Optical enhancement mode 2 improves the detection rate of gastric neoplastic lesion in high-risk populations: A multicenter randomized controlled clinical study.

OBJECTIVES: Detection of early neoplastic lesions is crucial for improving the survival rates of patients with gastric cancer. Optical enhancement mode 2 is a new image-enhanced endoscopic technique that offers bright images and can improve the visibility of neoplastic lesions. This study aimed to compare the detection of neoplastic lesions with optical enhancement mode 2 and white-light imaging (WLI) in a high-risk population. METHODS: In this prospective multicenter randomized controlled trial, patients were randomly assigned to optical enhancement mode 2 or WLI groups. Detection of suspicious neoplastic lesions during the examinations was recorded, and pathological diagnoses served as the gold standard. RESULTS: A total of 1211 and 1219 individuals were included in the optical enhancement mode 2 and WLI groups, respectively. The detection rate of neoplastic lesions was significantly higher in the optical enhancement mode 2 group (5.1% vs. 1.9%; risk ratio, 2.656 [95% confidence interval, 1.630-4.330]; p < 0.001). The detection rate of neoplastic lesions with an atrophic gastritis background was significantly higher in the optical enhancement mode 2 group (8.6% vs. 2.6%, p < 0.001). The optical enhancement mode 2 group also had a higher detection rate among endoscopists with different experiences. CONCLUSIONS: Optical enhancement mode 2 was more effective than WLI for detecting neoplastic lesions in the stomach, and can serve as a new method for screening early gastric cancer in clinical practice. CLINICAL REGISTRY: United States National Library of Medicine (https://www. CLINICALTRIALS: gov), ID: NCT040720521.

Differential Diagnosis of Post Pancreatitis Diabetes Mellitus Based on Pancreatic and Gut Hormone Characteristics.

CONTEXT: Distinguishing different types of diabetes is important in directing optimized treatment strategies and correlated epidemiological studies. OBJECTIVE: Through detailed analysis of hormone responses to mixed meal tolerance test (MMTT), we aimed to find representing characteristics of post-acute pancreatitis diabetes mellitus (PPDM-A) and post-chronic pancreatitis diabetes mellitus (PPDM-C). METHODS: Participants with PPDM-A, PPDM-C, type 1 diabetes, type 2 diabetes, and normal controls (NCs) underwent MMTT. Fasting and postprandial responses of serum glucose, C-peptide, insulin, glucagon, pancreatic polypeptide (PP), ghrelin, gastric inhibitory peptide (GIP), glucagon like peptide-1 (GLP-1), and peptide YY (PYY) were detected and compared among different groups. Focused analysis on calculated insulin sensitivity and secretion indices were performed to determine major causes of hyperglycemia in different conditions. RESULTS: Participants with PPDM-A were characterized by increased C-peptide, insulin, glucagon, and PP, but decreased ghrelin, GIP, and PYY compared with NCs. Patients with PPDM-C showed secretion insufficiency of C-peptide, insulin, ghrelin, and PYY, and higher postprandial responses of glucagon and PP than NCs. In particular, both fasting and postprandial levels of ghrelin in PPDM-C were significantly lower than other diabetes groups. PYY responses in patients with PPDM-A and PPDM-C were markedly reduced. Additionally, the insulin sensitivity of PPDM-A was decreased, and the insulin secretion for PPDM-C was decreased. CONCLUSION: Along with the continuum from acute to chronic pancreatitis, the pathological mechanism of PPDM changes from insulin resistance to insulin deficiency. Insufficient PYY secretion is a promising diagnostic marker for distinguishing PPDM from type 1 and type 2 diabetes. Absent ghrelin secretion to MMTT may help identify PPDM-C.

Predictive value of adipokines for the severity of acute pancreatitis: a meta-analysis.

