ABSTRACT
@#【Objective】To analyze the risk factors of delayed hemorrhage after colon polyp resection.【Methods】We retrospectively analyzed the clinical data of patients who underwent endoscopic polypectomy between January 2010 and December 2018，in which 106 patients with delayed hemorrhage were hemorrhage group，while 3 856 patients who did not bleed were the controlled group，and Logistic regression model was applied to screen the risk factors of hemorrhage after polyp resection.【Results】Of the 3 962 patients included in the study，106 had delayed post polypectomy hemorrhage， the hemorrhage rate being 2.68%. 89.6% delayed hemorrhage occurred within 3 days after polypectomy. Logistic regression analysis showed that the difference of polyp size，complicated hypertension，combined with chronic nephropathy，aspirin drug history and warfarin drug history in hemorrhage group and control group was statistically significant（P values were 0.011，0.009，0.028，0.001，0.023，respectively）.【Conclusion】The size of polyps，comorbidity of hypertension，chronic renal disease ，application of aspirin and warfarin were considered to be independent risk factors for post-polypectomy delayed hemorrhage，most of hemorrhage occurred within 3 days. According to the risk factors of patients，we may predict the risk of delayed hemorrhage.
ABSTRACT
<p><b>OBJECTIVE</b>To investigate the effects of shikonin on the proliferation, expression of CXCR4 and the migratory responses to CXCL12 in colorectal carcinoma cell line SW480.</p><p><b>METHODS</b>The proliferation of SW480 cells was assessed by MTT assay. Cell surface expression of CXCR4 was determined by flow cytometry. The migratory ability was determined by Transwell.</p><p><b>RESULTS</b>Shikonin inhibited the proliferation of SW480 cells in time- and concentration-dependent manner. The expression rate of CXCR4 in SW480 cells was 99.1%. After application of shikonin 0.01 micromol/L, 0.1 micromol/L and 1.0 micromol/L for 24 h, the expression rate of CXCR4 decreased to 76.0%, 59.1% and 35.5% respectively (F=1098.041, P <0.001), and the CXCL12-induced SW480 cell migratory inhibition rate was 25.2%, 38.5% and 55.7% respectively (F=48.970, P <0.001).</p><p><b>CONCLUSION</b>Besides having inhibiting tumor cell proliferation effect, Shikonin may also play a role in anti-metastasis via down-regulating the expression of CXCR4 and reducing the CXCL12-induced migratory response in colorectal carcinoma cell.</p>
Subject(s)
Humans , Cell Line, Tumor , Cell Proliferation , Chemokine CXCL12 , Metabolism , Down-Regulation , Naphthoquinones , Pharmacology , Receptors, CXCR4 , MetabolismABSTRACT
<p><b>OBJECTIVE</b>To investigate the relationship of Toll-like receptor 2 (TLR2) and viral hepatitis B through testing the expression of TLR2 in liver tissues of patients infected with HBV and in HepG2 and HepG2.2.15 cell lines.</p><p><b>METHODS</b>Expression of TLR2 was determined by Elivision immunohistochemistry in liver tissues from patients with chronic viral hepatitis B (CHB), chronic severe hepatitis (CSH), from healthy controls and from cells of HepG2 and HepG2.2.15 hepatocellular carcinoma cell lines. Direct immunofluorescence flow cytometry was used to detect TLR2+ cell percentage and mean fluorescence intensity (MFI).</p><p><b>RESULTS</b>The intensity of TLR2 expression in liver tissues of CHB and CSH was significantly higher than that of the healthy controls (probability value less than 0.01). The positive staining was mainly located in the cytoplasm and on some cell membranes. In CHB, the intensity of TLR2 expression was positively correlated with the grade of necroinflammatory activity (r=0.597, P less than 0.01). There were significant differences of serum total bilirubin levels with different grades of positive staining of TLR2 (P less than 0.05). In liver tissues of the CHB patients, the positive staining of TLR2 was shown in small foci. MFI of TLR2 (10.7+/-2.8) and TLR2+ cell percentage (16.3%+/-7.0%) of HepG2.2.15 cells were both significantly higher than those of HepG2 cells (1.0+/-0.3, 0.4%+/-0.1%, P less than 0.01).</p><p><b>CONCLUSIONS</b>Expression of TLR2 is closely correlated with hepatitis B, especially to the grades of its necroinflammatory activity.</p>