Search

Recryopreservation (recryo) is occasionally applied in clinical, while the underlying mechanism of impaired clinical outcomes after recryo remains unclear. In this study, frozen embryo transfer (FET) cycles of single blastocyst transfer in an academic reproductive medicine center were enrolled. According to the number of times blastocysts experienced cryopreservation, they were divided into the cryopreservation (Cryo) group and the Recryo group. Donated human blastocysts were collected and detected for mechanism exploration. It was found that recryo procedure resulted in impaired blastocyst developmental potential, including decreased implantation rate, reduced biochemical pregnancy rate, declined clinical pregnancy rate, higher early miscarriage rate, and lower live birth rate. Moreover, recryo led to impaired trophectoderm (TE) function, exhibiting lower human chorionic gonadotropin levels 12 days after FET. In addition, single‐cell RNA sequencing showed that the expression of genes involved in cell adhesion and embryo development were altered. More specifically, activated endoplasmic reticulum (ER) pathway and induced apoptosis were further verified by immunofluorescence and terminal deoxynucleotidyl transferase‐mediated dUTP nick‐end labeling (TUNEL) assay involving in the recryo procedure. In conclusion, recryo could interfere with the process of blastocyst implantation by impairing TE function, affecting blastocyst adhesion, activating ER stress pathway and inducing apoptosis. It provides caution to embryologists about the potential risk of recryopreservation. [ABSTRACT FROM AUTHOR]

Atherosclerosis (AS) is a chronic inflammatory arterial disease, in which abnormal lipid metabolism and foam cell formation play key roles. Histamine is a vital biogenic amine catalyzed by histidine decarboxylase (HDC) from L-histidine. Histamine H1 receptor (H1R) antagonist is a commonly encountered anti-allergic agent in the clinic. However, the role and mechanism of H1R in atherosclerosis have not been fully elucidated. Here, we explored the effect of H1R on atherosclerosis using Apolipoprotein E-knockout (ApoE−/−) mice with astemizole (AST, a long-acting H1R antagonist) treatment. The results showed that AST increased atherosclerotic plaque area and hepatic lipid accumulation in mice. The result of microarray study identified a significant change of endothelial lipase (LIPG) in CD11b+ myeloid cells derived from HDC-knockout (HDC−/−) mice compared to WT mice. Blocking H1R promoted the formation of foam cells from bone marrow-derived macrophages (BMDMs) of mice by up-regulating p38 mitogen-activated protein kinase (p38 MAPK) and LIPG signaling pathway. Taken together, these findings demonstrate that blocking H1R signal aggravates atherosclerosis by promoting abnormal lipid metabolism and macrophage-derived foam cell formation via p38 MAPK-LIPG signaling pathway. Key messages: Blocking H1R signal with AST aggravated atherosclerosis and increased hepatic lipid accumulation in high-fat diet (HFD)-fed ApoE−/− mice. Blocking H1R signal promoted macrophage-derived foam cell formation via p38 MAPK-LIPG signaling pathway. [ABSTRACT FROM AUTHOR]

The persulfate-based advanced oxidation process has been an effective method for refractory organic pollutants' degradation in aqueous phase. Herein, α-MnO2 with nanowire morphology was facially fabricated via a one-step hydrothermal method and successfully activated peroxymonosulfate (PMS) for Rhodamine B (RhB) degradation. Influencing factors, including the hydrothermal parameter, PMS concentration, α-MnO2 dosage, RhB concentration, initial pH, and anions, were systematically investigated. The corresponding reaction kinetics were further fitted by the pseudo-first-order kinetic. The RhB degradation mechanism via α-MnO2 activating PMS was proposed according to a series of quenching experiments and the UV-vis scanning spectrum. Results showed that α-MnO2 could effectively activate PMS to degrade RhB and has good repeatability. The catalytic RhB degradation reaction was accelerated by increasing the catalyst dosage and the PMS concentration. The effective RhB degradation performance can be attributed to the high content of surface hydroxyl groups and the greater reducibility of α-MnO2, and the contribution of different ROS (reactive oxygen species) was 1O2 > O 2 · − > SO 4 · − > ·OH. [ABSTRACT FROM AUTHOR]

