Cerebrospinal Fluid Rhinorrhea ; surgery ; Endoscopy ; methods ; Female ; Humans ; Male

Objective To investigate the role of glargine in glucose metabolism improvement and antiinflammation of skeletal muscle in Caveolin-1 silenced type 2 diabetic mice.Methods Multiple low doses of streptozotocin (STZ) intraperitoneal injection and high-fat high-glucose (HFHG) were used to induce type 2 diabetic mice model.The mice were divided into normal control group (NC group) and type 2 diabetic model group (T group).Then according to virus injection and glargine treatment,T group were further divided into type 2 diabetes group (T2DM group),type 2 diabetes with insulin treatment group (insulin group),Caveolin-1 silenced with insulin treatment group (LV-CAV1 group),and scramble virus with insulin treatment group (LV-GFP group).Glucose metabolism was accessed by the fluctuation of blood glucose.TNF-α protein expression in skeletal muscle was detected by Western blot.Results The glycemic control of LV-CAV1 group needed more dosages of glargine (P ＜ 0.05).The expression of TNFαin skeletal muscle was elevated in LV-CAV 1 group than that in LV-GFP and insulin group (P ＜ 0.05).Conclusion The anti-inflammation function and glycemic metabolism improvement of glargine may be associated with the expression of Caveoin-1 in skeletal muscle.

Objective To investigate the relationship between blood glucose levels and severity of coronary stenosis in hypertensive patients. Methods Blood pressure, fasting plasma glucose, 2 h plasma glucose, clinical features and coronary angiographic findings were analyzed retrospectively in 540 patients with essential hypertension. Acoording 2 h plasma glucose, patients were stratified into three group: group 1: 2h plasma glucose

Animals ; Chlorine Compounds ; toxicity ; Dose-Response Relationship, Drug ; Female ; Lung ; drug effects ; metabolism ; RNA, Messenger ; genetics ; Rats ; Rats, Sprague-Dawley ; Transforming Growth Factor beta1 ; biosynthesis ; genetics ; Tumor Necrosis Factor-alpha ; biosynthesis ; genetics

The aim was to construct and identify the mammalian expression vector of pCAG-IRES-SHIP-GFP and to detect whether it could express in human acute leukemia cell line K562.The cDNA fragment of SHIP obtained by RT-PCR was inserted into pCAG-IRES-GFP.The recombinant plasmid was confirmed by restriction enzyme digesiton,PCR and DNA sequecing.pCAG-IRES-SHIP-GFP was transfected into K562 cells with lipofectamine 2000.The expression of SHIP was determined by GFP fluorescence and Western blot analysis.FQ-PCR was used to quantitate SHIP mRNA.The expression of p-Akt,Akt were determined by Western blot.PI were tested by flow cytometry and MTT to verify whether exogenous SHIP could inhibit proliferation of K562 cells.The results showed that the correct constrution of the recombinant plasmid pCAG-IRES-SHIP-GFP has been shown by restriction enzyme digestion,PCR and DNA sequencing.pCAG-IRES-SHIP-GFP could express SHIP protein in K562 cells.The K562 cells viability after transfected with SHIP gene droped down.Western blot analysis showed that phospha-Akt308 and Akt473 were reduced to 38.7% and 68% respectively.It was concluded that the vector of pCAG-IRES-SHIP-GFP has been successfully constructed and it can be expressed in K562 cells.The expression of exogenous SHIP gene can lead to apoptosis of K562 cells by down-regulating the p-Akt expression.What found here might be one of the mechanisms involved in the pathogenesis of leukemia.

Gallbladder cancer occurs insidiously and is usually induced by basic gallbladder diseases accompanied with chronic inflammation. Surgical operation can remove cancerous focus but further treatment should be applied to relieve complications and prevent recurrence and metastasis. According to TCM theory, the basic pathogenesis of post-operation of gallbladder cancer is the combination of blood stasis and heat. Blood stasis arises from surgical operations, failure of liver-gallbladder in keeping smooth flow of qi, and dampness retention in middle-Jiao. Heat arises from qi-stagnation, phlegm-dampness, blood stasis and yin-blood deficiency. Therefore, this article proposed that the therapeutic methods should include Qingre Huoxue Method (clearing away heat and promoting blood circulation), keeping smooth qi-flow of liver-gallbladder, and removing dampness and discharging waste, with typical clinical cases for illustration.

