Xianfei Wang

Association between Diet and Lifestyle Habits and Irritable Bowel Syndrome: A Case-Control Study

Background/Aims Recent papers have highlighted the role of diet and lifestyle habits in irritable bowel syndrome (IBS), but very few population-based studies have evaluated this association in developing countries. The aim of this study was to evaluate the association between diet and lifestyle habits and IBS. Methods A food frequency and lifestyle habits questionnaire was used to record the diet and lifestyle habits of 78 IBS subjects and 79 healthy subjects. Cross-tabulation analysis and logistic regression were used to reveal any association among lifestyle habits, eating habits, food consumption frequency, and other associated conditions. Results The results from logistic regression analysis indicated that IBS was associated with irregular eating (odds ratio [OR], 3.257), physical inactivity (OR, 3.588), and good quality sleep (OR, 0.132). IBS subjects ate fruit (OR, 3.082) vegetables (OR, 3.778), and legumes (OR, 2.111) and drank tea (OR, 2.221) significantly more frequently than the control subjects. After adjusting for age and sex, irregular eating (OR, 3.963), physical inactivity (OR, 6.297), eating vegetables (OR, 7.904), legumes (OR, 2.674), drinking tea (OR, 3.421) and good quality sleep (OR, 0.054) were independent predictors of IBS. Conclusions This study reveals a possible association between diet and lifestyle habits and IBS.

Low molecular weight heparin relieves experimental colitis in mice by downregulating IL-1β and inhibiting syndecan-1 shedding in the intestinal mucosa.

Low molecular weight heparin (LMWH) exhibits anti-inflammatory properties, but its effect on inflammation in colitis remains unclear. This study aimed to evaluate the therapeutic effects of LMWH on dextran sulfate sodium (DSS)-induced colitis in mice, in which acute colitis progresses to chronic colitis, and to explore the potential mechanism involved in this process. C57BL/6 mice were randomly divided into control, DSS, and DSS plus LMWH groups (n = 18). Disease activity was scored by a disease activity index (DAI). Histological changes were evaluated by hematoxylin and eosin (HE) staining. The mRNA levels of syndecan-1, interleukin (IL)-1β, and IL-10 were determined by quantitative reverse transcription polymerase chain reaction. Protein expression of syndecan-1 was detected by immunohistochemistry. The serum syndecan-1 level was examined by a dot immunobinding assay. LMWH ameliorated the disease activity of colitis induced by DSS administration in mice. Colon destruction with the appearance of crypt damage, goblet cell loss, and a larger ulcer was found on day 12 after DSS administration, which was greatly relieved by the treatment of LMWH. LMWH upregulated syndecan-1 expression in the intestinal mucosa and reduced the serum syndecan-1 level on days 12 and 20 after DSS administration (P<0.05 vs. DSS group). In addition, LMWH significantly decreased the expression of both IL-1β and IL-10 mRNA on days 12 and 20 (P<0.05 vs. DSS group). LMWH has therapeutic effects on colitis by downregulating inflammatory cytokines and inhibiting syndecan-1 shedding in the intestinal mucosa.

Activated Syndecan-1 Shedding Contributes to Mice Colitis Induced by Dextran Sulfate Sodium

BackgroundSyndecan-1(Sdc1) plays important roles in many steps of inflammatory responses. In ulcerative colitis patients, decreased Sdc1 expression was observed and Sdc1 analogue heparin could improve the disease course. A better understanding of how Sdc1 functions in colitis will benefit the disease intervention.AimsTo evaluate the role of Sdc1 in dextran sulfate sodium (DSS)-induced colitis.MethodsBALB/c mice were grouped randomly into control, DSS, and heparin+DSS. The DSS group was given 4% DSS orally and heparin+DSS group was given 4% DSS with heparin (enoxaparin) subcutaneously, while the control was given distilled water orally. All mice were killed at day 7. Disease activities, histopathological changes, membrane-bound and free Sdc1 level and mRNA expression of Sdc1, IL-1, and IL-10 in colon mucosa were detected.ResultsSignificant colitis was observed in the DSS group, but disease activity index and histological score showed significant lower in the heparin+DSS group than those in the DSS group. Compared to the control group, decreased Sdc1 protein expression was detected in colon mucosa of DSS-induced colitis while Sdc1 ectodomain level in serum was much higher. Inhibited Sdc1 ectodomain shedding was detected in the heparin+DSS group compared to the DSS group. RT-PCR demonstrated that both IL-1 and IL-10 expression were up-regulated in DSS-induced colitis while heparin lessened the up-regulation extent.ConclusionsSdc1 shedding is activated in DSS-induced colitis and heparin, which mimics Sdc1 functions, relieves colitis severity by inhibiting Sdc1 shedding and down-regulating cytokines expression.

