0.05). Conclusions Cyclin D1 and p16 are important factors modulating cell cycle. The interrupt of balance between these two factors derived from abnormal expression of cyclin D1 may be one of the causes of vulvar white lesion.

Objective To observe the expression profiles of miR-200b/c and their targets ZEB1/2 in early pulmonary fibrosis caused by acute lung injury induced by lipopolysaccharide in mice.Methods Early pulmonary fibrosis caused by acute lung injury is built via a lipopolysaccharide three-hit regimen.Mice were sacrificed at post-injective day 3,7,14,21 respectively and the lung tissue specimens were collected.The lung tissue sections were stained with HE and Masson staining and pathological changes were observed by optical microscope.The expression profiles of miR-200b,miR-200c,ZEB1 mRNA and ZEB2 mRNA were detected by real-time PCR.Western blot was utilized to detect the levels of ZEB1,ZEB2,E-cadherin,Vimentin,α-SMA proteins.Results (1) pathological findings:compared with the control group,the collagen fibers deposited on on the third day after LPS treatment and pulmonary fibrosis gradually worsened;(2) Real time-PCR results:With the aggravation of pulmonary fibrosis,miR-200b and miR-200c levels were declined and the levels of miR-200b/c at post-injective day 7,14,21 were significantly lower than that of control group (P＜0.01).ZEB1 mRNA and ZEB2 mRNA levels were gradually increased in the process of pulmonary fibrosis and the increased magnitude of ZEB2 mRNA was more significant than that of ZEB1 mRNA;(3) Western blot results:ZEB1 and ZEB2 protein levels were also gradually increased,consistent with their mRNA levels and the expression of E-cadherin protein was decreased while Vimentin and oα-SMA protein levels increased with the evolution of pulmonary fibrosis caused by acute lung injury.Conclusion miR-200b and miR-200c promote epithelial-mesenchymal transition by inhibiting their targets ZEB1/2 in early pulmonary fibrosis caused by acute lung injury induced by LPS.

Acute kidney injury (AKI) is the complex clinical syndrome attributed to multiple causes and risk factors, which is characterized by an abrupt loss of renal function. Metabonomics, recently advances in the field of omics, is the nontargeted measurement of all of the low-molecularweight compounds that appear in a particular cell, tissue, organ or biofluid in a living organism. Compared to genomics, transcriptomics and proteomics,metabonomics has its unique advantages, including fewer metabolites than genes, transcripts and proteins, the most accurate predictors of the signature of the actual processes, easy access to biofluids. Thus, metabonomics makes it possible to find new biomarkers for AKI on early diagnosis, identifying new metabolic pathways, finding new targets for drug therapy and individual medical treatment.

BACKGROUND: Tendon injury and dysfunction often occurs in military training, but the exactly epidemiological, pathological, physiological, healing and remodeling mechanisms of tendonopathy is still unclear, even the pain due to chronic tendon dysfunction should be further studied.OBJECTIVE: To evaluate the effect of forced training on the muscular strength of ankle joint and the cross-sectional area (CSA) of achilles tendon of infantry soldiers, and look for effective training methods.DESIGN: One-sample contrasting study.SETTING: Fourth Military Medical University of Chinese PLA; InStitute of Military Training-related Medical Sciences, the 150 Hospital of Chinese PLA.PARTICIPANTS: The study was carried out in the Institute of Military Training-related Medical Sciences, the 150 Hospital of Chinese PLA from March to June 2004. Thirty male light infantry recruits and thirty one-year-trained male soldiers were regarded as recruit group and one-year soldier group. The enlisted age ranged from 17 to 18 years. Recruits did not have the history of special training and injury of ankle joints. All of them were able to undertake routinely physical training.METHODS: The recruits participated in routinely physical trainings, such as grenade throwing and 5 km cross-country race, and forced trainings, such as dorsiflexors and plantarflexors on ankle joint, twice a day for each training item for 8 successive weeks. The forced training included calf raise for 50 times and sit-ups for 50 times on 45° arched board.Moreover, one-year soldiers were undertaken routinely physical trainings. Eight weeks later, the isokinetic testing of ankle joint and CSA of achilles tendon were measured before and after trainings.MAIN OUTCOME MEASURES: Comparisons of CSA of achilles tendon and changes of muscular strength of ankle joint between recruits before routine training and after 8-week forced training and one-year soldiers after routine training.RESULTS: All 60 soldiers were involved in the final analysis. Partial correlation was showed between CSA and body weight (r =0.446, P=0.015), and there was no difference in CSA before and after training. The relative peak torque, endurance and torque acceleration energy of plantarflexors, dorsiflexors and evertors were distinctively higher in recruit group and one-year soldier group after training than those in recruit group before training (P ＜ 0.05); however, there was no difference between recruit group and one-year soldier group after training.CONCLUSION: Forced training method can improve physical readiness in a short time. No changes of CSA of achilles tendon after training show that the improvement of ankle muscular strength may be through the rebuilding of its inner-structure rather than through the hypertrophy of the tendon.