The hexane extract from marine actinomycetes 124092 showed potent inhibition on B16 cell line by MTT assay. The hexane extract was fractionationed on silica gel column by vacuum liquid chromatography to afford 6 fractions(Fr1~Fr6), and Fr6 showed cytotoxic activity. To determine the bioacitve components of hexane extract, Fr6 was analyzed by GC/MS. The main components were identified as palmitic acid (11.76%), oleic acid (12.16%), linoleic acid (14.77%), and lactobacillic acid (61.31%). It have been reported that palmitic acid, oleic acid, and linoleic acid possess cytotoxic activity on rat ascites tumor cells and linoleic acid have suppressive effect on human lung adenocarcinoma cells.

Objective To study the relationship among apoptosis,NF-KB activation and uPA expres- sion in human colon carcinoma cell line HCTll6 induced by 5-fluorouracil,and to observe the effect of in- hibiting activity of NF-KB by PDTC on apoptosis as well as expression of uPA.Methods Cell apoptosis was analysed by Annexin V-FITC.Fluctuation of NF-KB and uPA was detected by semi-quantitative immuno- histochemistry.Results 5-fluorouracil could induce apoptosis and activate NF-KB.PDTC could significantly increase the apoptosis and suppress the activation of NF-KB induced by 5-fluorouracil.There was a positive correlation between the changes of uPA and NF-KB.Conclusion 5-fluorouracil could induce apoptosis,ac- tivate NF-KB and up-regulate expression of uPA of HCT116 cells.The mechanism of enhanced apoptosis by PDTC may be related to suppressing activation of NF-?B and down-regulating expression of uPA.

Objective To investigate the level and value of serum IgE, anti-IgE, FcεRⅠα, anti-FcεRⅠin autoimmune liver disease ( AILD) .Methods In this case-control study, the serum samples and clinical data of 77 patients with hepatosis were collected between May and November 2014 from the department of gastroenterology of Shanghai First People′s Hospital.These patients had positive results about the liver-related autoimmune antibodies, including 33 cases of AILD, 44 cases of other chronic liver disease. 64 healthy persons were collected as control group.Serum mast cell-associated anti-IgE, FcεRⅠα, anti-FcεRⅠwere detected by Enzyme-linked Immuno sorbent Assay ( ELISA) .Serum IgE, IgM and IgG were detected by rate scatter nephelometry.Differences among AILD, other chronic liver disease and healthy control were assessed.Results were compared using Mann-Whitney U test.Results Mast cell-associated anti-IgE, FcεRⅠα, anti-FcεRⅠin liver-related autoimmune antibodies positive patients were significantly higher than healthy control [1.74(1.16 -2.88)mg/L, 14.86(4.39 -26.23)mg/L, 47.22(36.89 -55.29)mg/L and 1.23(0.95-1.58)mg/L, 1.87(1.52-2.33)mg/L, 35.40(24.74-44.89)mg/L, respectively;U=1614,556.5,1319.5, P<0.01].FcεRⅠαwas significantly higher in other chronic liver disease patients than AILD patients [18.40(7.35-30.64)mg/L and 6.25(2.49-22.29), respectively;U=445, P<0.01] .Conclusion Mast cell-associated anti-IgE, FcεRⅠα, anti-FcεRⅠwere increased in liver-related autoimmune antibodies positive hepatosis patients.However, FcεRⅠαwas lower in AILD than other chronic liver disease.Mast cell-associated anti-IgE、FcεRⅠαand anti-FcεRⅠ molecules involved in the inflammatory lesion of liver disease.

0.05).However,phosphor-ERK and phosphor-STAT3,NF-?B were higher in CVB_3 group than those in control groups(P