Successful closure of lateral duodenal perforation by endoscopic band ligation after endoscopic clipping failure.

Successful Closure of Lateral Duodenal Perforation by Endoscopic Band Ligation After Endoscopic Clipping Failure

Clinicopathological characteristics of laterally spreading colorectal tumor.

Background and Aims Laterally spreading tumor (LST) is a colorectal pre-cancerous lesion. Previous studies have demonstrated distinct LST clinicopathological characteristics in different populations. This study evaluated clinicopathological characteristics of LST in a Chinese population. Methods A total of 259 Chinese LST patients with 289 lesions were recruited for endoscopic and clinicopathological analyses. Results Among these 289 lesions, 185 were granular type (LST-G), whereas 104 were non-granular type (LST-NG). LST-G lesions were further classified into homogeneous G-type and nodular mixed G-type, while LST-NG lesions were further classified into flat elevated NG-type and pseudo-depressed NG-type. Clinically, these four LST subtypes showed distinct clinicopathological characteristics, e.g., lesion size, location, or histopathological features (high-grade intraepithelial neoplasia and submucosal carcinoma). The nodular mixed G-type showed larger tumor size and higher incidence of high-grade intraepithelial neoplasia compared to the other three subtypes, while pseudo-depressed NG-type lesions showed the highest incidence of submucosal carcinoma. Noticeably, no diffidence was detected between the lesions of homogeneous G-type and flat elevated NG-type with regard to the histopathological features. Histology of the malignancy potential was associated with nodular mixed G-type [OR = 2.41, 95% CI (1.09–5.29); P = 0.029], flat elevated NG-type [OR = 3.49, 95% CI (1.41–8.22); P = 0.007], Diameter ≥30 mm [OR = 2.56, 95% CI (1.20–5.20); P = 0.009], Villous adenoma [OR = 2.76, 95% CI (1.01–7.58); P = 0.048] and serrated adenoma [OR = 6.99, 95% CI (1.81–26.98); P = 0.005]. Conclusion Chinese LSTs can be divided into four different subtypes, which show distinct clinicopathological characteristics. Morphology, size and pathological characteristics are all independent predictors of advanced histology.

iTRAQ-Based Proteomics Screen identifies LIPOCALIN-2 (LCN-2) as a potential biomarker for colonic lateral-spreading tumors

The improvement and implementation of a colonoscopy technique has led to increased detection of laterally spreading tumors (LSTs), which are presumed to constitute an aggressive type of colonic neoplasm. Early diagnosis and treatment of LSTs is clinically challenging. To overcome this problem, we employed iTRAQ to identify LST-specific protein biomarkers potentially involved in LST progression. In this study, we identified 2,001 differentially expressed proteins in LSTs using iTRAQ-based proteomics technology. Lipocalin-2 (LCN-2) was the most up-regulated protein. LSTs expression levels of LCN-2 and matrix metallopeptidase-9 (MMP-9) showed positive correlation with worse pathological grading, and up-regulation of these proteins in LSTs was also reflected in serum. Furthermore, LCN-2 protein overexpression was positively correlated with MMP-9 protein up-regulation in the tumor tissue and serum of LST patients (former rs = 0.631, P = 0.000; latter rs = 0.815, P = 0.000). Our results suggest that LCN-2 constitutes a potential biomarker for LST disease progression and might be a novel therapeutic target in LSTs.

CDK5 functions as a tumor promoter in human colorectal cancer via modulating the ERK5–AP-1 axis

Abnormal expression of cyclin-dependent kinase 5 (CDK5) has been found in several human cancers, whereas the role of CDK5 in the malignant development of colorectal cancer (CRC) has not been well characterized. Here we investigated the role of CDK5 in CRC and found that its expression was much higher in CRC tissues than that in normal tissues with a higher expression level of CDK5 closely correlating to advanced American Joint Committee on Cancer (AJCC) stage, poor differentiation, increased tumor size and poor prognosis of CRC. Biological function experiments showed that CDK5 regulated CRC cell proliferation and metastasis ability. Whole-genome microarray analysis, co-immunoprecipitation, in vitro kinase assay, western blotting, luciferase reporter assays and electrophoretic mobility shift assay (EMSA) showed that CDK5 could directly phosphorylate ERK5 at threonine (Thr) 732 and finally modulate the oncogenic ERK5–AP-1 axis. Further researches showed that CDK5–ERK5–AP-1 axis could promote progression of CRC carcinogenesis and had a significant correlation in human CRC samples. In summary, this study revealed the functional and mechanistic links between CDK5 and the oncogenic ERK5–AP-1 signaling pathway in the pathogenesis of CRC. These findings suggest that CDK5 has an important role in CRC development and may serve as a potential therapeutic target for CRC.