BACKGROUND: Severe acute pancreatitis (SAP) is a dangerous condition with a high mortality rate. Many studies have found an association between adipokines and the development of SAP, but the results are controversial. Therefore, we performed a meta-analysis of the association of inflammatory adipokines with SAP. METHODS: We screened PubMed, EMBASE, Web of Science and Cochrane Library for articles on adipokines and SAP published before July 20, 2023. The quality of the literature was assessed using QUADAS criteria. Standardized mean differences (SMD) with 95% confidence intervals (CI) were calculated to assess the combined effect. Subgroup analysis, sensitivity analysis and publication bias tests were also performed on the information obtained. RESULT: Fifteen eligible studies included 1332 patients with acute pancreatitis (AP). Pooled analysis showed that patients with SAP had significantly higher serum levels of resistin (SMD = 0.78, 95% CI:0.37 to 1.19, z = 3.75, P = 0.000). The difference in leptin and adiponectin levels between SAP and mild acute pancreatitis (MAP) patients were not significant (SMD = 0.30, 95% CI: -0.08 to 0.68, z = 1.53, P = 0.127 and SMD = 0.11, 95% CI: -0.17 to 0.40, z = 0.80, P = 0.425, respectively). In patients with SAP, visfatin levels were not significantly different from that in patients with MAP (SMD = 1.20, 95% CI: -0.48 to 2.88, z = 1.40, P = 0.162). CONCLUSION: Elevated levels of resistin are associated with the development of SAP. Resistin may serve as biomarker for SAP and has promise as therapeutic target.

A prognostic and immunotherapy effectiveness model for pancreatic adenocarcinoma based on cuproptosis-related lncRNAs signature.

Pancreatic adenocarcinoma (PAAD) results in one of the deadliest solid tumors with discouraging clinical outcomes. Growing evidence suggests that long non-coding RNAs (lncRNAs) play a crucial role in altering the growth, prognosis, migration, and invasion of pancreatic cancer cells. Cuproptosis is a novel type of cell death induced by copper (Cu) and is associated with mitochondrial respiration during the tricarboxylic acid cycle. However, the relationship between lncRNAs related to cuproptosis and PAAD is poorly studied. In this study, we investigated the association between a signature of cuproptosis-related lncRNAs and the diagnosis of PAAD. Genomic data and clinical information were obtained using the TCGA dataset, while cuproptosis-related genes (CRGs) from previous studies. Co-expression analysis was utilized to identify lncRNAs associated with cuproptosis. We developed and verified a prognostic risk model following a classification of patients into high- and low-risk categories. The prediction capacity of the risk model was assessed using a number of methods including Kaplan-Meier analysis, receiver operating characteristic (ROC) curves, nomograms, and principal component analysis (PCA). Furthermore, differentially expressed genes (DEGs) were used to perform functional enrichment analyses, and to examine the behaviors of various risk groups in terms of immune-related activities and medication sensitivity. We identified 7 cuproptosis-related lncRNA signatures, including CASC19, FAM83A-AS1, AC074099.1, AC007292.2, AC026462.3, AL358944.1, and AC009019.1, as overall survival (OS) predictors. OS and progression-free survival (PFS) showed significant differences among patients in different risk groups. Independent prognostic analysis revealed that the cuproptosis-related lncRNA signatures can independently achieve patient prognosis. The risk model demonstrated strong predictive ability for patient outcomes, as evidenced by ROC curves, nomograms, and PCA. Higher tumor mutation burden (TMB) and lower tumor immune dysfunction and exclusion (TIDE) scores were observed in the high-risk group. Additionally, the low-risk group was hypersensitive to 3 anti-cancer medications, whereas the high-risk group was hypersensitive to one. A prognostic risk model with a good predictive ability based on cuproptosis-related lncRNAs was developed, providing a theoretical basis for personalized treatment and immunotherapeutic responses in pancreatic cancer.

Comparison of the efficacy and safety of an oral sulfate solution and 3-L polyethylene glycol on bowel preparation before colonoscopy: a phase III multicenter randomized controlled trial.

