Objective To investigate the value of Cells Free Ferrous Protoporphyrin (FH) detection in cervical cancer screening.Methods Retrospective analysis of December 2013 to 2014 year in December to accept the clinical data of 368 cases of female cervical cancer screening in Ningxia People's Hospital of Zhongwei Prefecture, divided into normal group (n=210), cervical precancerous lesions group (n=130) and cervical carcinoma group (n=28).The liquid based thin-layer cell detection (TCT) and FH detection were carried out, and the detection effects of the 2 detection methods were observed and compared.Results The statistics and comparison, in the detection of normal cervix, the false positive rate of FH detection was 19.05%, significantly higher than the detection of TCT 4.76% (P< 0.05);in the detection of cervical precancerous lesions, FH positive detection rate was 86.15%, lower than the detection of TCT 86.92%, and with the degree of cervical lesions continuously improve the positive rate of the 2 detection methods are showing a rising situation;in the detection of cervical cancer, the positive rate of FH detection was 96.43%, higher than the detection of TCT 92.86%, but the difference was not significant.Conclusion With ThinPrep cytology test (TCT), FH in the detection of relative detection effect of normal cervix of the poor, but in precancerous lesions and cervical cancer detection and detection of TCT are basically the same, therefore, FH still has a certain application value in screening of cervical cancer.

Hepatitis C virus (HCV)was easily developed into hepatitis,cirrhosis and liver cancer after infecting human.Cur-rently,the traditional method of treatment of HCV was pegylated interferon and ribavirin program,which was ineffective and had poor side effects,while the new direct antiviral drugs were expensive.Therefore,looking for cheap and non-toxic side effects of treatment was the focus of current research.More and more evidence indicate that micro-Ribose Nucleic Acid (miRNAs)play an important role in the development of liver disease,regeneration and functional regulation.This review studies the relationship between miR-122 and Hepatitis C virus and hepatocellular carcinoma.

High mobility group box 1 protein,a kind of damage-associated molecular patterns,is a group of nonhistone DNA-binding protein in the nuclear.It not only involves in DNA replication,recombination,repair,regulation of gene transcription,but also induces activation of innate immunity and T cell generation and activates the adaptive immune response through Toll-like receptor.It is also more closely related to autoimmune diseases,inflammatory diseases,tumors and so on.Currently there are many researches on the role of TLR-mediated HMGB1 signaling pathway in diseases,which is involved in a variety of pathological processes and has a broad clinical outlook.

Objective To detect the expression of retinoic acid-inducible gene Ⅰ ( RIG-Ⅰ) in peripheral blood mononuclear cells (PBMCs) of patients with chronic hepatitis C (CHC), and to explore its correlations with type Ⅰinterferon gene expression and serum level of hepatitis C virus .Methods A total of 101 na?ve patients with CHC were enrolled from Renmin Hospital of Wuhan University during July 2014 and July 2015, and 69 healthy subjects served as controls .The expressions of RIG-Ⅰ, IFNαand IFNβmRNA in PBMCs and serum level of HCV RNA were detected by real-time quantitative polymerase chain reaction.Pearson correlation analysis was performed to investigate the correlations of RIG-Ⅰ mRNA expression with IFNα/βmRNA expression and serum level of HCV RNA .Results The relative expressions of RIG-Ⅰ, IFNα, IFNβmRNA to healthy controls in CHC group were 0.082, 0.022 and 0.156, respectively (t=7.83, 3.65 and 2.13, all P<0.05).RIG-Ⅰ mRNA expression in patients with HCV loads <(1 ×106 ) IU/mL was 1.79 times higher than that in patients with HCV loads≥(1 ×106 ) IU/mL (t=2.60, P <0.05).Pearson correlation analysis showed that the expression of RIG-Ⅰ mRNA was positively correlated with that of IFNαmRNA and IFNβmRNA (r=0.247 and 0.489, P<0.05), but not correlated with HCV load (r=0.187, P>0.05).Conclusion Expression of RIG-ⅠmRNA decreases in patients with CHC , and is positively correlated with that of IFNαand IFNβmRNA.

