Objective To investigate the effects of dexmedetomidine on serum inflammatory factor and oxidative stress response in septic rats.Methods Thirty healthy male SD rats,aged 10-14 weeks,weighing 250-300 g,were randomly divided into 3 groups( n =10 each): sham operation group (group S),sepsis group (group CLP) and sepsis + dexmedetomidine group (group CLP + D).Sepsis was induced by cecal ligation and puncture in groups CLP and CLP + D.Group CLP + D received intravenous infusion of dexmedetomidine at 10 μg· kg- 1 ·h- 1 from the end of operation until dead or 12 h after operation.Groups S and CLP received equal volume of normal saline at 1 ml·kg-1 ·h-1.Arterial blood samples were taken from 5 rats in each group before (basline) and at 1,6 and 12 h after operation for determination of serum IL-6,IL-10,SOD and MDA levels.The survival rate within 12 h after operation was recorded.Results Compared with group S,serum IL-6,IL-10 and MDA concentrations at 1,6 and 12 h after operation were increased,while serum SOD activity at 1,6 and 12 h after operation and survival rate were decreased in group CLP ( P ＜ 0.05 ).Compared with group CLP,serum IL-6 and MDA concentrations at 6 and 12 h after operation were decreased,while serum SOD activity at 12 h after operation and survival rate were increased in group CLP + D ( P ＜ 0.05 ).Conclusion Dexmedetomidine can increase the survival rate of septic rats by inhibiting inflammatory factor release and oxidative stress response.

An anaerobic sequencing batch reactor (ASBR) was used to treat thermal denitration tail liquid and microbial community was studied. Activated sludge was taken from the reactor for scanning electron microscope analysis. The images showed that the dominant cells in the flora were oval cocci. Its diameter was about 0.7 μm. Through a series of molecular biology methods such as extracting total DNA from the sludge, PCR amplification, positive clone authentication and sequencing, we obtained the 16S rDNA sequences of the flora. Phylogenetic tree and clone library were established. The universal bacteria primers of 27F-1492R PCR amplification system obtained 85 clones and could be divided into 21 OTUS. The proportions were as follows: Proteobacteria 61.18%; Acidobacteria 17.65%; Chlorobi 8.24%; Chlorofexi 5.88%; Gemmatimonadetes 3.53%; Nitrospirae 2.35% and Planctomycetes 1.18%. The specific anammox bacterial primers of pla46rc-630r and AMX368-AMX820 PCR amplification system obtained 45 clones. They were divided into 3 OTUS. Candidatus brocadia sp. occupied 95.6% and unknown strains occupied 4.4%.
Ammonia ; chemistry ; Bacteria ; Phylogeny ; Polymerase Chain Reaction ; RNA, Ribosomal, 16S ; Sewage ; microbiology

Objective To explore the nursing interventions of paronychia caused by Erlotinib therapy for advanced non-small-cell lung cancer patients. Methods A total of 78 patients who diagnosed as advanced non-small-cell lung cancer and treated by oral Erlotinib were selected. The occurrence of paronychia among them was observed and the curative effect of certain nursing interventions on paronychia was evaluated. Results Seven out of 78 cases occurred various degrees of paronychia,and certain nursing interventions could effectively prevent and treat paronychia. Conclusions Targeted drug Erlotinib in patients with advanced non-small cell lung cancer can cause adverse reactions like paronychia,but effective nursing interventions are capable of controlling the adverse reactions, thus further improve the quality of life and ensure the smooth progress of treatment.

Objective To investigate the role of Stathmin in pancreatic cancer invasion and metastasis and its relationship with DNA methylation. Methods Immunohistochemical detection of MBDI and Stathmin protein expression in 40 cases of pancreatic cancer and 15 cases ot normal pancreatic tissue were performed,followed by analysis of their clinical and pathological relationship with pancreatic cancer; Human pancreatic cancer cell line BxPC-3 was treated with 5-Aza-2-dC (AZA).Both qRT-PCR and Western blot analysis of Stathmin expression were used before and after AZA treatment; Stathmin-siRNA transfected BxPC-3 cells were divided into the Stathmi-siRNA group and the empty vector control group.Transwell chamber invasion assay and animal experiment were performed to measure the changes in cell invasion and metastatic capability. Results lmmunohistochemistry showed positive MBDI and Stathmin expressions in 28 (70％) and 24 (60％) out of 40 cases of pancreatic cancer,respectively,which were significantly higher than that in the normal pancreatic tissue (P＜ 0.05); MBDI and Stathmin protein expressions were positively correlated (r =0.356,P =0.037),so were MBDI expression and lymph node metastasis (P=0.023).Stathmin expression was significantly correlated with clinical staging and lymph node metastasis (P =0.002,and P =0.001,respectively).After AZA treatment,both Stathmin mRNA and protein expression in BxPC-3 were significantly decreased.Transwell chamber invasion assay showed that compared with the control group,the cell invasion capability of the Stathmin-siRNA group was significantly decreased (P＜0.05).Animal experiment showed that the incidence of liver metastasis was significantly lower in the Stathmin-siRNA transfected group than the empty vector control group (P＜0.05).Conclusion Demethylation may contribute to the reduction of Stathmin expression in pancreatic cancer and further improve the prognosis of pancreatic cancer patients.