BACKGROUND AND AIMS: Adequate bowel preparation is crucial for clear mucosal visualization during colonoscopy. We aimed to comprehensively compare oral sulfate solution (OSS) and 3-L split-dose polyethylene glycol (PEG) for bowel preparation before colonoscopy. METHODS: This randomized, active-controlled, noninferiority study was performed in 10 medical centers. Eligible subjects were enrolled to receive OSS or 3-L PEG in a split-dose regimen. The quality of bowel preparation, adverse reactions, and acceptability were evaluated. The quality of bowel preparation was evaluated using the Boston Bowel Preparation Scale. Safety was evaluated by adverse reactions. The study population was divided into the full analysis set (FAS), the safety set, the modified FAS (mFAS), and the per-protocol set (PPS). RESULTS: Three hundred forty-eight potentially eligible subjects were enrolled. Three hundred forty-four subjects were included in the FAS and safety set, 340 subjects were included in the mFAS, and 328 subjects were included in the PPS. Adequate bowel preparation of the OSS was not inferior to 3-L PEG in the mFAS (98.22% vs 97.66%) and the PPS (98.17% vs 98.78%). There was no significant difference in acceptability between the 2 groups (94.74% vs 94.80%, P = .9798). Overall adverse reactions were similar (50.88% vs 44.51%, P = .2370) between the 2 groups. CONCLUSIONS: The split-dose OSS regimen was not inferior to the split-dose 3-L PEG regimen for the quality of bowel preparation in a Chinese adult population. The safety and acceptability of the 2 groups were similar. (Clinical trial registration number: NCT05465889.).

Acute pancreatitis as initial presentation of acute myeloid leukemia-M2 subtype: A case report.

BACKGROUND: Direct infiltration of the pancreas by acute myeloid leukemia (AML) with acute pancreatitis (AP) as an initial symptom is extremely rare. Only once in the literature, the leukemia cells in AML have been implicated as the cause of AP. Pancreatitis caused by a rare predisposing factor is often misdiagnosed as idiopathic pancreatitis or pancreatitis of other common causes. Severe AP (SAP) progresses rapidly with a high fatality rate. Therefore, it is important to identify the predisposing factors in the early stage of SAP, evaluate the condition, determine prognosis, formulate treatment plans, and prevent a recurrence. Here, we describe a case of SAP due to AML. CASE SUMMARY: A 61-year-old man presented to the hospital with fever and persistent abdominal pain. Blood analysis presented significantly elevated serum amylase and severe thrombocytopenia. Computed tomography examination of the abdomen revealed peripancreatic inflammatory effusion. The patient had no common etiologies and risk factors for AP, but the concurrent severe thrombocytopenia could not be explained by pancreatitis. Finally, the bone marrow aspirate and biopsy inspection revealed the underlying reason for pancreatitis, AML (M2 type based on the French-American-British classifications system). CONCLUSION: Direct infiltration of the pancrease by acute leukemia, particularly AML cells, is an infrequent cause of AP. Therefore, although AP is a rare extramedullary infiltration characteristic for AML patients, it should be considered when determining the etiology of AP.

NPTX1 inhibits pancreatic cancer cell proliferation and migration and enhances chemotherapy sensitivity by targeting RBM10.

Pancreatic cancer (PC), one of the deadliest diseases worldwide, has exhibited an increasing incidence rate in recent years. The present study aimed to explore the biological mechanism of PC. Therefore, the expression levels of neuronal pentraxin 1 (NPTX1) and RNA-binding protein 10 (RBM10) were detected in PC cell lines using reverse transcription-quantitative PCR (RT-qPCR) and western blot analyses prior to or following NPTX1 and RBM10 overexpression. Additionally, the proliferative ability of PANC-1 and BxPC-3 cells treated with or without gemcitabine (GEM) and cisplatin (DDP) was evaluated using Cell Counting Kit-8 assay. Cell apoptosis and the expression levels of apoptosis-related proteins were determined by TUNEL assay and western blot analysis, respectively. Furthermore, wound healing and Transwell assays were performed to measure the migration and invasion abilities of PANC-1 and BxPC-3 cells. The interaction between RBM10 and NPTX1 mRNA was detected by RNA binding protein immunoprecipitation (RIP) assay. Additionally, cells were treated with actinomycin D to verify the regulatory effect of RBM10 on NPTX1 expression. This effect was further confirmed by RT-qPCR analysis. The results showed that NPTX1 was downregulated in PC cell lines. In addition, NPTX1 overexpression inhibited the proliferation and promoted apoptosis in PC cells. The results from the wound healing and Transwell assays revealed that the migration and invasion abilities of PANC-1 and BxPC-3 cells were reduced following NPTX1 overexpression. However, treatment of NPTX1-overexpressing cells with GEM or DDP attenuated PC cell viability. In addition, the results of the RIP assay revealed that RBM10 could bind with NPTX1. Furthermore, RBM10 overexpression could regulate NPTX1 expression, as evidenced by actinomycin D experiments. Overall, the results of the present study suggested that NPTX1 could inhibit PC and enhance the sensitivity of PC cells to chemotherapy. Additionally, NPTX1 was found to interact with RBM10, indicating that NPTX1 could inhibit PC via targeting RBM10.