Objective To investigate the expression of NKG2D and related signaling molecules adaptor protein(DAP10) and extracellular signal-regulated kinase(ERK) in the inflammatory cells of gastric adenocarcinoma and para-carcinoma tissues,the effects of vasoactive intestinal peptide(VIP) on the expression of NKG2D,DAP10 and ERK in natural killer(NK) cells of healthy volunteers.Methods The expression of NKG2D,DAP10 and ERK in the inflammatory cells of 36 gastric adenocarcinoma and para-carcinoma tissues were detected by immunohistochemistry.The peripheral blood NK cells of healthy volunteers were isolated and purified with CDC method.The expressions of NKG2D,DAP10 and ERK in NK cells were determined by immunocytochemistry and reverse transcription-polymerase chain reaction(RT-PCR) methods before and after VIP intervention.The ttest was used for comparison between two groups and rank transformation nonparametric test (Kruskal-Wallis H test) for count data analysis.Results The expression levels of NKG2D,DAP10 and ERK in the inflammatory cells of gastric adenocarcinoma were significantly lower than those of para-carcinoma tissues (H=30.640,24.910,20.320,all P＜0.01).The expression levels of NKG2D,DAP10 and ERK were much lower in poorly differentiated gastric adenocarcinoma (H =4.049,11.830,8.118),at stage Ⅲ-Ⅳ (H=4.275,11.560,7.686),and the expression levels of NKG2D,ERK were lower with lymph nodes metastasis (H=6.513,6.064,all P＜0.05).The expression levels of NKG2D,DAP10 and ERK in gastric adenocarcinoma tissues and inflammatory cells were not correlated with gender,age and the location of lesions (all P＞0.05).The expression levels of NKG2D,DAP10 and ERK in NK cells was decreased after VIP intervention (protein:H=12.438,4.798,13.745,mRNA:F=337.640,638.579,1055.015,all P＜0.05).Conclusion Gastric adenocarcinoma may downregulate the expression of NKG2D,DAP10 and ERK in NK cells through VIP secretion,which may be involved in the immune escape of gastric cancer.

With the expanding development of engineering of medical service,medical engineering department should adapt to hospital development.Expanding principle and the goal of medical engineering department are expounded.The fundamental content of the expanding strategy includes mechanism of purchasing and purveying,construction and management of both equipment maintenance and medical metrological organization,training to faculty of specialized subject,orientation of scientific research,etc.

Objective To detect mRNA expressions of STING and type Ⅰ interferons(IFN-α and IFN-β) in peripheral blood mononuclear ceils (PBMCs) of patients with chronic hepatitis C(CHC).Methods 113 patients with CHC and 94 healthy controls were collected from Renmin Hospital of Wuhan University during January 2015 and January 2016.Expressions of mRNA of STING,RIG-1,IFN-α and IFN-β were detected by real-time quantitative PCR,and their relative expression values were obtained by 2-△△Ct method and the results were statistically analyzed.Results The expression of mRNA of STING,RIG-1,IFN-α and IFN-β in CHC were 0.018,0.361,0.578 and 0.573 times than its in healthy controls respectively and the differences were statistically significant (t-8.28,4.26,2.18 and 2.07,all P ＜ 0.05).Pearson correlation analysis showed that mRNA expressions of STING in healthy controls were positively correlated with that of IFN-α mRNA and IFN-β mRNA (r=0.487 and 0.207,all P＜0.05),which had no correlation in CHC (r=0.174 and 0.091,all P＞0.05).The expressions of STING mRNA was positively correlated with that of RIG-1 mRNA in healthycontrols (r=0.222,P＜0.05),but there was no correlation of expression in CHC between STING mRNA and RIG-1 mRNA (r=-0.029,P＞0.05).Conclusion Compared with healthy controls,the expression of STING,RIG-1,IFN-α and IFN-β mRNA were all reduced.There was positive correlation between STING and RIG-1,IFN-α and IFN-β in healthy controls,but no correlation in CHC.

