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Introduction: Multiple sclerosis (MS) is a chronic inflammatory condition that impacts the central nervous system. It is distinguished by processes like demyelination, gliosis, neuro-axonal harm, and inflammation. The prevailing theory suggests that MS originates from an immune response directed against the body's own antigens within the central nervous system., Aim: The main aim of this research paper "Neuroinflammation-on-a-Chip" for studying multiple sclerosis is to enhance our comprehension of MS development, demonstrate the application of cutting-edge technology, and potentially provide valuable insights for therapeutic approaches., Methods: The available literature for this Narrative Review was searched on various bibliographic databases, PubMed, NCBI, and many other medical references using an individually verified, prespecified approach. Studies regarding the significance of MS and its neuroinflammatory pathogenesis in addition to the development and optimization of neuroinflammatory-on-a-chip and the advancement in innovations in this field have been reviewed in this research for a better understanding of "Neuroinflammation-on-a-chip for multiple sclerosis". The level of evidence of the included studies was considered as per the Centre for Evidence-Based Medicine recommendations., Results: Several studies have indicated that the brain-chip model closely mimics cortical brain tissue compared to commonly used conventional cell culture methods like the Transwell culture system. Additionally, these studies have clearly demonstrated that further research using brain chips has the potential to enhance our understanding of the molecular mechanisms and roles of blood-brain barrier (BBB) transporters in both normal and disease conditions., Conclusion: Understanding neuroinflammation processes remains essential to establish new MS treatments approaches. The utilization of brain chips promises to advance our understanding of the molecular processes involving BBB transporters, both in normal and diseased states. Further research needs to be addressed in order to enhance the performance and understanding of neuroinflammation on a chip, hence aiming to provide more effective treatments for all CNS diseases., Competing Interests: Not applicable.Sponsorships or competing interests that may be relevant to content are disclosed at the end of this article., (Copyright © 2024 The Author(s). Published by Wolters Kluwer Health, Inc.)

Introduction: Sleeve gastrectomy is the most commonly performed bariatric operation globally. The main complication is GERD. In the medium term, it can increase the incidence of Barrett's esophagus (BE), which is a risk factor for esophageal adenocarcinoma. Following conventional sleeve gastrectomy, BE is noted in up to 16% of patients postoperatively. Recently, Nissen sleeve gastrectomy (NSG) has been shown to reduce the frequency of postoperative GERD compared to conventional sleeve gastrectomy. This study aims to evaluate the impact of NSG on the incidence and remission of BE in the long term., Material and Method: This bicentric retrospective study included 692 patients who received NSG from September 2013 to July 2021. All patients underwent preoperative upper GI endoscopy and were then scheduled to receive upper GI endoscopy between 1 and 2 years and then between 3 and 5 years postoperatively. BE was systematically confirmed by biopsies., Results: Seventy-four patients had endoscopic suspicion of BE, which was confirmed on 54/692 patients by histology. The BE lesions consisted of 18.5% intestinal metaplasia and 75.9% fundal metaplasia. Among these 54 patients, 38 underwent endoscopic investigation within 2 years postoperatively. The biopsies showed healed BE in 25/38 patients (64.1%). At 5 years, two patients had proven BE. Concerning the incidence of BE post NSG: 234 performed the follow-up endoscopy within 2 years. The incidence of de novo BE is nil., Conclusion: The NSG is associated with healing of known BE in approximately two-thirds of patients at 2-year follow-up. This is consistent with the GERD improvement that has been shown with NSG., (© 2024. The Author(s), under exclusive licence to Springer Science+Business Media, LLC, part of Springer Nature.)

Introduction: Obesity is a chronic disease that increases cardiovascular and metabolic morbidity and mortality, decreases quality of life, and increases health care costs. While the role of lifestyle behavioral factors in the development of obesity is well established, the role of traumatic life events, including violence, is unclear. The purpose of this study was to describe situations of traumatic life events reported by patients undergoing a bariatric surgery program, with a particular focus on sexual violence and its clinical correlates., Methods: In this cross-sectional study, patients with grade II or III obesity, admitted to our digestive surgery department for bariatric surgery from August 01, 2019, to December 31, 2020, underwent a structured interview by a trained psychologist to describe the history of traumatic life events self-reported by the patients. The primary endpoint was the presence of a history of sexual violence (SV). Multivariate logistic regressions were applied to identify independent risk factors for SV., Results: Of the 408 patients interviewed, 87.1% reported at least one traumatic life event and 33.1% reported having had an SV in the past. Female gender (aOR = 7.44, 95% confidence interval: 3.85-15.73; p < 0.001) and higher body mass index (1.05, 1.02-1.08; p = 0.002) were associated with an increased risk of SV. Male gender was associated with a higher risk of difficulties including sports cessation, depression, and work-related distress., Conclusion: In the context of obesity, psychosocial trauma is characterized by a high frequency and several gender specificities that must be taken into account in the management of these patients., (© 2024 The Author(s). Published by S. Karger AG, Basel.)

