The purpose of this study is to develop bioimpedance spectroscopy methods for diagnosing pancreatic diseases. We developed a descriptor approach using impedance spectroscopy results, generating four amplitude-phase-frequency responses from four quasi-orthogonal leads. They create the feature spaces required for our hybrid classifier for diagnosing pancreatic diseases, consisting of five macro levels, the first of which is based on probabilistic neural networks, and the remaining four are based on fuzzy inference. We also presented a device structure for generating informative feature spaces. The use of multi-frequency sensing in classifiers based on fully connected neural networks made it possible to develop a clinical decision support system for diagnosing pancreatic diseases. The results were confirmed in groups of patients aged from 25 to 80 years, male and female, at different stages of pancreatic disease. The training and testing samples were formed using various diagnostic methods, including medical history, physical examination, assessment of comorbidities, laboratory tests, ultrasound, laparoscopy, intraoperative revision, and computed tomography. An assessment of the diagnostic quality indicators of a hybrid neural network for three classes of diseases: "pancreatic cancer," "chronic pancreatitis" and "without pancreatic pathology" showed that their maximum value for differentiating these classes of diseases was 89%, the minimum -63%. Experimental software studies and clinical trials of our decision support system demonstrated diagnostic sensitivity and specificity comparable to existing methods, validating the practicality of our methods. This research opens new possibilities for accessible and objective diagnosis of pancreatic diseases, expanding the ability to make intelligent medical decisions.

Blood purification plays an important role in the treatment of severe acute pancreatitis. Extracorporeal blood anticoagulation is an important strategy to achieve smooth circulation in blood purification circuits. We aimed to investigate the efficacy, safety, and impact on circulating cytokines of using heparin or nafamostat mesylate anticoagulation in patients with severe acute pancreatitis during continuous renal replacement therapy.

Pancreatic ductal adenocarcinoma (PDAC) is often diagnosed at an advanced stage, highlighting the need for minimally invasive biomarkers capable of distinguishing it from related risk conditions. This study evaluated relative leukocyte telomere length (LTL) and gut microbiome profiles as potential biomarkers for PDAC. The study included 244 participants with PDAC (n = 37), chronic pancreatitis (CP; n = 56), type 2 diabetes mellitus (T2DM; n = 99), or no related risk conditions (controls; n = 52). LTL was measured by monochrome multiplex quantitative polymerase chain reaction (qPCR), while gut microbiome composition was assessed by 16S ribosomal RNA (rRNA) gene sequencing in a subset of participants with PDAC (n = 12), CP (n = 13), and controls (n = 7). LTL varied with age, sex, and smoking status. After adjustment for these factors, patients with PDAC had significantly longer LTL than controls (p = 0.029), whereas differences between PDAC and CP or T2DM were not significant. LTL showed limited ability to discriminate PDAC from controls (area under the receiver operating characteristic curve = 0.651) and was not associated with overall survival. Gut microbiome diversity and taxonomic composition did not differ significantly among the analyzed groups. These findings indicate that LTL has limited utility as a standalone diagnostic or prognostic biomarker for PDAC but may warrant further evaluation as a complementary marker in larger prospective studies. The exploratory microbiome findings also require validation in adequately powered cohorts.

Nephrocalcinosis refers to the deposition of calcium oxalate or calcium phosphate in the kidney, most commonly within the renal medulla, and is frequently linked with underlying metabolic abnormalities. Roux-en-Y gastric bypass (RYGB) is a well-established risk factor for enteric hyperoxaluria secondary to fat malabsorption, thereby increasing the risk of nephrolithiasis, oxalate nephropathy, and nephrocalcinosis. Despite this association, nephrocalcinosis following RYGB remains an uncommon and underrecognized clinical entity. A 36-year-old male with a history of complicated peptic ulcer disease, multiple prior abdominal surgeries, and previous RYGB presented with acute abdominal pain and distention. Laboratory evaluation revealed an elevated creatinine of 2.27 mg/dL, a suppressed parathyroid hormone level of 6.3 pg/mL, and hypocalcemia with serum calcium of 8.1 mg/dL. Imaging studies revealed bilateral renal medullary calcifications, consistent with nephrocalcinosis. Given the patient's history of RYGB, chronic pancreatitis, multiple GI surgeries, and evidence of chronic malnutrition, chronic malabsorptive physiology leading to enteric hyperoxaluria was hypothesized to be the most plausible explanation. However, measurements of 24-hour urinary oxalate, calcium, citrate, and vitamin D, as well as a renal biopsy, were not obtained, thereby precluding definitive confirmation of this proposed mechanism. This case highlights the importance of considering metabolic and renal complications in patients with complex GI disease following bariatric surgery and emphasizes the role of comprehensive metabolic evaluation and renal imaging in improving early recognition, diagnostic accuracy, and long-term kidney outcomes.

