eGastroenterology最新文献

{"title":"Gasdermin D deletion prevents liver injury and exacerbates extrahepatic damage in a murine model of alcohol-induced ACLF.","authors":"Martí Ortega-Ribera, Yuan Zhuang, Veronika Brezani, Radhika S Joshi, Zsuzsanna Zsengeller, Prashanth Thevkar Nagesh, Aditi Datta, Gyongyi Szabo","doi":"10.1136/egastro-2024-100151","DOIUrl":"10.1136/egastro-2024-100151","url":null,"abstract":"<p><strong>Background: </strong>Gasdermin D (GSDM-D), a key executor of pyroptosis, is increased in various liver diseases and contributes to disease progression. Alcohol induces inflammasome activation and cell death, which are both linked to GSDM-D activation. However, its role in alcohol-induced acute-on-chronic liver failure (ACLF) remains unclear.</p><p><strong>Methods: </strong>ACLF was induced in GSDM-D-deficient or wild-type (WT) mice by 28-day bile duct ligation surgery plus a single 5 g/kg alcohol binge leading to acute decompensation. Nine hours after the alcohol binge, blood, liver, kidney and cerebellum specimens were collected for analysis.</p><p><strong>Results: </strong>Active GSDM-D was significantly increased in humans and mice ACLF livers compared with both healthy controls and cirrhotic livers. GSDM-D-deficient mice with ACLF showed decreased inflammation, neutrophil infiltration and fibrosis in the liver, together with a reduction in pyroptotic, apoptotic and necroptotic death, compared with WT ACLF mice. Notably, GSDM-D-deficient mice also showed decreased liver regeneration and hepatocyte function. This was associated with an increase in senescence and expression of stem-like/cholangiocyte markers in the liver. Interestingly, in the kidney, GSDM-D-deficient mice showed an increase in histopathological damage score, decreased function and increased expression of necroptosis-related genes. In the cerebellum, GSDM-D deficiency increased the expression of neuroinflammation markers, astrocyte activation and apoptosis-related genes.</p><p><strong>Conclusion: </strong>Our data indicate that GSDM-D deficiency has organ-specific effects in ACLF. While it reduces inflammation, neutrophil activation, cell death and fibrosis in the liver, GSDM-D deficiency impairs the synthetic function and increases senescence in hepatocytes. GSDM-D deficiency also increases kidney injury and neuroinflammation in ACLF.</p>","PeriodicalId":72879,"journal":{"name":"eGastroenterology","volume":"3 1","pages":"e100151"},"PeriodicalIF":0.0,"publicationDate":"2025-03-22","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://www.ncbi.nlm.nih.gov/pmc/articles/PMC11934631/pdf/","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"143712457","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":0,"RegionCategory":"","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"OA","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

{"title":"Bacterial dysbiosis and decrease in SCFA correlate with intestinal inflammation following alcohol intoxication and burn injury.","authors":"Caroline J Herrnreiter, Mary Grace Murray, Marisa Luck, Chirag Ganesa, Paulius V Kuprys, Xiaoling Li, Mashkoor A Choudhry","doi":"10.1136/egastro-2024-100145","DOIUrl":"10.1136/egastro-2024-100145","url":null,"abstract":"<p><strong>Background: </strong>Patients intoxicated at the time of burn experience increased rates of sepsis and death compared with that observed in similarly sized burns alone. We sought to characterise changes in the intestinal microbiome and short-chain fatty acids (SCFAs) following alcohol intoxication and burn injury and to determine whether these changes are associated with intestinal inflammation.</p><p><strong>Methods: </strong>10-12-week-old C57BL/6 male and female mice were subjected to ethanol intoxication and a 12.5% total body surface area scald burn injury. The following day, mice were euthanised and faecal contents from the caecum and small intestine (SI) were harvested for 16S sequencing for microbial analysis and caecum contents underwent high-performance liquid chromatography mass spectroscopy to assess SCFAs.</p><p><strong>Results: </strong>The intestinal microbiome of ethanol burn (EB) mice exhibited decreased alpha diversity and distinct beta diversity compared with sham vehicle (SV). EB faeces were marked by increased Proteobacteria and many pathobionts. EB caecum faeces exhibited a significant decrease in butyrate and a downward trend in acetate and total SCFAs. SCFA changes correlated with microbial changes particularly in the SI. Treatment of murine duodenal cell clone-K (MODE-K) cells with faecal slurries led to upregulation of interleukin-6 (IL-6) from EB faeces compared with SV faeces which correlated with levels of Enterobacteriaceae. However, supplementation of butyrate reduced faecal slurry-induced MODE-K cells IL-6 release.</p><p><strong>Conclusion: </strong>Together, these findings suggest that alcohol and burn injury induce bacterial dysbiosis and a decrease in SCFAs, which together can promote intestinal inflammation and barrier disruption, predisposing to postinjury pathology.</p>","PeriodicalId":72879,"journal":{"name":"eGastroenterology","volume":"3 1","pages":"e100145"},"PeriodicalIF":0.0,"publicationDate":"2025-03-14","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://www.ncbi.nlm.nih.gov/pmc/articles/PMC11911813/pdf/","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"143652410","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":0,"RegionCategory":"","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"OA","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

