Numerical Simulation and Optimization of a Phase-Change Energy Storage Box in a Modular Mobile Thermal Energy Supply System

Featuring phase-change energy storage, a mobile thermal energy supply system (M-TES) demonstrates remarkable waste heat transfer capabilities across various spatial scales and temporal durations, thereby effectively optimizing the localized energy distribution structure—a pivotal contribution to the attainment of objectives such as “carbon peak” and “carbon neutral”. To heighten the efficiency of energy transfer for mobile heating, this research introduces the innovative concept of modular storage and transportation. This concept is brought to life through the development of a meticulously designed modular mobile phase-change energy storage compartment system. Employing computational fluid dynamics (CFD), an in-depth exploration into the performance of the modular M-TES container and the adapted phase-change material (PCM) is conducted. By implementing fin arrangements on the inner wall of the heat storage module, a remarkable upsurge in the liquid phase-transition rate of the phase-change material is achieved in comparison to the design lacking fins—this improvement approximating around 30%. However, it is essential to acknowledge that the augmentation in heat transfer gradually recedes with the proliferation of fins or an escalation in their height. Moreover, the integration of expanded graphite into erythritol emerges as profoundly effective in amplifying the thermal conductivity of the PCM. Notably, with the addition of a 15.2% volume fraction of expanded graphite to erythritol, the duration of heat storage experiences a drastic reduction to nearly 10% of its original duration, thereby signifying a momentous advancement in thermal performance

QSOX1 regulates trophoblastic apoptosis in preeclampsia through hydrogen peroxide production.

OBJECTIVE: Oxidative stress plays a significant role in the pathogenesis of preeclampsia (PE), by inducing trophoblast cell death and consequent placental dysfunction. Quiescin sulfhydryl oxidase 1 (QSOX1) is upregulated in many types of cancer cells; it promotes disulfide bond formation as well as hydrogen peroxide (H2O2) production. The aims of present study are to investigate the expression pattern of QSOX1 in placentae of pregnancies complicated by PE and the role of QSOX1 in the regulation of trophoblastic function, thus providing in-depth understanding of the putative involvement of QSOX1 in the development of PE. METHODS: Human term placenta from normal pregnancies and from pregnancies complicated by PE were collected to measure QSOX1 expression and H2O2 levels. Down-regulation of QSOX1 in HTR-8/Svneo cells was achieved by siRNA interference. An in vitro cellular PE model was generated by hypoxic incubation. Protein expression levels were assessed by Western blotting, and H2O2 levels were determined in the cell culture medium as well as in the cell lysate. Trophoblast apoptosis was evaluated by TUNEL staining. RESULTS: QSOX1 was overexpressed in the PE placenta. Inhibition of QSOX1 expression in HTR-8/Svneo cells attenuated cell apoptosis and intracellular H2O2 levels. Hypoxia induced QSOX1 expression in HTR-8/Svneo cells and led to apoptosis of HTR-8/Svneo cells, and knock-down of QSOX1 rescued hypoxia induced trophoblast apoptosis. CONCLUSIONS: Hypoxia induced up-regulation of QSOX1 and a consequent elevation in intracellular H2O2 increased apoptosis in placentae of pregnancies complicated by PE

Phosphorylation of Yes-associated protein impairs trophoblast invasion and migration: implications for the pathogenesis of fetal growth restriction

Fetal growth restriction (FGR) is a condition in which a newborn fails to achieve his or her prospective hereditary growth potential. This condition is associated with high newborn mortality, second only to that associated with premature birth. FGR is associated with maternal, fetal, and placental abnormalities. Although the placenta is considered to be an important organ for supplying nutrition for fetal growth, research on FGR is limited, and treatment through the placenta remains challenging, as neither proper uterine intervention nor its pathogenesis have been fully elucidated. Yes-associated protein (YAP), as the effector of the Hippo pathway, is widely known to regulate organ growth and cancer development. Therefore, the correlation of the placenta and YAP was investigated to elucidate the pathogenic mechanism of FGR. Placental samples from humans and mice were collected for histological and biomechanical analysis. After investigating the location and role of YAP in the placenta by immunohistochemistry, we observed that YAP and cytokeratin 7 have corresponding locations in human and mouse placentas. Moreover, phosphorylated YAP (p-YAP) was upregulated in FGR and gradually increased as gestational age increased during pregnancy. Cell function experiments and mRNA-Seq demonstrated impaired YAP activity mediated by extracellular signal-regulated kinase inhibition. Established FGR-like mice also recapitulated a number of the features of human FGR. The results of this study may help to elucidate the association of FGR development with YAP and provide an intrauterine target that may be helpful in alleviating placental dysfunction