[Progress in the immunometabolism in the regulation of macrophage function in sepsis].

Macrophages are widely distributed in peripheral blood, lungs, liver, brain, kidneys, skin, testes, vascular endothelial cells, and other parts of the body. As sentinel cells of innate immunity, they play an important role in the occurrence and development of sepsis. Recent research in immune metabolism has revealed the complicated relationship between specific metabolic pathways of macrophages and their phenotype and function in sepsis.

Dexmedetomidine attenuates sepsis-associated acute lung injury by regulating macrophage efferocytosis through the ROS/ADAM10/AXL pathway.

Background: The lungs are highly susceptible to damage during sepsis, with severe lung injury potentially progressing to acute respiratory distress syndrome and even fatal sepsis. Effective efferocytosis of apoptotic cells is crucial in alleviating inflammation and tissue injury.

Methods: We established a septic lung injury mouse model via intraperitoneal injection of lipopolysaccharide.

tBHQ mitigates fatty liver ischemia-reperfusion injury by activating Nrf2 to attenuate hepatocyte mitochondrial damage and macrophage STING activation.

Background: Liver ischemia-reperfusion (IR) injury is an inevitable pathophysiological process in various liver surgeries. Previous studies have found that IR injury is exacerbated in fatty liver due to significant hepatocellular damage and macrophage inflammatory activation, though the underlying mechanisms are not fully understood. In this study, we aim to explore the role and mechanism of Nrf2 (Nuclear factor erythroid 2-related factor 2) signaling in regulating hepatocellular damage and macrophage immune response in fatty liver IR injury.

ER stress promotes mitochondrial calcium overload and activates the ROS/NLRP3 axis to mediate fatty liver ischemic injury.

Background: Fatty livers are widely accepted as marginal donors for liver transplantation but are more susceptible to liver ischemia and reperfusion (IR) injury. Increased macrophage-related inflammation plays an important role in the aggravation of fatty liver IR injury. Here, we investigate the precise mechanism by which endoplasmic reticulum (ER) stress activates macrophage NOD-like receptor thermal protein domain-associated protein 3 (NLRP3) signaling by regulating mitochondrial calcium overload in fatty liver IR.

Defective efferocytosis by aged macrophages promotes STING signaling mediated inflammatory liver injury.

Aged livers have shown aggravated liver ischemia and reperfusion (IR) injury. Timely efferocytosis of apoptotic cells is a key mechanism for avoiding excessive inflammation and tissue injury. Here, we investigated the alteration of efferocytosis by aged macrophages and its role in regulating macrophage STING (stimulator of interferon genes) signaling and liver IR injury.

Macrophage STING signaling promotes NK cell to suppress colorectal cancer liver metastasis via 4-1BBL/4-1BB co-stimulation.

Background And Aims: Macrophage innate immune response plays an important role in tumorigenesis. However, the role and mechanism of macrophage STING signaling in modulating tumor microenvironment to suppress tumor growth at secondary sites remains largely unclear.

Methods: STING expression was assessed in liver samples from patients with colorectal cancer (CRC) liver metastasis.

Exosome-Encapsulated miR-31, miR-192, and miR-375 Serve as Clinical Biomarkers of Gastric Cancer.

In recent years, microRNAs (miRNAs) derived from exosomes have been attracting attention as novel clinical biomarkers in a variety of cancers. In this study, plasma samples from 60 gastric cancer (GC) patients and 63 healthy individuals were collected, and the exosomal microRNAs (ex-miRNAs) were isolated. We determined the specific ex-miRNAs through miRNA microarray and a database of differentially expressed miRNAs called dbDEMC.

MLKL deficiency attenuated hepatocyte oxidative DNA damage by activating mitophagy to suppress macrophage cGAS-STING signaling during liver ischemia and reperfusion injury.

