Computed tomography-based radiomics and body composition analysis for predicting clinically relevant postoperative pancreatic fistula after pancreaticoduodenectomy.

Background: Preoperative risk assessment of clinically relevant postoperative pancreatic fistula (CR-POPF) is still lacking. This study aimed to develop and validate a combined model based on radiomics, pancreatic duct diameter, and body composition analysis for the prediction of CR-POPF in patients undergoing pancreaticoduodenectomy (PD).

Methods: Multivariable logistic regression was used to construct a combined model in conjunction with radiomics score (Rad-score), pancreatic duct diameter, and visceral fat area/total abdominal muscle area index (VFA/TAMAI).

Interventional therapy combined with tyrosine kinase inhibitors with or without immune checkpoint inhibitors as initial treatment for hepatocellular carcinoma with portal vein tumor thrombosis: a systematic review and meta-analysis.

Background: Interventional therapy, in conjunction with tyrosine kinase inhibitors (TKIs), has shown promising outcomes for treating hepatocellular carcinoma (HCC) with portal vein tumor thrombosis (PVTT). With the advent of immunotherapy, the combined use of immune checkpoint inhibitors (ICIs) has attracted great attention due to their potential effectiveness in advanced HCC. This study aims to compare the efficacy and safety of a triple therapy regimen (Interventional therapy, TKIs and ICIs, IT-TKI-ICI) with a dual therapy regimen (Interventional therapy and TKIs, IT-TKI) in the treatment of HCC and PVTT (HCC-PVTT).

Association between gut microbiota and NAFLD/NASH: a bidirectional two-sample Mendelian randomization study.

Background: Recent studies have suggested a relationship between gut microbiota and non-alcoholic fatty liver disease (NAFLD)/nonalcoholic steatohepatitis (NASH). However, the nature and direction of this potential causal relationship are still unclear. This study used two-sample Mendelian randomization (MR) to clarify the potential causal links.

Human islet amyloid polypeptide-induced β-cell cytotoxicity is linked to formation of α-sheet structure.

Type 2 diabetes (T2D) results from insulin secretory dysfunction arising in part from the loss of pancreatic islet β-cells. Several factors contribute to β-cell loss, including islet amyloid formation, which is observed in over 90% of individuals with T2D. The amyloid is comprised of human islet amyloid polypeptide (hIAPP).

Liver Abscess Disguised as Biliary Disease: A Report of Two Cases and a Review of the Literature.

Liver abscesses caused by are rare but rapidly fatal. In only a few days, patients progress from liver abscess to sepsis, intravascular hemolysis, multiple organ failure, and even death. These abscesses often occur in patients after trauma or surgery or in those with immunodeficiency.

Designed α-sheet peptides disrupt uropathogenic E. coli biofilms rendering bacteria susceptible to antibiotics and immune cells.

Uropathogenic Escherichia coli account for the largest proportion of nosocomial infections in the United States. Nosocomial infections are a major source of increased costs and treatment complications. Many infections are biofilm associated, rendering antibiotic treatments ineffective or cause additional complications (e.

Comprehensive multimodal management of borderline resectable pancreatic cancer: Current status and progress.

Borderline resectable pancreatic cancer (BRPC) is a complex clinical entity with specific biological features. Criteria for resectability need to be assessed in combination with tumor anatomy and oncology. Neoadjuvant therapy (NAT) for BRPC patients is associated with additional survival benefits.

Research trends and hotspots of neoadjuvant therapy in pancreatic cancer: a bibliometric analysis based on the Web of Science Core Collection.

Neoadjuvant therapy (NAT) for pancreatic cancer (PC) has achieved certain results. This article was aimed to analyze the trends in NAT in PC over the past 20 years using bibliometric analysis and visualization tools to guide researchers in exploring future research hotspots. Articles related to NAT for PC were retrieved from the Web of Science Core Collection for the period 2002-2021.

Impact of Surgery on Non-Functional Pancreatic Neuroendocrine Tumors ≤2 cm: Analyses With Propensity Score-Based Inverse Probability of Treatment Weighting.

Purpose: The impact of surgery on non-functional pancreatic neuroendocrine tumors (NF-PNETs) ≤2 cm is controversial. This study sought to demonstrate the impact of surgery on the prognosis of NF-PNETs ≤2 cm with different biological behaviors.

Methods: Patients with NF-PNETs ≤2 cm from 2004 to 2015 in the Surveillance, Epidemiology, and End Results database were included in this study.

Kupffer cells depletion alters cytokine expression and delays liver regeneration after Radio-frequency-assisted Liver Partition with Portal Vein Ligation.

Radio-frequency-assisted Liver Partition with Portal Vein Ligation (RALPP) induces comparable hypertrophy of the liver remnant compared to Associating Liver Partition and Portal vein ligation for Staged hepatectomy (ALPPS) in humans. However, whether it is significantly improved compared to ALPPS is unclear, and the underlying mechanisms of liver regeneration after RALPP need to further investigate. The present study was to develop an animal model mimicking RALPP and explore mechanisms of liver regeneration.

SCARF1 promotes M2 polarization of Kupffer cells via calcium-dependent PI3K-AKT-STAT3 signalling to improve liver transplantation.

Objectives: This study aimed to investigate the protective effect of SCARF1 on acute rejection (AR), phagocytic clearance of Kupffer cells (KCs), M2 polarization and the exact mechanism underlying these processes.