Introduction: Sleep is an important neurophysiological condition that is intricately linked to general health, laying the basis for both physiological and psychological well-being. A thorough examination of sleep disorders and cardiovascular health demonstrates their deep relationship, emphasizing the numerous diagnostic tools and treatment techniques available., Aim: This study aims to examine the impact, mechanisms, diagnostic techniques, treatment strategies, implications, and healthcare interventions of the sleep-cardiovascular connection, to better understand the relationship between sleep disorders and cardiovascular health., Methods: The paper reviews key studies conducted from 2015-till date, investigating the impact of sleep disorders on the cardiovascular system. It looked into data relating to cardiovascular outcomes based on the degree of sleep disorders, considered potential confounding factors, and addressed current research constraints., Results: The findings highlight a strong link between sleep problems and poor cardiovascular outcomes. Emerging diagnostic tools, such as enhanced sleep-related technology and biomarkers, open up new avenues for determining the impact of sleep disturbances on cardiovascular health. In addition, the research discusses several treatment options, ranging from cognitive behavioral therapy to pharmaceutical therapies, and their potential benefits in addressing sleep-related cardiovascular risks., Conclusion: The complex association between sleep disturbances and cardiovascular health emphasizes the need to recognize sleep as a critical component of overall well-being. Thus collaboration among medical disciplines, as well as individualized therapies, are critical to improving patient care. Moreover, Understanding and managing the consequences of sleep problems on cardiovascular health can lead to more effective interventions, better outcomes, and improved public health as research advances., Competing Interests: The authors declare no conflict of interest., (© 2023 The Authors. Health Science Reports published by Wiley Periodicals LLC.)

Purpose: The development of gastroesophageal reflux disease (GERD) is a commonly encountered scenario after sleeve gastrectomy. A recently reported technical amendment to incorporate a Nissen fundoplication is discussed in this multimedia article focussing on optimising outcomes and reducing complications., Materials and Methods: An intraoperative video has been edited to demonstrate the Nissen-Sleeve Gastrectomy and important technical considerations in its technical performance., Results: Gastrolysis is performed proximally from 6 cm proximal to the pylorus. Routine full mediastinal mobilisation of the oesophagus (5 cm) is completed. Cruroplasty is routinely performed. A short Nissen fundoplication is completed calibrated on a 37 French bougie and then sleeve gastrectomy is performed. Our team's experience suggests that careful manipulation of the fundus and using reproducible measurements of the fundus are key to completing the fundoplication whilst minimising complications. A control test with mobilisation of the bougie through the wrap is recommended at the end of the procedure., Conclusion: The Nissen-Sleeve Gastrectomy, as presented in this video, is safe and has good short-term efficacy outcomes. Longer term and randomised studies are ongoing., (© 2023. The Author(s), under exclusive licence to Springer Science+Business Media, LLC, part of Springer Nature.)

Background: Gastrogastric fistula (GGF) occurs in 1-6% of patients who undergo Roux-en-Y gastric bypass (RYGB) for morbid obesity. The pathophysiology may be related to gastric ischemia, fistula, or ulcer., Objectives: The purposes of the study are to describe the principles of management and to review the literature of this uncommon complication., Setting: The setting of this study is University Hospital, France., Materials and Methods: We conducted a retrospective review of all patients' records with a diagnosis of GGF after RYGB between January 2004 and November 2014., Results: During the study period, 1273 patients had RYGB for morbid obesity. Fifteen patients presented with a symptomatic GGF (1.18%). The average interval from surgery to presentation was 28 months (22-62). A history of marginal ulcer or anastomotic leak was present in nine patients (60%). The most common presentation was weight regain (80%), followed by pain (73.3%). Two types of fistulas were identified, an exclusively GGF (high) and a gastro-jejuno-gastric fistula (low). High GGF, frequently associated with dilatation of the gastric pouch, was treated by a sleeve of the pouch and sleeve resection of the remnant stomach (nine patients). Low GGF was treated with gastric resection coupled with a revision of the gastrojejunal anastomosis (six patients). All patients were treated laparoscopically with no conversion to laparotomy. The average length of postoperative hospital stay was 5.2 days (range 3-10)., Conclusion: GGF after RYGB is a rare complication. Its pathophysiology remains unclear. Surgical management is the definitive treatment.

CD24 is an extensively glycosylated membrane protein that is linked to the membrane via a glycosyl-phosphatidylinositol (GPI)-anchor. In mice, CD24 is expressed by hematopoietic and non-hematopoietic cells. CD24-/- mice do not have gross immunological defects, but detailed analysis revealed strongly reduced responses in an experimental autoimmune encephalomyelitis (EAE) model and a massive proliferation of T cells under lymphopenic conditions. It was also demonstrated that preB cells from CD24-/- mice are impaired in α4-integrin-mediated cell binding. Here we report that CD24-/- mice have strongly reduced numbers of leukocytes in the colon compared to wildtype mice. The reduction comprized all subpopulations. Leukocyte counts in spleen, mesenteric lymph nodes or small intestine were not significantly different. We find that beside leukocytes, CD24 is widely expressed in EpCAM+ epithelial and CD31+ endothelial cells of colon and small intestine. However, in CD24-/- mice the number of CD31+ endothelial cells in colons was strongly reduced and the number of epithelial cells was augmented. Leukocyte transfer experiments provided evidence that the CD24 status of recipient mice, rather than of the transferred cells, is crucial for leukocyte recruitment to the colon. We hypothesize that CD24 on colonic epithelial and endothelial cells is required for the retention and positioning of leukocytes most likely by affecting integrin function., (Copyright © 2014 Elsevier B.V. All rights reserved.)

