Objective To investigate the abnormity of blood lipids and uric acid ,and to analyze their relationship in health exami-nation population over 18 years in Yangzhou .Methods Totally 28 202 individuals receiving the health examination from October 2011 to August 2012 in the physical examination center of this hospital were enrolled in our study .Total cholesterol(TC) ,triglycer-ide(TG) ,low density lipoprotein cholesterol(LDL-C) ,high density lipoprotein cholesterol(HDL-C) and blood uric acid(UA) were detected ,and the relationship between age and sex with the abnormity of blood lipids and uric acid and the relationship between UA levels and blood lipids were analyzed .Results Among the detection population ,the detection rates of abnormal TG ,abnormal TC , abnormal HDL-C ,abnormal LDL-C and hyperuricemia were 31 .5% ,32 .1% ,15 .9% ,18 .4% and 17 .3% respectively .Compared with females ,males had the higher rates of abnormal blood lipids and UA (P<0 .05) .The rate of abnormal blood lipids was in-creased with age increase before 50 years old ,the > 50 -70 years old group had the highest abnormity rate of blood lipids ,then which was gradually decreased after 70 years old .The morbidity rate of hyperuricemia was increased with age .Compared with nor-mal UA group ,the hyperuricemia group had the higher rate of abnormal blood lipids (P<0 .01) .Conclusion The health examina-tion population over 18 years have the higher abnormity rate of blood lipids and uric acid ,which is significantly correlated with age and sex ;the increase of uric acid has certain correlation with abnormal blood lipids metabolism .Both blood lipids and uric acid are the risk factors of cardiocerebralvascular diseases ,rational dietary structure and periodic physical examination have the important significance to prevent the occurrence of these diseases .

Objective To explore the MRI features of primary spinal lymphoma,and aim at improving the understanding of the disease.Methods The MRI data of primary spinal lymphoma in 8 cases were analyzed retrospectively,which were confirmed by op-eration and pathology,all cases were experienced by the plain MRI scan and enhancement scan.Results There were 6 cases located in thoracic vertebra,5 cases located in lumbar spine,and 2 cases located in sacral vertebral,the MRI performance were the bone damage and bone marrow infiltration in vertebral bodies and accessories,which were showed low signal on T1 WI ,high signal on T2 WI;Compared to adjacent muscles,a obscure boundary of soft tissue masses were also showed low signal on T1 WI ,high signal on T2 WI,and were significantly enhanced.Conclusion MRI is helpful for localization and qualitative diagnosis of the primary spinal lymphoma.

Objective: To develop a healthy personality scale for undergraduates.Methods: A healthy personality scale was developed based on interviews,open questionnaires and theory hypothesis.The test-retest reliability,split-half reliability,internal consistency reliability,construct validity were examined.Results: Exploratory principle factor analysis of the items indicated that the scale had three factors: self consistency and congruence,self-social harmony,practical ability,which explained 54.8% of the total variance.The Cronbach's ? coefficient ranged from 0.82 to 0.94,split-half reliability ranged from 0.70 to 0.85,and retest reliability ranged from 0.73 to 0.84.In the confirmatory factor analysis of the three factor model,fit statistics(RMSEA=0.07,NFI=0.95,NNFI=0.96,CFI=0.94,GFI=0.95) for the model best explained the observed relationship.The three dimensions and the total scale had significant positive correlations with self-esteem and subjective well-being and significant negative correlations with SCL-90.Conclusion: The results suggest the healthy personality scale with eligible psychometric quality,can be applicable to Chinese undergraduates.