Non-Alcoholic Fatty Liver Disease (NAFLD) Is an Independent Risk Factor for Developing New-Onset Diabetes After Acute Pancreatitis: A Multicenter Retrospective Cohort Study in Chinese Population.

Background: Numerous studies validated frequent glucose dysfunction in patients with acute pancreatitis (AP). However, the prevalence of new-onset diabetes in individuals after a first episode of AP varies widely among previous studies. This study aims to determine the incidence of post-acute pancreatitis diabetes mellitus (PPDM-A) in Chinese people and further identify potential risk factors that influence diabetes development in patients with AP. Methods: This was a multi-center retrospective cohort study including 6009 inpatients with a first attack of AP. A total of 1804 patients with AP without known endocrine pancreatic disorders or other pancreatic exocrine diseases were eligible for analysis. Data was collected from medical records by hospital information system and telephone follow-ups after discharge. The multiple logistic regression analysis was established to evaluate the potential influencing factors of PPDM-A. Results: The prevalence of newly diagnosed diabetes after a first episode of AP in China was 6.2%. Data showed that patients who developed PPDM-A were more likely to be younger (X2 = 6.329, P = 0.012), experienced longer hospital stays (X2 = 6.949, P = 0.008) and had a higher frequency of overweight or obesity (X2 = 11.559, P = 0.003) compared to those with normal glycemia. The frequency of stress hyperglycemia on admission (X2 = 53.815, P < 0.001), hyperlipidemia (X2 = 33.594, P < 0.001) and non-alcoholic fatty liver disease (NAFLD) (X2 = 36.335, P < 0.001) were significantly higher among individuals with PPDM-A compared with control group. Also, patients with PPDM-A were more likely to be hyperlipidemic AP (X2 = 16.304, P = 0.001) and show a higher degree of severity (X2 = 7.834, P = 0.020) and recurrence rate (X2 = 26.908, P < 0.001) of AP compared to those without diabetes. In addition, multiple logistic regression analysis indicated that stress hyperglycemia, hyperlipidemia, NAFLD and repeated attacks of AP were the independent influence factors for developing PPDM-A. Conclusion: Our study first demonstrated the prevalence of secondary diabetes in Chinese patients after AP. The disorder of glucose metabolism in individuals with AP should be regularly evaluated in clinical practice. Further studies are needed to verify the relationship between liver and pancreas in keeping glucose homeostasis under AP condition.

Identification of Hub Genes and Potential ceRNA Networks of Diabetic Nephropathy by Weighted Gene Co-Expression Network Analysis.

Diabetic nephropathy (DN) is one of the most common microvascular complications in diabetic patients, and is the main cause of end-stage renal disease. The exact molecular mechanism of DN is not fully understood. The aim of this study was to identify novel biomarkers and mechanisms for DN disease progression by weighted gene co-expression network analysis (WGCNA). From the GSE142153 dataset based on the peripheral blood monouclear cells (PBMC) of DN, we identified 234 genes through WGCNA and differential expression analysis. Gene Ontology (GO) annotations mainly included inflammatory response, leukocyte cell-cell adhesion, and positive regulation of proteolysis. Kyoto Encyclopedia of Genes and Genomes (KEGG) pathways mostly included IL-17 signaling pathway, MAPK signaling pathway, and PPAR signaling pathway in DN. A total of four hub genes (IL6, CXCL8, MMP9 and ATF3) were identified by cytoscape, and the relative expression levels of hub genes were also confirmed by RT-qPCR. ROC curve analysis determined that the expression of the four genes could distinguish DN from controls (the area under the curve is all greater than 0.8), and Pearson correlation coefficient analysis suggested that the expression of the four genes was related to estimated glomerular filtration rate (eGFR) of DN. Finally, through database prediction and literature screening, we constructed lncRNA-miRNA-mRNA network. We propose that NEAT1/XIST/KCNQ1T1-let-7b-5p-IL6, NEAT1/XIST-miR-93-5p-CXCL8 and NEAT1/XIST/KCNQ1T1-miR-27a-3p/miR-16-5p-ATF3 might be potential RNA regulatory pathways to regulate the disease progression of early DN. In conclusion, we identified four hub genes, namely, IL6, CXCL8, MMP9, and ATF3, as markers for early diagnosis of DN, and provided insight into the mechanisms of disease development in DN at the transcriptome level.

