Gastrointestinal fistula is a serious complication after gastrectomy, leading to high morbidity and mortality. Early identification of high-risk patients is crucial for improving outcomes and reducing complications. However, a simple and effective scoring system for assessing postoperative fistula risk is still lacking. This multicenter retrospective study aimed to develop and validate a scoring system (F-index) for predicting gastrointestinal fistula risk after gastrectomy. A total of 83 patients diagnosed with postoperative gastrointestinal fistula after gastrectomy between Aug 2021 and Dec 2023 were included. Patients were divided into low-risk (0–3 points, 30 patients) and high-risk (4–7 points, 53 patients) groups. 58 patients from the Third Hospital of Jilin University were used as the training set, while 25 patients from Weifang People’s Hospital formed the validation set. Data collection included demographic information, surgical data, and postoperative outcomes. Univariate and multivariate logistic regression analyses were used to identify risk factors, and ROC curve analysis was performed to evaluate the F-index’s predictive performance. Sensitivity, subgroup analyses, and nomogram construction were also conducted to validate the model. The F-index showed good discriminatory ability for post-diagnosis risk stratification among patients with postoperative gastrointestinal fistula after gastrectomy. Multivariate analysis indicated that time to fistula recognition after surgery > 7 days (OR = 6.307, 95

Crohn's disease (CD) is a chronic inflammatory bowel disease characterized by periods of remission and relapse. Probiotics have been suggested as potential therapeutic agents for managing CD, but their effects on clinical outcomes remain unclear. This meta-analysis aimed to evaluate the efficacy and safety of probiotics in patients with CD. A systematic search was conducted across multiple databases, including Medline, Embase, Cochrane Library, Wanfang, and CNKI. Randomized controlled trials (RCTs) assessing probiotic interventions in patients with CD were included. The primary outcomes were clinical remission and relapse, while secondary outcomes included endoscopic recurrence and safety. Risk ratios (RR) and 95 % confidence intervals (CIs) were calculated using a random-effects model. Sixteen RCTs involving 1112 patients were included. Probiotics significantly increased the likelihood of clinical remission in patients with active CD (RR: 1.27, 95 % CI: 1.09-1.47, p = 0.002) with mild heterogeneity (I2 = 16 %). However, no significant effect on clinical relapse was found in patients in remission (RR: 0.93, 95 % CI: 0.68-1.28, p = 0.66). In addition, probiotics did not reduce the risk of endoscopic recurrence after ileocecal resection (RR: 0.86, 95 % CI: 0.63-1.18, p = 0.34), and the incidence of severe adverse events was comparable between patients receiving probiotics and controls (p = 0.82). Probiotics may help enhance clinical remission in active CD patients possibly by modulating gut microbiota. However, no significant effect on relapse or endoscopic recurrence in remission was observed.

Inflammatory bowel disease (IBD) is characterised by chronic inflammation in the gastrointestinal tract resulting from dysregulated immune responses to gut microflora. Intestinal macrophages play important roles in the pathogenesis of IBD. The progression of IBD is often associated with increased M1-like macrophages, whereas M2-like macrophages are linked to tissue repair and resolution of inflammation. Ferroptosis in macrophages is potentially involved in IBD pathogenesis. However, the mechanisms underlying the involvement of macrophages and ferroptosis in IBD remain incompletely understood. Here, we established a dextran sodium sulphate (DSS)-induced murine colitis model to recapitulate human IBD. We observed elevated Pannexin-1 (Panx1) expression and an increased M1/M2 macrophage ratio in colonic tissues of DSS-treated mice. Depletion of Panx1 improved DSS-induced colitis via promoting macrophage polarisation into the M2-like phenotype. Furthermore, Panx1 depletion significantly enhanced M2-like macrophage polarisation and moderately inhibited M1-like macrophage polarisation. We further found that depletion of Panx1 reduced ferroptosis in intestinal macrophages from DSS-treated mice, and Glutathione peroxidase 4 (GPX4), a suppressor of ferroptosis, was upregulated in M2-like macrophages rather than M1-like macrophages by Panx1 depletion. In vitro assays showed that depletion of Panx1 inhibited ferroptosis in bone marrow-derived macrophage (BMDM)-derived macrophages. Further analysis showed that Wilms' tumour 1-associating protein (WTAP) inhibited Panx1 expression. Collectively, Panx1 aggravates IBD by shifting macrophage polarisation towards a pro-inflammatory phenotype and enhancing ferroptosis. Our study provides a novel mechanism of IBD pathogenesis and suggests potential therapeutic targets such as Panx1 and macrophage polarisation for IBD.

