• Book : ()
• Pub. Date : 2025
• Page :
• Keyword :

Astrocytes are the most abundant type of glial cell in the central nervous system. Upon injury and inflammation, astrocytes become reactive and undergo morphological and functional changes. Depending on their phenotypic classification as A1 or A2, reactive astrocytes contribute to both neurotoxic and neuroprotective responses, respectively. However, this binary classification does not fully capture the diversity of astrocyte responses observed across different diseases and injuries. Transcriptomic analysis has revealed that reactive astrocytes have a complex landscape of gene expression profiles, which emphasizes the heterogeneous nature of their reactivity. Astrocytes actively participate in regulating central nervous system inflammation by interacting with microglia and other cell types, releasing cytokines, and influencing the immune response. The phosphoinositide 3-kinase (PI3K)/protein kinase B (AKT) signaling pathway is a central player in astrocyte reactivity and impacts various aspects of astrocyte behavior, as evidenced by in silico, in vitro, and in vivo results. In astrocytes, inflammatory cues trigger a cascade of molecular events, where nuclear factor-κB serves as a central mediator of the pro-inflammatory responses. Here, we review the heterogeneity of reactive astrocytes and the molecular mechanisms underlying their activation. We highlight the involvement of various signaling pathways that regulate astrocyte reactivity, including the PI3K/AKT/mammalian target of rapamycin (mTOR), αvβ3 integrin/PI3K/AKT/connexin 43, and Notch/PI3K/AKT pathways. While targeting the inactivation of the PI3K/AKT cellular signaling pathway to control reactive astrocytes and prevent central nervous system damage, evidence suggests that activating this pathway could also yield beneficial outcomes. This dual function of the PI3K/AKT pathway underscores its complexity in astrocyte reactivity and brain function modulation. The review emphasizes the importance of employing astrocyte-exclusive models to understand their functions accurately and these models are essential for clarifying astrocyte behavior. The findings should then be validated using in vivo models to ensure real-life relevance. The review also highlights the significance of PI3K/AKT pathway modulation in preventing central nervous system damage, although further studies are required to fully comprehend its role due to varying factors such as different cell types, astrocyte responses to inflammation, and disease contexts. Specific strategies are clearly necessary to address these variables effectively.

• Book : 20(4)
• Pub. Date : 2025
• Page : pp.1031-1041
• Keyword :

JOURNAL/nrgr/04.03/01300535-202506000-00028/figure1/v/2024-08-08T040853Z/r/image-tiff

The pathophysiology of Huntington’s disease involves high levels of the neurotoxin quinolinic acid. Quinolinic acid accumulation results in oxidative stress, which leads to neurotoxicity. However, the molecular and cellular mechanisms by which quinolinic acid contributes to Huntington’s disease pathology remain unknown. In this study, we established in vitro and in vivo models of Huntington’s disease by administering quinolinic acid to the PC12 neuronal cell line and the striatum of mice, respectively. We observed a decrease in the levels of hydrogen sulfide in both PC12 cells and mouse serum, which was accompanied by down-regulation of cystathionine β-synthase, an enzyme responsible for hydrogen sulfide production. However, treatment with NaHS (a hydrogen sulfide donor) increased hydrogen sulfide levels in the neurons and in mouse serum, as well as cystathionine β-synthase expression in the neurons and the mouse striatum, while also improving oxidative imbalance and mitochondrial dysfunction in PC12 cells and the mouse striatum. These beneficial effects correlated with upregulation of nuclear factor erythroid 2-related factor 2 expression. Finally, treatment with the nuclear factor erythroid 2-related factor 2 inhibitor ML385 reversed the beneficial impact of exogenous hydrogen sulfide on quinolinic acid-induced oxidative stress. Taken together, our findings show that hydrogen sulfide reduces oxidative stress in Huntington’s disease by activating nuclear factor erythroid 2-related factor 2, suggesting that hydrogen sulfide is a novel neuroprotective drug candidate for treating patients with Huntington’s disease.

