Objective To evaluate the correlation between the expression of C5b-9 and the gastric carcinoma.Methods In this study, the human gastric adenocarcinoma (HGAC)tissues (n =32 cases)from 32 patients were evaluated by immunohistochemistry and tissue chip.The result was analyzed and evaluated by Multinomial logistic regression and likelihood ratio.Results Multinomial logistic regression and likelihood ratio testing showed that over-expression of C5b-9 in HGAC tissue was significantly correlated with clinical stage (P =0.007) and tumor stage (P =0.005),but not with tumor metastasis,lymphoid nodal status,sex or age.Conclusion C5b-9 can be the criteria of di-agnosis and clinical staging for gastric adenocarcinoma,which may help in diagnosis and assessment disease severity of human gastric carcinoma.

Objective To evaluate the clinical,epidemiological,and viral molecular biology features of 26 patients infected with H7N9 avian influenza A virus. Methods Clinical and epidemiological data of 26 patients with con-firmed avian influenza A (H7N9)infection in 2013 and 2014 were collected,virus isolated from human and poultry were identified and typed through sequencing.Results Of 26 patients,fever and cough were the most common symptoms,all patients had pneumonia;20 patients (76. 92% )developed acute respiratory distress syndrome (ARDS);25 patients (96.15% )had leucopenia or normal leukocytes at the initial diagnosis;treatment with antivi-ral drugs was initiated in 25 patients at a median of 10 days after the onset of illness;10 patients (38.46% )died. Gene sequencing indicated Gln226Leu and Gly186Val substitutions in human virus H7 gene and the PB2 Asp701Asn mutation. Conclusion Acute respiratory system damage is the main clinical manifestation of avian influenza (H7N9)virus infection in humans,live poultry exposure is an important risk factor for H7N9 infection in humans, adaptive mutation occurred at partial site of avian virus gene,which can be more easily be spread from birds to hu-man and cause serious diseases,it is necessary to strengthen the pathogen monitoring.

Asian Continental Ancestry Group ; Drugs, Chinese Herbal ; pharmacology ; therapeutic use ; Female ; Humans ; Immune Tolerance ; drug effects ; Materia Medica ; therapeutic use ; Medicine, Chinese Traditional ; Pregnancy ; Pregnancy Complications ; drug therapy

BACKGROUND:Neural stem cel (NSC) transplantation is a common method for various ischemicencephalopathies, but inability to survive in the transplantation region limits its further use in clinical practice. OBJECTIVE:To explore the effect of vascular endothelial progenitor cel s (VEPCs) on the proliferation and apoptosis of co-cultured NSCs as wel as vascular remodeling in rats with ischemia reperfusion injury. METHODS:125 Sprague-Dawley rats were randomly divided into five groups, 25 rats in each group, including sham operation, ischemia, NSCs, co-culture, and VEPCs groups. Rat models of ischemia reperfusion injury were made in al groups except for the sham operation group, fol owed by corresponding interventions. The proliferation and apoptosis of neural stem cel s were detected, and vascular remolding in the ischemic region was observed in each group. RESULTS AND CONCLUSION:At different time points after transplantation, BrdU positive cel s were not observed in VEPCs, ischemia and sham operation groups;the number of BrdU positive cel s in the co-culture group was significantly higher than that in the NSCs group (P<0.05);BrdU+/Caspase-3+cel were observed in both co-culture and NSCs groups, and the apoptosis rate of the co-culture group was significantly lower than that in the NSCs group (P<0.05);there were new blood vessels in al the groups except for the sham operation group, and the number of new bone vessels was highest in the co-culture group. To conclude, our experimental results show that VEPCs promotes the proliferation of co-cultured NSCs, inhibits cel apoptosis and and promote angiogenesis in the ischemic penumbra of rats with ischemia reperfusion injury.

BACKGROUND:Mkx (Mohawk, transcription factor) is one of the crucial factors in tendon formation, development and differentiation.
OBJECTIVE:To summarize the molecular structure, distribution and function of Mkx and its research process in the signaling pathways during tendon differentiation.
METHODS:The first author retrieved the databases of CqVip, CNKI and Medline from1990 to 2016 using the keywords of“Mkx, Mohawk, Irxl, tendon, tendon differentiation, tissue engineering, TGFβ, stem cel”in Chinese and English, respectively. The articles related to research process of Mkx in tendon tissue engineering were retrieved, and a total of 55 literatures were enrol ed final y.
RESULTS AND CONCLUSION:Mkx that expresses in various mesoderm-derived tissues plays an important role in the formation and development of tendon and tissue-engineered tendon formation. Although Mkx does not directly act on Scx (Scleraxis), it can regulate the differentiation of tendon progenitor cel s via transforming growth factor-β2 signaling pathway. Cel s from different species and different cel lines as wel as various cytokines for certain make different effects on Mkx involved in tendon tissue engineering.

