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Abstract Background This study aims to evaluate the clinical efficacy of pancreatic duct stenting in the treatment of SAP, providing reference for clinical diagnosis and treatment. Methods A retrospective analysis was conducted on clinical data from patients with SAP admitted to the General Hospital of Ningxia Medical University from June 1, 2019 to December 31, 2022. A total of 51 patients were included (33 males, 18 females). Patients were divided into two groups based on treatment: the control group (n = 28) receiving conventional treatment and the stent group (n = 23) undergoing pancreatic duct stenting in addition to conventional treatment. Data collected and analyzed include demographic information, rates of late local complications, late surgical interventions, new-onset OF, infected pancreatic necrosis and new-onset systemic complications. Specific outcomes measured were incidences of new-onset respiratory, renal and circulatory failure, single and multiple OF, sepsis, ACS, abdominal hypertension, and pancreatogenic encephalopathy, as well as use of ≥ 3 types of antibiotics, time of antibiotic use, time of analgesic administration, oral refeeding, length of hospital stay, ICU care, and length of ICU stay. These indicators were used to assess the therapeutic efficacy of pancreatic duct stenting. Results All 23 patients in the stent group successfully underwent stenting. The incidence of new-onset OF and new-onset systemic complications was significantly lower in the stent group compared to the control group (χ2 = 4.96, 6.65, P 0.05). Notably, two patients in the control group required additional procedures due to inadequate drainage, with one undergoing endoscopic debridement and the other, laparotomy. Mortality rates were 3 (10.7%) in the control group and 4 (17.4%) in the stent group, with no statistically significant difference (P > 0.05). Furthermore, significant differences were noted in new-onset respiratory failure, single OF, sepsis, abdominal hypertension, time of analgesic administration, oral refeeding, length of enzyme inhibitor use, and hospitalization expenses (χ2 = 3.94, 4.37, 5.79, 4.79; Z = − 2.008, − 4.176, − 4.165, − 2.309; P 0.05). Conclusions Pancreatic duct stenting effectively reduces the incidence of new-onset systemic complications and OF in SAP, preventing further deterioration. Pancreatic duct stenting can alleviate symptoms, shorten oral refeeding, and promote patient recovery. Trial registration: This study was recorded as a single-center, retrospective case–control study (ChiCTR1900025833).

Acute biliary pancreatitis (ABP) is an acute inflammatory reaction that occurs as a result of abnormal reflux of bile into the pancreatic duct, which activates pancreatic digestive enzymes to produce pancreatic auto-digestion. Objectives: To explore the advantages of Endoscopic Retrograde Cholangiopancreatography (ERCP) treatment compared with laparoscopic surgery in the management of patients with mild and moderately severe ABP, and to study the risk factors for recurrence of ABP and construct a risk prediction model to assist in resolving clinical decision-making and improving prognosis. Methods: Patients with mild and moderately severe ABP treated at General Hospital of Ningxia Medical University from January 1, 2019 to July 1, 2022 were reviewed. A total of 327 patients were enrolled according to the inclusion criteria and exclusion criteria. According to the different treatment modalities, they were divided into the group treated via ERCP (n = 239) and the group treated via laparoscopic surgery (n = 88). Statistical analyses were performed to compare the differences between the average levels of preoperative and postoperative blood routine and blood biochemical indexes, as well as the time of recovery from clinical symptoms, length of hospital stay, and postoperative complications between the two groups of patients. The 280 patients who participated in the follow-up were divided into the recurrence group (n = 130) and the non-recurrence group (n = 150) according to whether they had recurrence or not. Independent samples t-test and binary logistic regression were used to analyze the causative monofactors and risk factors of recurrent biliary pancreatitis, and then to construct the model and assess the predictive accuracy of the model. Results: On postoperative day 2, the incidence of local complications, Balthazar CT score, and the number of analgesia were lower in the patients in the group treated by ERCP than in the group treated by laparoscopic surgery (P