The expression of the glycosyl phosphatidylinositol (GPI)-anchored protein CD24 correlates with poor prognosis in a variety of carcinomas. However, little is known about the cellular mechanisms of the CD24-mediated effects. In this study, we present evidence that CD24 affects the lateral localization of beta1 integrin. Using stably CD24-transfected A125 and MDA-MB-435S carcinoma cells we show that CD24 augments beta1-dependent cell motility and stimulates transmigration and invasion across a monolayer of endothelial cells. Furthermore, as demonstrated by sucrose density gradient centrifugation and Western Blot analysis, CD24 recruits beta1 integrin into lipid raft domains. We suggest that CD24 acts as a gate-keeper for lipid rafts, thereby regulating the activity of integrins and other proteins.

CD24 is a small, heavily glycosylated cell-surface protein which is linked to the membrane via a glycosyl-phosphatidylinositol (GPI-) anchor and therefore localizes in lipid rafts. CD24 is widely used as a cell-lineage marker for hematopoietic cells. CD24 is also expressed on a variety of human carcinomas, including epithelial ovarian, breast, prostate, colon and lung cancer and has been linked to poor prognosis. Except for its role as a ligand for P-selectin on carcinoma and myeloid cells, a specific function for CD24 has not been determined. Here we show that CD24 affects the function of the chemokine receptor CXCR4. Using isolated CD19-positive bone marrow B cells from CD24-knockout mice and CD24-/- pre-B lymphocytic cell lines, we demonstrate that CD24 expression reduces SDF-1-mediated cell migration and signalling via CXCR4. We observed that the loss of CD24 augmented cellular cholesterol levels and enhanced CXCR4 lipid raft association. Altered chemotactic migration and raft residence was also observed in MDA-MB-231 breast cancer cells expressing high and low levels of CD24 and CXCR4 receptor. MDA-MB-231 cells expressing low levels of CD24 also showed enhanced tumour formation in NOD/SCID mice compared with cells overexpressing CD24. These results demonstrate a novel role for CD24 as a regulator of CXCR4 function that could be relevant for breast cancer growth and metastasis.

L1 is a neural cell adhesion molecule involved in cell migration, axon growth and guidance. Recent data have shown that L1 is overexpressed in ovarian and endometrial tumors and is associated with bad prognosis. How L1 promotes tumor progression is presently unknown. Here we show that L1 expression is predominantly confined to the invasive front of ovarian carcinomas. Overexpression of L1 in carcinoma cell lines by adenovirus-mediated gene transfer enhanced the haptotactic cell migration on extracellular matrix proteins. Expression of L1 augmented tumor growth of carcinomas xenografted in nonobese diabetic/severe combined immunodeficient mice (NOD/SCID). A recent report has demonstrated L1-dependent upregulation of beta3 integrin involving activation of the extracellular signal-regulated kinase (erk) pathway. We find that L1 and beta3 integrin are not coexpressed in ovarian carcinoma tissues. Overexpression of L1 did not upregulate beta3 integrin in ovarian carcinoma cell lines but could do so in HEK293 cells. Our results suggest that L1 could drive progression by enhancing cell migration and tumor growth but that L1 dependent and erk-regulated gene expression requires cell-type specific elements., (Copyright 2005 Wiley-Liss, Inc.)

Cells can release membrane components in a soluble form and as membrane vesicles. L1, an important molecule for cell migration of neural and tumor cells, is released by membrane-proximal cleavage, and soluble L1 promotes cell migration. Release of L1 is enhanced by shedding inducers such as phorbol ester and pervanadate, but it is also enhanced by depletion of cellular cholesterol with methyl-beta-cyclodextrin (MCD). How such different compounds can induce shedding is presently unknown. We show here that ADAM10 is involved in L1 cleavage, which occurs at the cell surface and in the Golgi apparatus. MCD and pervanadate treatment induced the release of microvesicles containing full-length L1 and the active form of ADAM10. L1 cleavage occurred in isolated vesicles. L1-containing microvesicles could trigger haptotactic cell migration. Only the neural L1 form carrying the RSLE signal for clathrin-dependent endocytosis was recruited and cleaved in vesicles. Phorbol ester treatment activated L1 cleavage predominantly at the cell surface. Our results provide evidence for two pathways of L1 cleavage, based on ADAM10 localization, that can be activated differentially: 1) direct cleavage at the cell surface, and 2) release and cleavage in secretory vesicles most likely derived from the Golgi apparatus. The findings establish a novel role for ADAM10 as a vesicle-based protease.