Objective To study the dynamic change of high-sensitivity C-reactive protein(hCRP),interleukin-1(IL-1?)interleukin-6(IL-6)in acute traumatic brain injury,and the correlation between the dynamic change and the scale of brain injury and the prognosis of the patients.Methods 192 cases patients were divided into different groups according to the Glasgow Coma Scale(GCS)and the Glasgow outcome Scale(GOS)three months later discharged from hospital respectively.The concentration of serum CRP,IL-1?,IL-6 were detected with immunoturbidimetry and ABC-ELISA 24 with in hours after traumatic brain injury and the concentration of serum after iniwn at ond day,three days and seven days was detected as well.Results Serum hCRP levels were remarkably elevated and reached peak value within 24 hours,and then gradually decreased.There were a negative correlation between hCRP,IL-1?,IL-6 and the patient's GCS groups(r=-0.162,P

Objective:To investigate the effect of antlerbase on the radiation carcinogenesis by observing the effect of antlerbase on the expressions of Notch2 gene and immune function of the mice with thymic lymphomas induced by ionizing radiation.Methods:Ninety BALB/c mice were randomly divided into control group,irradiation group and irradiation combined with drug group (combined group)(n=30).The thymic lymphoma models of mice were made by X-ray irradiation in irradiation group and combined group;after establishing the animal models,the mice in combined group were fed with chow containing antlerbase superfine powder.After 6 months,the whole blood and thymic tissue were taken,then RT-PCR and Western blotting methods were used to detect the mRNA and protein expressions levels of Notch2 gene in the thymic lymphoma tissue;ELISA method was used to detect the serum immunoglobulin (IgG,IgA,IgM)levels and SOD kit was used to detect the serum SOD activities of the tumor mice.Results:The incidences of thymic lymphoma in irradiation group and combined group were 53.33%(16/30)and 36.67% (11/30),respectively.Compared with control group,the expression levels of mRNA and protein of Notch2 gene in thymic lymphoma of the mice in irradiation group were significantly increased (P <0.05);compared with irradiation group,the expression levels of mRNA and protein of Notch2 gene in combined group were decreased (P <0.05);compared with control group,the levels of IgG,IgA,and IgM in serum of the mice in irradiation group were decreased (P < 0.05 ); compared with irradiation group, the levels of IgG, IgM, hemoglobin and the activity of SOD in serum of the mice in combined group were increased (P < 0.05 ). Conclusion:Ionizing radiation can activate the high expression of Notch2 gene and protein and decrease the immune function of mice,it might be one of the mechanisms for the occurrence of radiation carcinogenesis;antlerbase can decrease the incidence of radiation carcinogenesis by inhibiting the expression of Notch2 gene and increasing the immune function of mice,which might play an role in restraining tumor.

Objective To investigate the regulatory effects of miR-145 on the proliferation,cell cycle and apoptosis of a human keratinocyte cell line HaCaT.Methods miR-145 mimics and negative control (NC) mimics were chemically synthesized and then transiently transfected into HaCaT cells respectively.After additional culture for different durations,real-time PCR was performed to determine the expression level of miR-145,MTS assay to estimate cell proliferation,and flow cytometry to detect cell apoptosis and cycle.Luciferase assay,real-time PCR and Western blot were conducted to determine whether NRAS was the target gene of miR-145.Results The miR-145 expression level in miR-145 mimic-transfected cells increased by 85.00 ± 1.21 folds compared with NC mimic-transfected cells (t =115.90,P ＜ 0.0001).The transfection with miR-145 mimics significantly inhibited the proliferation of HaCaT cells (F =8.76,P =0.008),and the inhibitory effect significantly varied with the duration (24-96 hours) of culture after transfection,with no interaction effect between the transfection with miR-145 mimics and culture duation (F =1.21,P =0.18).Compared with NC mimic-transfected cells,those transfected with miR-145 mimics showed a significant increase in the proportion of early apoptotic cells (18.9％ ± 4.1％ vs.4.3％ ± 1.2％,t =7.126,P ＜ 0.01),late apoptotic cells (9.3％ ± 2.3％ vs.3.6％ ± 1.6％,t =12.38,P ＜ 0.01),G1-phase cells (85.83％ ± 5.2％ vs.62.08％ ± 6.23％,t =11.78,P =0.007),but a significant decrease in the percentage of G2-phase cells (6.26％ ± 1.2％ vs.19.36％ ± 3.45％,t =7.610,P =0.017) and S-phase cells (7.91％ ± 1.3％ vs.18.56％ ± 5.23％,t =7.230,P=0.019).As luciferase assay showed,luciferase activity was significantly lower in HaCaT cells cotransfected with miR-145 mimics and a recombinant luciferase reporter vector psi-CHECK2-NRAS-wild carrying the wild-type 3'UTR of NRAS than in those cotransfected with NC mimics and the vector psi-CHECK2-NRAS-wild (t =11.09,P =0.008),but similar between cells cotransfected with miR-145 mimics and a recombinant luciferase reporter vector psi-CHECK2-NRAS-mut carrying the mutant-type 3'UTR of NRAS and those cotransfected with NC mimics and the vector psi-CHECK2-NRAS-mut (P ＞ 0.05).Real-time PCR and Western blot revealed that the overexpression of miR-145 mimics had no significant effect on NRAS mRNA expression (P ＞ 0.05),but significantly inhibited NRAS protein expression (1.52 ± 0.07 vs.0.20 ± 0.02,t =28.43,P＜ 0.01).Conclusion miR-145 might inhibit proliferation and promote apoptosis of HaCaT cells by influencing cell cycle via NRAS.

Objective:To investigate the association between catechol-O-methyl transferase (COMT)Vall58Met polymorphism and prepulse inhibition of the auditory startle reflex (PPI) in patients with schizophrenia.Methods:Totally 178 patients with schizophrenia and 190 healthy volunteers were recruited.The auditory startle reflex was detected by using SR-HLAB monitoring system.The indexed of the auditory startle reflex included the amplitude,habituation％ and PPI30,PPI60,PPI120 (the lead interval was set 30 ms,60 ms,120 ms).COMT Vall58Met polymorphism was genotyped by polymerase chain reaction-restriction fragment length polymorphism (PCR-RELP).The differences of PPI among COMT genotypes were compared.Results:Compared to the healthy volunteers,patients with schizophrenia had a significant lower the amplitude of auditory startle reflex[(563± 460) mV vs (695 ± 447) mY,P ＜ 0.05] and habituation％ [(32 ± 46) vs (48 ± 33),P ＜ 0.01] as well as the ％PPI120[(27 ± 5) vs (35 ± 3),P ＜ 0.05].The significant differences in COMT allelic and genotypic distribions were observed between patients with schizophrenia and healthy volunteers (x2 =8.16,11.74,Ps ＜ 0.05).The significant main effect of COMT genotype on habituation％ was observed (P ＜0.05) but no interaction genotype by diagnosis on the amplitude of auditory startle reflex,habituation％ and ％ PPI120 was observed (Ps ＞ 0.05).Conclusions:There may be a correlation between COMT genotype and adaptability,but not between COMT genotype and PPI deficit present in patients with schizophrenia

Objective To investigate the efficacy of treatment and prevention of VitE on vacuous chewing move-ments (VCMs) of haloperidol-induced tardive dyskinesia (TD) rats and serum levels of brain-derived neurotrophic fac-tor ( BDNF) and total antioxidant capacity ( TAC) , and to explore the possible mechanisms.Methods Thirty-two male Sprague-Dawley (SD) rats were randomly divided into TD, P-Vit E, T-Vit E and control group (n=8), receiving to-week treatment with Haloperidol (Hal)+NS, Hal+Vit E (medicated at the baseline), Hal+VitE (medicated at the fifth week) or normal saline (NS), respectively.VCM was evaluated at each week.ELISA and spectrophotometer were used to detect the serum levels of BDNF and TAC, respectively.Results The VCM score of both TD group and T-Vit E group increased at the 2nd weekend, reached the peak at the 5th weekend.VCM score of T-Vit E group declined gradually at the 6th weekend and was significantly lower than that in the TD group [(6.5 ±3.3) vs.(27.9 ±5.8), P<0.001] but was not significantly different from the control group (3.5 ±1.9) (P>0.05) at the 10th weekend.There was no significant difference in VCM score between P-Vit E group and control group for ten weeks(P>0.05).At the 10th weekend, serum BDNF [(6.9 ±1.0) pg/mL] and TAC [(11.9 ±3.2) U/mL] levels of TD group were significantly lower than those of the controls [BDNF (8.6 ±2.5) pg/mL, TAC (18.2 ±5.5) U/mL] and T-Vit E group [BDNF (8.7 ±2.0) pg/mL, (18.6 ±5.9) U/mL] (P<0.01).However, there was no significant difference in the BDNF and TAC levels between TD and P-Vit E groups (P>0.05).Conclusions Vit E may relieve and prevent VCM in TD model rats though alleviation of free radical damage.

