Although proton pump inhibitors (PPIs) are widely used in the prevention of gastric bleeding caused by endoscopic submucosal dissection (ESD), there is no consensus on the optimal regimen for these patients. Therefore, we aim to investigate whether intermittent use of low-dose PPI is sufficient to prevent post-ESD bleeding.This multicenter, non-inferiority, randomized controlled trial was conducted at 9 hospitals in China. Consecutive eligible patients with a diagnosis of gastric mucosal lesions after ESD treatment were randomly assigned (1:1) to receive either intermittent low-dose or continuous high-dose PPIs treatment. After three days, all patients administered orally esomeprazole 40 mg once a day for 8 weeks. The primary endpoint was post-ESD bleeding within 7 days. Analysis was done according to the intention-to-treat principle with the non-inferiority margin (Δ) of 5%.526 consecutive patients were assessed for eligibility from 30 September 2017 to 30 July 2019, of whom 414 were randomly assigned to low-dose (n = 209) or high-dose (n = 205) esomeprazole treatment group without dropouts within7 days. The total post-ESD bleeding is occurred in 13 (6.2 %, 95 % CI 3.3-9.6) of 209 within 7 days in the intermittent low-dose group, and 12 (5.9 %, 95 % CI 2.9-9.3) of 205 in the continuous high-dose group. The absolute risk reduction (ARR) was 0.4 % (-4.2, 4.9). One month after ESD, There are 44 patients (21.1 %, 95 % CI 15.8, 26.8) and 39 patients (19.0 % 95 % CI 13.7, 24.4) in scar stage respectively in low-dose group and high-dose group (P = 0.875).The hospital costs in the low-dose PPI group was lower than high -dose group (P = 0.005).The intermittent use of low-dose PPIs is sufficient to prevent post-ESD bleeding. It might be applied in clinical practice to prevent post-ESD bleeding and reduce the costs related to PPIs.
There are many endoscope-assisted techniques that have been reported for the removal of traditional foreign bodies in the digestive tract (e. g. rat-tooth grasper, mini-snare, and end loop, among others) [1] [2] [3]. However, for any long and bent metal foreign bodies incarcerated in the duodenum or stomach, the technical difficulty is how to make the angled and sharp ends pass through the physiological narrow areas (e. g. pyloric canal, cardia, and esophageal entrance) in a relatively safe way.
The cause of lower prevalence of duodenal ulcer in young women compared with men is largely unknown. We recently found that sex difference in duodenal mucosal HCO₃⁻ secretion existed in humans and mice, but the mechanisms are not clear. Prostaglandin E₂ (PGE₂) is an important endogenous mediator that plays an important role in the regulation of duodenal HCO₃⁻ secretion. Therefore, in the present study, we investigated the effect of estrogen on PGE₂-stimulated duodenal HCO₃⁻ secretion and the underlying mechanisms. The results showed that 17β-estradiol at the physiological concentration (1 nM) had no significant effects on duodenal mucosal HCO₃⁻ secretion or short-circuit current (I(sc)) in mice. However, the pretreatment of 17β-estradiol (1 nM) markedly potentiated PGE₂-stimulated duodenal HCO₃⁻ secretion and I(sc) (P < 0.01 and P < 0.05). Global estrogen receptor (ER) antagonist ICI-182,780 and ERα-specific antagonist MPP, but not the ERβ-specific antagonist PHTPP, abolished estrogen-potentiated PGE₂-stimulated duodenal HCO₃⁻ secretion and I(sc). 17β-Estradiol and PGE₂ additively increased phosphatidylinositol 3-kinase (PI3K) activity and Akt phosphorylation. Wortmannin, a specific PI3K inhibitor, inhibited estrogen-potentiated PGE₂-stimulated duodenal HCO₃⁻ secretion and I(sc). In conclusion, estrogen at the physiological concentration potentiates PGE₂-stimulated duodenal mucosal HCO₃⁻ secretion through the activation of ERα and the PI3K-dependent mechanism, which may contribute to the sex difference in duodenal mucosal HCO₃⁻ secretion and the lower prevalence of duodenal ulcer in young women.
Dopamine (DA) is a neurotransmitter synthesized in the human body that acts on multiple organs throughout the body, reaching them through the blood circulation. Neurotransmitters are special molecules that act as messengers by binding to receptors at chemical synapses between neurons. As ligands, they mainly bind to corresponding receptors on central or peripheral tissue cells. Signalling through chemical synapses is involved in regulating the activities of various body systems. Lack of DA or a decrease in DA levels in the brain can lead to serious diseases such as Parkinson's disease, schizophrenia, addiction and attention deficit disorder. It is widely recognized that DA is closely related to neurological diseases. As research on the roles of brain-gut peptides in human physiology and pathology has deepened in recent years, the regulatory role of neurotransmitters in digestive system diseases has gradually attracted researchers' attention, and research on DA has expanded to the field of digestive system diseases. This review mainly elaborates on the research progress on the roles of DA and DRs related to digestive system diseases. Starting from the biochemical and pharmacological properties of DA and DRs, it discusses the therapeutic value of DA- and DR-related drugs for digestive system diseases.
Autophagy is a process of degradation and catabolism in cells. By removing damaged or dysfunctional organelles, autophagy interacts with the ubiquitin‑proteasome degradation system to jointly regulate cell function and energy homeostasis. Since autophagy plays a key role in physiology, disorders of the autophagy mechanism are associated with various diseases. Therefore, thorough understanding of the autophagy regulatory mechanism are crucially important in the diagnosis and treatment of diseases. To date, ion channels may affect the development and treatment of diseases by regulating autophagy, especially calcium‑permeable ion channels, in the process of digestive system diseases. However, the mechanism by which calcium ions and their channels regulate autophagy is still poorly understood, thus emphasizing the need for further research in this field. The present review intends to discuss the association, mechanism and application of calcium ions, their channels and autophagy in the occurrence and development of digestive system diseases.