Objective To evaluate the effect of dietary ω-3 polyunsaturated fatty acid (PUFA) supplementation on lipopolysaccharide (LPS)-induced acute lung injury in rats.Methods Totally 58 male SD rats were divided into control group (n =10),model group (n =12),ω-3 PUFA high-dose group (n =12),ω-3PUFA medium-dose group (n =12),and ω-3 PUFA low-dose group (n =12).Seven days before model establishment,rats in the three ω-3 PUFA groups were orally given ω-3 PUFA at 1,0.5,and 0.25 g/kg body weight once per day,respectively,for seven consecutive days.Twenty-four hours after the last administration,all rats except those in the control group were given intravenous injection of LPS (6 mg/kg) at caudal vein to establish the model of acute lung injury.Body temperature was measured at 0,6,and 24 hour.Blood samples were collected from the eye venous plexus for routine blood tests and blood biochemical tests 24 hours after modeling.After the rats were sacrificed,the left lung was harvested for measuring the wet weight and dry weight and calculating the wet/dry weight ratio (W/D).The right lung was harvested for pathological observation under light microscope and calculation of semi-quantitative pathological index (PI).Results Twenty-four hours after modeling,deaths were noted in all groups except the control group.After injection of LPS,rats curled with little movements.At 6 hour,the body temperature was significantly higher in the model group than in the control group [(37.4 ±0.27)℃ vs.(35.9 ±0.05) ℃,P =0.00] ; it was (36.2 ±0.38)℃,(36.3 ±0.30)℃,and (36.3 ± 0.32) ℃ in the ω-3 PUFA high-,medium-,and low-dose groups,which were significantly lower than that in the model group (all P =0.01).The amounts of white blood cells,neutrophils,and lymphocytes increased in the model group,but showing no significant difference compared with the other groups.The serum glutamic oxalacetic transaminase (GOT) and glutamic pyruvic transaminase (GPT) levels were significantly higher in the model group than in the control group [(353 ± 235) U/L vs.(157 ± 55) U/L,P =0.02 ; (141± 103) U/L vs.(54 ±23) U/L,P =0.03] ; the ω-3 PUFA high-dose group had significantly lower GOT and GPT levels than the model group did [(167 ±94) U/L vs.(353 ±235) U/L,P =0.03 ; (63 ±57) U/L vs.(141 ± 103) U/L,P =0.04].The model group had significantly higher lung wet weight [(371 ±38) mg vs.(281 ±24) mg,P=0.01] and W/D value (7.34±1.40 vs.5.41 ±0.84,P=0.01) compared with the control group.Compared with the model group,the W/D value was significantly lower in the ω-3 PUFA high-,medium-,and low-dose groups (6.17 ±0.58,P =0.03; 6.17 ± 0.76,P =0.03; 6.13 ± 1.23,P =0.04).Light microscopy showed that the lung alveoli of the model group presented congestion,obvious expansion,and scattered inflammatory cell infiltration in interstitium,along with significantly increased PI compared with the control group (3.9±0.9 vs.0.0±0.0,P=0.00).The PI value was (2.1 ±0.3),(2.1 ±0.3),and (2.3 ± 0.5) in ω-3 PUFA high-,medium-,and low-dose groups,respectively,all significantly lower than that in the model group (all P =0.01).Conclusions The acute lung injury model could be successful established by intravenous injection of LPS.ω-3 PUFA at different doses can improve the acute lung injury of rats.It is therefore supposed that early enteral administration of ω-3 PUFA can alleviate LPS-induced acute lung injury,although the optimal dosage and timing need further research.

Objective To investigate whether functional electrical stimulation (FES) can improve the expression of proteins in the NMDAR1-pGLuR1 pathway so as to promote the recovery of motor function and sensation after stroke.Methods Eighty-one Wistar rats were used to make a photochemical brain model of local ischemia.Rats were randomly assigned into a sham, placebo stimulation or FES group.Rats in the placebo and FES groups had local ischemia induced in the M1 zone of the brain using the photosensitive dye Bengal rose.It was administered intravenously and a laser beam was then stereotactically positioned on the skull.The rats in the FES groups were stimulated for 30 minutes (10 minutes on, 10 minutes off, then 10 minutes on).The placebo group's treatment was similar, but without the electric current.The rats in the sham group received no intervention.The cylinder test and the adhesive-removal test were used to test the rats' motor function and sensation before the operation and before they were sacrificed.Cohorts were sacrificed after 3, 7 and 14 days of intervention.NMDA receptor and AMPA receptor were detected in the peri-ischemic cortex using western blotting.Results After 7 and 14 days the index of forelimb motor function in the cylinder test of the FES group was significantly better than that of the placebo group.The average adhesive-removal time of the FES group was also significantly faster compared with the placebo group.After 7 days the average expression of NMDAR1 in the FES group was significantly higher than in the placebo group.The average expression of GluR1 and pGluR1 in the FES group was significantly higher than in the placebo group after 14 days.Conclusion Functional electrical stimulation can improve motor function after ischemia through the NMDARAMPAR signal pathway, at least in rats.