Objective To investigate the level of serum vascular endothelial growth factor (VEGF) in stable schizophrenia patients, and to explore the relationship between serum VEGF level and clinical symptoms. Methods Seventy-five patients with stable schizophrenia and 40 healthy controls were enrolled. The levels of serum VEGF were detected by flow multiplex protein analysis. The clinical symptoms of patients were assessed by positive and negative symptom scale (PANSS). Results The level of serum VEGF was significantly lower in patients group than in healthy control group [medians (lower and upper quartiles) were 3.77 (2.61, 5.14) pg/mL vs. 6.21 (4.37, 11.16) pg/mL, P＜0.01]. There was no significant difference in serum VEGF levels between patients with different gender, smoking or family history of mental illness (P＞0.05). The level of VEGF was negatively correlated with the total score of PANSS (r=-0.27, P=0.03), negative symptom subscale score (r=-0.25, P=0.04), lack of response score (r=-0.26, P=0.02), but not with other PANSS scores (P＞0.05). Conclusion The serum level of VEGF in patients with stable schizophrenia is lower than that in healthy control group. There is, to some degree, a relationship between the level of VEGF and the severity of clinical symptoms in patients with stable schizophrenia.

Objective To compare the prevalence of HIV/STD and related health care seeking behaviors among male STD clinic attendees between Xi'an and Xianyang cities.Methods During June and July 2016,206 male STD clinic attendees were studied in Xi'an city,with another 221 male STD clinic attendees in Xianyang city.Cross-sectional questionnaire survey was used to collect attendees' behavioral information.Blood samples were collected via HIV/HCV/Syphilis testing.Results The prevalence rate of HIV infection was 2.4％ (5/206) in Xi'an and 0.9％ (2/221) in Xianyang,with no statistical significant difference between the two cities.The prevalence rate of syphilis was 4.9％ (10/206) in Xi'an,which was significantly lower than 13.6％ (30/221) in Xianyang.The proportion of respondents,diagnosed with other sexually transmitted diseases,in Xi'an was higher than that of Xianyang.The proportions of commercial heterosexual sex and sex with temporary sexual partners in the past 3 months were 18.0％ (37/206) and 15.5％ (32/206) in Xi'an,lower than 46.6％ (103/221) and 15.8％ (35/221) in Xianyang (x2 =39.70,P ＜0.01;x2 =-0.01,P=0.93).The proportions of condom use with commercial sex workers or temporary sexual partners in the past 3 months among Xi'an were 37.8％ (14/37) and 6.3％ (2/32),lower than 93.1％ (95/102)and 57.1％ (20/35) in Xianyang (x2=49.06,P＜0.01;x2=19.63,P＜0.01).Conclusion Differences were noticed between Xi'an and Xianyang city in terms of STD and HIV prevalences,behaviors related to commercial sex and use of condoms among the male STD clinic attendees that calling for targeted actions in control of high risk behaviors in both HIV/AIDS and STDs transmission.