{"title":"Steatosis is not associated with increased risk of chemotherapy-associated liver injury in metastatic colorectal cancer.","authors":"Rebecca Squires, Cameron Blair, Hedvig Karteszi, Pedram Modarres, Chloe Caws, Syamantak Mookherjee, Timothy Robinson, Kushala W Abeysekera","doi":"10.1136/egastro-2024-100157","DOIUrl":"10.1136/egastro-2024-100157","url":null,"abstract":"","PeriodicalId":72879,"journal":{"name":"eGastroenterology","volume":"3 1","pages":"e100157"},"PeriodicalIF":0.0,"publicationDate":"2025-03-07","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://www.ncbi.nlm.nih.gov/pmc/articles/PMC11911809/pdf/","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"143652417","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":0,"RegionCategory":"","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"OA","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

{"title":"Periodontal disease and cirrhosis: current concepts and future prospects.","authors":"David Hudson, Gustavo Ayares, Zahra Taboun, Gurpreet Malhi, Francisco Idalsoaga, Rokhsana Mortuza, Maite Souyet, Carolina Ramirez-Cadiz, Luis Antonio Díaz, Marco Arrese, Juan Pablo Arab","doi":"10.1136/egastro-2024-100140","DOIUrl":"10.1136/egastro-2024-100140","url":null,"abstract":"<p><p>Periodontal diseases are prevalent among the general population and are associated with several systemic conditions, such as chronic kidney disease and type 2 diabetes mellitus. Chronic liver disease and cirrhosis have also been linked with periodontal disease, an association with complex underlying mechanisms, and with potential prognostic implications. Multiple factors can explain this relevant association, including nutritional factors, alcohol consumption, disruption of the oral-gut-liver axis and associated dysbiosis. Additionally, patients with liver disease have been observed to exhibit poorer oral hygiene practices compared with the general population, potentially predisposing them to the development of periodontal disease. Therefore, it is recommended that all patients with liver disease undergo screening and subsequent treatment for periodontal disease. Treatment of periodontal disease in patients with cirrhosis may help reduce liver-derived inflammatory damage, with recent research indicating a potential benefit in terms of reduced mortality. However, further studies on periodontal disease treatment in patients with liver disease are still warranted to determine optimal management strategies. This narrative review describes current concepts on the association between periodontal disease and chronic liver disease.</p>","PeriodicalId":72879,"journal":{"name":"eGastroenterology","volume":"3 1","pages":"e100140"},"PeriodicalIF":0.0,"publicationDate":"2025-02-25","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://www.ncbi.nlm.nih.gov/pmc/articles/PMC11950965/pdf/","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"143756308","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":0,"RegionCategory":"","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"OA","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

{"title":"Attention to the misuse of Mendelian randomisation in medical research.","authors":"Lanlan Chen, Adrien Guillot, Carolin Victoria Schneider","doi":"10.1136/egastro-2025-100187","DOIUrl":"10.1136/egastro-2025-100187","url":null,"abstract":"","PeriodicalId":72879,"journal":{"name":"eGastroenterology","volume":"3 1","pages":"e100187"},"PeriodicalIF":0.0,"publicationDate":"2025-02-25","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://www.ncbi.nlm.nih.gov/pmc/articles/PMC11950933/pdf/","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"143756242","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":0,"RegionCategory":"","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"OA","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