Mixed-lineage kinase domain-like protein (MLKL)-mediated necroptosis has been implicated in aggravating liver ischemia and reperfusion (IR) injury. However, the precise role and mechanism of MLKL in regulating oxidative DNA damage of hepatocytes and subsequent activation of macrophage stimulator of interferon genes (STING) signaling remains unclear. In this study, we investigated the role of MLKL in regulating the interplay between hepatocyte injury and macrophage pro-inflammatory responses during liver IR injury.

CCAAT/Enhancer-binding Protein Homologous Protein Promotes ROS-mediated Liver Ischemia and Reperfusion Injury by Inhibiting Mitophagy in Hepatocytes.

Background: Liver ischemia and reperfusion (IR) injury represent a major risk factor in both partial hepatectomy and liver transplantation. CCAAT/enhancer-binding protein homologous protein (CHOP) is a key regulator of cell death, its precise molecular basis in regulating hepatocyte death during liver IR has not been delineated.

Methods: Hepatocellular CHOP deficient mice were generated by bone marrow chimera models using global CHOP knockout mice.

Defective mitophagy in aged macrophages promotes mitochondrial DNA cytosolic leakage to activate STING signaling during liver sterile inflammation.

Macrophage-stimulator of interferon genes (STING) signaling mediated sterile inflammation has been implicated in various age-related diseases. However, whether and how macrophage mitochondrial DNA (mtDNA) regulates STING signaling in aged macrophages remains largely unknown. We found that hypoxia-reoxygenation (HR) induced STING activation in macrophages by triggering the release of macrophage mtDNA into the cytosol.

Takotsubo syndrome after liver transplantation: An association with intraoperatively administered epinephrine and fentanyl.

Takotsubo syndrome (TTS) can develop after liver transplant (LT), but its predisposing factors are poorly understood. In this study, we aimed to determine if perioperative factors were associated with posttransplant TTS. Adult patients who underwent primary LT between 2006 and 2018 were included.

Obstructive jaundice secondary to fungal infection: a rare case report.

Obstructive jaundice is characterized by an obstruction of the intrahepatic or extrahepatic biliary system, and the most common causes include pancreatic and duodenal periampullary cancer. There have been some cases reporting obstructive jaundice caused by infection. Deep tissue infection usually develops in the individuals who are immunologically compromised or chronically ill, while a few cases reported in the immunocompetent patients.

Aging aggravated liver ischemia and reperfusion injury by promoting hepatocyte necroptosis in an endoplasmic reticulum stress-dependent manner.

Background: Aggravated liver ischemia and reperfusion (IR) injury has been reported in aged mice. Although necroptosis inhibition showed no crucial effect on hepatic IR injury in young mice, whether and how necroptosis affects liver IR injury in aged mice remains unclear.

Methods: Young and aged mice were subjected to liver IR modeling.

Aging aggravated liver ischemia and reperfusion injury by promoting STING-mediated NLRP3 activation in macrophages.

Although aggravated liver injury has been reported in aged livers post-ischemia and reperfusion (IR), the underlying mechanism of innate immune activation of aged macrophages is not well understood. Here, we investigated whether and how Stimulator of interferon genes (STING) signaling regulated macrophage proinflammatory activation and liver IR injury. Mice were subjected to hepatic IR in vivo.

Diabetes induces hepatocyte pyroptosis by promoting oxidative stress-mediated NLRP3 inflammasome activation during liver ischaemia and reperfusion injury.

Background: Although diabetes mellitus has been reported to aggravate liver ischaemia and reperfusion (IR) injury, the basic mechanism remains largely unknown. The object of the present study was to determine the role of oxidative stress and hepatocellular pyroptosis in liver IR injury in diabetic mice.

Methods: Db/db and C57BL/6 mice at 8 weeks of age were subjected to liver IR injury.

Dexmedetomidine preconditioning alleviated murine liver ischemia and reperfusion injury by promoting macrophage M2 activation via PPARγ/STAT3 signaling.

Background: Although a protective role of dexmedetomidine in liver ischemia and reperfusion (IR) injury has been reported, the underlying mechanism remains to be determined. The aim of this study is to analyze the effects of dexmedetomidine on the regulation of macrophage innate immune activation during liver IR.

