Inflammatory bowel disease (IBD), a chronic recurrent inflammatory bowel disease, is associated with depression and anxiety. Intestinal inflammation increases susceptibility to psychiatric disorders through a multidimensional network of immune-inflammatory, neuroendocrine, intestinal flora, and intestinal barrier abnormalities. Conversely, psychiatric stress exacerbates the pathology of IBD through immune regulation, intestinal barrier disruption, and microenvironmental alterations. Therefore, it is important to explore the mechanisms of comorbidity between IBD and depression and anxiety to optimise clinical management. This article reviews the comorbid mechanisms of IBD and depression and anxiety from the perspectives of immune-inflammatory axis, intestinal flora-metabolic pathway, intestinal barrier dysfunction, and neuroendocrine regulation in the context of rodent models, and explore potential intervention strategies, with the aim of providing new ideas and targets for therapeutic and transformation research in this field.

Inflammatory bowel disease (IBD), a chronic recurrent inflammatory bowel disease, is associated with depression and anxiety. Intestinal inflammation increases susceptibility to psychiatric disorders through a multidimensional network of immune-inflammatory, neuroendocrine, intestinal flora, and intestinal barrier abnormalities. Conversely, psychiatric stress exacerbates the pathology of IBD through immune regulation, intestinal barrier disruption, and microenvironmental alterations. Therefore, it is important to explore the mechanisms of comorbidity between IBD and depression and anxiety to optimise clinical management. This article reviews the comorbid mechanisms of IBD and depression and anxiety from the perspectives of immune-inflammatory axis, intestinal flora-metabolic pathway, intestinal barrier dysfunction, and neuroendocrine regulation in the context of rodent models, and explore potential intervention strategies, with the aim of providing new ideas and targets for therapeutic and transformation research in this field.

Objective:To systematically evaluate the qualitative study on the sexual health needs of patients with ostomy based on theoretical domains framework (TDF), providing reference for clinical care and practice.Methods:A comprehensive search was conducted for qualitative studies on the sexual experience of ostomy patients in the China National Knowledge Infrastructure, Wanfang Data, VIP database, China Biology Medicine, PubMed, Embase, Web of Science, Cochrane Library, Elton B. Stephens Company (EBSCO), Elsevier Scopus (SCOPUS), and Cumulative Index to Nursing and Allied Health Literature (CINAHL) databases, with a timeframe of from the creation of the databases to April 15, 2024. The Joanna Briggs Institute Evidence Based Healthcare Center Critical Appraisal Tool was used to evaluate the quality of eligible literature, and the theoretical domain framework was used to integrate the extracted results.Results:A total of 11 articles were included and 51 results were extracted. Based on the theoretical framework, map the sexual health needs of ostomy patients to six core areas: knowledge, skills, optimism, outcome beliefs, environment and resources, and emotions.Conclusions:Medical staff should pay attention to the sexual health needs of patients with intestinal stomas. Based on the six core areas of knowledge, skills, optimism, outcome beliefs, environment and resources, and emotions, they should deeply explore the factors that affect their sexual health, provide professional guidance and comprehensive care, and improve their sexual health level and quality of life.

UNC-51-like kinase 1 (ULK1), as a serine/threonine kinase, is an autophagic initiator in mammals and a homologous protein of autophagy related protein (Atg) 1 in yeast and of UNC-51 in Caenorhabditis elegans. ULK1 is well-known for autophagy activation, which is evolutionarily conserved in protein transport and indispensable to maintain cell homeostasis. As the direct target of energy and nutrition-sensing kinase, ULK1 may contribute to the distribution and utilization of cellular resources in response to metabolism and is closely associated with multiple pathophysiological processes. Moreover, ULK1 has been widely reported to play a crucial role in human diseases, including cancer, neurodegenerative diseases, cardiovascular disease, and infections, and subsequently targeted small-molecule inhibitors or activators are also demonstrated. Interestingly, the non-autophagy function of ULK1 has been emerging, indicating that non-autophagy-relevant ULK1 signaling network is also linked with diseases under some specific contexts. Therefore, in this review, we summarized the structure and functions of ULK1 as an autophagic initiator, with a focus on some new approaches, and further elucidated the key roles of ULK1 in autophagy and non-autophagy. Additionally, we also discussed the relationships between ULK1 and human diseases, as well as illustrated a rapid progress for better understanding of the discovery of more candidate small-molecule drugs targeting ULK1, which will provide a clue on novel ULK1-targeted therapeutics in the future.

Objective To determine the level of peripheral blood CD34 positive (CD34+) cells in patients with acute cerebral infarction (ACI),and to explore its clinical significance.Methods The level of peripheral blood CD34+ cells was determined by flow cytometry within 72 hours of onset of patients with acute cerebral infarction (infarct group,n=45),cerebrovascular risk factors in patients without cerebral infarction (high risk group,n=27) and healthy subjects (control group,n=20).The neural function defect score,infarction lesion volume and carotid artery intima-media thickness (IMT) were determined in patients with infarction group.Results The percentages of peripheral blood CD34 cells in infarction group (0.034 ±0.012)％ and the high risk group of patients (0.047±0.009)％ were lower than that of control group(0.063±0.009)％,and were lower in infarction group than in high-risk groups (all P＜0.05).The percentages of peripheral blood CD34+cells were significantly decreased compared with control group (P＜0.05) in infarction patients with mild [(0.047±0.009)％],moderate [(0.036±0.009)％],severe [(0.022±0.007)％] infarction nervous function defect score.Wherein,the percentages were lower in severe group than in the moderate group,moderate group was lower than in mild group (all P＜0.05).The percentages of peripheral blood CD34 cells in infarction patients with small,moderate,large infaret lesion volume were lower than in control group (P＜0.05),wherein,were lower in large group than in moderate group,lower in moderate group than in treatment group (all P＜0.05).Infarction patients were confirmed with carotid atherosclerosis (CAS) by carotid ultrasound.The extent of lesion were divided into carotid artery intimal thickening group [(0.043±0.010)％],carotid artery plaque group [(0.036±0.010)％],and carotid artery stenosis group [(0.023±0.009)％].The levels of peripheral blood CD34+ cells in three groups of patients were decreased compared with control group.The levels were lower in carotid artery stenosis group than in carotid artery plaque group,lower in carotid artery plaque group than in carotid artery intimal thickening group (all P＜0.05).Conclusions The level of peripheral blood CD34+ cells in acute cerebral ischemia is reduced,it can become a sensitive and early indicator of cerebral ischemia,and its level is related to neurologic impairment,infarction size and the degree of carotid artery atherosclerosis.