Objective To explore the effect of miR-1-3p on the malignant biological behavior of human esophageal squamous cell carcinoma cells and the potential mechanisms.Methods The Gene Expression Omnibus(GEO)database was analyzed to screen differentially expressed miRNAs in esophageal squamous cell carcinoma(ESCC).qRT-PCR was used to detect the expression of miR-1-3p in human ESCC cell lines(KYSE30,KYSE150,KYSE410,KYSE510,and Eca109)and normal esophageal epithelial cell line HET-1A.CCK-8,wound healing,Transwell assays,and flow cytometry were applied to detect the effect of miR-1-3p on the proliferation,migration,invasion,and apoptosis of ESCC cells.Bioinformatics tool was used to predict the target genes of miR-1-3p.A Kaplan-Meier survival curve was drawn to analyze the correlation between STC2 expression and overall survival of patients in the ESCC cohort of the TCGA database.Fluorescence in situ hybridization was performed to verify the subcellular location of miR-1-3p in ESCC cells,and dual-luciferase reporter gene assay was performed to validate the regulation of miR-1-3p on stanniocalcin 2(STC2).RNA immunoprecipitation assays were used to detect the binding of miR-1-3p and STC2.Western blot assay was performed to determine the effect of miR-1-3p on the expression of STC2 and endoplasmic reticulum stress pathway-related proteins,including p-PERK,p-eIF2α,and ATF4.CCK-8,wound healing,Transwell assays,and flow cytometry were applied to detect the effect of STC2 overexpression and knockdown on the proliferation,migration,invasion,and apoptosis of ESCC cells.Results The expression of miR-1-3p was lower in ESCC cell lines than in HET-1A cells(all P<0.05).The transfection of miR-1-3p mimic decreased the proliferation,invasion,and migration of ESCC cells(all P<0.05)and promoted the apoptosis of ESCC cells(all P<0.001).Bioinformatics tool showed that STC2 was a target gene of miR-1-3p.The expression of STC2 in ESCC tissues was higher than that in normal esophageal epithelial tissues in the ESCC cohort of TCGA database and was negatively correlated with prognosis(all P<0.05).miR-1-3p was located in the cytoplasm and can directly bind to STC2 mRNA.The transfection of miR-1-3p mimic downregulated the expression of STC2,p-PERK,p-eIF2α,and ATF4(all P<0.05).The overexpression of STC2 promoted the proliferation,invasion,and migration(all P<0.05)and inhibited the apoptosis of ESCC cells(all P<0.05).Knockdown of STC2 inhibited the proliferation,invasion,and migration(all P<0.05)and promoted the apoptosis of ESCC cells(all P<0.05).Conclusion miR-1-3p inhibits the malignant biological behavior and promotes the apoptosis of esophageal squamous cell carcinoma cells by regulating STC2 possibly by suppressing the endoplasmic reticulum stress.

Objective:To study the effects of reactive oxygen species (ROS)-responsive antibacterial microneedles (MNs) on the full-thickness skin defect wounds with bacterial colonization in diabetic mice.Methods:Experimental research methods were adopted. The ROS-responsive crosslinker N1-(4-boronobenzyl)-N3-(4-boronophenyl)-N1, N1, N3, N3-tetramethylpropane-1,3-diaminium (TSPBA) was first synthesized, and then the polyvinyl alcohol (PVA)-TSPBA MNs, PVA-ε-polylysine (ε-PL)-TSPBA MNs, PVA-TSPBA-sodium hyaluronate (SH) MNs, and PVA-ε-PL-TSPBA-SH MNs were prepared by mixing corresponding ingredients, respectively. The PVA-TSPBA MNs were placed in pure phosphate buffer solution (PBS) and PBS containing hydrogen peroxide, respectively. The degradation of MNs immersed for 0 (immediately), 3, 7, and 10 days was observed to indicate their ROS responsiveness. The standard strains of Staphylococcus aureus ( S. aureus) and Escherichia coli (E. coli) cultured in Luria-Bertani medium containing hydrogen peroxide were divided according to the random number table (the same grouping method below) into blank control group (without any treatment, the same below) and 0 g/L ε-PL group, 1.0 g/L ε-PL group, 5.0 g/L ε-PL group, and 10.0 g/L ε-PL group with which PVA-ε-PL-TSPBA MNs containing the corresponding concentration of ε-PL were co-cultured, respectively. Bacterial growth was observed after 24 h of culture, and the relative survival rate of bacteria was calculated ( n=3). The mouse fibroblast cell line 3T3 cells at logarithmic growth stage (the