Primary mucosa-associated lymphoid tissue (MALT) lymphoma of the gallbladder is an extremely rare disease. We describe a case of a 79-year-old man with chronic hepatitis C-related cirrhosis presenting with acute epigastric pain and laboratory findings consistent with gallstone pancreatitis. He underwent a cholecystectomy, and histopathology review of the surgical specimen revealed a primary MALT lymphoma of the gallbladder. Staging studies revealed no evidence of metastatic disease but incidentally identified a malignancy of the prostate. The patient's gallbladder MALT lymphoma was managed conservatively with surgery and active surveillance, and he remains disease-free at two years status post surgery. This case expands the clinical spectrum of gallbladder MALT lymphoma, with, to our knowledge, the first report of pancreatitis as the presenting symptom. It underscores the importance of considering lymphoid neoplasms in atypical gallbladder disease and highlights the need to further evaluate the potential role of chronic hepatic inflammation in its pathogenesis.

Metabolic dysfunction-associated steatotic liver disease (MASLD) is increasingly recognised as a systemic disorder with clinically relevant extrahepatic manifestations. Pancreatic diseases have gained particular attention in this context, as they share key metabolic and inflammatory mechanisms with MASLD and may influence each other's natural history and clinical outcomes. Beyond shared cardiometabolic risk factors, emerging evidence suggests that MASLD may actively contribute to pancreatic dysfunction and disease progression, supporting a bidirectional liver-pancreas relationship. Recognition of this association is essential to improve risk stratification, diagnostic assessment, and clinical management. This review summarises the current evidence linking MASLD with pancreatic disorders, focusing on acute and chronic pancreatitis, pancreatic cancer, and fatty pancreas. We examine shared pathophysiological pathways and discuss how these interactions may affect disease progression, nutritional status, diagnostic strategies, and therapeutic decision-making. We also address key clinical challenges, including alcohol assessment and MASLD-MetALD misclassification, highlight current knowledge gaps, and provide scenario-specific recommendations.

Regulation and screening of biomacromolecule (e.g., enzyme) activity is one of the core tasks in disease treatment and drug discovery. Natural products are an important source of enzyme inhibitors, but their complex composition makes it difficult to develop effective candidate drug molecules. As a typical biomacromolecular target, chymotrypsin (CHT) exhibits aberrant activity closely associated with diseases such as wound healing, chronic pancreatitis, and emphysema. Therefore, efficient screening of enzyme inhibitors from natural products holds significant importance for clinical diagnosis, treatment, and drug development. This study establishes an integrated screening platform for enzyme inhibitors by combining a Cu[2+]-casein-mediated fluorescence-enhanced biosensing system with targeted ligand capture technology, enabling highly sensitive screening and precise identification of chymotrypsin inhibitors from natural products. In this platform, Cu[2+]-casein functions as a biomacromolecular substrate while also acting as a peroxidase-mimetic enzyme, significantly enhancing the fluorescence signal amplification effect of o-phenylenediamine oxidation. When chymotrypsin hydrolyzes casein, the structure of casein is disrupted, reducing its copper ion-binding capacity. Which leads to decreased catalytic activity and subsequent changes in fluorescence intensity, allowing quantitative detection of chymotrypsin activity with a detection limit as low as 13.6 ng mL[-1]. In the targeted fishing module, immobilized chymotrypsin (CHT@NH2-SiO2) is employed as an affinity medium, and combined with HPLC and LC-MS analysis, enables precise identification of active components in complex samples. This integrated strategy mitigates certain limitations of individual techniques, providing a feasible approach for efficient, high-throughput screening of inhibitors targeting biomacromolecules from complex systems.

Pancreatic ductal adenocarcinoma (PDAC) is initiated by activating KRAS mutations, yet most pancreatic cells fail to survive the induced oncogenic stress. How a subset adapts to and initiates malignant transformation remains unclear. Here, we show that stress granules (SGs) formation is a key adaptive mechanism enabling these cells to tolerate oncogenic KRAS signaling. Although we determine that SGs are a generic response in stressed acinar cells, they are required for KRAS-mutant cells to progress to the preneoplastic stage. SGs blocking prevents KRAS-driven acinar-to-ductal metaplasia ex vivo and suppresses preneoplastic lesion formation in vivo. Importantly, SGs inhibition does not affect pancreatic damage during chronic pancreatitis, supporting its safety for selectively targeting KRAS-mutant cells. Finally, SGs are detected in pancreatic tissue from patients with chronic pancreatitis, confirming clinical relevance. Together, these findings identify SGs as a stress adaptation mechanism enabling tumor initiation and highlight them as a target for cancer interception in KRAS-driven PDACs.