N6022 attenuates cerebral ischemia/reperfusion injury-induced microglia ferroptosis by promoting Nrf2 nuclear translocation and inhibiting the GSNOR/GSTP1 axis.

Stroke poses a significant risk of mortality, particularly among the elderly population. The pathophysiological process of ischemic stroke is complex, and it is crucial to elucidate its molecular mechanisms and explore potential protective drugs. Ferroptosis, a newly recognized form of programmed cell death distinct from necrosis, apoptosis, and autophagy, is closely associated with the pathophysiology of ischemic stroke. N6022, a selective inhibitor of S-nitrosoglutathione reductase (GSNOR), is a "first-in-class" drug for asthma with potential therapeutic applications. However, it remains unclear whether N6022 exerts protective effects in ischemic stroke, and the precise mechanisms of its action are unknown. This study aimed to investigate whether N6022 mitigates cerebral ischemia/reperfusion (I/R) injury by reducing ferroptosis and to elucidate the underlying mechanisms. Accordingly, we established an oxygen-glucose deprivation/reperfusion (OGD/R) cell model and a middle cerebral artery occlusion/reperfusion (MCAO/R) mouse model to mimic cerebral I/R injury. Our data, both in vitro and in vivo, demonstrated that N6022 effectively protected against I/R-induced brain damage and neurological deficits in mice, as well as OGD/R-induced BV2 cell damage. Mechanistically, N6022 promoted Nrf2 nuclear translocation, enhancing intracellular antioxidant capacity of SLC7A11-GPX4 system. Furthermore, N6022 interfered with the interaction of GSNOR with GSTP1, thereby boosting the antioxidant capacity of GSTP1 and attenuating ferroptosis. These findings provide novel insights, showing that N6022 attenuates microglial ferroptosis induced by cerebral I/R injury through the promotion of Nrf2 nuclear translocation and inhibition of the GSNOR/GSTP1 axis.

Effect of Gut Microbiota-Mediated Tryptophan Metabolism on Inflammaging in Frailty and Sarcopenia.

Frailty syndrome refers to the nonspecific state of increased body vulnerability and decreased antistress and recovery abilities after stress during aging. Sarcopenia is the major component of frailty and is characterized by the gradual loss of muscle mass, strength, and function with age. Inflammaging is the gradual increase in inflammatory status during aging, and it disrupts immune tolerance, causes physiological changes in tissues, organs, and normal cells, and is related to frailty and sarcopenia. The gut microbiota is an extremely complex and diverse microbial community that coevolves with the host. The composition and structure of the gut microbiota and the metabolism of tryptophan (Trp) significantly change in older adults with frailty and sarcopenia. The gut microbiota participates in regulating the Trp metabolic pathways of kynurenine (Kyn), 5-hydroxytryptamine (5-HT), and indole in the gastrointestinal tract. The Trp metabolites derived from the gut microbiota may synergistically promote the occurrence of age-related frailty and sarcopenia by promoting inflammation in the intestines, nervous system, and muscles. The role and mechanisms of the gut microbiota, Trp metabolism, and inflammaging in age-related frailty and sarcopenia may be a worthwhile research direction to help promote healthy aging.

Effects of Aminomethylphosphonic Acid on the Transcriptome and Metabolome of Red Swamp Crayfish, Procambarus clarkii.

Red swamp crayfish, Procambarus clarkii (P. clarkii), is an important model crustacean organism used in many types of research. However, the effects of different doses of aminomethylphosphonic acid (AMAP) on the transcriptome and metabolites of P. clarkii have not been explored. Thus, this study investigated the molecular and metabolic mechanisms activated at the different exposure dosages of AMAP in P. clarkii to provide new insights into the strategies of P. clarkii in response to the high concentrations of AMAP in the environment. In the present study, the P. clarkii were divided into three groups (control group; low-dosage AMAP exposure; high-dosage AMAP exposure), and hepatopancreatic tissue samples were dependently taken from the three groups. The response mechanisms at the different dosages of AMAP were investigated based on the transcriptome and metabolome data of P. clarkii. Differentially expressed genes and differentially abundant metabolites were identified in the distinct AMAP dosage exposure groups. The genes related to ribosome cell components were significantly up-regulated, suggesting that ribosomes play an essential role in responding to AMAP stress. The metabolite taurine, involved in the taurine and hypotaurine metabolism pathway, was significantly down-regulated. P. clarkii may provide feedback to counteract different dosages of AMAP via the upregulation of ribosome-related genes and multiple metabolic pathways. These key genes and metabolites play an important role in the response to AMAP stress to better prepare for survival in high AMAP concentrations.