Objective To develop and validate a ultrasonographic (US)imaging agent with targeted microbubbles that attaches to chemokine receptor 2 (CCR2)and to compare the US single obtained from targeted microbubble with that from control microbubble in murine breast tumor model.Methods The microbubble which carried CCR2 antibody (MBCCR2 )and isotype-macthed immunoglobulin G-labled control microbubble (MBcontrol ) were prepared. The microbubble size and distribution were assessed by AccuSizer780.Binding specificities of targeted microbubble compared with control microbubble were tested with murine microvascular endothelial cells (bEnd.3 ).Orthotopic breast tumor model was estabished in BALB/c mice with mouse breast cancer 4T1 cell.In vivo imaging signals of contrast material-enhanced ultrasound by use these two different types of microbubble which were injected respectively into each mouse at random order and 30 min interval.Tumor tissue was stained for CCR2 and CD3 1 .Results Automatic Particle Sizer showed size uniform of two kinds of microbubbles,and narrow distribution of particle size (mean diameter of about 1 -2 μm),which were not significantly different (P >0.05).Adhension to bEnd. 3 endothelial cells was significantly higher (P < 0.001 )for MBCCR2 (mean,9.50 ± 1 .5 1 )than that for MBcontrol (mean,0.01 ±0.01).Imaging signal in the murine tumor model was significantly higher for MBCCR2 [mean,(6.76±0.26)dB]than that for MBcontrol [mean,(1 .06 ±0.62)dB,P <0.001 ].Immunofluorescence confirmed expression of CCR2 on tumor vasculature.Conclusions The targeted microbubbles with CCR2 monoclonal antibody had been successfully prepared,which precisely targeted to CCR2 of tumor angiogenesis in the murine breast cancer xenograft tumor models in vivo.These results suggest that the targeted microbubbles as a kind of ultrasound molecular imaging agent with a better specificity can be used for both evaluating tumor neovascularization and monitoring therapeutic effect of anti-angiogenesis.

To investigate the neuroprotective of ligustilide (LIG) against glutamate-induced apoptosis of PC12 cells, cell viability were examined by MTT assay. Flow cytometry was applied to assay cell apoptosis rate. Intracellular calcium concentration was measured by using fluorescent dye Fluo-3/AM. Cytochrome C (Cyt C), Caspase-3, Bax and Bcl-2 protein expression were assayed by western blot. The results showed that glutamate is cytotoxic with an inhibitory concentration 50 (ID50) of 15 mmol · L(-1). Pretreatment with LIG (1, 5, 15 μmol · L(-1)) significantly improved cell viability. The apoptosis rate in glutamate-induced PC12 cells was 13.39%, and decreased in the presence of LIG (1, 5, 15 μmol · L(-1)) by 9.06%, 6.48%, 3.82%, separately. Extracellular accumulation of Ca2+ induced by glutamate were significantly reduced by LIG. The results of western blot manifested that pretreatment LIG could decrease the release of Cyt C from mitochondria, down-regulate Caspase-3 protein expression and up-regulate Bcl-2/Bax ratio, thereby protects PC12 cells from apoptosis. In summary, LIG had protective effect on glutamate-induced apoptosis in PC12 cells through attenuating the increase in intracellular Ca2+ concentration, and inhibiting the release of Cyt C from mitochondria to cytoplasm.