AIM: To study the effect of rosiglitazone (RSG) to improve insulin sensitivity on myocardial energy substrate utilization as well as the cardiac function in a rat model of type 2 diabetes mellitus. METHODS: Sprague-Dawley rats were conducted into three groups: chow-fed rats were fed with normal chow (12% of calories as fat); fat-fed/STZ rats were fed with high-fat diet (40% of calories as fat) for 4 weeks and then injected with streptozotocin 35 mg/kg intraperitoneal; fat-fed/STZ/RSG rats were fat-fed/STZ rats treated with rosiglitazone (3 mg?kg~(-1)?d~(-1)) for 2 weeks. A cannula connected to a passive transducer was inserted the heart for the measurement of the cardiac function including heart rate (HR), left ventricular end-diastolic pressure (EDP) and ?dp/dt_(max). Then the isolated hearts were mounted onto a Langendorff perfusion apparatus to perfuse with Krebs-Henseleit buffer in the presence of 5 mmol/L glucose and 0.4 mmol/L [~3H] labelled palmitate. Glucose uptake and [~3H_2O] collection were measured to evaluate the rate of carbohydrate and fatty acid oxidation. RESULTS: Compared with the chow-fed rats, fat-fed/STZ rats had a significantly depression of glucose uptake in the hearts [(54.7?6.2 vs 69.0?5.7) ?mol?g~(-1) dry weight, P

Objective To build a method to simultaneously determine paeoniflorin, naringin, hesperidin, glycyrrhizic acid in Sinisan by HPLC, provide a reliable method for evaluation and effective quality control, and lay the foundation of material basis for efficacy research for TCM compound Sinisan.Methods The column was Kromasil C18 (4.6 mm×250 mm, 5μm);mobile phase was acetonitrile-0.05% phosphoric acid aqueous solution with gradient elution program;the flow rate was 1.0 mL/min;UV detection was performed at 240 nm;the detector drift tube temperature was set at 30℃.Results The linear ranges of paeoniflorin, naringin, hesperidin and glycyrrhizic acid were 0.00225-0.01125μg (r=0.999 7), 0.00390-0.00195μg (r=0.9997), 0.00198-0.00099μg (r=0.999 5), 0.00262-0.00131μg (r=0.999 7), respectively. The average recoveries of paeoniflorin, hesperidin, naringin and glycyrrhizic acid were 97.72% (RSD=1.02%), 98.45% (RSD=1.52%), 97.74% (RSD=1.63%), 98.34% (RSD=1.78%), respectively.Conclusion The method is accurate, simple, reliable and duplicable, and is available for the quality control of Sinisan.

Objective:To study immunosuppression mediated by the porcine FcγRⅢ in porcine reproductive and respiratory syndrome virus ( PRRSV ) infection to pulmonary alveolar macrophages ( PAMS ).Methods: In this study pulmonary alveolar macrophages cells were treated with containing 200 TCID50 PRRSV,lipopolysaccharide (LPS) (100 ng/ml) and purified mouse anti-pig FcγRⅢIgG (550 μg/ml) separately,simultaneously,PAM cells treated with purified mouse anti-pig FcγRⅢIgG (550 μg/ml) was infected by 200 TCID50 PRRSV ,untreated PAM cells as the control group.Each group were post-cultured 12,24,36,48,60,72 h, the cells and the supernatant were collected.The dynamic variation of PRRSV RNA copies in inoculation group were detected by using real-time fluorescence quantitative PCR method.mRNA level of IFN-αand TNF-αin each group were detected by using relative fluorescence quantitative PCR.Results:The result showed that mRNA level of IFN-αwas improved during PRRSV infection to PAMS 12-24 h,and mRNA level of IFN-αwas inhibited during 36-72 h,then mRNA level of IFN-αrecovered normally; mRNA level of TNF-αwas increased slightly post-infection 12-72 h.IFN-αand TNF-αmRNA levels of PAM cells treated with LPS were both up-regu-lated,using the purified mouse anti-pig FcγRⅢ IgG to treat the PAM cells,selective activation of porcine FcγRⅢ in the PAM cells down-regulated significantly mRNA levels of IFN-αand TNF-α.PRRSV infection assay mediated by selective activation FcγRⅢof the PAM cells inhibited antiviral cytokine ( IFN-αand TNF-α) mRNA levels.Conclusion:The results show selective activation of FcγRⅢinhibited significantly mRNA levels of the antiviral cytokine IFN-αand TNF-αof host cells,and innate antiviral immune response to PRRSV infection.