Abstract Bleeding is a major and potentially life-threatening complication of peptic ulcer. Despite endoscopic hemostatic therapy advance, conventional endoscopic hemostatic modalities remain refractory for peptic ulcer bleeding with big size, fibrous base or in difficult-to-access anatomical locations. In this study, we attempted to evaluate the efficacy and safety of endoscopic cyanoacrylate injection treatment (ECIT) for refractory high-risk peptic ulcer bleeding by conventional endoscopic therapy. The patients with refractory high-risk peptic ulcer bleeding by conventional endoscopic therapy were carried out ECIT. The data were retrospectively collected. A total of 119 patients accepted ECIT. 74 patients (62.18%) obtained successful intravascular injection and perivascular injection was performed in 45 patients (37.82%). Immediate hemostatic rate for active bleeding achieved 90.91%. Rebleeding rate within 30 days was 12.07%. Overall successful hemostasis rate achieved 87.93%. Immediate hemostatic rate and overall successful hemostasis rate in intravascular injection patients were markedly superior over perivascular injection. Rebleeding rate in intravascular injection patients was markedly lower than that in perivascular injection patients. 11 patients complicated abdominal pain and no other complication occurred. In conclusion, ECIT, especial intravascular injection, was effective and safe, with high successful hemostasis rate for refractory high-risk peptic ulcer bleeding by conventional endoscopic therapy.
Neurofibromatosis type 1 (NF-1) is commonly associated with benign or malignant tumors in both the central and peripheral nervous systems. However, rare cases of NF-1-associated multiple rectal neuroendocrine tumors have been reported. This report describes a case of a 39 year old female with NF-1 and intermittent hematochezia as a primary symptom. Physical examination showed multiple subcutaneous nodules and café au lait spots with obvious scoliosis of the back. Imaging examinations and colonoscopy found malformation of the left external iliac vein and multiple gray-yellow nodules with varying sizes and shapes in the rectal submucosal layer. Histological and immunohistochemical results suggested multiple rectal neuroendocrine tumors, a rare disease with few appreciable symptoms and a particularly poor prognosis. The patient with NF-1 presented here had not only multiple rectal neuroendocrine neoplasms but also vascular malformations, scoliosis and other multiple system lesions. This case therefore contributes to improving clinical understanding, diagnosis and treatment of related complications for patients with NF-1 who present with associated medical conditions.
Abstract Ginsenoside Rh2 (G-Rh2) has well-established potent antitumor activity; yet, the effects of G-Rh2 on immune and metabolism regulation in cancer treatment, especially non-small cell lung cancer (NSCLC) remain unclear. We showed that G-Rh2 had a synergistic antitumor effect with cyclophosphamide (CY) on mice with NSCLC, and improved the immune deficiency caused by CY. Consistently, G-Rh2 exhibited no inhibitory effect on tumor growth of T cells-deficient nude mice. Furthermore, G-Rh2 treatment triggered the oxidative decomposition of fatty acid (FA), suppressed FA synthesis, increased ketone level, and decreased glucocorticoid (CORT) secretion. G-Rh2 significantly down-regulated the expression of fatty acid synthase (FASN). Of note, in liver-specific FASN knockout mice G-Rh2 failed to show the same immune enhancement effects. Further mechanistic exploration revealed that G-Rh2 suppressed the expression and nuclear translocation of sterol regulatory element binding protein 1 (SREBP-1), and disturbed the SREBP-1–FASN interaction in vitro.
Neurotransmitters are special molecules that serve as messengers in chemical synapses between neurons, cells, or receptors, including catecholamines, serotonin, dopamine, and other neurotransmitters, which play an important role in both human physiology and pathology. Compelling evidence has indicated that neurotransmitters have an important physiological role in various digestive diseases. They act as ligands in combination with central or peripheral receptors, and transmits signals through chemical synapses, which are involved in regulating the physiological and pathological processes of the digestive tract organs. For instance, neurotransmitters regulate blood circulation and affect intestinal movement, nutrient absorption, the gastrointestinal innate immune system, and the microbiome. In this review, we will focus on the role of neurotransmitters in the pathogenesis of digestive tract diseases to provide novel therapeutic targets for new drug development in digestive diseases.
To analyze the clinicopathological data of 13 cases of small cell neuroendocrine carcinoma (SCNEC) of the uterine cervix who received treatment at this medical institutions over the past five years with patient survival as the primary endpoint.The clinicopathologic data of 13 cases were reviewed. Immunohistochemistry was performed using antibodies against synaptophysin and chromogranin A and Ki-67. Survival was analyzed using the Kaplan-Meier method and log-rank tests.The median age of these patients was 37 years (range 21-62). Immunohistochemistry showed that the positive rate of synaptophysin and chromogranin A was 100% (13/13) and 69.23% (9/13), respectively. The median survival of patients with early-Stage I-II SCNEC of the uterine cervix (17.5 months) was significantly higher than that of patients with advanced stage SCNEC of the uterine cervix (four months) (p < 0.05). There was no local recurrence in all 13 patients. Five patients died of distant metastasis in less than six months.SCNEC of the uterine cervix is a highly-malignant disease and early-stage patients showed significantly longer survival compared to late-stage patients. Early diagnosis and prompt combination treatment may improve the outcome of patients with SCNEC of the uterine cervix.
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