Therapeutic strategies targeting the NLRP3­mediated inflammatory response and pyroptosis in cerebral ischemia/reperfusion injury (Review).

Ischemic stroke poses a major threat to human health. Therefore, the molecular mechanisms of cerebral ischemia/reperfusion injury (CIRI) need to be further clarified, and the associated treatment approaches require exploration. The NOD­like receptor thermal protein domain associated protein 3 (NLRP3) inflammasome serves an important role in causing CIRI, and its activation exacerbates the underlying injury. Activation of the NLRP3 inflammasome triggers the maturation and production of the inflammatory molecules IL­1ß and IL­18, as well as gasdermin­D­mediated pyroptosis and CIRI damage. Thus, the NLRP3 inflammasome may be a viable target for the treatment of CIRI. In the present review, the mechanisms of the NLRP3 inflammasome in the intense inflammatory response and pyroptosis induced by CIRI are discussed, and the therapeutic strategies that target the NLRP3­mediated inflammatory response and pyroptosis in CIRI are summarized. At present, certain drugs have already been studied, highlighting future therapeutic perspectives.

Commensal Enterococcus faecalis W5 ameliorates hyperuricemia and maintains the epithelial barrier in a hyperuricemia mouse model.

OBJECTIVE: The intestine is responsible for approximately one-third of uric acid (UA) excretion. The effect of commensal Enterococcus faecalis (E. faecalis), one of the most colonized bacteria in the gut, on UA excretion in the intestine remains to be investigated. The aim of this study was to evaluate the effect of commensal E. faecalis on UA metabolism and gut microbiota. METHODS: The 16S rRNA gene sequencing was used to examine the species of Enterococcus in mouse fecal content. E. faecalis strain was isolated from mouse feces and identified to be E. faecalis W5. The hyperuricemia (HUA) animal model was established with yeast-rich forage and 250 mg·kg-1 ·day-1 potassium oxonate. Oral administration of E. faecalis W5 was given for 20 days, serving as the Efa group. RESULTS: Disrupted intestinal barrier, activated proinflammatory response and low UA excretion in the intestine were found in HUA mice. After E. faecalis W5 treatment, the gut barrier was restored and serum UA level was decreased. Additionally, fecal and intestinal UA levels were elevated, intestinal urate transporter ABCG2 and purine metabolism were upregulated. Moreover, short-chain fatty acid levels were increased, and intestinal inflammation was ameliorated. CONCLUSIONS: Commensal E. faecalis W5 ameliorated HUA through reversing the impaired gut barrier, promoting intestinal UA secretion by regulating ABCG2 expression, and decreasing intestinal UA synthesis by regulating purine metabolism. The results may provide the potential for developing treatments for HUA through the intestine.

Tumor-Derived Exosomal LINC01480 Upregulates VCAM1 Expression by Acting as a Competitive Endogenous RNA of miR-204-5p to Promote Gastric Cancer Progression.

Exosomes are a type of cell-derived vesicles that range in size from 30 to 100 nm. They are widely present in various organisms and participate in diverse biological processes, playing crucial roles in tumorigenesis and progression. This study aimed to investigate whether LINC01480 in tumor-derived exosomes is involved in the molecular mechanism of gastric cancer by competitively upregulating the VCAM1 expression through binding miR-204-5p. The study analyzed transcriptome data related to gastric cancer from the cancer genome atlas database and constructed a risk-scoring model for epithelial-mesenchymal transition (EMT)-related lncRNAs to identify eight EMT-related lncRNAs associated with prognosis. EMT-related mRNAs positively correlated with LINC01480 were screened in the ExoRBase database. In vitro cell experiments showed that exosomal LINC01480 can promote the proliferation, migration, invasion, and EMT of gastric cancer cells by upregulating VCAM1 expression through competitive binding with miR-204-5p. In vivo experiments on nude mice showed that exosomal LINC01480 promotes the development of gastric cancer. These results suggest that exosomal LINC01480 could be a potential therapeutic target for gastric cancer.