Thrombotic microangiopathy (TMA) is a group of acute clinical pathological syndromes with common pathological features, which include hemolytic uremic syndrome (HUS) and thrombotic thrombocytopenic purpura syndrome. They have many similarities in etiology and clinical presentation. The role of abnormal activation of complement bypass pathway in the genesis and development of HUS has been recognized. More than 100 kinds of complement regulatory factors or gene mutations of complement itself were found to be associated with the development of HUS, which resulted in the decrease of negative complement regulatory protein activity or the increase of complement activation protein function. Abnormal activation of complement system resulted in endothelial injury and thrombosis. Loss of ADAMTS13 activity (<10%) is the most important pathogenesis of TTP. However, there are more and more evidence that complement bypassing pathway is over-regulated and over-activated in the formation of TTP. At present, the research of TMA is focused on finding specific complement-activated biomarkers in patients with various forms of TMA and developing new targeted therapeutic drugs for the disease.

This study is to investigate the treatment of Jin Chai antiviral capsule for influenza virus FM1/47 (H1N1) infection. The model of pneumonia was established by dropping influenza virus into the nose of normal mice, real-time PCR and Western blot technique were used to detect the virus load and the interferoninducible transmembrane protein3 (IFITM3) in lung of mice at the 1st day, 3rd day, 5th day and 7th day after affected. The results showed that Jin Chai antiviral capsule in large, middle, small dose groups can decrease virus load significantly at each time point, after being affected (P<0.05, P<0.01), Jin Chai antiviral capsule can increase the interferoninducible transmembrane protein3 in lung of mice, large dose groups are significantly higher in expression of IFITM3 compared with model group at each time point (P<0.05, P<0.01). Middle dose groups are significantly higher in expression of IFITM3 compared with model group at the 3th day and the 5th day (P<0.05), small dose groups are significantly higher in expression of IFITM3 compared with model group at the 3th day (P<0.05). It can be concluded that Jin Chai antiviral capsule exerts antiviral effects against influenzavirus by raised expression of IFITM3.

OBJECTIVETo explore the effect of epidermal growth factor-like domain 7(EGFL7) on the migration and angiogenesis of endothelial cells.

METHODSEGFL7 overexpression vectors were constructed and transfected into human microvascular endothelial cells. The expression levels of EGFL7-mRNA and EGFL7 protein were examined by real-time RT-PCR and Western blot. Cell migration was analyzed by the wound healing. The capability of cell to form capillary-like tubes in vitro was evaluated on matrigel assay. Protein expression of p-AKT, AKT, p-ERK and ERK in endothelial cells was detected by Western blot upon transfection with EGFL7 overexpression vectors and vehicle control for 0, 10, 30 and 60 min.

RESULTSMigration and angiogenesis of endothelial cells were notably enhanced by EGFL7 overexpression. ERK pathway was strongly activated by EGFL7, whereas AKT remained constant in endothelial cells. Inhibition of ERK impaired EGFL7 induced ERK activation and endothelial cell migration and angiogenesis.

CONCLUSIONEGFL7 effectively promotes migration and angiogenesis through ERK signaling pathway in endothelial cells.

Blotting, Western ; Cell Movement ; Endothelial Cells ; physiology ; Endothelial Growth Factors ; genetics ; physiology ; Humans ; MAP Kinase Signaling System ; physiology ; Neovascularization, Physiologic ; RNA, Messenger ; metabolism ; Signal Transduction

OBJECTIVETo explore the mechanism of serotonin-promoted osteoblast differentiation.

METHODSExpression levels of collagen I and lysyl oxidase (LOX) in osteoblast were measured by RT-PCR after treated by (50, 100, 200 and 400 ng/L) serotonin. LOX siRNA effect was measured by Western blot, and protein levels of collagen I were determined by ELISA after treated by serotonin. Expression levels of Smad2 and Smad3 in osteoblasts were also measured by RT-PCR after treated by serotonin.Moreover, expression levels of LOX were measured by RT-PCR after Smad3 was knockout.

RESULTSSerotonin promoted collagen I and LOX expression. The expression level of collagen I was significantly decreased by LOX siRNA. Furthermore, serotonin up-regulated the expression of Smad2 and Smad3 in osteoblasts, and the expression level of LOX was inhibited by Smad3 siRNA.