Objective To investigate the distribution,epidemiologic feature and the related risk features of allergic rhinitis among college students in Kunming.Methods Stratified cluster sampling was conducted in each school as a unit.The investigated subjects included 1500 students aged from18 to 29 years old from 7 universities in Kunming,Yunnan Province.The epidemiological investigation was carried out using the designed questionnaire of allergic rhinitis.The results were analyzed.Restlts We had given out 1500 questionnaires and the response rate was 98.9％.The self-reported prevalence of allergic rhinitis was 25.4％ among college students in Kunming,in which,the males' prevalence rate was 29.3％ and the females' was 22.9％.And 3.7％ of the students with allergic rhinitis were combined with asthma and the 19.1％ combined with a history of familial inheritance.The main risk factor was dust.Concltsion The self-reported and prevalence of allergic rhinitis among college students in Kunming is 25.4％.Males' prevalence rate is slightly higher than the females'.The potential risk factors are bronchial asthma and the history of familial inheritance.The mainly inducement is dust,animal fur and plant pollen.

Objective To explore the feasibility of extending liver blood perfusion cessation by ultrasound combining microbubbles.Methods The livers of 9 healthy rabbits were treated with a pulsed therapeutic ultrasound device,in presence of microbubbles.For quantification of liver perfusion,contrastenhanced ultrasonography was performed on 6 rabbits before treatment and at different time points of 0 min,30 min,60 min and 48 hours after treatment.Pathological examination of the treated livers was performed immediately after treatment on the other 3 rabbits.Results The liver blood perfusion almost vanished immediately after treatment,remained at a low perfusion level from 30 to 60 min,and completely recovered 48 hours later.The peak intensity dropped from ( - 51.88 ± 4.26)dB to ( - 62.53 ± 4.83)dB after treatment and rose up to ( - 52.00 ± 4.60) dB 48 hours later.The peak intensities before treatment and 48 hours after treatment were significantly higher than those of 0 min,30 min and 60 min time points after treatment( P ＜0.05).Pathological examination showed significant swelling of hepatocytes and hemorrhage around portal veins.Conclusions Microbubbles enhanced ultrasound can induce liver blood perfusion cessation for up to 1 hours.The mechanism could be swelling of hepatocytes and hemorrhage of portal track.

With thousands of sequenced 16 S rRNA genes available,and advancements in oligonucleotide microarray technology,the detection of microorganisms in microbial communities consisting of hundreds of species may be possible.The existing algorithms developed for sequence-specific probe design are not suitable for applications in large-scale bacteria detection due to the lack of coverage,flexibility and efficiency.Many other strategies developed for group-specific probe design focus on how to find a unique group-specific probe that can specifically detect all target sequences of a group.Unique group-specific probe for each group can not always be found.Hence,it is necessary to design non-unique probes.Each probe can specifically detect target sequences of a different subgroup.Combination of multiple probes can achieve higher coverage.However,it is a time-consuming task to evaluate all possible combinations.A feasible algorithm using relative entropy and genetic algorithm (GA) to design group-specific non-unique probes was presented.