• Book : 20(6)
• Pub. Date : 2025
• Page : pp.1776-1788
• Keyword :

Abstract

The Zircaloy alloy system (1.2-1.7 wt.% Sn) provides an excellent basis to study the effect of temperature on Pourbaix diagrams, as Zircaloy fuel rods in a CANadian Deuterium UraniumTM (CANDU) reactor are exposed to an aqueous phase coolant in the range 250 °C (523.15 K) to 310 °C (583.15 K). In addition to its presence in Zircaloy, much of the thermochemical data for tin, particularly for the aqueous species, is unavailable or uncorroborated. This paper presents tin Pourbaix diagrams at 85 °C (358.15 K) alongside the reconstructed 25 °C (298.15 K) diagram. Solid-aqueous phase SnO2 equilibria were used to determine thermochemical data for tin +IV species in a batch vessel with in situ pH measurement. Solubilities were used to calculate the Gibbs energies of Sn complexes. The SnOH3+ and Sn(OH)5− species were incorporated into the 25 °C and 85 °C diagrams.

• Book : 11(2)
• Pub. Date : 2025
• Page : pp.021602
• Keyword :

Abstract

Concentrated solar energy can be used as the source of heat at above 1000 °C for driving key energy-intensive industrial processes, such as cement manufacturing and metallurgical extraction, contributing to their decarbonization. The cornerstone technology is the solar receiver mounted on top of the solar tower, which absorbs the incident high-flux radiation and heats a heat transfer fluid. The proposed high-temperature solar receiver concept consists of a cavity containing a reticulated porous ceramic (RPC) structure for volumetric absorption of concentrated solar radiation entering through an open (windowless) aperture, which also serves for the access of ambient air used as the heat transfer fluid flowing across the RPC structure. A heat transfer analysis of the solar receiver is performed by means of two coupled models: a Monte Carlo (MC) ray-tracing model to solve the 3D radiative exchange and a computational fluid dynamics (CFD) model to solve the 2D convective and conductive heat transfer. Temperature distributions computed by the iteratively coupled models were compared with experimental data obtained by testing a lab-scale 5 kW receiver prototype with a silicon carbide RPC structure exposed to 3230 suns flux irradiation. The receiver model is applied to optimize its dimensions for maximum efficiency and to scale-up for a 5 MW solar tower.

• Book : 147(2)
• Pub. Date : 2025
• Page : pp.021007
• Keyword :

Subarachnoid hemorrhage leads to a series of pathological changes, including vascular spasm, cellular apoptosis, blood-brain barrier damage, cerebral edema, and white matter injury. Microglia, which are the key immune cells in the central nervous system, maintain homeostasis in the neural environment, support neurons, mediate apoptosis, participate in immune regulation, and have neuroprotective effects. Increasing evidence has shown that microglia play a pivotal role in the pathogenesis of subarachnoid hemorrhage and affect the process of injury and the prognosis of subarachnoid hemorrhage. Moreover, microglia play certain neuroprotective roles in the recovery phase of subarachnoid hemorrhage. Several approaches aimed at modulating microglia function are believed to attenuate subarachnoid hemorrhage injury. This provides new targets and ideas for the treatment of subarachnoid hemorrhage. However, an in-depth and comprehensive summary of the role of microglia after subarachnoid hemorrhage is still lacking. This review describes the activation of microglia after subarachnoid hemorrhage and their roles in the pathological processes of vasospasm, neuroinflammation, neuronal apoptosis, blood-brain barrier disruption, cerebral edema, and cerebral white matter lesions. It also discusses the neuroprotective roles of microglia during recovery from subarachnoid hemorrhage and therapeutic advances aimed at modulating microglial function after subarachnoid hemorrhage. Currently, microglia in subarachnoid hemorrhage are targeted with TLR inhibitors, nuclear factor-κB and STAT3 pathway inhibitors, glycine/tyrosine kinases, NLRP3 signaling pathway inhibitors, Gasdermin D inhibitors, vincristine receptor α receptor agonists, ferroptosis inhibitors, genetic modification techniques, stem cell therapies, and traditional Chinese medicine. However, most of these are still being evaluated at the laboratory stage. More clinical studies and data on subarachnoid hemorrhage are required to improve the treatment of subarachnoid hemorrhage.

• Book : 20(7)
• Pub. Date : 2025
• Page : pp.1829-1848
• Keyword :

• Book : 210()
• Pub. Date : 2025
• Page : pp.110840
• Keyword :

• Book : 210()
• Pub. Date : 2025
• Page : pp.110885
• Keyword :

• Book : 210()
• Pub. Date : 2025
• Page : pp.110852
• Keyword :

• Book : 109()
• Pub. Date : 2025
• Page : pp.80-91
• Keyword :