{"title":"Gut cannabinoid receptor 1 regulates alcohol binge-induced intestinal permeability.","authors":"Luca Maccioni, Szabolcs Dvorácskó, Grzegorz Godlewski, Resat Cinar, Malliga R Iyer, Bin Gao, George Kunos","doi":"10.1136/egastro-2024-100173","DOIUrl":"10.1136/egastro-2024-100173","url":null,"abstract":"<p><strong>Background: </strong>Endocannabinoids acting via cannabinoid receptor 1 (CB1R) can elicit increased intestinal permeability (a condition also called 'leaky gut'). Alcohol binge can adversely affect digestive functions, including intestinal permeability; however, the underlying mechanisms remain incompletely understood. The current study aimed at examining whether CB1R is involved in alcohol binge-induced intestinal permeability.</p><p><strong>Methods: </strong>We developed intestinal epithelial-specific CB1R knockout (CB1^IEC-/-) mice and evaluated the <i>in vivo</i> contribution of gut CB1R in alcohol binge-induced intestinal permeability.</p><p><strong>Results: </strong>Alcohol binge increased anandamide levels in the proximal small intestine in association with increased intestinal permeability. Radioligand binding and functional assays confirmed that the genetic deletion of intestinal epithelial CB1R did not alter the density or functionality of CB1R in the brain. Additionally, a peripheral CB1R antagonist, (<i>S</i>)-MRI-1891 (INV-202/monlunabant), exhibited comparable binding affinity to CB1R in brain homogenates. An acute oral administration of (<i>S</i>)-MRI-1891 (3 mg/kg) reduced alcohol binge-induced intestinal permeability in littermate control CB1^f/f (CB1 floxed/floxed) mice but had no effect in CB1^IEC-/- mice, underscoring the role of intestinal CB1R in this phenomenon. Mechanistically, we found that alcohol activated intestinal epithelial CB1R-ERK1/2 pathway with subsequent downregulation of tight junction proteins and reduction in villi length. In addition, targeting intestinal CB1R and downstream ERK1/2 was able to reverse this process, with subsequent upregulation of tight junction proteins and increased villi length, thus improving gut barrier function. Despite the effects on intestinal permeability, deletion of intestinal CB1R did not significantly affect metabolic parameters and liver disease.</p><p><strong>Conclusion: </strong>Our findings suggest that alcohol promotes leaky gut via the activation of gut epithelial CB1R and demonstrate that inhibition of CB1R with peripheral-restricted selective CB1R antagonists can prevent alcohol binge-induced intestinal permeability.</p>","PeriodicalId":72879,"journal":{"name":"eGastroenterology","volume":"3 1","pages":"e100173"},"PeriodicalIF":0.0,"publicationDate":"2025-02-12","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://www.ncbi.nlm.nih.gov/pmc/articles/PMC11927431/pdf/","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"143694568","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":0,"RegionCategory":"","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"OA","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