Objective To explore the role of Kupffer cells( KCs)disorder on the occurrence and development of Nonalcoholic Fatty Liver Disease ( NAFLD) by means of rat model fed with high-fat diet. Methods Twenty-four male SD rats were random divided into model group ( n =12) and normal group( n = 12) , with a high-fat diet and standard diet for 12 weeks. The levels of body weight, liver weight, alanine aminotransferase( ALT), aspartate aminotransferase( AST) , triglyceride(TG) , and total cholesterol( TC) were measured. Routine histological features of hepatic section were observed by H. E staining. The shape changes of KCs in the liver were detected, and the levels of tumor necrosis factor-α(TNF-α) and nitric oxide (NO) secreted by KCs were measured. Results The weight, liver index, the levels of ALT, AST, TG, TC, and the levels of TNF-α and NO secreted by KCs in model group were higher than that in the normal group ( P < 0. 05). Histopathological examination showed hepatocellular macrovesicular steatosis, lobular inflammatory cell infiltration and necrosis. Compared with normal group, the shape and function of KCs in the liver changed largely. Furthermore, these changes of KCs were in accordance with the degree of steatosis, inflammation and necrosis in the liver of the model group. Conclusions The shape and function of KCs changed significantly in NAFLD induced by high-fat diet, and KCs disorder might be involved in the pathogenesis of NAFLD.

Objective To clone and express prokaryotic recombinant plasmid of nucleoside triphosphate hydrolase (NTPase) gene of Toxoplasma gondii, and analyze its antigenicity. Method NTPase gene was amplified by PCR from RH strain of T. gondii and cloned into pGEM-T Easy vector. Positive clones were screened and identified by BglⅡ, HindⅢ digestion and sequenced. The target gene was then subcloned into prokaryotic expression vector pBAD-HisB and transformed into E. coli BL21(DE3). The expressed recombinant protein was purified with Ni-NTA agarose and further analyzed by sodium dodecyl sulfate polyacrylamide gel electropheresis (SDS-PAGE) and Western blotting. Results NTPase-Ⅱ gene was specifically amplified, and the homology of DNA sequence was 100% to that in the GenBank. SDS-PAGE showed that the recombinant NTPase protein with correct molecular weight was expressed highly in E.coli BL21(DE3). Western blotting testified that the purified recombinant protein could be specifically recognized by mouse serum immunized with T. gondii and mouse anti-recombinant protein serum. Conclusion The NTPase-Ⅱ gene has been cloned and expressed in E.coli BL21(DE3), and the purified protein of NTPase-Ⅱ gene displays a specific antigenicity.

Objective To construct a recombinant expression vector of human interleukin-24(hIL-24) gene and express it in E.coli M15,and to evaluate the bioactivity of IL-24 fusion protein.Methods The human IL-24 cDNA fragment was amplified from plasmid by polymerase chain reaction(PCR),and sequenced.PQE/hIL-24 was constructed by gene rearrangement,then it was transformed into E.coli M15.The expression of the target protein was induced with IPTG and purified by Ni2+-NTA agarose column.The expressed recombinant hIL-24(rhIL-24) was identified by SDS-PAGE and Western blotting.Normal peripheral blood mononuclear cells(PBMCs) were cultivated with the expression protein for 48 and 72 h,the levels of IL-6,IFN-? and TNF-? of PBMCs stimulated with rhIL-24 were detected by ELISA.Results The recombinant prokaryotic expression vector PQE/IL-24 was constructed successfully and expressed stably in E.coli M15.At about 18 400 of molecular weight,there was an induced protein band.The levels of IFN-?,IL-6 and TNF-? in the group of cultivated with the expression protein were obviously higher than those in the groups without the expresson protein(P

llary-like mural nodules of PTC showed less enhancement on post-contrast CT and cervical lymph node metastases were more frequently seen in PTC.

Objective To test whether the prophylactic small dose amitriptyline has any beneficial influence on the rate of poststroke depression (PSD) by clinical experiment. Methods All 123 patients with first stroke were divided into the intervention group and the control group according to the block randomization tables. The patients in the intervention group were treated with 12. 5 mg amitriptyline every night for more than 1 month and the control group was blank Before and at the end of the observation, the rate of PSD and activities of daily living (ADL), degree of neurological deficit (NIHSS) of all the subjects were assessed. Results At the end of the one-month treatment, the intervention group had lower rate of PSD (16. 4% ) than the control (51.6%);and they had lower score in NIHSS (2. 83 ± 1.74 vs 3. 64 ±1.93) and higher score in ADL (93.0 ± 16. 1 vs 87.0 ± 37. 1) than the control. Multivariate Logistic regression analysis showed: the change of ADL score was closely related to the rate of PSD (RR =3.01 ,P =0. 04); the change of NIHSS score was closely related to the rate of PSD ( RR = 2. 42, P = 0. 03 );prophylactic small dose amitriptyline was closely related to PSD ( RR = 3.11, P = 0. 01 ). Conclusions Prophylactic small dose amitriptyline can decrease the rat of PSD, reduce the neurologic impairment and improve the activity of daily living.