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Background Esophageal and gastric varices bleeding (EGVB) is one of the most common and dangerous complications of liver cirrhosis. However, whether EGVB affects the one-year mortality of patients with liver cirrhosis remains unclear. Objective To explore the influence of EGVB on one-year mortality and influencing factors in patients with liver cirrhosis, providing guidance for follow-up for these patients. Methods This study selected liver cirrhosis patients who were admitted to the Affiliated Changsha Central Hospital, University of South China from January 2015 to May 2021. The patients were divided into EGVB group and non-bleeding (control group) by the prevalence of EGVB at the first consultation. One-year routine follow-up was conducted with them until the date of death from liver cirrhosis or the termination follow-up day. Logistic regression analysis was conducted for screening the factors affecting one-year mortality. Furthermore, the covariates between the two groups were matched in a 1∶2 ratio using propensity score matching (PSM) . Then, Logistic regression analyses were applied to identify and compare the influencing factors of one-year mortality in the groups. Results Among the 812 patients enrolled, 158 (19.5%) were diagnosed with EGVB, and the other 654 (80.5%) had no EGVB. The one-year mortality of the EGVB and control groups was 13.3% (21/158) and 13.9% (91/654) , respectively, showing no significant difference (P>0.05) . Before PSM, multivariate Logistic regression analysis showed that elevated serum sodium level〔OR=0.95, 95%CI (0.90, 0.99) 〕 and albumin level [OR=0.95, 95%CI (0.91, 0.99) 〕 were associated with a decreased risk of one-year mortality (P0.05) . Moreover, elevated blood urea nitrogen (BUN) 〔OR=1.15, 95%CI (1.02, 1.29) 〕 was an independent risk factor for one-year mortality in EGVB group (P

Despite the importance of tourist mobility for urban tourism, mechanisms as to how these tourist activities shift throughout the day remain scarcely explored. This study fills this gap by providing a three‐step analysis framework. First, aggregated trajectory data were transformed into a directed weighted network. Then, a new community detection method was proposed to capture the spatial interactions, and two approaches were employed to quantify the evolution patterns of tourist mobility. Finally, the capability of the framework and its potential applications were explored and implemented through a case study in Xiamen, China. [ABSTRACT FROM AUTHOR]

Endoplasmic reticulum stress (ERS) and Toll-like receptor 2 (TLR2) signaling play an important role in inflammatory bowel disease (IBD); however, the link between TLR2 and ERS in IBD is unclear. This study investigated whether Thapsigargin (TG) -induced ER protein expression levels contributed to TLR2-mediated inflammatory response. The THP-1 cells were treated with TLR2 agonist (Pam3CSK4), ERS inducer Thapsigargin (TG) or inhibitor (TUDCA). The mRNA expressions of TLR1-TLR10 were detected by qPCR. The production and secretion of inflammatory factors were detected by PCR and ELISA. Immunohistochemistry was used to detect the expressions of GRP78 and TLR2 in the intestinal mucosa of patients with Crohn's disease (CD). The IBD mouse model was established by TNBS in the modeling group. ERS inhibitor (TUDCA) was used in the treatment group. The expression of TLRs was detected via polymerase chain reaction (PCR) in THP-1 cells treated by ERS agonist Thapsigargin (TG). According to the findings, TG could promote TLR2 and TLR5 expression. Subsequently, in TLR2 agonist Pam3CSK4 induced THP-1 cells, TG could lead to increased expression of the inflammatory factors such as TNF-α, IL-1β and IL-8, and ERS inhibitor (TUDCA) could block this effect. However, Pam3CSK4 did not significantly impact the GRP78 and CHOP expression. Based upon the immunohistochemical results, TLR2 and GRP78 expression were significantly increased in the intestinal mucosa of patients with Crohn's disease (CD). For in vivo experiments, TUDCA displayed the ability to inhibit intestinal mucosal inflammation and reduce GRP78 and TLR2 proteins. ERS and TLR2 is upregulated in inflammatory bowel disease, ERS may promote TLR2 pathway-mediated inflammatory response. Moreover, ERS and TLR2 signaling could be novel therapeutic targets for IBD. [ABSTRACT FROM AUTHOR]