{"title":"Protein tyrosine phosphatase delta is a STAT3-phosphatase and suppressor of metabolic liver disease.","authors":"Armando Andres Roca Suarez, Frank Jühling, Julien Moehlin, Laurent Mailly, Alessia Virzì, Nicolas Brignon, Sarah C Durand, Marine A Oudot, Eugenie Schaeffer, Romain Martin, Laura Meiss-Heydmann, Charlotte Bach, Zakaria Boulahtouf, Lea Girard, Emma Osswald, Carole Jamey, Daniel Brumaru, Nassim Dali-Youcef, Atish Mukherji, Maria Saez-Palma, Barbara Testoni, Fabien Zoulim, Bhuvaneswari Koneru, Naoto Fujiwara, Yujin Hoshida, Emanuele Felli, Patrick Pessaux, Michel L Tremblay, Romain Parent, Catherine Schuster, Thomas F Baumert, Joachim Lupberger","doi":"10.1136/egastro-2024-100159","DOIUrl":"10.1136/egastro-2024-100159","url":null,"abstract":"<p><strong>Abstract: </strong></p><p><strong>Objective: </strong>Impaired hepatic expression of protein tyrosine phosphatase delta (<i>PTPRD</i>) is associated with increased STAT3 transcriptional activity and reduced survival from hepatocellular carcinoma in patients with chronic hepatitis C virus infection. However, the <i>PTPRD</i>-expressing hepatic cell types, signalling pathways responsive to PTPRD and their role in non-viral liver disease are largely unknown.</p><p><strong>Methods: </strong>We studied <i>PTPRD</i> expression in single-cell and bulk liver transcriptomic data from mice and humans, and established a <i>Ptprd</i>-deficient mouse model for metabolic dysfunction-associated steatohepatitis (MASH). Identified pathways were validated by perturbation studies in human hepatocytes and PTPRD substrates by pull-down assays. The clinical relevance was further explored in a cohort with metabolic disease by ranking patients according to <i>PTPRD</i> expression and analysing its association with metabolic disease markers.</p><p><strong>Results: </strong>The analysis of individuals ranked according to <i>PTPRD</i> expression and <i>Ptprd</i>-deficient mice, showed that <i>PTPRD</i> levels were associated with hepatic glucose/lipid signalling and peroxisome function. Hepatic <i>PTPRD</i> expression is impaired in aetiologies of chronic liver diseases that are associated with metabolic disease. We further validated PTPRD as a STAT3 phosphatase in the liver, acting as a regulator of peroxisomal fatty acid metabolism. During MASH, low PTPRD led to increased liver steatosis in <i>Ptprd</i>+/- mice and a pronounced unfolded protein response, which impacts insulin signalling. Accordingly, silencing of <i>PTPRD</i> blunted insulin-induced AKT phosphorylation. Patients with obesity and low hepatic <i>PTPRD</i> expression exhibit increased levels of metabolic risk factors.</p><p><strong>Conclusion: </strong>Our data revealed an important regulatory role of the hepatic PTPRD-STAT3 axis in maintaining glucose/lipid homeostasis, which is recapitulated in clinical manifestations of metabolic liver disease.</p>","PeriodicalId":72879,"journal":{"name":"eGastroenterology","volume":"3 1","pages":"e100159"},"PeriodicalIF":0.0,"publicationDate":"2025-01-27","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://www.ncbi.nlm.nih.gov/pmc/articles/PMC11927410/pdf/","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"143694569","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":0,"RegionCategory":"","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"OA","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

{"title":"Functional dyspepsia and gastroparesis: are they distinct disorders, a spectrum of diseases or one disease?","authors":"Stella-Maris Egboh, Kerith Duncanson, Michael Potter, Simon Keely, Nicholas J Talley","doi":"10.1136/egastro-2024-100119","DOIUrl":"10.1136/egastro-2024-100119","url":null,"abstract":"<p><p>Functional dyspepsia (FD) and gastroparesis (GP) are clinically managed as distinct upper gastrointestinal conditions but present with symptoms that are often indistinguishable. FD is a common disorder of gut-brain interaction that negatively impacts quality of life, while GP is considered a rare disease exclusively defined by delayed gastric emptying and symptoms. The degree of overlap between these disorders makes them hard to differentiate in clinical practice, thereby impacting treatment decisions. This review is focused on exploring the similarities and differences between FD and GP to guide clinician management and improve treatment outcomes. A comprehensive literature search was performed and the full texts of eligible articles were retrieved for the extraction of information reported in this review. This summary of evidence supports the hypothesis that GP and FD represent two ends of the same disease spectrum in a major subgroup. Improved understanding of the similarities, differences and overlap is likely to help guide the development of objective biomarkers and better-targeted therapies.</p>","PeriodicalId":72879,"journal":{"name":"eGastroenterology","volume":"3 1","pages":"e100119"},"PeriodicalIF":0.0,"publicationDate":"2025-01-23","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://www.ncbi.nlm.nih.gov/pmc/articles/PMC11770444/pdf/","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"143411985","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":0,"RegionCategory":"","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"OA","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

