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Background: Central nervous system (CNS) injury is the most prominent feature of heatstroke and the hippocampus is prone to damage. However, the mechanisms underlying the heatstroke-induced hippocampal injury remain unclear. Hyperbaric oxygen (HBO) therapy prevents CNS injury in heatstroke mice. However, the underlying mechanisms of HBO in heatstroke-induced hippocampal injury remain unclear. This study aimed to elucidate the protective effects of HBO against hippocampal injury and its potential role in microglial pyroptosis in heatstroke rats.Methods: A rat heatstroke model and a heat stress model with a mouse microglial cell line (BV2) were, respectively, used to illustrate the effect of HBO on heat-induced microglial pyroptosis in vivo and in vitro. We used a combination of molecular and histological methods to assess microglial pyroptosis and neuroinflammation both in vivo and in vitro.Results: The results revealed that HBO improved heatstroke-induced survival outcomes, hippocampal injury, and neurological dysfunction in rats. In addition, HBO mitigates microglial pyroptosis and reduces the expression of pro-inflammatory cytokines in the hippocampus of heatstroke rats. In vitro experiments showed that HBO attenuated BV2 cell injury under heat stress. Furthermore, HBO prevented heat-induced pyroptosis of BV2 cells, and the expression of pro-inflammatory cytokines IL-18 and IL-1β was reduced. Mechanistically, HBO alleviates heatstroke-induced neuroinflammation and hippocampal injury by preventing microglial pyroptosis. Conclusions: In conclusion, HBO attenuates heatstroke-induced neuroinflammation and hippocampal injury by inhibiting microglial pyroptosis.

BACKGROUND: The mechanisms underlying heat stroke (HS)-induced hippocampal injury remain unclear. This study aimed to evaluate the HS-induced metabonomics of hippocampal and cerebellar transmitters. METHODS: The HS model was established with male Sprague-Dawley rats subjected to heat exposure of up to 42 °C at a humidity of (55.0±5.0)%. The hippocampal and cerebellar transmitters and metabolites of rats were tested via ultra-high-performance liquid chromatography--mass spectrometry (UPLC-MS/MS). The primary transmitters and metabolites were identified by principal component analysis (PCA) and orthogonal partial least square-discriminant analysis (OPLS-DA). The major metabolic pathways for HS were selected after enrichment. The brain injury was evaluated by histological tests. RESULTS: HS induced hippocampal and cerebellar injuries in rats. HS upregulated the protein levels of hippocampal glutamate, glutamine, gamma-aminobutyric acid, L-tryptophan (Trp), 5-hydroxy-indoleacetic acid, and kynurenine; however, it downregulated asparagine, tryptamine, 5-hydroxytryptophan, melatonin, 3,4-dihydroxyphenylalanine (L-DOPA), and vanillylmandelic acid. HS also sharply elevated the protein levels of cerebellar methionine and Trp, and decreased the levels of serotonin, L-alanine, L-asparagine, L-aspartate, cysteine, norepinephrine, spermine, spermidine, and tyrosine. Hippocampal glutamate, monoamine transmitters, cerebellar aspartate acid, and catecholamine transmitters' metabolic pathways were identified as the main metablic pathways in HS. CONCLUSION: The hippocampus and cerebellum were injured in rats with HS, possibly induced the disorder of hippocampal glutamate and serotonin metabolism, cerebellar aspartate acid and catecholamine transmitter metabolism, and related metabolic pathways. [ABSTRACT FROM AUTHOR]

This paper introduces the research advances on replacement of CH4 in Natural Gas Hydrates (NGHs) by use of CO2 and discusses the advantages and disadvantages of the method on the natural gas production from such hydrates. Firstly, the feasibility of replacement is proven from the points of view of kinetics and thermodynamics, and confirmed by experiments. Then, the latest progress in CH4 replacement experiments with gaseous CO2, liquid CO2 and CO2 emulsion are presented Moreover, the superiority of CO2 emulsion for replacement of CH4 is emphasized. The latest experiment progress on preparation of CO2 emulsions are introduced. Finally, the advancements in simulation research on replacement is introduced, and the deficiencies of the simulations are pointed. The factors influencing on the replacement with different forms of CO2 are analyzed and the optimum conditions for the replacement of CH4 in hydrated with different forms of CO2 is suggested.

