Objective To investigate the correlation of changes in peripheral natural killer T(NKT) cells and fatty liver disease(NAFLD).Methods Peripheral blood samples were obtained from 60 NAFLD patients and 60 age and gender matched healthy controls.The frequency of peripheral NKT cells was detected by flow cytometry.The differences of clinical presentation and laboratory data in two groups were analyzed.The risk factors of NAFLD were screened by Logistic regression analysis. Results NAFLD patients had lower frequency of peripheral NKT cells than healthy controls [median fre- quency was 1.12%(IQR0.87%～1.54%)in patients vs.1.48%(1.23%～1.98%) in controls,P

Non-alcoholic fatty liver disease (NAFLD) has become one of the major metabolic diseases.In view of the defects of traditional animal models, this study was the first to establish the NAFLD model of Mongolian gerbil (Meriones unguiculatus) with simple feed formula which is similar to human (from simple fatty liver to steatohepatitis, fibrosis,Liver cirrhosis).This study discussed the mechanism of rapid fatty liver deposition in Mongolian gerbil, revealed its molecular mechanism,main regulatory target and network function of fatty liver susceptibility.We provide a new animal model of NAFLD with relatively clear background and less time-consuming for clinical treatment and new drug development.The theoretical and practical basis for the breeding of inbred strain NAFLD gerbil was established.

Aim To study the effects of total saponins of Panax japonicus(TSPJ) on liver inflammation of natural aging rats.Methods The experimental rats were allocated into seven groups (twelve rats in each group): three months group, nine months group, fifteen months group, twenty-four months group, and TSPJ low-, mid-and high-dose groups(10, 30, 60 mg·kg-1).When the rats were eighteen months old, the TSPJ low-, mid-and high-dose groups of rats were given lavage treatments with TSPJ 10,30, 60 mg·kg-1 respectively until twenty-four months.During lavage, we stopped a day every week for six consecutive months.HE staining was used to observe the pathological morphological changes.Western blot was utilized to test IL-1β and TNF-α protein expressions.RT-PCR method was adopted to test IL-1β, IL-6, IL-12, IL-17α, TNF-α, IFN-γ mRNA expressions.Results HE staining observation showed that as the rats grew older the hepatic cord and sinusoid were arranged in more severe disorder, and the fat vacuole and inflammatory cells were increased significantly.While every dose group of TSPJ could improve these pathological changes distinctly.The IL-1β, TNF-α protein and IL-1β, IL-6, IL-12, IL-17α, TNF-α, IFN-γ mRNA expressions were increased gradually as the rats grew older, and every dose group of TSPJ could reduce their expressions to some extent.Conclusion TSPJ could protect the aging rat liver to some extent by inhibiting the liver inflammation.

Objective:To investigate the effects of airborne fine particle on cell viability and inflammation in human bronchial epithelial cells.Methods:Atmospheric PM2.5 samples were collected by PM2.5 sampler.PM2.5 morphology was observed by scanning electron microscope (SEM).Human bronchial epithelial cells (BEAS-2B) were treated with PM2.5 at different concentrations (0,50,100,200,400,800 μg/mL) for 12,24 or 48 hours,and the cell activity were evaluated by cell counting kit-8 (CCK-8).The mRNA expression levels of (granulocyte-macrophage colony stimulating factor,GM-CSF) and TNF-α were detected by quantitative real-time PCR (qRT-PCR).Western blot was used to detect the protein expressions of GM-CSF and TNF-α.Results:According to SEM,the shape of PM2.5 varied,and the diameter was different and mostly equal to or less than 2.5 μm.CCK-8 assay showed that different concentrations of PM2.5 exposure for 12 hours,24 hours and 48 hours resulted in loss of cell viability of BEAS-2B cells (P＜0.05).Different concentrations of PM2.5 increased the mRNA and protein expression of GM-CSF and TNF-α,and the higher concentration of PM2.5 induced higher expression,which have statistical significant difference between the groups (P＜0.05).Conclusion:Atmospheric PM2.5 can cause inflammatory response in human bronchial epithelial cells.They can reduce cell viability,which may be related to the PM2.5 trigger and aggravation of bronchopulmonary inflammatory diseases.

OBJECTIVETo explore the platelet count in prediction of the efficacy of infliximab for active Crohn's disease.

METHODSA total of 74 patients with Crohn's disease, including 50 males and 24 females with mean age of 27 years, receiving infliximab therapy from January 2011 to June 2015 were retrospectively included. Clinical variables including routine blood test, erythrocyte sedimentation rate, C-reactive protein and Crohn's disease activity index were measured before treatment and after 3rd, 6th treatments.

RESULTSCompared with baseline, the Crohn's disease activity index score, white blood cell count, platelet count, erythrocyte sedimentation rate, C-reactive protein significantly decreased (all (P<0.01), while hemoglobin and red blood cell hematocrit increased (P<0.01) in patients after 3 treatments of infliximab. These variables were further improved after 6 treatments. Further analysis showed that platelet count was positively associated with disease severity of Crohn's disease. Fifty-three patients achieved clinical remission (Crohn's disease activity index score<150) after 3 treatments of infliximab. Logistic regression analysis showed that baseline platelet count, Crohn's disease activity index, and disease course were three predictors for clinical remission of Crohn's disease.

CONCLUSIONPlatelet count is positively associated with disease severity of Crohn's disease, and baseline platelet count is an important predicator for the early response of infliximab therapy.

Adult ; C-Reactive Protein ; analysis ; Crohn Disease ; blood ; drug therapy ; Disease Progression ; Female ; Humans ; Infliximab ; therapeutic use ; Male ; Platelet Count ; Retrospective Studies

Adult ; Humans ; Non-alcoholic Fatty Liver Disease/complications* ; Cross-Sectional Studies ; Folic Acid/therapeutic use* ; Risk Factors