Neferine induces apoptosis by modulating the ROS­mediated JNK pathway in esophageal squamous cell carcinoma.

Current treatments for esophageal squamous cell carcinoma (ESCC) have limited efficacy. Therefore, the development of novel therapeutic targets to effectively manage the disease and boost survival rates is imperative Neferine, a natural product extracted from Nelumbo nucifera (lotus) leaves, has been revealed to inhibit the growth of hepatocarcinoma, breast cancer and lung cancer cells. However, its effect on ESCC is unknown. In the present study, it was revealed that neferine exerted anti­proliferative effects in ESCC. It was also revealed that it triggered arrest of the G2/M phase and enhanced apoptosis of ESCC cell lines. Moreover, its ability to trigger accumulation of reactive oxygen species (ROS) and activate the c­Jun N­terminal kinase (JNK) pathway was demonstrated. Further study revealed how N­acetyl cysteine (NAC), a ROS inhibitor, attenuated these effects, demonstrating that ROS and JNK inhibitors mediated a marked reversal of neferine­triggered cell cycle arrest and apoptosis in ESCC cells. Finally, it was revealed that neferine was involved in the inhibition of Nrf2, an antioxidant factor. Collectively, these findings demonstrated the antitumor effect of neferine in ESCC, through the ROS­mediated JNK pathway and inhibition of Nrf2, indicating its potential as a target for development of novel and effective therapeutic agents against ESCC.

[Antibiotic resistance of Helicobacter pylori clinical isolates in Hebei Province].

OBJECTIVE: To evaluate the resistance of Helicobacter pylori (H.pylori) clinical isolates to various antibiotics, in order to guide rational drug use in Hebei Province. METHODS: From January 2014 to July 2015, 260 patients with H. pylori infection who had not received eradication treatment were enrolled in Third Hospital of Hebei Medical University. Gastric mucosa biopsy tissue samples were collected from these patients before treatment for isolation and culture of H. pylori. Kirby-Bauer method was used to detect drug-resistance rate of the H. pylori clinical isolates to metronidazole, clarithromycin, amoxicillin, levofloxacin, and furazolidone. RESULTS: A total of 155 H. pylori strains were isolated from tissue samples of the 260 patients (positive rate, 59.6%). The drug-resistance rate of H. pylori isolated to metronidazole, clarithromycin, amoxicillin, levofloxacin, and furazolidone was 94.2%(146/155), 21.3%(33/155), 2.6%(4/155), 5.8% (9/155), and 1.9%(3/155), respectively. There was no statistically significant difference in positive culture rate and drug-resistance rate between different sex, age, and disease category(all P>0.05). CONCLUSION: In Hebei Province, the resistance rates of H. pylori to metronidazole and clarithromycin appear to be higher than those to amoxicillin, levofloxacin, and furazolidone.

Pyoderma gangrenosum of articulations carpi associated with ulcerative colitis: one case report.

Pyoderma gangrenosum (PG), an extra-intestinal manifestation of ulcerative colitis (UC), is extremely rare. Up to now, there is no any data reported the occurrence of PG in joints, especially in China. The management of PG associated with UC is a therapeutic challenge. Our report here showed that a female patient diagnosed as UC complained a pustule in the dorsal side of left wrist, primarily was diagnosed as bone tuberculosis. The pustule progressed rapidly into a severe painful necrolytic cutaneous ulcer with a pale purple irregular destructive ulcer edge, this patient was diagnosed by UC complicated with PG, and skin lesions were cured by UC treatment. Here, we for the first time present a case acquired correct diagnosis and successful treatment of UC associated with PG of articulations carpi. We report this case here in order to provide more information about this disease to more doctors, furthermore, to decrease the rates of misdiagnosis and missed diagnosis.