Abstract Background This study aimed to investigate the feasibility, effectiveness, and safety of pancreatic duct stenting in managing acute biliary pancreatitis (ABP) necessitating endoscopic retrograde cholangiopancreatography (ERCP). It further aimed to provide valuable insights for subsequent clinical diagnosis and treatment. Methods This research employs an observational retrospective case–control study design, encompassing patients with ABP who underwent ERCP at the hepatobiliary surgery department of the General Hospital of Ningxia Medical University between August 1, 2018, and December 31, 2020. A total of 229 cases were screened based on inclusion and exclusion criteria. Regardless of ABP severity, patients were categorized into the stent group (141) and the non-stent group (88). Changes in blood amylase (Amy), lipase (LIP), leukocyte count (WBC), total bilirubin (TBIL), alanine aminotransferase (ALT), hematocrit (HCT), and creatinine (CR) were compared between the two groups. Moreover, variables such as recovery time for oral feeding, hospitalization duration, hospitalization costs, local complications, systemic complications, and new organ failure were recorded to assess the therapeutic effect of pancreatic duct stenting. Results No significant differences were observed in gender, age, Acute Physiology and Chronic Health Evaluation (APACHE) II score, ABP severity grade, organ failure (OF), cholangitis, or biliary obstruction between the pancreatic stent and non-stent groups (P > 0.05). There was no significant difference in the incidence of complications related to acute pancreatitis between the two groups (P > 0.05). The median fasting and hospitalization times of patients in the stent group were significantly shorter than those in the non-stent group (P 0.05). There were no significant variations in white blood cell (WBC) count, TBIL, ALT, and creatinine (Cr) at admission, 72 h, and in the differences between the two groups (P > 0.05). The levels of Amy at admission and 72 h in the stent group were significantly higher than those in the non-stent group (P 0.05), the mean 72-h HCT in the stent group was 38.39% (95% confidence interval [CI] 37.82%–38.96%) was lower than that in the non-stent group (39.44%, 95% CI 38.70–40.17%) (P

ObjectiveThis study aims to retrieve, evaluate, and summarize domestic and foreign evidence on the prevention and treatment of embolism syndrome following transcatheter arterial chemoembolization (TACE) for primary liver cancer and to provide an evidence-based foundation for clinical practice.MethodsUtilizing the “6S” model, we conducted a systematic search of UpToDate, BMJ Best Practice, domestic and foreign guidelines, and related databases on the prevention and treatment of embolism syndrome following TACE for primary liver cancer. This search included clinical decision-making, guidelines, systematic reviews, evidence summaries, randomized controlled trials, and expert consensus. The search time frame extended from January 1, 2013 to May 1, 2023. Evidence was synthesized after an independent review of the included studies by two investigators.ResultsA total of 11 articles were included in the analysis, comprising one clinical decision-making article, three clinical guidelines, six expert consensus articles, and one randomized controlled trial. We summarized 31 pieces of evidence across three categories: preoperative preparation, intraoperative interventions, and postoperative symptom management.ConclusionThis study presents a comprehensive summary of the best available evidence on the prevention and treatment of embolism syndrome following TACE for primary liver cancer. These findings can serve as a valuable reference for clinical practitioners, enabling nurses to deliver individualized care based on the symptoms and specific needs of liver cancer patients.Systematic review registrationhttp://ebn.nursing.fudan.edu.cn, identifier ES20232398.

Abstract Background The expression of cytoplasmic poly (A) binding protein‐1 (PABPC1) has been reported in multiple cancer types. This protein is known to modulate cancer progression. However, the effects of PABPC1 expression in pancreatic adenocarcinoma (PAAD) have not been investigated. Here, we investigate the regulatory targets and molecular mechanisms of PABPC1 in PAAD. Methods PABPC1 and collagen type XII α1 chain (COL12A1) expression in PAAD and their role in tumor prognosis and tumor stage were investigated using The Cancer Genome Atlas database analysis. After silencing PABPC1, messenger RNA sequencing and Gene Ontology (GO) and Kyoto Encyclopedia of Genes and Genomes (KEGG) analyses were performed. The expression of differentially expressed genes (DEGs), cell viability, apoptosis, and cell migration and invasion were explored using reverse transcription‐quantitative polymerase chain reaction, Cell Counting Kit‐8 assay, flow cytometry assay, and transwell assay, respectively. The relationship between PABPC1 and COL12A1 expression was assessed by Pearson's correlation analysis. The regulatory function of COL12A1 in PABPC1‐affected BXPC3 cell behavior was studied after COL12A1 was overexpressed. Results PABPC1 and COL12A1 expression was upregulated in patients with PAAD and was linked to poor prognosis. Four hundred and seventy‐four DEGs were observed in BXPC3 cells after PABPC1 silencing. GO and KEGG analyses revealed that the top 10 DEGs were enriched in cell adhesion pathways. Additionally, PABPC1 silencing inhibited cell viability, migration, and invasion and accelerated apoptosis in BXPC3 cells. PABPC1 silencing increased AZGP1 and ARHGAP30 expression and decreased CAV1 and COL12A1 expression in BXPC3 cells. PABPC1 positively mediated COL12A1 expression, whereas PABPC1 knockdown induced the inhibition of BXPC3 cell proliferation, migration, and invasion. Conclusion The results of this study indicate that PABPC1 may function as a tumor promoter in PAAD, accelerating BXPC3 cell proliferation and metastasis by regulating COL12A1 expression.

