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Objective To investigate the risk factors associated with post-implantation syndrome (PIS) in Stanford type B aortic dissection (TBAD) patients undergoing thoracic endovascular aortic repair (TEVAR) and the relationship of PIS with short-term outcomes. Methods A case-control trial was conducted on the clinical data of patients undergoing TEVAR treatment for TBAD in our department from December 2013 to December 2022. They were divided into 2 groups based on the occurrence of PIS. Independent risk factors were analyzed according to the different clinical characteristics between the 2 groups. The overall 30-day mortality following TEVAR was assessed in both groups. Kaplan-Meier survival curves were utilized to evaluate the 30-day postoperative survival. Logistic regression models were constructed to investigate the relationship between PIS and overall mortality occurring within 30 d after TEVAR. Results A total of 373 TBAD patients, with an average age of 57.9±12.1 years and a male ratio of 77.5% (289 cases), were enrolled in this study. There were 106 cases (28.4%) experiencing PIS following TEVAR. Significantly larger proportions of implanted stents ≥2, operation duration ≥2 h and implantation of polyethylene terephthalate (PET)-coverted stents were observed in the PIS group than the non-PIS group (P < 0.05). Multivariate logistic regression analysis suggested that implanted stents ≥2 (OR=1.886, 95%CI: 1.049~3.389, P=0.034), operation duration ≥2 h (OR=1.938, 95%CI: 1.147~3.275, P=0.013) and implantation of PET-coverted stents (OR=2.131, 95%CI: 1.263~3.597, P=0.005) were independent risk factors for PIS after TEVAR. Within 30 d after TEVAR, 15 (4.0%) cases dead, including 10 (9.4%) from the PIS group and 5 (1.9%) from the non-PIS group. Kaplan-Meier survival curve indicated a significantly lower survival in the PIS group (Log-rank P=0.000 7). The results of multivariate logistic regression model indicated that cystatin C (OR=1.486, 95%CI: 1.053~2.097, P=0.024) and PIS (OR=5.628, 95%CI: 1.836~17.248, P=0.002) were independent risk factors for 30-day mortality after TEVAR in TBAD patients. Conclusion Implanted stents ≥2, operation duration ≥2 h and implantation of PET-coverted stents are closely associated with the occurrence PIS in TBAD patients after TEVAR. Cystatin C level and PIS are primary risk factors for poor 30-day prognosis after TEVAR.

Taste quality is one of the most important indicators for assessing the quality of rice. However, there has been a lack of systematic studies investigating the impact factors of taste quality. In this study, chromosomal segment substitution lines (CSSLs) with notable differences in physicochemical properties were obtained by screening the CSSL population. A correlation analysis between the physicochemical properties and the taste qualities of rice revealed that amylose and protein content are significantly negatively correlated with the taste value of both freshly cooked and rehydrated instant rice. The alkali spreading value (ASV) had limited impact on the taste value of rice, but low-ASV rice is more resistant to cooking. Grain chalkiness played a critical role in maintaining the integrity of freshly cooked rice and instant rice grains after rehydration. In summary, our study provides crucial insights and guidance for rice breeding, with the goal of developing excellent quality and enhancing the processing of instant rice. [ABSTRACT FROM AUTHOR]

Objective To investigate the predictive value of D-dimer combined with activated partial thromboplastin time (APTT) for slow/no-reflow of percutaneous coronary intervention (PCI) in patients with acute coronary syndrome(ACS). Methods A total of 181 ACS patients undergoing emergency PCI in our department from November 2015 to June 2018 were recruited in this study. Their plasma D-dimer level and APTT were tested before surgery. According to thrombolysis in myocardial infarction (TIMI), the patients were divided into slow/no-reflow group and normal blood flow group. The correlations of D-dimer level and APTT were analyzed with the incidence of slow/no-reflow. According to the cutoff values of the 2 indicators, the patients were assigned into high-risk group and non-high-risk group, and the incidence of slow/no-reflow was compared between the 2 groups. Results Logistics multivariate regression analysis showed preoperative D-dimer (OR=2.801, 95% CI=1.399~5.610, P=0.004) was positively, and APTT (OR=0.881, 95%CI=0.810~0.959, P=0.003) was negatively correlated with slow/no-reflow phenomenon. According to ROC curve, D-dimer AUC=0.612 (95% CI=0.537~0.683, P=0.036), APTT AUC=0.653 (95% CI=0.579~0.722, P=0.004), and AUC increased to 0.697 (95% CI=0.624~0.763, P < 0.001) when D-dimer was combined with APTT index. According to the cutoff values of D-dimer and APTT, the incidence of slow/no-reflow in high-risk and non-high-risk groups was 36.17% and 14.92%, respectively (P=0.002). Conclusion Higher preoperative D-dimer indicates higher incidence of slow/no-reflow in ACS patients after emergency PCI, while preoperative APTT is negatively correlated with the incidence. So combined detection of the 2 indicators helps predict the occurrence of slow/no-reflow in the patients.

