Fructose-1,6-diphosphate inhibits viral replication by promoting the lysosomal degradation of HMGB1 and blocking the binding of HMGB1 to the viral genome.

Fructose-1,6-diphosphate (FBP), a key glycolytic metabolite, is recognized for its cytoprotective effects during stress. However, the role of FBP in viral infections is unknown. Here, we demonstrate that virus-infected cells exhibit elevated FBP levels.

Riboflavin kinase binds and activates inducible nitric oxide synthase to reprogram macrophage polarization.

Riboflavin kinase (RFK) is essential in riboflavin metabolism, converting riboflavin to flavin mononucleotide (FMN), which is further processed to flavin adenine dinucleotide (FAD). While RFK enhances macrophage phagocytosis of Listeria monocytogenes, its role in macrophage polarization is not well understood. Our study reveals that RFK deficiency impairs M(IFN-γ) and promotes M(IL-4) polarization, both in vitro and in vivo.

Biodegradation of Crude Oil by Nitrate-Reducing, Sulfate-Reducing, and Methanogenic Microbial Communities under High-Pressure Conditions.

Carbon capture, utilization, and storage (CCUS) is an important component in many national net-zero strategies, and ensuring that CO can be safely and economically stored in geological systems is critical. Recent discoveries have shown that microbial processes (e.g.

Progress of Crude Oil Gasification Technology Assisted by Microorganisms in Reservoirs.

Crude oil gasification bacteria, including fermenting bacteria, hydrocarbon-oxidizing bacteria, reducing bacteria, and methanogenic bacteria, participate in multi-step reactions involving initial activation, intermediate metabolism, and the methanogenesis of crude oil hydrocarbons. These bacteria degrade crude oil into smaller molecules such as hydrogen, carbon dioxide, acetic acid, and formic acid. Ultimately, they convert it into methane, which can be utilized or stored as a strategic resource.

Induction of MTHFD2 in Macrophages Inhibits Reactive Oxygen Species-mediated NF-κB Activation and Protects against Inflammatory Responses.

The one-carbon metabolism enzyme methylenetetrahydrofolate dehydrogenase 2 (MTHFD2) is critical for cancer cell proliferation and immune cell phenotypes, but whether it can contribute to macrophage inflammatory responses remains unclear. In this study, we show that MTHFD2 was upregulated by LPS in murine macrophages upon activation of the TLR4-MyD88-IKKα/β-NF-κB signaling pathway. MTHFD2 significantly attenuated LPS-induced macrophage proinflammatory cytokine production through its enzymatic activity.

Gallbladder cancer: current and future treatment options.

Surgery remains the preferred treatment option for early-stage gallbladder cancer (GBC). According to the anatomical position of the primary tumor, accurate preoperative stage and strict control of surgical indications, appropriate surgical strategies are selected to achieve the optimal surgical effect. However, most patients have already been at the locally advanced stage or the tumor has metastasized at the initial diagnosis.

Predictive Factors of Treatment Outcomes After Percutaneous Radiofrequency Ablation of Hepatocellular Carcinoma in the Hepatocaval Confluence: A Propensity Score Matching Analysis.

Rationale And Objectives: To compare the efficacy and complications of ultrasound-guided percutaneous radiofrequency ablation of hepatocellular carcinoma (HCC) in the hepatocaval confluence with those of HCC in the non-hepatocaval confluence and to explore the risk factors that lead to radiofrequency ablation failure and patient local tumor progression (LTP).

Materials And Methods: From January 2017 to January 2022, 86 patients with HCC in the hepatocaval confluence who had radiofrequency ablation were included. A 1:1 propensity-matched group of patients with HCC in the non-hepatocaval confluence with comparable clinical baseline traits, such as tumor diameter and tumor number, served as the control group.

MTHFD2 reprograms macrophage polarization by inhibiting PTEN.

The one-carbon metabolism enzyme methylenetetrahydrofolate dehydrogenase 2 (MTHFD2) is involved in the regulation of tumor oncogenesis and immune cell functions, but whether it can contribute to macrophage polarization remains elusive. Here, we show that MTHFD2 suppresses polarization of interferon-γ-activated macrophages (M(IFN-γ)) but enhances that of interleukin-4-activated macrophages (M(IL-4)) both in vitro and in vivo. Mechanistically, MTHFD2 interacts with phosphatase and tensin homolog (PTEN) to suppress PTEN's phosphatidylinositol 3,4,5-trisphosphate (PIP3) phosphatase activity and enhance downstream Akt activation, independent of the N-terminal mitochondria-targeting signal of MTHFD2.

Molecular Dynamics Insight into the CO Flooding Mechanism in Wedge-Shaped Pores.

Because of the growing demand for energy, oil extraction under complicated geological conditions is increasing. Herein, oil displacement by CO2 in wedge-shaped pores was investigated by molecular dynamics simulation. The results showed that, for both single and double wedge-shaped models, pore Ⅱ (pore size from 3 to 8 nm) exhibited a better CO2 flooding ability than pore Ⅰ (pore size from 8 to 3 nm).

Serine metabolism orchestrates macrophage polarization by regulating the IGF1-p38 axis.

Serine metabolism is reportedly involved in immune cell functions, but whether and how serine metabolism regulates macrophage polarization remain largely unknown. Here, we show that suppressing serine metabolism, either by inhibiting the activity of the key enzyme phosphoglycerate dehydrogenase in the serine biosynthesis pathway or by exogenous serine and glycine restriction, robustly enhances the polarization of interferon-γ-activated macrophages (M(IFN-γ)) but suppresses that of interleukin-4-activated macrophages (M(IL-4)) both in vitro and in vivo. Mechanistically, serine metabolism deficiency increases the expression of IGF1 by reducing the promoter abundance of S-adenosyl methionine-dependent histone H3 lysine 27 trimethylation.

and evaluation of virus-induced innate immunity in mouse.

Innate immunity is the first line of host defense against viral infection. As one of the innate immune cell types, antigen-presenting cells play an important role in the process of antiviral immunity. This protocol describes the analysis of innate immunity induced by vesicular stomatitis virus infection of peritoneal macrophages and detection of IFN-β production and lung injury.

Serine metabolism antagonizes antiviral innate immunity by preventing ATP6V0d2-mediated YAP lysosomal degradation.

Serine metabolism promotes tumor oncogenesis and regulates immune cell functions, but whether it also contributes to antiviral innate immunity is unknown. Here, we demonstrate that virus-infected macrophages display decreased expression of serine synthesis pathway (SSP) enzymes. Suppressing the SSP key enzyme phosphoglycerate dehydrogenase (PHGDH) by genetic approaches or by treatment with the pharmaceutical inhibitor CBR-5884 and by exogenous serine restriction enhanced IFN-β-mediated antiviral innate immunity in vitro and in vivo.