Objective Fecal biomarkers have emerged as an important tool for assessing and monitoring disease activity in patients with inflammatory bowel disease ( IBD) .We aimed to investigate the diagnostic value of fecal neopterin and calprotectin in pa-tients with active inflammatory bowel disease and made comparison with that of serum C-reactive protein ( CRP) . Methods A total of 151 consecutive patients with IBD (84 CD and 67 UC) provided 2 gram fecal samples for the measurement of fecal neopterin( FNP) and calprotectin( FCP) concentrations and 2 milliliter blood samples for the serum C-reactive protein measurement before undergoing a colonoscopy.ELISA was applied in the measurement.Clinical disease activities were scored independently according to the Best Crohn′s Disease Activity Index(CDAI) in patients with CD, while the Modi-fied Mayo Scores in patients with UC.Comaprison was made in the relativity of each fecal marker and IBD activity score, the optimum value of diagnosing IBD acitivity as to each fecal marker, as well as sensitivity, specificity, moreover, receiver operating characteristic curve ( ROC) was drawn.50 healthy volunteers who received a normal colonoscopy were also enrolled as the control group and asked to give a 2 gram fresh stool sample. Results The FNP and FCP concentrations in patients with IBD were significantly higher than those in healthy control group(P<0.05).Both FNP and FCP concentrations differed significantly in clinically active IBD when compared with those in patients with inactive disease( P<0.001) .In CD patients, the correlation coefficients of FNP and FCP with CDAI were 0.55 and 0.59, respectively(P<0.001).In UC patients, the correlation coefficients of FNP and FCP with Mayo scores were 0.74 and 0.77, respectively( P<0.001) .The correlation coefficients of serum CRP in CD and UC patients with clinical scores were 0.49 and 0.60, respectively(P<0.001).The area under the ROC curve(AUC) of FNP and FCP for the diagnosis of clinical activity in pa-tients with CD were 0.75 and 0.80, respectively.The AUC of FNP and FCP in UC patients were 0.85 and 0.90, respectively.The AUC of serum CRP in patients with CD and UC were 0.65 and 0.74, respectively.When combined FNP with FCP, the AUC in pa-tients with CD and UC were 0.85 and 0.92, respectively. Conclusion FNP is a novel reliable and non-invasive biomarker to evalu-ate clinical disease activity in patients with IBD as accurate as FCP, It is advisable to combine FNP with FCP to evaluate disease activi-ty in patients with IBD.

Objective To study the effects of Toll-like receptor 4(TLR4) on oxidized low density lipoprotein ( ox-LDL) induced macrophage apoptosis and its possible mechanism .Methods THP-1 derived macrophages were divided into four groups including untreated control group , ox-LDL treated group , ox-LDL+LPS treated group and tunicamycin treated group .MTT assay and flow cytometry analysis were performed to measure cell vitality and cell apoptosis , respectively .Oil red O staining was used to observe the phagocytosis of lipids by macrophages .The persistent and intense endoplasmic reticulum ( ER) stress markers were de-tected by analyzing the expression of glucose-regulated protein 78 ( GRP78 ) and CCAAT/enhancer-binding protein homologous protein ( CHOP) at mRNA and protein levels by q-RT-PCR and Western blot .Small in-terfering RNA ( siRNA) was used to silence the expression of TLR 4 to further elucidate its possible mecha-nism.Results Flow cytomotry and MTT assay showed that the number of apoptotic cells in ox-LDL+LPS treated group were increased more significantly than that in ox-LDL treated group (P<0.01), and cell apop-tosis in both two groups were greater than that in control group (P<0.01).Compared with control group, the expression of GRP78 and CHOP at mRNA and protein levels were up-regulated in ox-LDL+LPS treated group and ox-LDL treated group (P<0.01), and the expression of GRP78 and CHOP in ox-LDL+LPS treated group was significantly higher than that in ox-LDL treated group (P<0.01).Silenced expression of TLR4 al-leviated the endoplasmic reticulum stress (P<0.05).Conclusion Increased expression of CHOP contribu-ted to cell apoptosis .TLR4 might promote ox-LDL induced macrophage apoptosis through accelerating endo-plasmic reticulum stress .

Objective To investigate the effects of TLR7 on imiquimod induced apoptosis of THP-1 derived macrophages.Methods Three cell lines ( THP-1 derived macrophages, MDCK cell line and HUVEC cell line) with different capabilities of expressing TLR7 were selected.The survival rates of cells af-ter the treatment with different concentrations of imiquimod were detected by MTT assay.The levels of IL-6 in the supernatants of TLR7 inhibitor chloroquine or TLR7-siRNA treated cells were detected by enzyme-linked immunosorbent assay.The apoptosis of cells was detected by flow cytometry after inhibiting the ex-pression of TLR7.Results Imiquimod induced the apoptosis of THP-1 derived macrophages, MDCK cell lines and HUVEC cell lines.The levels of IL-6 were significantly decreased as the expression of TLR7 was inhibited by treating THP-1 derived macrophages with chloroquine or TLR7-siRNA.Treating THP-1 derived macrophages with chloroquine or TLR7-siRNA did not affect the cell apoptosis induced by imiquimod.Con-clusion Imiquimod could induce the apoptosis of THP-1 derived macrophages through TLR7 independent pathway.