Glutamine addiction and therapeutic strategies in pancreatic cancer.

Pancreatic cancer remains one of the most lethal diseases worldwide owing to its late diagnosis, early metastasis, and poor prognosis. Because current therapeutic options are limited, there is an urgent need to investigate novel targeted treatment strategies. Pancreatic cancer faces significant metabolic challenges, principally hypoxia and nutrient deprivation, due to specific microenvironmental constraints, including an extensive desmoplastic stromal reaction. Pancreatic cancer cells have been shown to rewire their metabolism and energy production networks to support rapid survival and proliferation. Increased glucose uptake and glycolytic pathway activity during this process have been extensively described. However, growing evidence suggests that pancreatic cancer cells are glutamine addicted. As a nitrogen source, glutamine directly (or indirectly via glutamate conversion) contributes to many anabolic processes in pancreatic cancer, including amino acids, nucleobases, and hexosamine biosynthesis. It also plays an important role in redox homeostasis, and when converted to α-ketoglutarate, glutamine serves as an energy and anaplerotic carbon source, replenishing the tricarboxylic acid cycle intermediates. The present study aims to provide a comprehensive overview of glutamine metabolic reprogramming in pancreatic cancer, focusing on potential therapeutic approaches targeting glutamine metabolism in pancreatic cancer.

Comparative analysis of e-cigarette prevalence and influencing factors among adolescents in Jiangsu Province, China.

Objective: The objectives of this study were to investigate electronic cigarette (e-cigarette) and cigarette use in Jiangsu Province, China, by analyzing the two-year trends of e-cigarette using and to explore the factors influencing the experimentation and use of e-cigarettes. Methods: We conducted a cross-sectional study following the standard methodology of the Global Youth Tobacco Survey in 2019 and 2021. A three-stage cluster sampling design was applied. Eighty-two schools in 14 districts (counties) in Jiangsu Province were surveyed. All computations were performed using the SPSS 21.0 complex samples procedure. Multivariate logistic regression was used to explore the factors influencing e-cigarette experimentation and use. Results: A total of 12,410 and 12,880 students were surveyed in 2019 and 2021, respectively. E-cigarette experimentation increased from 9.34% in 2019 to 13.07% in 2021 (P < 0.001). E-cigarette use increased from 2.23% in 2019 to 3.74% in 2021 (P < 0.001). The main factors associated with e-cigarette use were cigarette experimentation (OR = 2.700, P < 0.001); male gender (OR = 1.416, P = 0.011); junior high school students (OR = 1.551, P = 0.005) and vocational high school students (OR = 1.644, P = 0.001); more pocket money per week (OR1 = 1.214, P = 0.187; OR2 = 1.686, P = 0.001); exposure to second-hand smoke (SHS) at home (OR = 1.239, P < 0.001); exposure to e-cigarette advertising (OR = 1.855, P < 0.001); believe SHS is harmful (OR = 0.933, P = 0.026); closest friends smoking (OR = 2.501, P < 0.001); believe smoking makes youth look more attractive (OR1 = 1.469, P = 0.040; OR2 = 1.305, P = 0.049); believe tobacco helps youth feel more comfortable in social situations (OR1 = 2.161, P < 0.001; OR2 = 1.635, P = 0.001); will use an e-cigarette product if offered by best friends (OR = 1.322, P < 0.001); intend to use an e-cigarette product in the next 12 months (OR = 1.486, P < 0.001). Conclusion: E-cigarette use among adolescents has been on the rise in recent years. E-cigarette use is associated with past cigarette use and a strong desire to smoke. It is crucial to take health education and tobacco control efforts to reduce adolescents' e-cigarette use rate.

Application of artificial intelligence in endoscopic gastrointestinal tumors.