Methods: AAV was transfected into the portal vein of rats, and AR and immune tolerance (IT) models of liver transplantation were established. Liver tissue and blood samples were collected.

Left-sided portal hypertension caused by peripancreatic lymph node tuberculosis misdiagnosed as pancreatic cancer: a case report and literature review.

Background: Left-sided portal hypertension (LSPH) is an extremely rare clinical syndrome, and it is the only form of curable portal hypertension. It is primarily caused by pancreatic disease, and is associated with complications that cause spleen vein compression. Specific symptoms are often lacking, rendering it difficult to diagnose.

IL-4 Alleviates Ischaemia-Reperfusion Injury by Inducing Kupffer Cells M2 Polarization via STAT6-JMJD3 Pathway after Rat Liver Transplantation.

Background: Liver ischaemia-reperfusion injury (IRI) remains a problem in liver transplantation. Interleukin-4 (IL-4) has been found to reduce liver IRI, but the exact mechanism remains unclear.

Methods: Donor livers were infused with recombinant IL-4 or normal saline during cold storage, and the hepatocellular apoptosis and the inflammatory response were detected.

α-ketoglutarate attenuates ischemia-reperfusion injury of liver graft in rats.

Objective: The α-ketoglutarate (αKG), a metabolite of glutaminolysis, is reported to orchestrate macrophages activation. This study aims to clarify whether the αKG / glutaminolysis metabolism can suppress Kupffer cells (KCs) activation during liver transplantation and attenuate hepatic ischemia-reperfusion injury (IRI).

Methods: Donor livers were perfused with DM-αKG (a cell-permeable analog of αKG) or BPTES (an inhibitor of glutaminase 1) via portal vein during cold preservation, and controls were perfused with UW solution.

VEGF-C attenuates ischemia reperfusion injury of liver graft in rats.

Background: Vascular endothelial growth factor receptor-3 (VEGFR-3) / vascular endothelial growth factor -c (VEGF-C) signaling is reported to negatively regulate TLR4-triggered inflammation of macrophages. This study aims to clarify whether the VEGFR-3/VEGF-C signaling can suppress Kupffer cells (KCs) activation and attenuate hepatic ischemia-reperfusion injury (IRI) after liver transplantation.

Methods: A rat model of liver transplantation was performed.

Tauroursodeoxycholic acid alleviates hepatic ischemia reperfusion injury by suppressing the function of Kupffer cells in mice.

The aim of this study is to investigate the protective effect and the mechanism of tauroursodeoxycholic acid (TUDCA) against hepatic ischemia reperfusion (IR) injury. Male Balb/c mice were intraperitoneally injected with tauroursodeoxycholic acid (400 mg/kg) or saline solution, once per day for 3 days before surgery, and then the model of hepatic I/R injury was established. Blood and liver samples were collected from each group at 3, 6, and 24 h after surgery.

TIM‑4 blockade of KCs combined with exogenous TGF‑β injection helps to reverse acute rejection and prolong the survival rate of mice receiving liver allografts.

An acute reaction response (AR) following liver transplantation (LT) is caused by immune responses that are primarily mediated by T lymphocytes. Kupffer cells (KCs) are the largest antigen presenting cell (APC) group in vivo and are the primary modulators of the inflammatory or tolerogenic immune response in liver tissues. T cell immunoglobulin‑domain and mucin‑domain-4 (TIM‑4), the only TIM protein not expressed on T cells, is expressed on APCs; suggesting that it mediates the various immune responses.

Liver X Receptors Activation Attenuates Ischemia Reperfusion Injury of Liver Graft in Rats.

: Suppression of the Toll like receptor 4 (TLR4)-nuclear factor-κB (NF-κB) signaling was critical in protection against liver IRI. Previous studies revealed that Liver X receptors (LXRs) activation could antagonize TLR4-NF-κB signaling. The purpose of this study is to determine whether LXRs agonist GW3965 can suppress the TLR4-NF-κB signaling during liver transplantation and protect ischemia-reperfusion injury (IRI).

Differential metabonomic profiles of primary hepatocellular carcinoma tumors from alcoholic liver disease, HBV-infected, and HCV-infected cirrhotic patients.

Our objective was to comparatively profile the metabolite composition of primary hepatocellular carcinoma (HCC) tumors from alcoholic liver disease (ALD), hepatitis B virus (HBV)-infected, and hepatitis C virus (HCV)-infected cirrhotic patients. Primary HCC tumors were collected from ALD, HBV-infected, and HCV-infected cirrhotic patients (n=20 each). High-resolution magic-angle spinning proton nuclear magnetic resonance spectroscopy and metabonomic data analysis were performed to compare HCC tumors from the three groups.

NLRP3 Deletion Inhibits the Non-alcoholic Steatohepatitis Development and Inflammation in Kupffer Cells Induced by Palmitic Acid.

The cleavage and secretion of pro-inflammatory cytokines IL-1β and IL-18 is regulated by NLRP3 (NACHT, LRR, and PYD domain-containing protein 3) inflammasome activation. Kupffer cells (KCs) are implicated in the pathogenesis of various liver diseases, such as non-alcoholic fatty liver disease (NAFLD), alcoholic liver disease, and liver fibrosis. However, the role of NLRP3 played in the non-alcoholic steatohepatitis (NASH) has yet to be evaluated.