group was significantly thicker than that the NMBPS group[(1.27 ± 0. 12)mm vs (0.92 ± 0.33 )mm], P ＜ 0. 05 ) ;②Compared with the NMBPS group,the severity of carotid arteries plaque of the MBPS group was significantly higher (72. 15% vs 54.21% ), ( P ＜0. 01 ) ;③Pearson relation analysis showed CCA-IMT level positively correlated with age (r = 0.288, P ＜ 0.001 ) ,the average of 24h SBP ( r = 0. 768 ,P ＜ 0. 001 ), and MBPS ( r = 0. 768, P ＜ 0.001 ). Conclusion The study showed that MBPS was closely related with carotid atherosclerosis in elder patients with essential hypertension and was an important risk factor in the process of atheresclerosis.