Objective To investigate anti-ulcerative drug use in patients undergoing arthroscopic operation against stress ulcer. Methosds A total of 297 patients undergoing arthroscopic operation during Jan. to Aug. 2013 in our hospital were recruited and retrospectively analyzed with Excellspreadsheet. Results Among 297 patients in the study, ninety-four patients (31.6%) used AUD before operation, most (94.9%) administered by intravenous, and drug utilization index was 1.35. Ninety-eight point nine patients used proton pump inhibitors (PPIs) in which Lansoprazole was prescribed most. Conclusion This study highlights the overuse of PPIs in patients undergoing arthroscopic operation.

Objective This study was carried out to compare chnical efficiency of methylprednisolone (MP) and dexamethasone (Dex) and their effects on Th cytokines in asthmatic children.Methods A total of 39 children with moderate and severe asthma at acute exacerbation were randomly divided into two groups, one (A) with MP 1 -2 mg/kg (n=21) and the other (B) with Dex 0.25 -0.75 mg/kg (n= 18),every 12 -24 h by intravenous drip.Scores of respiratory effort and peak expiratory flow rate prior to and three days after treatment in the asthmatic children aged over five years were evaluated,respectively,as well as the time of wheezing vanishing after treatment.Serum levels of interleukin-2 (IL-2) and IL-4 were determined by radioimmunoassay (RIA) prior to and three days after treatment,respectively.Results There was statistically significant difference in the time of wheezing vanishing between groups A and B (P = 0.042).Three days after treatment,PEER was significantly higher in group A than that in group B (P = 0.025).No statistically significant difference in serum IL-2 and IL-4,as well as ratio of IL-2/IL-4,was found in group B prior to and three days after treatment (P>0.05).Statistically significant difference in serum IL-2 was not observed in group B prior to and three day after treatment (P>0.05),and serum IL-4 decreased significantly (P=0.001) and ratio of serum IL-2/IL-4 (P=0.027) increased significantly three days after treatment than those prior to treatment.No significant correlation between respiratory-effort scores and ratio of serum IL-2/IL-4 prior to treatment was found (P=0.613).Conclusions Up-regulation of IL-2,or inhibition of release of IL-4,probably is not the main anti-inflammatory mechanism of dexamethasone.Methylprednisolone has little effect on serum IL-2,but can effectively reduce serum IL-4, thus increasing the ratio of serum IL-2/IL-4 and counterbalancing function of the Thl/Th2 cells.

The incidence of stroke increases year by year.It seriously affects the quality of life in patients.The pathogenesis of stroke is related to a variety of factors,involving genetic polymorphisms,biochemical mechanisms,and inflammatory effect.Among them,vascular endothelial growth factor (VEGF) has become one of the hotspots of research on the pathogenesis of stroke in recent years.This article reviews the correlation between VEGF gene polymorphism and stroke.

