Gastroparesis is a syndrome characterized by delayed gastric emptying with associated symptoms. It was reported that the symptoms of diabetic gastroparesis had been greatly improved by transpyloric stent placement. However, the use of stents in benign conditions is considered to be contraindicated because of the increasing risk of complications, such as stent migration, reflux, perforation, bleeding, and, most importantly, new strictures caused by stent-induced tissue hyperplasia. While temporary placement of a self-expanding metallic stent (SEMC) can drastically reduce the risk of complications, few reports are available on the treatment of refractory PSG by temporary transpyloric stent. Does it have a long-term clinical effect after the stent being retrieved? After accepting partial resection of the lesser curvature in another hospital, a patient developed refractory gastroparesis. The symptoms hadn’t been improved after long-term drug therapy and balloon dilation therapy. Four months after surgery, a fully covered SEMC was placed by endoscopy in our hospital. Gastroparesis had been greatly improved. Two weeks later, the transpyloric stent was retrieved and the patient didn’t show recurrent symptoms. Follow-ups were arranged at 3 months, 6 months and 1 year respectively, and there was no evidence of recurrence was found. This case indicates that temporary transpyloric SEMC is a safe, effective and less invasive alternative for post-surgical gastroparesis patients.

Hydrogen sulfide (H₂S) is a gaseous signaling molecule that influences digestive and nervous system functions. Enteric glial cells (EGCs) are integral to the enteric nervous system and play a role in regulating gastrointestinal motility. This study explored the dual effects of exogenous H₂S on EGCs and the influence of apoptosis-related pathways and ion channels in EGCs. We also administered honokiol for further interventional studies. The results revealed that low-concentration H₂S increased the mitochondrial membrane potential (MMP) of EGCs, decreased the whole-cell membrane potential, downregulated BAX and caspase-3, upregulated Bcl2 expression, reduced apoptosis, and promoted cell proliferation. The Ca²⁺ concentration, Cx43 mRNA, and protein expression were also increased. A high concentration of H₂S had the opposite effect. In addition, GFAP mRNA expression was upregulated in the test-low group, downregulated in the test-high group, and upregulated in the test-high + Hon group. Honokiol treatment increased MMP, reduced whole-cell membrane potential, inhibited BAX and caspase-3 expression, increased Bcl2 expression, decreased cell apoptosis, and increased cell proliferation. The Ca²⁺ concentration, Cx43 mRNA, and protein expression were also upregulated. In conclusion, our study showed that exogenous H₂S can bidirectionally regulate EGC proliferation and apoptosis by affecting MMP and cell membrane potential via the Bcl2/BAX/caspase-3 pathway and modulate Cx43-mediated Ca²⁺ responses in EGCs to regulate colonic motility bidirectionally. Honokiol can ameliorate the damage to EGCs induced by high H₂S concentrations through the Bcl2/BAX/caspase-3 pathway and improve colon motility by increasing Cx43 expression and Ca²⁺ concentration.

Ulcerative colitis (UC) is a chronic inflammatory bowel disease associated with disrupted lipid metabolism. This study aimed to uncover novel molecular subtypes and biomarkers by integrating sphingolipid metabolism-related genes (SMGs) with machine learning approaches. Using data from the GEO and GeneCards databases, 29 UC-related SMGs were identified. Consensus clustering was employed to define distinct molecular subtypes of UC, and a diagnostic model was developed through various machine learning algorithms. Further analyses—including functional enrichment, transcription factor prediction, single-cell localization, potential drug screening, molecular docking, and molecular dynamics simulations—were conducted to investigate the underlying mechanisms and therapeutic prospects of the identified genes in UC. The analysis revealed two molecular subtypes of UC: C1 (metabolically dysregulated) and C2 (immune-enriched). A diagnostic model based on three key genes demonstrated high accuracy in both the training and validation cohorts. Moreover, the transcription factor FOXA2 was predicted to regulate the expression of all three genes simultaneously. Notably, mebendazole and NVP-TAE226 emerged as promising therapeutic agents for UC. In conclusion, SMGs are integral to UC molecular subtyping and immune microenvironment modulation, presenting a novel framework for precision diagnosis and targeted treatment of UC.

肠神经胶质细胞(enteric glial cells, EGCs)是肠神经系统的重要组成部分, 在维持胃肠道功能方面发挥着重要作用. 营养和支持胃肠神经元, 参与胃肠道内神经活动的整合和调节以及参与肠道炎症反应, 直接或间接调节胃肠道运动功能. 研究肠神经胶质细胞对胃肠神经的影响以及在肠道炎症所致胃肠道运动障碍中的作用, 有助于揭示肠神经胶质细胞对胃肠道动力影响的作用机制.在临床上, EGCs具有作为多种胃肠道运动功能障碍性疾病的治疗靶点的应用前景.本文将对EGCs对胃肠道运动功能的影响进行综述.

肠神经胶质细胞(enteric glial cells, EGCs)是肠神经系统的重要组成部分, 其数量约是肠神经元数量的4倍. 在形态和功能上与中枢神经系统的星形胶质细胞相似. 在营养、支持肠神经、维持胃肠道稳态、调节胃肠道功能等方面发挥着重要作用. 由于其在肠道中发挥的作用复杂而多样, 成为研究的焦点. 对其形态学的观察和研究是非常重要的. EGCs发现至今, 针对其发挥功能的作用机制已得到深入研究, 相应的研究方法也在不断的进步与改进中. 本文主要介绍EGCs在胃肠道生理及病理状态下形态学特点及目前形态学研究方法, 以期对未来研究EGCs提供实验方法的借鉴及参考意义, 推进这一领域的发展.