CONCLUSIONSerotonin promoted collagen I expression by activating Smads signaling pathway and up-regulating the LOX expression.

Blotting, Western ; Cell Differentiation ; Cells, Cultured ; Collagen Type I ; metabolism ; Humans ; Osteoblasts ; drug effects ; metabolism ; Protein-Lysine 6-Oxidase ; metabolism ; RNA, Small Interfering ; Serotonin ; pharmacology ; Signal Transduction ; Smad2 Protein ; metabolism ; Smad3 Protein ; metabolism ; Up-Regulation

OBJECTIVETo identify risk factors of hepatocellular carcinoma (HCC) in cirrhotic patients with chronic hepatitis B (CHB).

METHODSA total of 715 cirrhotic patients with CHB were recruited from the Zhongshan Hospital Affiliated to Fudan University and enrolled in this case-control study between January 2009 and September 2014. All participants were Chinese Han residing in Shanghai and the surrounding areas. The patients were divided into a cirrhosis group (n =281) and a HCC group (n=434). History of hepatitis B infection and HCC, as well as clinical data from serological, imaging and pathological examinations were collected for analysis.SPSS software, version 19.0, was used for all statistical comparisons.

RESULTSSingle factor analysis indicated that development of HCC in cirrhotic patients with CHB was significantly associated with male sex, age of 50 years or more, family history of HCC, alcohol consumption,fatty liver, detectable levels of hepatitis B virus (HBV) DNA, and history of HBV infection without effective antiviral treatment. Multivariate logistic regression analysis indicated that age of 50 years or more (P =0.005, odds ratio [OR] =1.766), history of alcohol consumption (P =0.002, Or = 2.570), family history of HCC (P =0.014, Or = 2.268), fatty liver (P =0.023, Or = 3.390), and history of HBV infection without effective antiviral treatment (P < 0.001,Or = 5.389) were risk factors of HCC.The risk factors for development of HCC in cirrhotic patients with hepatitis B after achieving sustained virologic suppression (SVS) were family history of HBV infection (P =0.014, Or = 2.537), family history of HCC (P =0.037,Or = 3.339) and fatty liver (P =0.018, Or = 11.646).

CONCLUSIONRisk factors of HCC in cirrhotic patients with CHB include age,drinking history,family history of HCC, fatty liver, and ineffective antiviral treatment of CHB.Family history of HBV infection or HCC, and fatty liver disease, were significantly associated with HCC development after SVS in patients with hepatitis B-related cirrhosis.

Alcohol Drinking ; Antiviral Agents ; Carcinoma, Hepatocellular ; Case-Control Studies ; China ; Fatty Liver ; Hepatitis B virus ; Hepatitis B, Chronic ; Humans ; Liver Cirrhosis ; Liver Neoplasms ; Male ; Odds Ratio ; Risk Factors

Objective There is still a lack of effective clinical prognostic factors for predicting outcomes and guiding treatments in extranodal nasal-type NK/T-cell lymphoma (NKTCL).This study was aimed to investigate the clinical features and prognostic role of primary tumor burden (PTB).Methods A total of 1383 patients were recruited from ten hospitals, including 947 stage Ⅰ patients (68.5%), 326 stage Ⅱ patients (23.6%), and 110 stage Ⅲ-IV patients (8.0%).There were 751 patients (54.3%) presenting with high PTB (H-PTB).The Kaplan-Meier method was used to calculate survival rates, and the log-rank test was conducted for survival difference analysis.Meanwhile, a multivariate analysis was performed using the Cox regression model.Results H-PTB was associated with high invasive potential, high frequency of B symptoms, advanced stage, regional lymph node involvement, lactate dehydrogenase elevation, and poor performance status.The patients with H-PTB had significantly lower 5-year overall survival (OS) and progression-free survival (PFS) rates than those with low PTB (L-PTB)(OS:50.2% vs.72.1%, P=0.000;PFS:41.8% vs.62.5, P=0.000).PTB was an independent prognostic factor for both OS (HR=1.851) and PFS (HR=1.755) according to the Cox multivariate analysis.Moreover, H-PTB was associated with significantly lower locoregional control (LRC) in early-stage NKTCL, and the 5-year LRC rate was 71.6% in patients with H-PTB and 84.3% in those with L-PTB (P=0.000).Conclusions H-PTB is associated with multiple adverse clinical features in NKTCL, and it is an independent indicator for poor outcomes and LRC.H-PTB can be used as a reliable indicator for risk stratification and treatment decision.