With an increasing number of patients with gastrointestinal cancer, effective and accurate early diagnostic clinical tools are required provide better health care for patients with gastrointestinal cancer. Recent studies have shown that artificial intelligence (AI) plays an important role in the diagnosis and treatment of patients with gastrointestinal tumors, which not only improves the efficiency of early tumor screening, but also significantly improves the survival rate of patients after treatment. With the aid of efficient learning and judgment abilities of AI, endoscopists can improve the accuracy of diagnosis and treatment through endoscopy and avoid incorrect descriptions or judgments of gastrointestinal lesions. The present article provides an overview of the application status of various artificial intelligence in gastric and colorectal cancers in recent years, and the direction of future research and clinical practice is clarified from a clinical perspective to provide a comprehensive theoretical basis for AI as a promising diagnostic and therapeutic tool for gastrointestinal cancer.

Effects of Behavioral Interventions for Salt Reduction on Blood Pressure and Urinary Sodium Excretion: A Systematic Review and Meta-Analysis of Randomized Controlled Trials.

Hypertension is a prevalent cardiovascular condition, with excessive sodium intake being a significant risk factor. Various studies have investigated measures to reduce salt intake, including integrated lifestyle interventions and health education. However, the effectiveness of behavioral interventions focused solely on salt reduction remains unclear. This systematic review and meta-analysis aimed to investigate the effects of a behavioral intervention based on salt reduction on blood pressure and urinary sodium excretion. A comprehensive search of the Cochrane Central Register of Controlled Trials, EMBASE, PubMed, and Web of Science was conducted to identify relevant literature. Study and intervention characteristics were extracted for descriptive synthesis, and the quality of the included studies was assessed. A total of 10 studies, comprising 4,667 participants (3,796 adults and 871 children), were included. The interventions involved the provision of salt-restriction spoons or devices, salt-reduction education, self-monitoring devices for urinary sodium, and salt-reduction cooking classes. Meta-analysis results showed that behavioral interventions focused on salt reduction significantly reduced systolic blood pressure (SBP) (-1.17 mmHg; 95% CI, -1.86 to -0.49), diastolic blood pressure (DBP) (-0.58 mmHg; 95% CI, -1.07 to -0.08) and urinary sodium excretion (-21.88 mmol/24 hours; 95% CI, -32.12 to -11.64). These findings suggest that behavioral change interventions centered on salt reduction can effectively lower salt intake levels and decrease blood pressure levels. However, to enhance effectiveness, behavioral interventions for salt reduction should be combined with other salt-reduction strategies.

A practical nomogram included hyperlipidemia for predicting lymph node metastasis in patients with superficial esophageal squamous cell carcinoma.

To select an optimal treatment, it is crucial to evaluate the risk of lymph node metastasis (LNM) in patients with superficial esophageal squamous cell carcinoma (SESCC). The research aimed to explore more risk factors than before and construct a practical nomogram to predict LNM in patients with SESCC. We retrospectively reviewed 1080 patients diagnosed with esophageal cancer who underwent esophagectomy with lymphadenectomy between January 2013 and October 2021 at the Affiliated Hospital of Qingdao University. The clinical parameters, endoscopic features, and pathological characteristics of the 123 patients that were finally enrolled in this study were collected. The independent risk factors for LNM were determined using univariate and multivariate analyses. Using these factors, a nomogram was constructed to predict LNM. LNM was observed in 21 patients. Univariate analysis showed that the absence or presence of hypertriglyceridemia, tumor location, lesion size, macroscopic type, invasion depth, differentiation, absence or presence of lymphovascular invasion (LVI), and perineural invasion were significantly associated with LNM. According to the multivariate analysis, hypertriglyceridemia, tumors located in the lower thoracic esophagus, lesion size > 20 mm, submucosal invasion, and LVI were independent risk factors for LNM. A nomogram was established using these 5 factors. It showed good calibration and discrimination. Hypertriglyceridemia, tumors located in the lower thoracic esophagus, lesion size > 20 mm, submucosal invasion, and LVI were independent risk factors for LNM. A nomogram was constructed using these 5 factors. This model can help clinicians assess the risk of LNM in patients with SESCC for optimal treatment selection.