This paper introduces the research advances on replacement of CH4 in Natural Gas Hydrates (NGHs) by use of CO2 and discusses the advantages and disadvantages of the method on the natural gas production from such hydrates. Firstly, the feasibility of replacement is proven from the points of view of kinetics and thermodynamics, and confirmed by experiments. Then, the latest progress in CH4 replacement experiments with gaseous CO2, liquid CO2 and CO2 emulsion are presented Moreover, the superiority of CO2 emulsion for replacement of CH4 is emphasized. The latest experiment progress on preparation of CO2 emulsions are introduced. Finally, the advancements in simulation research on replacement is introduced, and the deficiencies of the simulations are pointed. The factors influencing on the replacement with different forms of CO2 are analyzed and the optimum conditions for the replacement of CH4 in hydrated with different forms of CO2 is suggested. [ABSTRACT FROM AUTHOR]

Background: Central nervous system (CNS) injury is the most prominent feature of heatstroke and the hippocampus is prone to damage. However, the mechanisms underlying the heatstroke-induced hippocampal injury remain unclear. Hyperbaric oxygen (HBO) therapy prevents CNS injury in heatstroke mice. However, the underlying mechanisms of HBO in heatstroke-induced hippocampal injury remain unclear. This study aimed to elucidate the protective effects of HBO against hippocampal injury and its potential role in microglial pyroptosis in heatstroke rats.Methods: A rat heatstroke model and a heat stress model with a mouse microglial cell line (BV2) were, respectively, used to illustrate the effect of HBO on heat-induced microglial pyroptosis in vivo and in vitro. We used a combination of molecular and histological methods to assess microglial pyroptosis and neuroinflammation both in vivo and in vitro.Results: The results revealed that HBO improved heatstroke-induced survival outcomes, hippocampal injury, and neurological dysfunction in rats. In addition, HBO mitigates microglial pyroptosis and reduces the expression of pro-inflammatory cytokines in the hippocampus of heatstroke rats. In vitro experiments showed that HBO attenuated BV2 cell injury under heat stress. Furthermore, HBO prevented heat-induced pyroptosis of BV2 cells, and the expression of pro-inflammatory cytokines IL-18 and IL-1β was reduced. Mechanistically, HBO alleviates heatstroke-induced neuroinflammation and hippocampal injury by preventing microglial pyroptosis. Conclusions: In conclusion, HBO attenuates heatstroke-induced neuroinflammation and hippocampal injury by inhibiting microglial pyroptosis. [ABSTRACT FROM AUTHOR]

Acidic gas penetration through the internal pressure sheath of a flexible riser tends to cause a corrosive environment in the annulus, reducing the service life of the flexible riser. Nanoparticles can act as gas barriers in the polymer matrix to slow down the gas permeation. Herein, we prepared PA11/SiO2 composites by the melt blending method. The effect of adding different amounts of SiO2 to PA11 on its gas barrier properties was investigated by conducting CO2 permeation tests between 20 °C and 90 °C. As the temperature increased, the lowest value of the permeability coefficient that could be achieved for the PA11 with different contents of SiO2 increased. The composites PA/0.5% SiO2 and PA/1.5% SiO2 had the lowest permeation coefficients in the glassy state (20 °C) and rubbery state (≥50 °C). We believe that this easy-to-produce industrial PA/SiO2 composite can be used to develop high-performance flexible riser barrier layers. It is crucial for understanding riser permeation behavior and enhancing barrier qualities. [ABSTRACT FROM AUTHOR]

Extensive research focused on finding effective strategies to prevent or improve recovery from myocardial ischaemia/reperfusion (I/R) injury. Basic fibroblast growth factor (b FGF) has been shown to have therapeutic potential in some heart disorders, including ischaemic injury. In this study, we demonstrate that b FGF administration can inhibit the endoplasmic reticulum ( ER) stress and mitochondrial dysfunction induced in the heart in a mouse model of I/R injury. In vitro, b FGF exerts a protective effect by inhibiting the ER stress response and mitochondrial dysfunction proteins that are induced by tert-Butyl hydroperoxide ( TBHP) treatment. Both of these in vivo and in vitro effects are related to the activation of two downstream signalling pathways, PI3K/Akt and ERK1/2. Inhibition of these PI3K/Akt and ERK1/2 pathways by specific inhibitors, LY294002 and PD98059, partially reduces the protective effect of b FGF. Taken together, our results indicate that the cardioprotective role of b FGF involves the suppression of ER stress and mitochondrial dysfunction in ischaemic oxidative damage models and oxidative stress-induced H9C2 cell injury; furthermore, these effects underlie the activation of the PI3K/Akt and ERK1/2 signalling pathways. [ABSTRACT FROM AUTHOR]