{"title":"Modifiable factors for irritable bowel syndrome: evidence from Mendelian randomisation approach.","authors":"Di Liu, Meiling Cao, Shanshan Wu, Yiwen Jiang, Weijie Cao, Tengfei Lin, Fuxiao Li, Feng Sha, Zhirong Yang, Jinling Tang","doi":"10.1136/egastro-2024-100126","DOIUrl":"10.1136/egastro-2024-100126","url":null,"abstract":"<p><strong>Abstract: </strong></p><p><strong>Background: </strong>The potential modifiable factors influencing irritable bowel syndrome (IBS) have not been thoroughly documented. We aimed to systematically investigate the modifiable factors associated with IBS, while accounting for the impact of unobserved confounders and coexisting disorders.</p><p><strong>Methods: </strong>Genetic correlation and Mendelian randomisation (MR) analyses were integrated to identify potential modifiable factors and coexisting disorders linked to IBS. Subsequently, multiresponse MR (MR²) was employed to further examine these associations. Summary-level genome-wide association data were used. Modifiable factors and coexisting disorders (ie, gastrointestinal and psychiatric disorders) were identified based on evidence from cohort studies and meta-analysis. In all analyses, IBS was the primary outcome, while in the MR² analysis, coexisting disorders were also treated as outcomes alongside IBS.</p><p><strong>Results: </strong>Most identified modifiable factors and coexisting disorders exhibited genetic correlations with IBS. MR analyses revealed strong causation between IBS and multisite chronic pain (OR=2.20, 95% CI 1.82 to 2.66), gastro-oesophageal reflux disease (OR=1.31, 95% CI 1.23 to 1.39), well-being spectrum (OR=0.17, 95% CI 0.13 to 0.21), life satisfaction (OR=0.31, 95% CI 0.25 to 0.38), positive affect (OR=0.30, 95% CI 0.24 to 0.37), neuroticism score (OR=1.20, 95% CI 1.16 to 1.25) and depression (OR=1.50, 95% CI 1.37 to 1.66). Additionally, smoking, alcohol frequency, college or university degree, intelligence, childhood maltreatment, frailty index, diverticular disease of the intestine and schizophrenia were suggestively associated with IBS. Robust associations were found between multisite chronic pain and both IBS and coexisting disorders.</p><p><strong>Conclusions: </strong>Our study identified a comprehensive array of potential modifiable factors and coexisting disorders associated with IBS, supported by genetic evidence, including genetic correlation and multiple MR analyses. The presence of multisite chronic pain may offer a promising avenue for the concurrent prevention of IBS and its coexisting disorders.</p>","PeriodicalId":72879,"journal":{"name":"eGastroenterology","volume":"3 1","pages":"e100126"},"PeriodicalIF":0.0,"publicationDate":"2025-01-20","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://www.ncbi.nlm.nih.gov/pmc/articles/PMC11770431/pdf/","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"143411986","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":0,"RegionCategory":"","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"OA","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

{"title":"Essential roles of the unfolded protein response in intestinal physiology.","authors":"Claudio Hetz, Juan Francisco Silva-Agüero, Lisa M Ellerby","doi":"10.1136/egastro-2024-100129","DOIUrl":"10.1136/egastro-2024-100129","url":null,"abstract":"<p><p>The intestinal epithelium serves as an essential interface between the host and microbiota, regulating innate and adaptive immunity, absorption of nutrients and systemic metabolism, and mediating bidirectional communication with the nervous system. The intestinal epithelium suffers constant challenges to the proteostasis machinery due to its exposure to the dynamically changing and microbial laden lumenal gut environment and to the high secretory demand placed on multiple epithelial cell types to accommodate gut and systemic physiology-especially goblet, enteroendocrine and Paneth cells. In all cases, intestinal cells require an active unfolded protein response (UPR) to sustain their physiological function, the main pathway that monitors and adjusts secretory function changes in the environment. A specialised endoplasmic reticulum (ER) stress sensor uniquely expressed in epithelial cells lining mucosal surfaces, termed inositol-requiring transmembrane kinase/endoribonuclease β, has specific roles in intestinal epithelial homeostasis, regulating mucus production and communication with microbiota. Chronic ER stress or genetic mutations affecting key UPR mediators contribute to the occurrence of inflammatory bowel disease and ulcerative colitis, in addition to colon cancer. Here, we review recent advances linking the UPR and ER stress with gut physiology and intestinal disease. Therapeutic strategies to alleviate ER stress or enforce UPR function to improve intestinal function in ageing and in bowel diseases are also discussed.</p>","PeriodicalId":72879,"journal":{"name":"eGastroenterology","volume":"2 4","pages":"e100129"},"PeriodicalIF":0.0,"publicationDate":"2024-12-31","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://www.ncbi.nlm.nih.gov/pmc/articles/PMC11770430/pdf/","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"143411982","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":0,"RegionCategory":"","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"OA","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}