Gut microbiota causally affects cholelithiasis: a two-sample Mendelian randomization study.

Background: The gut microbiota is closely linked to cholesterol metabolism-related diseases such as obesity and cardiovascular diseases. However, whether gut microbiota plays a causal role in cholelithiasis remains unclear. Aims: This study explored the causal relationship between gut microbiota and cholelithiasis. We hypothesize that the gut microbiota influences cholelithiasis development. Methods: A two-sample Mendelian randomization method was combined with STRING analysis to test this hypothesis. Summary data on gut microbiota and cholelithiasis were obtained from the MiBioGen (n=13,266) and FinnGen R8 consortia (n=334,367), respectively. Results: Clostridium senegalense, Coprococcus3, and Lentisphaerae increased the risk of cholelithiasis and expressed more bile salt hydrolases. In contrast, Holdemania, Lachnospiraceae UCG010, and Ruminococcaceae NK4A214 weakly expressed bile salt hydrolases and were implied to have a protective effect against cholelithiasis by Mendelian randomization analysis. Conclusion: Gut microbiota causally influences cholelithiasis and may be related to bile salt hydrolases. This work improves our understanding of cholelithiasis causality to facilitate the development of treatment strategies.

Effect of fucoidan on gut microbiota and its clinical efficacy in Helicobacter pylori eradication: A randomized controlled trial.

OBJECTIVE: To assess the clinical efficacy of fucoidan-assisted standard quadruple therapy (SQT) in Helicobacter pylori (H. pylori) eradication and the improvement of gut microbiota. METHODS: An open-label randomized controlled trial was conducted at the Affiliated Hospital of Qingdao University in Shandong Province, China. Ninety patients who tested positive for H. pylori were randomized to the standard quadruple therapy (SQT) group (SQ), SQT + fucoidan combination group (SF), and fucoidan + sequential SQT group (FS), respectively. Stool samples were collected for gut microbiota composition at baseline and after treatment. RESULTS: After H. pylori eradication, the relative abundances of most conditional pathogens in the SQ decreased, while those of several beneficial bacteria increased or decreased (P < 0.05). In FS, the abundances of most beneficial bacteria increased gradually from baseline to week 12, while those of the conditional pathogens decreased (P < 0.05). The abundance of Bifidobacterium had a decreasing trend in SQ, but remained unchanged in SF and increased in FS (P < 0.05). The abundances of most beneficial bacteria were significantly higher in FS than in SQ and SF (P < 0.05). Addition of fucoidan enhanced symptom improvement during H. pylori eradication compared with SQT alone. CONCLUSIONS: Fucoidan considerably improved gut dysbiosis during SQT for H. pylori eradication. Gut microbiota can be maintained by the addition of fucoidan before eradication therapy with SQT rather than by concomitant addition with therapy. Fucoidan-assisted SQT could relieve gastrointestinal symptoms during H. pylori eradication.

Characteristic analysis of early gastric cancer after Helicobacter pylori eradication: a multicenter retrospective propensity score-matched study.

BACKGROUND: Helicobacter pylori (H. pylori) is recognized as a type I carcinogen in gastric cancer (GC). However, GC still occurs after H. pylori eradication, and its diagnosis is more complicated. This study aimed to summarize the characteristics of early GC (EGC) after H. pylori eradication to help accurately identify EGC and avoid missed diagnosis and misdiagnosis. METHODS: A total of 81 patients of EGC after H. pylori eradication (Hp-eradicated group), resected by endoscopic submucosal dissection (ESD), and 105 cases of H. pylori infection-related EGC (control group) were assessed. After propensity-score matching, the clinical characteristics, endoscopic manifestations, and histopathological features of the 62 matched patients in each group were analyzed. We also conducted specific analyses in combination with endoscopic and histopathological images. RESULTS: There were more patients in the Hp-eradicated group who received proton pump inhibitor (PPI) for >1 year compared to the control group (p < 0.001). More patients at OLGA stages I-II before the diagnosis of EGC were in the control group (p = 0.045), especially at stage II. The mucosa in the Hp-eradicated group showed more moderate-to-severe atrophy (p = 0.047), map-like redness (p < 0.001) and mild activity (p < 0.001). The predominant histopathological types differed between the two groups (p < 0.001), and the majority of cases in the Hp-eradicated group were high-grade intraepithelial neoplasia (HGIN). Ki-67 expression was lower in the Hp-eradicated group (p = 0.025). But different eradication intervals of H. pylori have little effect on the characteristics of EGC. Furthermore, PPI uses for >1 year (p = 0.005), mucosal map-like redness (p < 0.001), moderate mucosal atrophy (p = 0.017), and mild activity of gastric mucosa (p = 0.005) were independent characteristics of EGC after H. pylori eradication. CONCLUSION: Our multicenter study revealed that EGC after H. pylori eradication was characterized by long-term PPI use, moderate mucosal atrophy, mucosal map-like redness, the mild activity of gastric mucosa, a higher proportion of HGIN cases, and lower levels of Ki-67.

