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 :

• Book : 41(3)
• Pub. Date : 2025
• Page : pp.124258
• Keyword :

Reperfusion following cerebral ischemia causes both structural and functional damage to brain tissue and could aggravate a patient’s condition; this phenomenon is known as cerebral ischemia-reperfusion injury. Current studies have elucidated the neuroprotective role of the sirtuin protein family (Sirtuins) in modulating cerebral ischemia-reperfusion injury. However, the potential of utilizing it as a novel intervention target to influence the prognosis of cerebral ischemia-reperfusion injury requires additional exploration. In this review, the origin and research progress of Sirtuins are summarized, suggesting the involvement of Sirtuins in diverse mechanisms that affect cerebral ischemia-reperfusion injury, including inflammation, oxidative stress, blood-brain barrier damage, apoptosis, pyroptosis, and autophagy. The therapeutic avenues related to Sirtuins that may improve the prognosis of cerebral ischemia-reperfusion injury were also investigated by modulating Sirtuins expression and affecting representative pathways, such as nuclear factor-kappa B signaling, oxidative stress mediated by adenosine monophosphate-activated protein kinase, and the forkhead box O. This review also summarizes the potential of endogenous substances, such as RNA and hormones, drugs, dietary supplements, and emerging therapies that regulate Sirtuins expression. This review also reveals that regulating Sirtuins mitigates cerebral ischemia-reperfusion injury when combined with other risk factors. While Sirtuins show promise as a potential target for the treatment of cerebral ischemia-reperfusion injury, most recent studies are based on rodent models with circadian rhythms that are distinct from those of humans, potentially influencing the efficacy of Sirtuins-targeting drug therapies. Overall, this review provides new insights into the role of Sirtuins in the pathology and treatment of cerebral ischemia-reperfusion injury.

• Book : 20(8)
• Pub. Date : 2025
• Page : pp.2199-2217
• Keyword :