Alzheimer!s disease (AD) is one of the commonest neurodegenerative diseases affected mainly theelderly. AD is characterized by the formation of neuritic plaque in brain, which is composed mainly of extracellular?amyloid deposion, the A?. A?is deprived from serial hydrolysis of amyloid precursor protein (APP) by twosecretases, the ?and ?-secretase respectively. Alternatively, APP can also be sequential processed by ?-secretaseand ?-secretase, which not only preclude the formation of A?, but also generate a large ectodomain (sAPP?) whohas several neuroprotective properties. Thus the secondary processing pathway has become the focus of ADresearch. Many results have indicated that members of the adamalysin family of proteins, mainly the ADAM 10,ADAM 17 and ADAM 9, fulfill some of the criteria required of ?-secretase. Here the biological characteristics of?-secretase, its activity regulation and its potential function as targets for the treatment of AD were summerized.

Objective To investigate the distribution of hepatitis B virus(HBV) genotypes ,drug resistance situation of hepatitis B patients and the relation between HBV genotype with drug resistance and mutation sites .Methods Three hundred serum samples of HBV patients were collected and HBV‐DNA was extracted by adopting the centrifugal column method .The HBV genotype and drug resistant mutant were detected by using PCR‐reverse dot blot hybridization method .Results In 300 cases of HBV‐DNA posi‐tive ,genotye B ,C ,B/C and other undetected genotypes were detected out ,but genotype D was not detected out ,in which genotype C was predominant ,accounting for 81 .8% ;in the HBV patients ,the resistant drugs were dominated by‐lamivudine and telbivudine , accounting for 43 .6% ;the HBV drug resistant mutation genotypes were mainly rt204I(24 .35% ) ,rt204V (17 .39% ) and rt180M (17 .39% );the drug resistance mutation rates of genotype B and C were 30 .77% and 42 .42% respectively ;the difference was sta‐tistically significant(P<0 .05) .Conclusion HBV genotype C in Dongying area is more than genotype B ,genotype C is prone to produce drug resistance ,rt204I ,rt204V and rt180M gene mutations are common ,lamivudine and telbivudine combined resistance is common ,the suitable treatment scheme should be selected according to genotyping and drug resistance mutations results .

Objective: To evaluate the effectiveness of unstable pelvic fractures treated by cannulated screw internal fixation with the assistance of three-dimensional (3D) printing insertion template.

Objective To investigate the effects of exercise on memory impairment in demented mice and possible molecular mechanisms.Methods Thirty Kunming nice were divided into a normal control group,a dementia group and a dementia plus exercise training group (exercise training group),10 mice/group. Dementia models were established by intraperitoneal injection of scopolamine.Exercise training was begun 30 min after the injection and lasted for a 6-week period. A water maze test was performed after the exercise training. Brain-derived neurotrophic factor (BDNF) expression and protein kinase (Akt) phosphorylation in the hippocampus were detected by Western blot analysis.Nitric oxide (NO) content and superoxide dismutase (SOD) activity in the hippocampus were also measured.ResultsDementia models were successfully induced as indicated by prolonged escape latency in the water maze test.After exercise training the escape latency had shortened significantly and hippocanpal BDNF expression and Akt phosphorylation had increased.NO content increased and SOD activity decreased after the injections,but these effects were partially reversed after exercise training.Conclusions Exercise can improve spatial memory significantly after scopolanine-induced dementia in mice.The increased hippocampal BDNF expression and Akt phosphorylation,increased SOD activity and decreased NO content may partially explain the behavior improvement induced by exercise.

levels are elevated in patients with NAFL and correlated with HOMA-IR, suggesting RBP4 may participate in the development of IR and NAFL.

BACKGROUND:Traditional external fixation of tibial fractures exhibits obvious stress shielding that delays fracture healing. Polyetheretherketone (PEEK) material has a similar elastic modulus to the bone, and it wil be possible to address this clinical problem.
OBJECTIVE:To compare the outcome of PEEK external fixator versus traditionaly external fixator in the treatment of tibial fractures.
METHODS:Clinical data of 86 patients with tibial fractures, including 64 males and 22 females, aged 24-78 years (mean age of 56 years), were retrospectively reviewed. There were 30 cases of closed fractures and 56 cases of open fractures; 32 cases received flat-patient surgery and 54 cases underwent emergency surgery. Al the patients were divided into two groups according to different fixation methods: PEEK group and traditional external fixator group. After operation, patients were checked regularly and at the last folow-up, functional recovery was evaluated according to Johner-Wruhs criteria.
RESULTS AND CONCLUSION:Al the patients were folowed up for 5-20 months. The mean fixator removal time of the PEEK group was 8.7 weeks and the mean duration of fracture healing was 4.2 months. The mean fixator removal time of the traditional external fixator group was 10.6 weeks and the mean duration of fracture healing was 6.1 months. At the last folow-up, in the PEEK group, 26 cases were assessed as excelent, 13 as good, 4 as poor; in the traditional external fixator group, 19 cases were assessed as excelent, 13 as good, 11 as poor. These findings indicate that PEEK external fixator for different types of tibial fractures can maintain the fracture stability, promote fracture healing and contribute to the functional recovery of the affected limbs.