Laryngopharyngeal reflux disease (LPRD) is an inflammatory condition in the laryngopharynx and upper aerodigestive tract mucosa caused by reflux of stomach contents beyond the esophagus. LPRD commonly presents with sym-ptoms such as hoarseness, cough, sore throat, a feeling of throat obstruction, excessive throat mucus. This complex condition is thought to involve both reflux and reflex mechanisms, but a clear understanding of its molecular mechanisms is still lacking. Currently, there is no standardized diagnosis or treatment protocol. Therapeutic strategies for LPRD mainly include lifestyle modifications, proton pump inhibitors and endoscopic surgery. This paper seeks to provide a comprehensive overview of the existing literature regarding the mechanisms, patho-physiology and treatment of LPRD. We also provide an in-depth exploration of the association between LPRD and gastroesophageal reflux disease.

Cholangiocarcinoma (CCA) is an aggressive tumor characterized by a poor prognosis. Therapeutic options are limited in patients with advanced stage of CCA, as a result of the intrinsic or acquired resistance to currently available chemotherapeutic agents, and the lack of new drugs entering into clinical application. The challenge in translating basic research to the clinical setting, caused by preclinical models not being able to recapitulate the tumor characteristics of the patient, seems to be an important reason for the lack of effective and specific therapies for CCA. So, there seems to be two ways to improve patient outcomes. The first one is developing the combination therapies based on a better understanding of the mechanisms contributing to the resistance to currently available chemotherapeutic agents. The second one is developing novel preclinical experimental models that better recapitulate the genetic and histopathological features of the primary tumor, facilitating the screening of new drugs for CCA patients. In this review, we discussed the evidence implicating the mechanisms underlying treatment resistance to currently investigated drugs, and the development of preclinical experiment models for CCA.

Cholangiocarcinoma (CCA) is an aggressive tumor characterized by a poor prognosis. Therapeutic options are limited in patients with advanced stage of CCA, as a result of the intrinsic or acquired resistance to currently available chemotherapeutic agents, and the lack of new drugs entering into clinical application. The challenge in translating basic research to the clinical setting, caused by preclinical models not being able to recapitulate the tumor characteristics of the patient, seems to be an important reason for the lack of effective and specific therapies for CCA. So, there seems to be two ways to improve patient outcomes. The first one is developing the combination therapies based on a better understanding of the mechanisms contributing to the resistance to currently available chemotherapeutic agents. The second one is developing novel preclinical experimental models that better recapitulate the genetic and histopathological features of the primary tumor, facilitating the screening of new drugs for CCA patients. In this review, we discussed the evidence implicating the mechanisms underlying treatment resistance to currently investigated drugs, and the development of preclinical experiment models for CCA.

在全球范围内,肝细胞癌（hepatocellular carcinoma,HCC）是癌症相关死亡第二大肿瘤,占90% [1] 。其特点为病死率、致死率高,侵袭性强,对化疗药物敏感性低,易产生耐药性 [2] 。晚期HCC化疗方案主要得益于阿霉素（adriamycin,DOX）,5-氟尿嘧啶（5-Fluorouracil,5-FU）和铂类等药物。但是由于肝细胞癌的多药耐药性（Multi-drug Resistant,MDR）,

黄疸是由于血清中胆红素升高导致皮肤巩膜发黄的症状和体征。在正常情况下,胆红素进入和离开血液循环保持动态平衡,因其代谢异常导致血清中胆红素升高而出现黄疸。引起黄疸的原因很多,按病因可分为溶血性黄疸、胆汁淤积性黄疸、肝细胞性黄疸、先天性非溶血性黄疸等。而心功能不全患者由于严重心脏疾病导致有效循环血量减少、肝

正>胆管导管内乳头状黏液性肿瘤(B-IPMN)是一种罕见的胆道肿瘤,为胆管内乳头状瘤(IPNB)的一种特殊病理类型,其临床主要特点为:胆管内乳头状肿物和大量的黏液分泌。临床上较为罕见,本文结合文献对1例胆管导管内乳头状黏液性肿瘤进行报道。1临床资料患者男性,50岁,因"皮肤及巩膜黄染,伴皮肤瘙痒和尿色深黄2周"于2016年10月来我院进行就诊。入院超声提

变应性鼻炎（过敏性鼻炎,AR）的发病率不断增高 [1-3] ,环境及病毒感染等成为重要的相关影响因素 [4-6] 。研究显示,包括EB病毒（EBv）以及鼻病毒等因素可能参与变应性鼻炎及哮喘的调节,可能通过促进Th2方向IL-4以及IL-13等细胞因子的表达,参与到变应性鼻炎以及哮喘的发生、发展进程中 [7] 。EB病毒主要特征基因潜伏膜蛋白1（LMP1）

<正>急性胆囊炎是普外科常见的急腹症之一,大多数急性胆囊炎是因为胆汁淤积并继发细菌感染,当机体抵抗力下降时引发急性胆囊炎症,而胆汁淤积的原因主要是由于机械性梗阻,如胆囊内结石形成,急性胆囊炎分为急性非结石性胆囊炎、结石,