Objective:To investigate the synergistic antitumor effect of pyrotinib in combination with 5-fluorouracil(5-Fu)on human epidermal growth factor receptor 2(HER2)positive breast cancer cells and its underlying molecular mechanism. Methods:HER2 positive breast cancer cells were screened by Western blotting.HER2 positive SKBR-3 and BT474 cells were treated with pyrotinib and 5-Fu individually or in combination for the following experiments.MTT assay was used to assess the effect of different drugs on the proliferation of the treated cells,and the combination index(CI)values were calculated using Combidrug software.Colony formation assay was used to evaluate the effect of different drugs on the colony-forming ability of the treated cells.FCM assay was used to analyze the effect of different drugs on the apoptosis rate and cell cycle of the treated cells.Western blotting was used to examine the effect of different drugs on the expression levels of proteins in the proliferation-and apoptosis-related signaling pathways.SKBR-3-cell-based tumor xenograft model was established using BALB/c nude mice.After treatment with pyrotinib and 5-Fu individually or in combination,the growth profiles of the xenograft tumors were recorded and the expression levels of proteins in the proliferation-and apoptosis-related signaling pathways were examined in the tumor tissues. Results:HER2 positive breast cancer cell lines SKBR-3 and BT474 were selected for further experiments after screening.The proliferation SKBR-3 and BT474 cells could be inhibited after treatment with pyrotinib and 5-Fu individually or in combination(all P＜0.05).Compared with pyrotinib or 5-Fu single drug treatment,pyrotinib in combination with 5-Fu had higher inhibition rate on the proliferation of SKBR-3 and BT474 cells with a Cl value of＜1,indicating the synergistic effect of pyrotinib and 5-Fu.In addition,in contrast to pyrotinib or 5-Fu single drug treatment,there was a further decrease in the number of colonies formed,increase in apoptosis rate,and increase in the percentage of G0/G,cells in SKBR-3 and BT474 cells after treatment with pyrotinib in combination with 5-Fu(all P＜0.01).Animal experiment results showed that the growth rate of xenograft tumors in mice treated with pyrotinib in combination with 5-Fu was significantly slower than that of the single-drug treated mice(P＜0.05).Western blotting analysis showed that the expression levels of HER2,HER4,AKT and phosphorylated ERK were significantly decreased after treatment with pyrotinib in combination with 5-Fu both in vitro and in vivo(all P＜0.01),indicative of the blockage of proliferation-related signaling pathways.Meanwhile,analysis of the apoptosis-related proteins revealed a decrease in the expression levels of caspase 3,poly ADP-ribose polymerase(PARP),and Bcl-2(all P＜0.01),while an increase in the expression levels of cleaved-caspase 3,cleaved-PARP,and p21(all P＜0.01). Conclusion:Pyrotinib and 5-Fu had synergistical antitumor effect on HER2 positive breast cancer cells,and the underlying mechanism may be related to the blockage of proliferation-associated signaling pathways and the induction of apoptosis and cell cycle arrest.

OBJECTIVE: To investigate the role of cathepsin B in hepatic Kupffer cells (KCs) in activating Toll-like receptor 4(TLR- 4)-independent inflammatory pathways in mice with lipopolysaccharide (LPS)-induced sepsis. METHODS: Eighteen wild-type (WT) mice and 18 TLR4-knockout (TLR4) mice were both divided into 3 groups for intraperitoneal injections of a lethal dose (54 mg/kg) of LPS, LPS and CA-074(a cathepsin B inhibitor), or normal saline, and the survival of the mice were observed. Another 36 WT mice and 36 TLR4mice were also divided into 3 groups and subjected to intraperitoneal injections of normal saline, 20 mg/kg LPS, or LPS with CA-074 pretreatment.After the treatments, KCs were collected from the mice for assessing the protein level and activity of cathepsin B.The histopathological changes of the liver were observed with HE staining, and the serum levels of IL-1α, IL-1β, TNF-α and IL-18 were detected. RESULTS: Compared with the WT mice,TLR4mice receiving the lethal dose of LPS had significantly longer survival time (up to 84 h) after the injection,but were still unable to fully resist LPS challenge.CA-074 pretreatment prolonged the survival time of WT mice and TLR4mice to 60 h and 132 h,respectively.In the mouse models of sepsis,20 mg/kg LPS induced significantly enhanced activity of cathepsin B without affecting its expression level in the KCs (<0.05) and increased the serum levels of the inflammatory cytokines.CA-074 pretreatment of the mice obviously lessened the detrimental effects of LPS in TLR4mice by significantly lowering cathepsin B activity in the KCs,alleviating hepatocyte apoptosis and reducing the serum levels of inflammatory cytokines. CONCLUSIONS Cathepsin B plays an important role in activating TLR4-independent inflammatory pathways in mice with LPS-induced sepsis.
Animals ; Cathepsin B ; antagonists & inhibitors ; physiology ; Dipeptides ; pharmacology ; Gene Knockout Techniques ; Hepatocytes ; Inflammation ; metabolism ; Interleukin-18 ; blood ; Interleukin-1alpha ; blood ; Interleukin-1beta ; blood ; Kupffer Cells ; metabolism ; Lipopolysaccharides ; Liver ; pathology ; Mice ; Sepsis ; etiology ; metabolism ; Toll-Like Receptor 4 ; genetics ; Tumor Necrosis Factor-alpha ; blood