Objective To investigate platelet α and β secretase activities and the amounts of platelet soluble fragment of APP (sAPPα) produced by α-secretase in patients with mild cognitive impairment (MCI) and Alzheimer's disease (AD).Methods The neurological functions of 48 nondemented patients,42 MCI and 40 AD patients were evaluated by neuropsychological examinations.The platelet α and β secretase activities and sAPPα production in each group were measured by fluorescence and Western blotting analysis respectively.Results The α secretase activities in non-demented,MCI and AD group were 100.0％ ± 10.6％,78.2％ ± 9.4％ and 61.8％ ± 7.2％ respectively.As compared with nondemented group,the α secretase activities in MCI and AD group were decreased (F =22.935,P =0.001).The α secretase activity in AD group was significantly lower than MCI group.The β secretase activities in non-demented,MCI and AD group were 100.0％ ± 11.2％,145.8％ ± 12.7％ and 189.8％ ± 14.2％respectively.The β secretase activities in MCI and AD group were significantly higher than that in nondemented group (F =16.368,P =0.001).The β secretase activity in AD group was significantly decreased as compared with MCI group.The sAPPα amounts in MCI group and AD group were all decreased as compared with that in control group; the sAPPo amount in AD patients was significantly decreased as compared with that in MCI group.Conclusions The platelet α secretase activity and its production sAPPα in MCI and AD patients are decreased,while β secretase activity is increased,as compared with that in control group; the altered α and β secretase activities may participate in the pathogenesis of MCI and AD patients and may have diagnostic potential for them.

Objective: To study the effect of zinc deficiency on the growth and concentrations of related hormones in serum of pregnant rats. Methods: Pregnant Wistar rats were assigned to zinc deficiency(ZD),pair-fed(PF),zinc supplement(ZS) and control(Cont) group and fed for 21 days with zinc deficient(0.7 mg/kg)diet(ZD rats)or a similar diet supplemented with 100 mg Zn/kg.The growth of pregnant rats was observed and the concentrations of triiodothyronine(T 3),thyroxine(T 4),thyrotropin(TSH) and growth hormone(GH) in serum of rats were determined with radioimmunoassay. Results: The ZD rats didn't gain weight.The birth weight of fetuses in ZD group was significantly lower than that of other groups (P

Ischemic stroke has become one of the leading causes of disability and death in China.A number of studies have confirmed that hypoalbuminemia is an independent risk factor for ischemic stroke.It affects the severity of ischemic stroke and outcomes.This article reviews the rehtionship between serum albumin and ischemic stroke,the cause of low albumin level,the effect of albumin on ischemic stroke,and how to supplement albumin in order to improve the clinician's attention for hypoalbuminemia in patients with ischemic stroke and supplement nutrition timely and reasonably.

Objective To investigate the effect of quercetin on suppressing the proliferation, migration and invasion of A549 cells via the signal transducer and activator of transcription 3 (STAT3) signaling pathway. Methods The A549 cells were cultured in vitro and treated with quercetin at various concentrations (0,7.5,15,30,60 and 120 µmol/L) for 24 h,48 h and 72 h. The proliferation of A549 and the 50% inhibitory concentration (IC50) were measured by the cell counting kit-8 (CCK-8). The A549 cells treated for 24 h were randomly divided into 4 groups: the blank control, 15 and 30 µmol/L quercetin, and 3 µg/ml cisplatin(the positive control) groups. The effect of quercetin on adhesion rate was detected by the cell adhesion assay; the cell migration ability was evaluated by the wound healing assay; the cell invasion ability was evaluated by the Transwell chamber assay; the expression of STAT3 and phosphorylated-STAT3 (p-STAT3) proteins were detected by Western blot assay. Results Quercetin inhibited A549 cell growth dose-dependently. Compared with the blank control group, quercetin could significantly inhibit the adhesion rate, migration ability and invasion of A549 cells (P<0.05 or P<0.01); compared with the blank control group, quercetin significantly inhibited STAT3 and p-STAT3 expression level (P<0.05 or P<0.01). Conclusion Quercetin could inhibit the proliferation, migration and invasion of A549 cells, and the mechanism is libely related to the STAT3 signal pathway.