Objective. Microfold cells (M cells) are specific intestinal epithelial cells for monitoring and transcytosis of antigens, microorganisms, and pathogens in the intestine. However, the mechanism for M-cell development remained elusive. Materials and Methods. Real-time polymerase chain reaction, immunofluorescence, and western blotting were performed to analyze the effect of sorbitol-regulated M-cell differentiation in vivo and in vitro, and luciferase and chromatin Immunoprecipitation were used to reveal the mechanism through which sorbitol-modulated M-cell differentiation. Results. Herein, in comparison to the mannitol group (control group), we found that intestinal M-cell development was inhibited in response to sorbitol treatment as evidenced by impaired enteroids accompanying with decreased early differentiation marker Annexin 5, Marcksl1, Spib, sox8, and mature M-cell marker glycoprotein 2 expression, which was attributed to downregulation of receptor activator of nuclear factor kappa-В ligand (RANKL) expression in vivo and in vitro. Mechanically, in the M-cell model, sorbitol stimulation caused a significant upregulation of phosphodiesterase 4 (PDE4) phosphorylation, leading to decreased protein kinase A (PKA)/cAMP-response element binding protein (CREB) activation, which further resulted in CREB retention in cytosolic and attenuated CREB binds to RANKL promoter to inhibit RANKL expression. Interestingly, endogenous PKA interacted with CREB, and this interaction was destroyed by sorbitol stimulation. Most importantly, inhibition of PDE4 by dipyridamole could rescue the inhibitory effect of sorbitol on intestinal enteroids and M-cell differentiation and mature in vivo and in vitro. Conclusion. These findings suggested that sorbitol suppressed intestinal enteroids and M-cell differentiation and matured through PDE4-mediated RANKL expression; targeting to inhibit PDE4 was sufficient to induce M-cell development. [ABSTRACT FROM AUTHOR]

Background: Metabolic reprogramming is a critical event for cell fate and function, making it an attractive target for clinical therapy. The function of metabolic reprogramming in Helicobacter pylori (H. pylori)-infected gastric intestinal metaplasia remained to be identified. Methods: Xanthurenic acid (XA) was measured in gastric cancer cells treated with H. pylori or H. pylori virulence factor, respectively, and qPCR and WB were performed to detect CDX2 and key metabolic enzymes expression. A subcellular fractionation approach, luciferase and ChIP combined with immunofluorescence were applied to reveal the mechanism underlying H. pylori mediated kynurenine pathway in intestinal metaplasia in vivo and in vitro. Results: Herein, we, for the first time, demonstrated that H. pylori contributed to gastric intestinal metaplasia characterized by enhanced Caudal-related homeobox transcription factor-2 (CDX2) and mucin2 (MUC2) expression, which was attributed to activation of kynurenine pathway. H. pylori promoted kynurenine aminotransferase II (KAT2)-mediated kynurenine pathway of tryptophan metabolism, leading to XA production, which further induced CDX2 expression in gastric epithelial cells. Mechanically, H. pylori activated cyclic guanylate adenylate synthase (cGAS)-interferon regulatory factor 3 (IRF3) pathway in gastric epithelial cells, leading to enhance IRF3 nuclear translocation and the binding of IRF3 to KAT2 promoter. Inhibition of KAT2 could significantly reverse the effect of H. pylori on CDX2 expression. Also, the rescue phenomenon was observed in gastric epithelial cells treated with H. pylori after IRF3 inhibition in vitro and in vivo. Most importantly, phospho-IRF3 was confirmed to be a clinical positive relationship with CDX2. Conclusion: These finding suggested H. pylori contributed to gastric intestinal metaplasia through KAT2-mediated kynurenine pathway of tryptophan metabolism via cGAS-IRF3 signaling, targeting the kynurenine pathway could be a promising strategy to prevent gastric intestinal metaplasia caused by H. pylori infection. 2STnY-xvxhAA5nGkWu7hrz Video Abstract [ABSTRACT FROM AUTHOR]

Rabeprazole is a representative of proton pump inhibitors and widely used in anti‐ulcer treatment. However, the effect of Rabeprazole on gut barrier function remains to be identified. In this study, we show that ZO‐1 expression is decreased in patients receiving Rabeprazole by immunofluorescence (IF) analysis. Western blotting (WB) and real‐time PCR (qPCR) results demonstrate that Rabeprazole treatment leads to a significant downregulation of ZO‐1 expression through inhibition of the FOXF1/STAT3 pathway, leading to destroy barrier function, which illustrates a novel pathway that Rabeprazole regulates barrier function in gastric epithelial cells. Mechanistically, Rabeprazole treatment led to a downregulation of STAT3 and FOXF1 phosphorylation, leading to inhibit nuclear translocation and decrease the binding of STAT3 and FOXF1 to ZO‐1 promoter, respectively. Most important, endogenous FOXF1 interacted with STAT3, and this interaction was dramatically abolished by Rabeprazole stimulation. Overexpression of STAT3 and FOXF1 in GES‐1 cells reversed the inhibitory effect of Rabeprazole on ZO‐1 expression, respectively. These finding extended the function of Rabeprazole and established a previously unappreciated mechanism by which the Rabeprazole/FOXF1/STAT3 axis facilitated ZO‐1 expression to regulate barrier function, and a comprehensive consideration and evaluation was required in treatment of patients. [ABSTRACT FROM AUTHOR]