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How corporate strategic disclosure affects investor evaluations is a crucial and widely discussed question. Although prior literature has spent efforts analyzing the information effect of strategic alliances on investor reactions, whether this effect can extend to the cost of equity capital still needs to be explored. Using data from China's A‐share listed firms from 2007 to 2021, we examine the impact of disclosing strategic collaborative agreements on equity capital costs. We find that disclosing strategic collaborative agreements relates to lower equity capital costs. These results hold after several robustness checks. The mechanism test reveals that announcing strategic collaborative agreements alleviates equity capital costs mainly through the information effect. Moreover, this effect is more salient in firms with lower agency costs, lower media coverage, positive media sentiment, and higher media quality. These findings suggest that strategic collaborative agreements provide investors with valuable information. [ABSTRACT FROM AUTHOR]

Background: Lacunar stroke accounts for a quarter of all strokes, but little is known about the underlying pathological mechanisms. Analysis of serum metabolites may allow better understanding of the underlying biological processes. Mendelian randomization (MR) can provide information on the causality of associations. Aims: To identify causal relationships between serum metabolites and lacunar stroke. Methods: We applied a two-sample MR analysis to evaluate relationships between 486 serum metabolites and lacunar stroke. The inverse-variance weighted (IVW) method was used to estimate the causal relationship of the exposure on the outcome, while sensitivity analyses were performed using MR-Egger, weighted median, and MR-PRESSO to eliminate the pleiotropy. We also performed a metabolic pathway analysis to identify potential metabolic pathways. Results: We identified 15 known (8 risk and 7 protective) and 14 unknown serum metabolites associated with lacunar stroke. Among the known risk metabolites, two were lipids (1-linoleoylglycerophosphoethanolamine and dihomo-linolenate (20:3n3 or n6)), five amino acids (kynurenine, isobutyrylcarnitine, aspartate, trans-4-hydroxyproline, and 3-methyl-2-oxovalerate), and one peptide (ADSGEGDFXAEGGGVR). The known protective metabolites included four lipids (4-androsten-3beta,17beta-diol disulfate 1, 1-palmitoleoylglycerophosphocholine, adrenate (22:4n6), and glycodeoxycholate), one amino acid (methionine), and two exogenous metabolites (homostachydrine and 2-methoxyacetaminophen sulfate). Metabolic pathway analysis identified several pathways that might be involved in the disease. Conclusion: We identified eight risk and seven protective human serum metabolites associated with lacunar stroke. Isobutyrylcarnitine was positively associated with an increased risk of lacunar stroke. In addition, 3-methyl-2-oxovalerate and aspartate may be involved in the disease pathogenesis through metabolic pathways. [ABSTRACT FROM AUTHOR]

Background: The functions of infiltrating CD8 + T cells are often impaired due to tumor cells causing nutrient deprivation in the tumor microenvironment. Thus, the mechanisms of CD8 + T cell dysfunction have become a hot research topic, and there is increased interest on how changes in metabolomics correlate with CD8 + T cell dysfunction., Aim: To investigate whether and how glutamine metabolism affects the function of infiltrating CD8 + T cells in hepatocellular carcinoma., Methods: Immunohistochemical staining and immunofluorescence were performed on surgically resected liver tissues from patients. Differentially expressed genes in infiltrating CD8 + T cells in hepatocellular carcinoma were detected using RNA sequencing. Activated CD8 + T cells were co-cultured with Huh-7 cells for 3 d. The function and mitochondrial status of CD8 + T cells were analyzed by flow cytometry, quantitative real-time polymerase chain reaction, and transmission electron microscopy. Next, CD8 + T cells were treated with the mitochondrial protective and damaging agents. Functional alterations in CD8 + T cells were detected by flow cytometry. Then, complete medium without glutamine was used to culture cells and their functional changes and mitochondrial status were detected., Results: There were a large number of infiltrating PD-1 + CD8 + T cells in liver cancer tissues. Next, we co-cultured CD8 + T cells and Huh-7 cells to explore the regulatory effect of hepatoma cells on CD8 + T cells. Flow cytometry results revealed increased PD-1 expression and decreased secretion of perforin (PRF1) and granzyme B (GZMB) by CD8 + T cells in the co-culture group. Meanwhile, JC-1 staining was decreased and the levels of reactive oxygen species and apoptosis were increased in CD8 + T cells of the co-culture group; additionally, the mitochondria of these cells were swollen. When CD8 + T cells were treated with the mitochondrial protective and damaging agents, their function was restored and inhibited, respectively, through the mitochondrial damage and apoptotic pathways. Subsequently, complete medium without glutamine was used to culture cells. As expected, CD8 + T cells showed functional downregulation, mitochondrial damage, and apoptosis., Conclusion: Glutamine deprivation impairs the function of infiltrating CD8 + T cells in hepatocellular carcinoma through the mitochondrial damage and apoptotic pathways., Competing Interests: Conflict-of-interest statement: All the authors report no relevant conflicts of interest for this article., (©The Author(s) 2022. Published by Baishideng Publishing Group Inc. All rights reserved.)