Methods: Mice were randomly divided into dexmedetomidine preconditioning (DEX) and phosphate buffered saline vehicle control (VEH) groups.

Dexamethasone and dexmedetomidine as adjuvants to local anesthetic mixture in intercostal nerve block for thoracoscopic pneumonectomy: a prospective randomized study.

Background And Objectives: Perineural dexamethasone or dexmedetomidine prolongs the duration of single-injection peripheral nerve block when added to the local anesthetic solution. In a randomized, controlled, double-blinded study in patients undergoing thoracoscopic pneumonectomy, we tested the hypothesis that combined perineural dexamethasone and dexmedetomidine prolonged the duration of analgesia as compared with either perineural dexamethasone or perineural dexmedetomidine after intercostal nerve block (INB).

Methods: Eighty patients were randomized to receive INB using 28 mL 0.

Combined ischemic and rapamycin preconditioning alleviated liver ischemia and reperfusion injury by restoring autophagy in aged mice.

Old livers are more damaged by hepatic ischemia and reperfusion (IR) injury than young livers. The aim of this study was to investigate the effects of ischemic and rapamycin preconditioning on IR injury in old livers. Young (8-week-old) and aged (60-week-old) mice were subjected to IR or a sham control procedure.

Precoagulation with microwave ablation for hepatic parenchymal transection during liver partial resection.

Purpose: To evaluate the feasibility of precoagulation with microwave ablation (MWA) for hepatic parenchymal transection during liver partial resection.

Methods: A total of 66 eligible patients were enrolled in this double-blind, randomized, controlled study. Patients were randomized to receive either the traditional clamp-crushing method (Control group) or the MWA precoagulation method (MWA group) for hepatic parenchymal transection during liver partial resection.

Ropivacaine wound infiltration: a fast-track approach in patients undergoing thoracotomy surgery.

Background: Postoperative pain impairs enhanced recovery in patients after various surgeries. Local use of ropivacaine has become an effective strategy for postoperative pain management. The aim of this study was to assess the effectiveness and safety of wound infiltration with ropivacaine for postoperative analgesia as a fast-track approach in patients undergoing thoracotomy surgery.

Hyperglycemia Aggravates Hepatic Ischemia and Reperfusion Injury by Inhibiting Liver-Resident Macrophage M2 Polarization C/EBP Homologous Protein-Mediated Endoplasmic Reticulum Stress.

Aggravated liver ischemia and reperfusion (IR) injury has been observed in hyperglycemic hosts, but its underlying mechanism remains undefined. Liver-resident macrophages (Kupffer cells, KCs) and endoplasmic reticulum (ER) stress play crucial roles in the pathogenesis of liver IR injury. In this study, we evaluated the role of ER stress in regulating KC activation and liver IR injury in a streptozotocin-induced hyperglycemic/diabetic mouse model.

Isoflurane Preconditioning Alleviated Murine Liver Ischemia and Reperfusion Injury by Restoring AMPK/mTOR-Mediated Autophagy.

Background: Isoflurane has a pharmacological preconditioning effect against ischemia injury in the heart, kidney, and brain, but whether and how isoflurane preconditioning protects livers against ischemia and reperfusion (IR) injury is unclear.

Methods: Mice were randomly divided into an isoflurane preconditioning (ISO) group and control group, receiving 1.5% isoflurane or carrier gas for 40 minutes, respectively (n = 8/group).

Effect of dobutamine on extravascular lung water index, ventilator function, and perfusion parameters in acute respiratory distress syndrome associated with septic shock.

Background: The role of dobutamine in the relief of pulmonary edema during septic shock-induced acute respiratory distress syndrome (ARDS) remains undetermined, due to a lack of controllable and quantitative clinical studies. Our objective was to assess the potential effects of dobutamine on extravascular lung water index (ELWI) in septic shock-induced ARDS, reflecting its importance in pulmonary edema. At the same time, ventilator function and perfusion parameters were evaluated.