EGC after H. pylori eradication was characterized by long-term PPI use, moderate mucosal atrophy, mucosal map-like redness, mild activity of gastric mucosa, a higher proportion of HGIN cases, and lower levels of Ki-67.H. pylori-positive patients at OLGA stages I-II are also more likely to progress to EGC.According to the current data, different eradication intervals of H. pylori have little effect on the characteristics of EGC.

Titin as a potential novel therapeutic target in colorectal cancer.

Colorectal cancer (CRC) is identified as a primary cause of death around the world. The current chemotherapies are not cost-effective. Therefore, finding novel potential therapeutic target is urgent. Titin (TTN) is a muscle protein that is critical in hypertrophic cardiomyopathy. However, its role in CRC is not well understood. The study focused on exploring the possible role of TTN in CRC carcinogenesis. TTN mRNA and protein expression levels presented an obvious downregulation in CRC tissue samples, relative to normal control (p < 0.05). TTN expression significantly correlated with the clinical stage (normal vs. Stage 1, p < 0.05; normal vs. Stage 4, p < 0.05), node metastasis (normal vs. N1, p < 0.05; N1 vs. N2, p < 0.05), histological type (normal vs. adenocarcinoma, p < 0.05), race (Caucasian vs. Asian, p < 0.05; African-American vs. Asian, p < 0.05) and TP53 mutation (normal vs. TP53 mutation, p < 0.05), considering The Cancer Genome Atlas database. However, for patients who had higher TTN expression, the overall survival was remarkably shorter than patients who had low TTN expression. Furthermore, TTN was lowly expressed in four CRC cell lines. TTN overexpression facilitated CRC cells in terms of the proliferation, metastasis and invasion. Based on gene set enrichment analysis, the ERB pathway might be responsible for TTN-related CRC. Besides, TTN was involved in the response to azacitidine. Overall, TTN might serve as a potential novel therapeutic target for treating and overcoming chemotherapy resistance in CRC.

Fecal microbial biomarkers in older adults with autoimmune diseases.

Aim: To analyze the alterations in the fecal microbiota of older adults with autoimmune disease and determine the diagnostic capabilities of microbial biomarkers. Methods: The raw data of fecal samples from 444 older adults from the publicly available American Gut Project database was analyzed. Results: It was found that there were no significant differences in the microbiota richness and evenness between older adults with autoimmune disease and healthy controls. However, significant differences were observed in the microbiota composition and structure. The subject operating characteristic curve of the eight key microbiota was obtained, and the area under curve value was 70.0%. Conclusion: Older adults with autoimmune disease showed changes in intestinal microbiota composition, which can be used as microbial biomarkers.

Update on diagnosis and treatment of early signet-ring cell gastric carcinoma: A literature review.

Gastric signet-ring cell gastric carcinoma (GSRC) is an unfavorable subtype of gastric cancer (GC) that presents with greater invasiveness and poorer prognosis in advanced stage than other types of GC. However, GSRC in early stage is often considered an indicator of less lymph node metastasis and more satisfying clinical outcome compared to poorly differentiated GC. Therefore, the detection and diagnosis of GSRC at early stage undoubtedly play a crucial role in the management of GSRC patients. In recent years, technological advancement in endoscopy including narrow-band imaging and magnifying endoscopy has significantly improved the accuracy and sensitivity of the diagnosis under endoscopy for GSRC patients. Researches have confirmed that early stage GSRC that meets the expanded criteria of endoscopic resection showed comparable outcomes to surgery after receiving endoscopic submucosal dissection (ESD), indicating that ESD could be considered standard treatment for GSRC after thorough selection and evaluation. This article summarizes the current knowledge and updates pertaining to the endoscopic diagnosis and treatment of early stage signet-ring cell gastric carcinoma.

