The etiology of gastrointestinal (GI) diseases is intricate and multifactorial, encompassing complex interactions between genetic predisposition and gut microbiota. The cell fate change, immune function regulation, and microenvironment composition in diseased tissues are governed by microorganisms and mutated genes either independently or through synergistic interactions. A comprehensive understanding of GI disease etiology is imperative for developing precise prevention and treatment strategies. However, the existing models used for studying the microenvironment in GI diseases-whether cancer cell lines or mouse models-exhibit significant limitations, which leads to the prosperity of organoids models. This review first describes the development history of organoids models, followed by a detailed demonstration of organoids application from bench to clinic. As for bench utilization, we present a layer-by-layer elucidation of organoid simulation on host-microbial interactions, as well as the application in molecular mechanism analysis. As for clinical adhibition, we provide a generalized interpretation of organoid application in GI disease simulation from inflammatory disorders to malignancy diseases, as well as in GI disease treatment including drug screening, immunotherapy, and microbial-targeting and screening treatment. This review draws a comprehensive and systematical depiction of organoids models, providing a novel insight into the utilization of organoids models from bench to clinic.

Diabetes, commonly known for its metabolic effects, also critically affects the enteric nervous system (ENS), which is essential in regulating gastrointestinal (GI) motility, secretion, and absorption. The development of diabetes-induced enteric neuropathy can lead to various GI dysfunctions, such as gastroparesis and irregular bowel habits, primarily due to disruptions in the function of neuronal and glial cells within the ENS, as well as oxidative stress and inflammation. This editorial explores the pathophysiological mechanisms underlying the development of enteric neuropathy in diabetic patients. Additionally, it discusses the latest advances in diagnostic approaches, emphasizing the need for early detection and intervention to mitigate GI complications in diabetic individuals. The editorial also reviews current and emerging therapeutic strategies, focusing on pharmacological treatments, dietary management, and potential neuromodulatory interventions. Ultimately, this editorial highlights the necessity of a multidisciplinary approach in managing enteric neuropathy in diabetes, aiming to enhance patient quality of life and address a frequently overlooked complication of this widespread disease.

In this editorial, we comment on an article titled \"Morphological and biochemical characteristics associated with autophagy in gastrointestinal diseases\", which was published in a recent issue of the World Journal of Gastroenterology. We focused on the statement that \"autophagy is closely related to the digestion, secretion, and regeneration of gastrointestinal cells\". With advancing research, autophagy, and particularly the pivotal role of the macroautophagy in maintaining cellular equilibrium and stress response in the gastrointestinal system, has garnered extensive study. However, the significance of mitophagy, a unique selective autophagy pathway with ubiquitin-dependent and independent variants, should not be overlooked. In recent decades, mitophagy has been shown to be closely related to the occurrence and development of gastrointestinal diseases, especially inflammatory bowel disease, gastric cancer, and colorectal cancer. The interplay between mitophagy and mitochondrial quality control is crucial for elucidating disease mechanisms, as well as for the development of novel treatment strategies. Exploring the pathogenesis behind gastrointestinal diseases and providing individualized and efficient treatment for patients are subjects we have been exploring. This article reviews the potential mechanism of mitophagy in gastrointestinal diseases with the hope of providing new ideas for diagnosis and treatment.

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OBJECTIVE: Mammoplasty, a common cosmetic procedure involving breast augmentation and reduction surgeries, has gained global popularity. Recently, attention has shifted towards understanding the prevalence and significance of gastrointestinal (GI) symptoms following mammoplasty. This systematic review aims to consolidate existing literature to provide a comprehensive overview of the type and frequency of GI problems associated with various mammoplasty procedures.
METHODS: A systematic search of PubMed and Scopus databases was conducted until January 22, 2024, identifying observational and interventional studies examining GI symptoms post-mammoplasty. Inclusion criteria covered human studies, while exclusion criteria ensured specificity. Two independent investigators performed screening, and data extraction included study characteristics, surgical procedures, anesthesia methods, and interventions.
RESULTS: Nineteen studies, involving 2,487 subjects, were included in the review. Breast reconstruction emerged as the most studied procedure, followed by breast reduction, augmentation, mastectomy, and breast cancer surgery. Predominant GI symptoms included nausea and vomiting, with varying rates across mammoplasty types. Anesthesia modality influenced symptomatology, with general, local, and combined anesthesia associated with GI disturbances. Antiemetics, notably ondansetron and droperidol, showed variable efficacy. Non-pharmacological approaches, such as preoperative hypnosis, were explored for symptom management.
CONCLUSIONS: Our systematic review reveals insights into GI symptoms post-mammoplasty, emphasizing the common occurrence of symptoms such as nausea and vomiting, alongside less frequent manifestations such as constipation, dry mouth, retching, abdominal pain, and tightness. Variations in symptom prevalence were noted across diverse mammoplasty surgeries, anesthesia methods, and the use of antiemetics, underscoring the complex nature of post-mammoplasty GI disturbances.

