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: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.

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.

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To study the mechanisms of total flavonoid from Glycyrrhizae Radix et Rhizoma (TFGR) and its ingredient isoliquiritigenin (ISL) on their regulation of M2 phenotype polarization of macrophages. IL-4 (60 μg x L(-1)) induced RAW264.7 cells for 6 h to establish the M2 macrophage model. TFGR and ISL restrained breast cancer cells migration with the aid of M2 macrophages in vitro. TFGR and ISL inhibited gene and protein expression of Arg-1, up-regulated gene of HO-1 and protein expression of iNOS, enhanced the expression of microRNA 155 and its target gene SHIP1, meanwhile down-regulated.the phosphorylation of STAT3 and STAT6. So TFGR and ISL were the bioactive fraction and ingredient in Glycyrrhizae Radix et Rhizoma to reverse M2 phenotype macrophages polarization. TFGR and ISL inhibited the promotion of M2 macrophages to breast cancer cells migration in vitro, STAT signal pathways and miR155 were partly involved.
Animals ; Cell Line, Tumor ; Cell Movement ; drug effects ; Cell Polarity ; drug effects ; Chalcones ; pharmacology ; Flavonoids ; pharmacology ; Glycyrrhiza ; chemistry ; Interleukin-4 ; genetics ; metabolism ; Macrophages ; cytology ; drug effects ; metabolism ; Mice ; RAW 264.7 Cells ; Rhizome ; chemistry

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.

Foreign student education is an important task in medical colleges and universities.Clinical neurology teaching is very difficult because of its complex discipline.Neurologists in the First Affiliated Hospital of Chongqing Medical University summarized and analyzed the common problems including the training of teachers' ability to use language,teaching of basic subjects,clinical skills training,promotion of patients' compliance and implementation of regular tests so as to provide references for improving the quality of neurology teaching.

Objective:To examine the expression and function of thrombonspondin-1 (TSP-1) in oxygen-induced retinopathy in new-born mice, and to investigate its role in retinal neovascularization. Methods:A total of 40 C57BL/6J newborn mice were divided equally into a model group (n=20)andanormalcontrolgroup(n=20).Miceinthemodelgroupwereexposedto75%oxygentoestablish the oxygen-induced retinopathy (OIR) model. On the 7th, 9th, and 11th day after the birth of mice, 5 mice were randomly selected each time from the 2 groups to examine the expression of TSP-1 mRNA with reverse transcription polymerase chain reaction (RT-PCR). After that, 5 mice were selected on the 11th day to observe the retinal neovascularization by fluorescein angiography retinal flatmount. Results:On the 11th day, fluorescein angiography retinal flatmount showed that the retinal blood vessels presented mean network distribution in the normal control group, while in the model group, a lot of dilatated areas in the retinal main vessels surrounded the optic disc. Meanwhile lots of new blood vessels were found surrounding the optic disc with irregular distribution but well distributed peripherial retinal small vessels, which was typical of early stage OIR. There was no signiifcant difference in the retinal TSP-1 mRNA level between the model group and the normal control group in the postnatal 7-day mice (P>0.05). Compared with the normal control group, the expression of TSP-1 mRNA in the model group was signiifcantly lower in postnatal 9-day and 11-day mice (P<0.05, P<0.01) , and the expression of TSP-1 mRNA in postnatal 9-day mice was lower than that in the postnatal 11-day mice(P<0.05).
Conclusion:In the early stage of OIR model (retinal vascular growth and development stage), the expression of TSP-1 mRNA in the retinal tissue is gradually decreased, implying that TSP-1 (as a negative regulatory factor) may be involved in the formation of retinal neovascularization in the early stage.