BackgroundAngiostrongylus cantonensis (A. cantonensis), is a food-borne zoonotic parasite that can cause central nervous system (CNS) injury characterized by eosinophilic meningitis. However, the pathogenesis of angiostrongylosis remains elusive. Natural killer cells (NK cells) are unique innate lymphocytes important in early defense against pathogens. The aim of this study was to investigate the role of NK cells in A. cantonensis infection and to elucidate the key factors that recruit NK cells into the CNS.MethodsMouse model of A. cantonensis infection was established by intragastric administration of third-stage larvae. The expression of cytokines and chemokines at gene and protein levels was analyzed by qRT-PCR and ELISA. Distribution of NK cells was observed by immunohistochemistry and flow cytometry. NK cell-mediated cytotoxicity against YAC-1 cells was detected by LDH release assay. The ability of NK cells to secrete cytokines was determined by intracellular flow cytometry and ELISA. Depletion and adoptive transfer of NK cells in vivo was induced by tail vein injection of anti-asialo GM1 rabbit serum and purified splenic NK cells, respectively. CX3CL1 neutralization experiment was performed by intraperitoneal injection of anti-CX3CL1 rat IgG.ResultsThe infiltration of NK cells in the CNS of A. cantonensis-infected mice was observed from 14 dpi and reached the peak on 18 and 22 dpi. Compared with uninfected splenic NK cells, the CNS-infiltrated NK cells of infected mice showed enhanced cytotoxicity and increased IFN-γ and TNF-α production ability. Depletion of NK cells alleviated brain injury, whereas adoptive transfer of NK cells exacerbated brain damage in A. cantonensis-infected mice. The expression of CX3CL1 in the brain tissue and its receptor CX3CR1 on the CNS-infiltrated NK cells were both elevated after A. cantonensis infection. CX3CL1 neutralization reduced the percentage and absolute number of the CNS-infiltrated NK cells and relieved brain damage caused by A. cantonensis infection.ConclusionsOur results demonstrate that the up-regulated CX3CL1 in the brain tissue recruits NK cells into the CNS and aggravates brain damage caused by A. cantonensis infection. The findings improve the understanding of the pathogenesis of angiostrongyliasis and expand the therapeutic intervention in CNS disease.

BACKGROUND: 2,4,6-Trichlorophenol (TCP), 2,4,6-tribromophenol (TBP) and 2,4,6-triiodophenol (TIP) are three widely detected trihalophenolic disinfection by-products (DBPs). Previous studies have mainly focused on the carcinogenic risk and developmental toxicity of 2,4,6-trihalophenols. Very little is known about their immunotoxicity in mammals. OBJECTIVES: We investigated the effects of 2,4,6-trihalophenols on mammalian immunity using a mouse macrophage model infected with bacteria or intracellular parasites and aimed to elucidate the underlying mechanisms from an epitranscriptomic perspective. The identified mechanisms were further validated in human peripheral blood mononuclear cells (PBMCs). METHODS: The mouse macrophage cell line RAW264.7 and primary mouse peritoneal macrophages were exposed to different concentrations of TCP, TBP, and TIP. The pro-inflammatory marker Ly6C, the survival of the bacterium Escherichia coli (E. coli), and the parasite burden of Toxoplasma gondii (T. gondii) were assessed. Furthermore, the global gene expression profiling of macrophages following exposure to 2,4,6-trihalophenols was obtained through RNA-sequencing (RNA-seq). The effects of 2,4,6-trihalophenols on RNA 푁[sup 6]-methyladenosine (m[sup 6]A) methyltransferases and total RNA m[sup 6]A levels were evaluated using Western blotting and dot blot, respectively. Transcriptome-wide m[sup 6]A methylome was analyzed by m[sup 6]A-seq. In addition, expression of m[sup 6]A regulators and total RNA m[sup 6]A levels in human PBMCs exposed to 2,4,6-trihalophenols were detected using quantitative reverse transcriptase polymerase chain reaction and dot blot, respectively. RESULTS: Mouse macrophages exposed to TCP, TBP, or TIP had lower expression of the pro-inflammatory marker Ly6C, with a greater difference from control observed for TIP-exposed cells. Consistently, macrophages exposed to such DBPs, especially TIP, were susceptible to infection with the bacterium E. coli and the intracellular parasite T. gondii, indicating a compromised ability of macrophages to defend against pathogens. Intriguingly, macrophages exposed to TIP had significantly greater m[sup 6]A levels, which correlated with the greater expression levels of m[sup 6]A methyltransferases. Macrophages exposed to each of the three 2,4,6-trihalophenols exhibited transcriptome-wide redistribution of m[sup 6]A. In particular, the m[sup 6]A peaks in genes associated with immune-related pathways were altered after exposure. In addition, differences in m[sup 6]A were also observed in human PBMCs after exposure to 2,4,6-trihalophenols. DISCUSSION: These findings suggest that 2,4,6-trihalophenol exposure impaired the ability of macrophages to defend against pathogens. This response might be associated with notable differences in m[sup 6]A after exposure. To the best of our knowledge, this study presents the first m[sup 6]A landscape across the transcriptome of immune cells exposed to pollutants. However, significant challenges remain in elucidating the mechanisms by which m[sup 6]A mediates immune dysregulation in infected macrophages after 2,4,6-trihalophenol exposure. [ABSTRACT FROM AUTHOR]