Cardiac fibrosis is an important pathological basis of various cardiovascular diseases. The roles of STAT6 signal in allergy, immune regulation, tumorigenesis, and renal fibrosis have been documented. However, the function and mechanism of STAT6 signal in sympathetic overactivation-induced cardiac fibrosis have not been fully elucidated. This study explores the novel role of STAT6 signal in isoproterenol (ISO)–induced cardiac fibrosis through the regulation of inflammatory response and the differentiation of macrophages from immature myeloid cells. The expression levels of STAT6, β1-adrenergic receptor (β1-AR), and inflammatory factors [interleukin α (IL-1α), IL-6, IL-18, and transforming growth factor β (TGF-β)] in CD11b+ myeloid cells were analyzed with a microarray study. The levels of IL-6 and TGF-β1 in the CD11b+ myeloid cells–derived macrophages were detected with reverse transcriptase–polymerase chain reaction (RT-PCR). STAT6–knockout (KO) and WT mice were used to establish a murine cardiac fibrosis model by ISO injection. Cardiac fibroblasts were isolated from the hearts of newborn STAT6-KO and WT mice, and STAT6 expression was measured by Western blotting and RT-PCR after ISO stimulation, while α-smooth muscle actin (α-SMA) expression was detected by immunofluorescence and immunohistochemistry staining. Cardiac function and pathological characteristics were examined by echocardiography and immunohistochemistry staining, respectively. Immunohistochemistry staining with anti-CD11b was performed to detect the infiltration of CD11b+ myeloid cells in heart tissue. Flow cytometry analysis was used to measure the percentages of CD11b+ myeloid cells and CD11b+Ly6C+ macrophages in the peripheral blood. The results showed that STAT6 was highly expressed in CD11b+ myeloid cells located in injured hearts, and STAT6 expression in cardiac fibroblasts was down-regulated after ISO treatment. STAT6 deficiency further aggravated ISO-induced increased expression of α-SMA in cardiac fibroblasts, myocardial fibrosis, and cardiac dysfunction. The activation of ISO/β1-AR signal aggravated cardiac inflammatory infiltration, promoted CD11b+ myeloid cell mobilization, and enhanced CD11b+Ly6C+/low macrophage differentiation, which was further exacerbated by STAT6 deficiency. Furthermore, β1-AR mRNA expression significantly increased in splenic CD11b+ myeloid cells compared to their bone marrow–derived controls, and STAT6 deficiency promoted β1-AR expression in an MI-induced sensitive cardiac fibrosis mouse model. The spleen-derived CD11b+ myeloid cells of STAT6-KO mice produced more IL-1α, IL-18, and TGF-β than their WT counterparts. Taken together, these results suggest that STAT6 signal plays a critical role in ISO-induced β1-AR overactivation and systemic inflammatory cascades, contributing to cardiac fibrogenesis. STAT6 should be a promising cardioprotective target against myocardial fibrosis and heart failure after β1-AR overactivation–induced myocardial injury. [ABSTRACT FROM AUTHOR]

Designing defect‐rich MoS2/C architectures with three‐dimensional (3D) porous frame effectively improve the electrochemical performance of lithium‐ion batteries (LIBs) owing to the improved conductivity and decreased diffusion distance of Li+ ions for lithium storage. Herein, we report a reliable morphology engineering method combining with tunable defects to synthesize defect‐rich MoS2 nanosheets with a few layers entrapped carbon sheath, forming a 3D porous conductive network architecture. The defect‐rich MoS2 nanosheets with expanded interlayers can provide a shortened ion diffusion path, and realize the 3D Li+ diffusion with faster kinetics. A 3D conductive interconnected carbon network is able to improve interparticle conductivity, concurrently maintaining the structural integrity. Benefiting from these intriguing features, the as‐prepared MoS2/C architectures exhibit excellent electrochemical performance: a high reversible capacity of 1163 mAh g−1 at a current density of 0.1 A g−1 after 100 cycles and a high rate capability of 800 mAh g−1 at 5 A g−1. Defect content in MoS2/C architectures can be obtained by changing H2 concentration. Compared with the counterparts with few defects, the defect‐rich MoS2/C architectures show improved electrochemical stability with a superior cycle life, illustrating a highly reversible capacity of 751 mAh g−1 at 0.5 A g−1 after 500 cycles. [ABSTRACT FROM AUTHOR]