same growth stage below) were divided into blank control group and 0 g/L ε-PL group, 1.0 g /L ε-PL group, 5.0 g /L ε-PL group, and 10.0 g /L ε-PL group in which cells were cultured in medium with the extract from PVA-ε-PL-TSPBA MNs containing the corresponding concentration of ε-PL, respectively. Cell growth was observed after 24 h of culture by optical microscopy, and the relative survival rate of cells was detected and calculated by cell counting kit 8 (CCK-8) assay to indicate the cytotoxicity ( n=6). Both PVA-TSPBA MNs and PVA-TSPBA-SH MNs were taken, the morphology of the two kinds of MNs was observed by optical microscopy, and the mechanical properties of the two kinds of MNs were tested by microcomputer controlled electronic universal testing machine (denoted as critical force, n=6). Six male BALB/c mice aged 6-8 weeks (the same gender and age below) were divided into PVA-TSPBA group and PVA-TSPBA-SH group, with 3 mice in each group. After pressing the skin on the back of mice vertically with the corresponding MNs for 1 minute, the skin condition was observed at 0, 10, and 20 min after pressing. Another batch of 3T3 cells were divided into blank control group, 0 g/L ε-PL group and simple 5.0 g/L ε-PL group which were cultured with the extract of PVA-ε-PL-TSPBA MNs containing the corresponding concentration of ε-PL, and 5.0 g/L ε-PL+SH group which were cultured with the extract of PVA-ε-PL-TSPBA-SH MNs with 5.0 g/L ε-PL. The CCK-8 assay was performed to detect and calculate the relative survival rate of cells cultured for 24, 48, and 72 h to indicate the cell proliferation activity ( n=6). Eighteen BALB/c mice were induced into diabetic mice model by high-sugar and high-fat diet combined with streptozotocin injection and then divided into sterile dressing group, 0 g/L ε-PL+SH group, and 5.0 g/L ε-PL+SH group, with 6 mice in each group. A full-thickness skin defect wound was made on the back of each mouse, and S. aureus solution was added to make a full-thickness skin defect wound with bacterial colonization model for diabetic mouse. The wounds of mice in 0 g/L ε-PL+SH group and 5.0 g/L ε-PL+SH group were covered with PVA-ε-PL-TSPBA-SH MNs with the corresponding concentration of ε-PL, and the wounds of mice in the 3 groups were all covered with sterile surgical dressings. The wound healing was observed on post injury day (PID) 0, 3, 7, and 12, and the wound healing rate on PID 3, 7, and 12 was calculated. On PID 12, the skin tissue of the wound and the wound margin were stained with hematoxylin and eosin to observe the growth of new epithelium and the infiltration of inflammatory cells. Data were statistically analyzed with one-way analysis of variance, analysis of variance for repeated measurement, Mann-Whitney U test, and Bonferroni test. Results:With the extension of the immersion time, the PVA-TSPBA MNs in PBS containing hydrogen peroxide gradually dissolved and completely degraded after 10 days of immersion. The PVA-TSPBA MNs in pure PBS only swelled but did not dissolve. After 24 h of culture, there was no growth of S. aureus in 5.0 g/L ε-PL group or 10.0 g/L ε-PL group, and there was no growth of E. coli in 10.0 g/L ε-PL group. The relative survival rate of S. aureus was significantly lower in 1.0 g/L ε-PL group, 5.0 g/L ε-PL group, and 10.0 g/L ε-PL group than in blank control group ( P<0.05 or P<0.01). The relative survival rate of E. coli was significantly lower in 5.0 g/L ε-PL group and 10.0 g/L ε-PL group than in blank control group ( P<0.01). After 24 h of culture, the cells in blank control group, 0 g/L ε-PL group, 1.0 g/L ε-PL group, 5.0 g/L ε-PL group, and 10.0 g/L ε-PL group all grew well, and the relative survival rate of cells was similar among the groups ( P>0.05). The needle bodies of PVA-TSPBA MNs and PVA-TSPBA-SH MNs were both quadrangular pyramid-shaped and neatly arranged, and the needle bodies of PVA-TSPBA-SH MNs was more three-dimensional and more angular. The critical force of PVA-TSPBA-SH MNs was significantly higher than that of PVA-TSPBA MNs ( Z=3.317, P<0.01). The MNs in PVA-TSPBA+SH group penetrated the skin of mice at 0 min after pressing, and the pinholes partially disappeared after 10 min and completely disappeared after 20 min, while the MNs in PVA-TSPBA group failed to penetrate the skin of