Fetal MR imaging has been shown to be a useful tool for the diagnosis of fetal gastro-intestinal pathologies. To recognize the various pathologies, it is, however, essential to know the normal MR imaging appearance of the fetal bowel at various gestational ages. By providing additional information to ultrasound in case of a fetal gastrointestinal anomaly, MR imaging helps to improve planning for the delivery, postnatal management, and improves parental counseling.

It is well known that municipal drinking water may be the cause of gastrointestinal illness (GII) outbreaks, but it is still unclear to what extent drinking water contributes to endemic GII. To explore this, we conducted a prospective cohort study among 6,955 adults in five municipalities in Sweden, collecting monthly GII episodes and mean daily cold drinking water consumption through SMS (Short Message Service). When the association between drinking water consumption and GII (all symptoms) and acute gastrointestinal illness (AGI, vomiting and/or three loose stools during a 24-h period) were assessed, there were indications that the association departed from linearity, following a unimodal shape. Among consumers in surface water areas, the highest risk of GII and AGI was generally seen among the average consumers, while the opposite was seen among groundwater consumers. The association however also seemed to be affected by neighbouring communities. The results of the study indicate that there is indeed an association between drinking water consumption and endemic GII, but the nature of this association is complex and likely affected by multiple factors, for example, water source type in the home and degree of exposure to drinking water from additional sources.

Cannabinoids and their receptors play a significant role in the regulation of gastrointestinal (GIT) peristalsis and intestinal barrier permeability. This review critically evaluates current knowledge about the mechanisms of action and biological effects of endocannabinoids and phytocannabinoids on GIT functions and the potential therapeutic applications of these compounds. The results of ex vivo and in vivo preclinical data indicate that cannabinoids can both inhibit and stimulate gut peristalsis, depending on various factors. Endocannabinoids affect peristalsis in a cannabinoid (CB) receptor-specific manner; however, there is also an important interaction between them and the transient receptor potential cation channel subfamily V member 1 (TRPV1) system. Phytocannabinoids such as Δ9-tetrahydrocannabinol (THC) and cannabidiol (CBD) impact gut motility mainly through the CB1 receptor. They were also found to improve intestinal barrier integrity, mainly through CB1 receptor stimulation but also via protein kinase A (PKA), mitogen-associated protein kinase (MAPK), and adenylyl cyclase signaling pathways, as well as by influencing the expression of tight junction (TJ) proteins. The anti-inflammatory effects of cannabinoids in GIT disorders are postulated to occur by the lowering of inflammatory factors such as myeloperoxidase (MPO) activity and regulation of cytokine levels. In conclusion, there is a prospect of utilizing cannabinoids as components of therapy for GIT disorders.

Infections with gastrointestinal nematodes (GINs) reduce the economic efficiency of sheep operations and compromise animal welfare. Understanding the host\'s response to GIN infection can help producers identify animals that are naturally resistant to infection. The objective of this study was to characterize the hepatic transcriptome of sheep that had been naturally exposed to GIN parasites. The hepatic transcriptome was studied using RNA-Sequencing technology in animals characterized as high (n = 5) or medium (n = 6) based on their innate immune acute-phase (AP) response phenotype compared with uninfected controls (n = 4), and with biased antibody-mediated (AbMR, n = 5) or cell-mediated (CMR, n = 5) adaptive immune responsiveness compared to uninfected controls (n = 3). Following the assessment of sheep selected for innate responses, 0, 136, and 167 genes were differentially expressed (DE) between high- and medium-responding animals, high-responding and uninfected control animals, and medium-responding and uninfected control animals, respectively (false discovery rate (FDR) < 0.05, and fold change |FC| > 2). When adaptive immune responses were assessed, 0, 53, and 57 genes were DE between antibody- and cell-biased animals, antibody-biased and uninfected control animals, and cell-biased and uninfected control animals, respectively (FDR < 0.05, |FC| > 2). Functional analyses identified enriched gene ontology (GO) terms and metabolic pathways related to the innate immune response and energy metabolism. Six functional candidate genes were identified for further functional and validation studies to better understand the underlying biological mechanisms of host responses to GINs. These, in turn, can potentially help improve decision making and management practices to increase the overall host immune response to GIN infection.

The management of gastrointestinal disease in animals represents a significant challenge in veterinary and zootechnic practice. Traditionally, acute symptoms have been treated with antibiotics and high doses of zinc oxide (ZnO). However, concerns have been raised regarding the potential for microbial resistance and ecological detriment due to the excessive application of this compound. These concerns highlight the urgency of minimizing the use of ZnO and exploring sustainable nutritional solutions. Hydrolysable tannins (HTs), which are known for their role in traditional medicine for acute gastrointestinal issues, have emerged as a promising alternative. This study examined the combined effect of food-grade HTs and subtherapeutic ZnO concentration on relevant biological functions of Caco-2 cells, a widely used model of the intestinal epithelial barrier. We found that, when used together, ZnO and HTs (ZnO/HTs) enhanced tissue repair and improved epithelial barrier function, normalizing the expression and functional organization of tight junction proteins. Finally, the ZnO/HTs combination strengthened enterocytes\' defense against oxidative stress induced by inflammation stimuli. In conclusion, combining ZnO and HTs may offer a suitable and practical approach for decreasing ZnO levels in veterinary nutritional applications.