Immune cells and immune cell-targeted therapy in chronic pancreatitis.

In recent years, studies have attempted to understand the immune cells and mechanisms underlying the pathogenesis of chronic pancreatitis (CP) by constructing a model of CP. Based on these studies, the innate immune response is a key factor in disease pathogenesis and inflammation severity. Novel mechanisms of crosstalk between immune and non-immune pancreatic cells, such as pancreatic stellate cells (PSC), have also been explored. Immune cells, immune responses, and signaling pathways in CP are important factors in the development and progression of pancreatitis. Based on these mechanisms, targeted therapy may provide a feasible scheme to stop or reverse the progression of the disease in the future and provide a new direction for the treatment of CP. This review summarizes the recent advances in research on immune mechanisms in CP and the new advances in treatment based on these mechanisms.

The behavior between fluid and structure from coupling system of bile, bile duct, and polydioxanone biliary stent: A numerical method.

The performance and effects of 12 different structures of stents in the bile duct were compared and used the finite element method. Numerical models of the 12 kinds of fluid-structure interaction(FSI) coupling systems were established to investigate the relationship between three aspects (velocity distribution of bile, wall shear stress (WSS) distribution of bile, and Von Mises Stress(VMS) distribution on the stent and bile duct) and the structural parameters of the stent (monofilament diameter and the number of braiding heads). After calculating and analyzing the simulation results yielding distributions of velocity, WWS, and VMS and regions of bile duct susceptibility to stenosis, they were consistent with previous findings on the locations of restenosis occurring after stent removal, indicating that the simulation results could provide a useful reference for studying biliary stents. The results of the simulations showed that (i) eddy currents were prone to occur at the stent ends regions; (ii) the WSS distribution of the bile fluid in contact with the stent and bile duct related to the stent structure; (iii) the high VMS on the stent and bile duct was prone to occur at the stent ends. The simulation results of 12 FSI coupling systems were studied and two superior stent model structures were obtained by comprehensive evaluation.

Ruptured small pancreaticoduodenal artery aneurysm-clinical features similar to pancreatitis: A case report.

BACKGROUND: Pancreaticoduodenal artery aneurysm (PDAA) is rare and has high rupture risks. PDAA rupture has a wide range of clinical symptoms, including abdominal pain, nausea, syncope, and hemorrhagic shock, which is difficult to differentiate from other diseases. PATIENT CONCERNS: A 55-year-old female patient was admitted to our hospital due to abdominal pain for 11 days. DIAGNOSIS: Acute pancreatitis was initially diagnosed. The patient's hemoglobin decreased compared to before admission, suggesting that active bleeding may occur. CT volume diagram and maximum intensity projection diagram show that a small aneurysm with a diameter of about 6 mm can be seen at the pancreaticoduodenal artery arch. The patient was diagnosed with a rupture and hemorrhage of the small pancreaticoduodenal aneurysm. INTERVENTIONS: Interventional treatment was performed. After the microcatheter was selected for the branch of the diseased artery for angiography, the pseudoaneurysm was displayed and embolized. OUTCOMES: The angiography showed that the pseudoaneurysm was occluded, and the distal cavity was not redeveloped. CONCLUSION: The clinical manifestations of PDAA rupture were significantly correlated with the aneurysm diameter. Because of small aneurysms, the bleeding is limited around the peripancreatic and duodenal horizontal segments, accompanied by abdominal pain, vomiting, and elevated serum amylase, similar to the clinical manifestations of acute pancreatitis but accompanied by the decrease of hemoglobin. This will help us to improve our understanding of the disease, avoid misdiagnosis, and provide the basis for clinical treatment.