mice. After 24, 48, and 72 h of culture, the proliferation activity of the cells in 5.0 g/L ε-PL+SH group was significantly higher than that of blank control group ( P<0.05 or P<0.01). In sterile dressing group, the wounds of mice healed slowly and exuded more. The wound healing speed of mice in 0 g/L ε-PL+SH group was similar to that of sterile dressing group in the early stage but was faster than that of sterile dressing group in the later stage, with moderate exudation. The wound healing of mice in 5.0 g/L ε-PL+SH group was faster than that in the other two groups, with less exudation. The wound healing rates of mice in 5.0 g/L ε-PL+SH group were (40.6±4.2)%, (64.3±4.1)%, and (95.8±2.4)% on PID 3, 7, and 12, which were significantly higher than (20.4±2.7)%, (38.9±2.2)%, and (59.1±6.2)% in sterile dressing group and (21.6±2.6)%, (44.0±1.7)%, and (82.2±5.3)% in 0 g/L ε-PL+SH group ( P<0.01). The wound healing rates of mice in 0 g/L ε-PL+SH group on PID 7 and 12 were significantly higher than those in sterile dressing group ( P<0.05 or P<0.01). On PID 12, the wounds of mice in 5.0 g/L ε-PL+SH group were almost completely epithelialized with less inflammatory cell infiltration, the wounds of mice in 0 g/L ε-PL+SH group were partially epithelialized with a large number of inflammatory cell infiltration, and no obvious epithelialization but a large number of inflammatory cell infiltration was found in the wounds of mice in sterile dressing group. Conclusions:The composite MNs prepared by TSPBA, PVA, ε-PL, and SH can successfully penetrate mouse skin and slowly respond to ROS in the wound to resolve and release antibacterial substances, inhibit bacterial colonization, and promote the repair of full-thickness skin defect wounds with bacterial colonization in diabetic mice.

Objective: To study the expression of miR-142-5p in lung adenocarcinoma tissues, and to explore its effect on proliferation, invasion, migration and epithelieal-mesenchymal transition (EMT) of H1650 cells and the potential mechanisms. Methods:Atotal of 107 pairs of lung adenocarcinoma tissues and corresponding para-cancerous tissues from patients, who underwent tumor resection and were pathologically confirmed at the Department of Thoracic Surgery, the Fourth Hospital of Hebei Medical University between Jan. 2014 and Jan. 2015, were collected for this study; in addition, human lung adenocarcinoma cell lines (H1650, HCC827, A549, H1975, PC9) and human bronchial epithelial BEAS-2B cells were also used in this study. qPCR was used to detect the expression of miR-142-5p in lung adenocarcinoma tissues and cell lines. The correlation between expression of miR-142-5p and clinical features was analyzed.After transfection with miR-142-5p mimics or miR-negative control (miR-NC) plasmid, the proliferation, invasion and migration of H1650 cells were detected with CCK-8, Transwell invasion assay and Wound healing assay, respectively. The bioinforamtics tool was used to predict the target genes of miR-142-5p, and Luciferase reporter gene assay was performed to validate the regulation of miR-142-5p on target gene. Western blotting (WB) was used to detect the expressions of cyclin-dependent kinase 5 (CDK5) and EMTrelated protein. Results: Compared to Para-cancerous tissues and BEAS-2B cells, the expression of miR-142-5p was lower in lung adenocarcinoma tissues and cell lines (all P<0.01). Of the 107 cases of lung adenocarcinoma tissues, 61 cases (57.01%) showed decreased miR-142-5 expression, which was correlated with the TNM stage and lymph node metastasis (both P<0.01). Transfection of miR-142-5p mimics significantly up-regulated the expression of miR-142-5p and decreased the proliferation, invasion and migration of H1650 cells (all P<0.05 or P<0.01). Bioinformatics showed that CDK5 was a target gene of miR-142-5p. Luciferase reporter gene assay and WB validated that miR-142-5p could significantly down-regulate CDK5 expression in H1650 cells, up-regulate the expression of E-cadherin and down-regulate the expressions of N-cadherin, Twist and Snail in H1650 cells (all P<0.01). Conclusion: miR-142-5p is low expressed in lung adenocarcinoma tissues and cell lines; it suppresses the EMT process to inhibit, invasion and migration of H1650 cells via down-regulating the expression of CDK5.