The influence of sleep factors and dietary habits on the disease pattern of ulcerative colitis patients with long and short disease courses - a multicentre cross-sectional analysis.

BACKGROUND: Ulcerative colitis (UC) is a disease characterized by chronic relapsing-remitting inflammatory disorders and is associated with environmental changes. AIM: To explore the disease patterns of Chinese UC patients and to determine controllable related environmental factors. METHODS: This multicentre cross-sectional study was performed using a questionnaire survey. Data on clinical characteristics and environmental factors were collected. Patients with a disease course ≥5 years were defined as the long course group, and those with a disease course < 5 years were defined as the short course group. RESULTS: A total of 588 effective questionnaires were collected. The proportion of the chronic continuous pattern was the highest among patients with a long disease course (46.8%), and in patients with a short disease course, the proportion of the active to remission pattern was the highest (53.3%). In patients with a long disease course, a higher proportion of patients with adequate sleep was found in the active to remission pattern than in the chronic intermittent (72.1% vs. 43.3%, p = 0.008) and chronic continuous (72.1% vs. 52.4%, p = 0.016) patterns. In patients with a short disease course, the frequency of shellfish and shrimp was higher in the chronic continuous pattern group than in the active to remission pattern group (P = 0.001 and 0.017 respectively). CONCLUSIONS: For early diagnosis patients, dietary guidance should be actively carried out. With the prolongation of the disease course, attention should be given to the sleep quality of patients.

1.UC exhibits various disease patterns, which may be associated with differences in patient prognosis and treatment response.2.Environmental factors, especially sleep and dietary factors, correlated strongly with disease patterns, which varied in different disease courses.3.Early diagnosis patients should receive active dietary guidance, while patients with a prolonged disease course require attention to their sleep quality and appropriate drug interventions when necessary.

Research progress on the predictive role of sarcopenia in the course and prognosis of inflammatory bowel disease.

Sarcopenia is a syndrome characterized by a progressive and extensive decrease in skeletal muscle quality and function. With the development of imaging technology in recent years, the understanding and research on the pathogenesis, diagnosis, and evaluation of sarcopenia have gradually improved. More than one-third of patients with inflammatory bowel disease (IBD) have sarcopenia (Ryan et al., 2019), and as a new and unique body composition evaluation index, it is critical for predicting the clinical course, prognosis and postoperative complications of patients with IBD. However, there are limited research summarizing the prevalence of sarcopenia among IBD. Furthermore, there is a scarcity of studies establishing the precise criteria for diagnosing sarcopenia in these patients. This article summarizes the evaluation of sarcopenia and its recent advancements in predicting the course and prognosis of IBD.

Analysis of a pedigree of Peutz-Jeghers syndrome and RET proto-oncogene mutation: one case report and literature review.

Peutz-Jeghers syndrome (PJS) is a rare autosomal dominant inherited disorder characterised by gastrointestinal (GI) hamartomatous polyposis and mucocutaneous pigmentations. PJS is associated with an increased cancer risk, including GI and various extra-GI malignancies. In this study, we tracked this family for 8 years, and analyzed the clinical data of the PJS pedigree including two generations. In our research, the studied family members, including the proband, older daughter and younger daughter, all detected to have three heterozygous mutations in the RET gene that were inherited from the proband. The existed three mutant spots included exon 5 (GTG>ATG, Val292Met), exon 2 (CGC>CAC, Arg67His) and exon 18 (CGC>TGC, Arg982Cys) in RET. Our study provides an observation of the genetic heterogeneity of PJS. This pedigree investigation showed that it is critical to establish a long-term follow-up system for PJS patients and their families.

Lentiviral vector-mediated IL-9 overexpression stimulates cell proliferation by targeting c-myc and cyclin D1 in colitis-associated cancer.

Colorectal cancer caused by inflammatory bowel disease is referred as colitis-associated cancer (CAC). The mechanism underling CAC is not fully understood. In the present study, the role of interleukin-9 (IL-9) in CAC was examined. The current study included 12 colorectal tissue specimens and matched adjacent tissues from CAC. The expression of IL-9 protein was examined using immunohistochemical staining. The expression of IL-9 in cancer tissues was markedly higher compared with that in adjacent tissues. Furthermore, IL-9 gene overexpression lentiviral vectors were constructed to overexpress IL-9 in RKO and Caco-2 cell lines. The role of IL-9 in cell proliferation was investigated using a Cell Counting Kit-8 assay, and MYC proto-oncogene bHLH transcription factor (c-Myc) and cyclinD1 expression levels were detected by reverse transcription-quantitative polymerase chain reaction. Notably, IL-9 overexpression promoted the proliferation of colonic epithelial cells by upregulating of the expression of c-Myc and cyclinD1. In conclusion, the present results suggested that IL-9 may exhibit an essential role in the pathogenesis of CAC, and IL-9 promotes the proliferation of colonic epithelial RKO and Caco2 cells, partially via the upregulation of c-Myc and cyclinD1 expression.

IL-9 promotes the pathogenesis of ulcerative colitis through STAT3/SOCS3 signaling.

Ulcerative colitis (UC) is a chronic condition in which the overreacting immune system may play an important role. It has been confirmed that the interleukin (IL) 9 (IL-9) participates in the pathogenesis of UC but the molecular mechanism is not fully illustrated. Here, we show that levels of peripheral blood cytokines IL-9, IL-8, IL-10, IL-6, IL-1ß, IL-12, and tumor necrosis factor (TNF) were higher in patients with UC than normal control, and serum and local IL-9 levels were positively correlated with the disease activity grade. Moreover, IL-9 stimulation inhibited suppressor of cytokine signaling 3 (SOCS3) expression and wound healing ability in colonic epithelial cells and promoted the phosphorylation level of signal transducers and activators of transcription 3 (STAT3). And IL-9 stimulation promoted claudin-2 expression while inhibited claudin-3 and occludin expression. Furthermore, SOCS3 overexpression rescued the IL-9-induced effects. Altogether, IL-9 participates in the pathogenesis of UC through STAT3/SOCS3 signaling pathway and has the potential to serve as a possible therapeutic candidate in patients with UC.