Objective To study the biofilm-forming ability and the distribution of biofilm-related genes in Acinetobacter baumannii clinical isolates as well as antimicrobial resistance,to analyze their relationships with the bacterial resistance phenotype.Methods A prospective study was conducted.Biofilm models of 70 strains Acinetobacter baumannii collected in Chengwu County People's Hospital from October 2012 to October 2013 were constructed using 96-well polystyrene plate.In order to analyze the biofilm-forming ability,a qualitative and quantitative analysis was conduct by crystal violet staining assay.And the antimicrobial resistance of different biofilm-forming ability strains was compared including imipenem,amikacin,meropenem,cefepime,sulbactam cefoperazone,trimethoprim,levofloxacin,gentamicin,ciprofloxacin,cefotaxime,ceftizoxime,aztreonam,piperacillin,ceftriaxone,cefuroxime.In addition,the expressions of biofilm-related gene Bap,bfs and intI1 were tested with polymerase chain reaction (PCR) assay.Results Among 70 strains Acinetobacter baumannii,40 strains were multi-drug resistant (57.14％) and 6 strains were pan-drug resistant (8.57％); 68 strains had biofilm-forming ability (97.14％),14 of which were weakly positive,20 were positive and 34 were strongly positive.The antimicrobial resistant rate of Acinetobacter baumannii to imipenem,amikacin,meropenem and cefepime was decreased,it was 30.00％,32.86％,38.57％ and 41.43％,respectively.However,the antimicrobial resistant rates to other commonly used antibiotics were all higher than 50％.The drug resistance of Acinetobacter baumannii to levofloxacin (85.71％,45.00％,38.24％,x2=9.225,P=0.010),cefepime (71.43％,45.00％,29.41％,x2=7.222,P=0.027),gentamicin (78.57％,55.00％,38.24％,x2 =6.601,P=0.037) was significantly decreased when biofilm-forming ability reinforced (weakly positive,positive,hadro-positive).Bap gene positive rate of weakly positive,positive and strong positive biofilm-forming strains Acinetobacter baumannii was 50.00％,65.00％ and 79.41％ (x2=4.244,P=0.120),respectively.Bfs gene positive rate was 35.71％,65.00％ and 88.24％,respectively (x2=13.602,P=0.001) and intI1 gene positive rate was 42.86％,75.00％ and 91.18％,respectively (x2 =12.902,P=0.002).Moreover,the antimicrobial resistances of biofilm-related gene positive strains were higher than the negative,of which the drug resistance of intI1 positive group to amikacin was significantly higher than the negative group (40.38％ vs.11.11％,x 2=5.194,P=0.023).Conclusions The Acinetobacter baumannii collected from the hospital had strong multi-drug resistance as well as strong biofilm-forming ability.The drug resistance of Acinetobacter baumannii decreased when biofilm-forming ability reinforced.In addition,genes,such as Bap,bfs,and intI1,contributed to biofilm formation.

Early diagnosis and early intervention for cognitive impairment after ischemic stroke can delay disease progression and prevent the occurrence of dementia.This article reviews the advances in research on ischemic stroke caused each risk factor for cognitive impairment.

Objective To evaluate the effects of interleukin-22(IL-22)on the expression of tazarotene-induced gene 3(TIG3)in HaCaT cells. Methods Cultured HaCaT cells were randomly divided into several groups to be treated with different concentrations (12.5, 25, 50, 100 μg/L)of IL-22 alone, or the combination of 50 μg/L IL-22 with the MAPK-ERK1/2 inhibitor PD98059 or the JAK/STAT inhibitor AG490 for 24 hours. Those HaCaT cells treated with phosphate buffered saline served as the control group. Subsequently, total proteins and mRNAs were extracted from the HaCaT cells. An immunofluorescence assay, Western blot and enzyme-linked immunosorbent assay (ELISA) were performed to determine the protein expression level of TIG3, and real-time fluorescence-based quantitative PCR to quantify the mRNA expression of TIG3 in HaCaT cells. Results The immunofluorescence assay showed that TIG3 protein was mainly expressed in the cytoplasm of HaCaT cells. As Western blot revealed, the protein expression level of TIG3 was 0.743 ± 0.035, 0.678 ± 0.040, 0.582 ± 0.041 and 0.328 ± 0.032 in HaCaT cells treated with IL-22 of 12.5, 25, 50 and 100μg/L, respectively, significantly lower than that in the control group (0.839 ± 0.045, all P<0.05). ELISA also showed a decrease in the protein expression of TIG3 in IL-22-treated HaCaT cells, which was consistent with Western blot results. Further more, the mRNA expression level (2-△△Ct)of TIG3 was significantly weaker in HaCaT cells treated with IL-22 of 12.5, 25, 50 and 100μg/L than in the control group (0.838 ± 0.036, 0.686 ± 0.061, 0.565 ± 0.047 and 0.457 ± 0.033 vs. 1.000, all P< 0.05). The decrease in TIG3 mRNA and protein expressions was significantly attenuated in HaCaT cells treated with the combination of 50 μg/L IL-22 with PD98059 or AG490 compared with those treated with 50 μg/L IL-22 alone. Conclusion IL-22 can dose-dependently inhibit the expression of TIG3 in HaCaT cells, likely through the MAPK-ERK1/2 and JAK2/STAT3 signaling pathways.