Objective:To investigate the heterogeneity of peripheral blood neutrophils in sepsis and provide reference for the diagnosis of sepsis.Methods:Twenty-four male C57BL/6 mice were divided into two groups, control and sepsis groups, with 12 mice in each group using a completely randomized design. The mice in the control group were injected with 100 μl saline through the tail vein, while the mice in the sepsis group were injected with an equal amount of Escherichia coli solution (3.33 McFarland turbidity standards) through the tail vein to establish the sepsis model. Peripheral blood samples were collected, and the proportions of neutrophils expressing different surface markers were detected using mass cytometry. GO and KEGG analyses were performed on neutrophil subsets with high CD62L expression, and public datasets were used for verification. The protein-protein interaction networks of CD62L were investigated to assess the value of neutrophil heterogeneity in the diagnosis of sepsis. Results:There were significant differences in the expression of markers in peripheral blood samples between the sepsis group and the control group. CD62L + neutrophil subsets were found in mice with sepsis. GO and KEGG analyses showed that CD62L + neutrophil subsets were associated with multiple biological processes and signaling pathways such as cell adhesion, migration, surface receptor activation, and immune regulation. Clinical results confirmed the correlation of neutrophil CD62L expression with the severity and prognosis of sepsis. The number of subpopulations expressing CD62L in peripheral blood neutrophils in the sepsis group was higher than that in the control group, but the expression level of CD62L in single cells in the sepsis group was significantly lower than that in the control group ( P<0.01). Protein-protein interaction network analysis showed strong interaction between CD62L and multiple important proteins such as P-selectin, P-selectin ligand, E-selectin, and vascular cell adhesion molecule-1. Conclusion:There is heterogeneity in the surface markers of neutrophils between sepsis mice and control mice, which may be a potential indicator for the diagnosis of sepsis.

Objective:To investigate the heterogeneity of peripheral blood neutrophils in sepsis and provide reference for the diagnosis of sepsis.Methods:Twenty-four male C57BL/6 mice were divided into two groups, control and sepsis groups, with 12 mice in each group using a completely randomized design. The mice in the control group were injected with 100 μl saline through the tail vein, while the mice in the sepsis group were injected with an equal amount of Escherichia coli solution (3.33 McFarland turbidity standards) through the tail vein to establish the sepsis model. Peripheral blood samples were collected, and the proportions of neutrophils expressing different surface markers were detected using mass cytometry. GO and KEGG analyses were performed on neutrophil subsets with high CD62L expression, and public datasets were used for verification. The protein-protein interaction networks of CD62L were investigated to assess the value of neutrophil heterogeneity in the diagnosis of sepsis. Results:There were significant differences in the expression of markers in peripheral blood samples between the sepsis group and the control group. CD62L + neutrophil subsets were found in mice with sepsis. GO and KEGG analyses showed that CD62L + neutrophil subsets were associated with multiple biological processes and signaling pathways such as cell adhesion, migration, surface receptor activation, and immune regulation. Clinical results confirmed the correlation of neutrophil CD62L expression with the severity and prognosis of sepsis. The number of subpopulations expressing CD62L in peripheral blood neutrophils in the sepsis group was higher than that in the control group, but the expression level of CD62L in single cells in the sepsis group was significantly lower than that in the control group ( P<0.01). Protein-protein interaction network analysis showed strong interaction between CD62L and multiple important proteins such as P-selectin, P-selectin ligand, E-selectin, and vascular cell adhesion molecule-1. Conclusion:There is heterogeneity in the surface markers of neutrophils between sepsis mice and control mice, which may be a potential indicator for the diagnosis of sepsis.

Anatomic resection aims to improve the surgical efficacy of hepatocellular carcinoma by systematic resection of portal territory. However, due to its deviation of traditional theory and practice, the oncology effect is questionable. Anatomic resection based on portal territory(PT-AR) is planned by the analysis of real portal vein territory, and performed complete resection of tumor-bearing portal territory by fluorescent guidance, while exposing typical inter-territory hepatic vein, so as to ensure the complete function of future liver remnant. PT-AR is based on the core theory of classical anatomic resection, which will correct the deviation of traditional theory and practice from the technical level, so as to lead a better surgical oncology outcomes for hepatocellular carcinoma.

Microglia-mediated neuroinflammation is widely perceived as a contributor to numerous neurological diseases and mental disorders including depression. Discs large homolog 1 (Dlg1), an adaptor protein, regulates cell polarization and the function of K
Animals ; Depression/chemically induced* ; Inflammation ; Lipopolysaccharides/toxicity* ; Mice ; Mice, Inbred C57BL ; Mice, Knockout ; Microglia ; NF-kappa B ; Neuroinflammatory Diseases

Microglia-mediated neuroinflammation is widely perceived as a contributor to numerous neurological diseases and mental disorders including depression. Discs large homolog 1 (Dlg1), an adaptor protein, regulates cell polarization and the function of K

Mitochondrial calcium uniporter (MCU) is a conserved Ca(2+) transporter at mitochondrial in eukaryotic cells. However, the role of MCU protein in oxidative stress-induced cell death remains unclear. Here, we showed that ectopically expressed MCU is mitochondrial localized in both HeLa and primary cerebellar granule neurons (CGNs). Knockdown of endogenous MCU decreases mitochondrial Ca(2+) uptake following histamine stimulation and attenuates cell death induced by oxidative stress in both HeLa cells and CGNs. We also found MCU interacts with VDAC1 and mediates VDAC1 overexpression-induced cell death in CGNs. This finding demonstrates that MCU-VDAC1 complex regulates mitochondrial Ca(2+) uptake and oxidative stress-induced apoptosis, which might represent therapeutic targets for oxidative stress related diseases.
Animals ; Apoptosis ; Biological Transport ; Calcium ; metabolism ; Calcium Channels ; metabolism ; Cerebellum ; cytology ; HeLa Cells ; Humans ; Mice ; Mitochondria ; metabolism ; Neurons ; cytology ; metabolism ; Oxidative Stress ; Voltage-Dependent Anion Channels ; metabolism