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CO2 storage in basalt formation has received much attention as one of the new CO2 geological storage methods worldwide. It has been successfully implemented in Iceland and the United States. During the process of carbon storage in basalt, CO2 is transformed into solid minerals, which differs significantly from carbon storage in sandstone reservoirs in terms of CO2 injection method, burial depth, and physical property requirements of reservoir cap. Significant differences are also found in both monitoring schemes. By studying the Wallula basalt storage project in the United States and the Carbfix mineralization storage project in Iceland, this study compared and summarized the monitoring schemes of basalt storage for different CO2 injection phases (supercritical and gas dissolved state). The monitoring systems of basalt storage, saline aquifer storage, oil and gas reservoir storage were further compared. The storage monitoring system for sandstone reservoir focuses on the structural integrity of the CO2 reservoir and evaluating the change of CO2 concentration along the potential leakage path. The monitoring period is usually more than 50 years. In contrast, basalt mineralization and storage technology focus on the mineralization reaction of “water-CO2-basalt”. Its monitoring system is mainly to describe the property changing pattern of each substance from downhole fluid (chemical compositions, tracer concentrations, pH, etc.) during the storage cycle. Moreover, it evaluates the degree of mineralization reaction and the storage efficiency of basalt qualitatively and quantitatively. Finally, based on the systematic and comprehensive monitoring scheme of saline aquifer and oil and gas reservoir storage, the basalt-CO2 mineralization storage monitoring technology is analyzed systematically and a complete set of basalt-CO2 mineralization storage monitoring scheme and process is summarized. By comparing different CO2 storage monitoring systems, this study proposes a universal “subsurface-wellbore-surface-ground” monitoring scheme for basalt-CO2 mineralization: monitoring scope, purpose, program, and alert system. This provides basic information for the future basalt-CO2 mineralization storage demonstration project.

Summary: Hyperfunction of the dopamine system has been implicated in manic episodes in bipolar disorders. How dopaminergic neuronal function is regulated in the pathogenesis of mania remains unclear. Histaminergic neurons project dense efferents into the midbrain dopaminergic nuclei. Here, we present mice lacking dopaminergic histamine H2 receptor (H2R) in the ventral tegmental area (VTA) that exhibit a behavioral phenotype mirroring some of the symptoms of mania, including increased locomotor activity and reduced anxiety- and depression-like behavior. These behavioral deficits can be reversed by the mood stabilizers lithium and valproate. H2R deletion in dopaminergic neurons significantly enhances neuronal activity, concurrent with a decrease in the γ-aminobutyric acid (GABA) type A receptor (GABAAR) membrane presence and inhibitory transmission. Conversely, either overexpression of H2R in VTA dopaminergic neurons or treatment of H2R agonist amthamine within the VTA counteracts amphetamine-induced hyperactivity. Together, our results demonstrate the engagement of H2R in reducing VTA dopaminergic activity, shedding light on the role of H2R as a potential target for mania therapy.

ObjectiveEmerging evidence has shown that gut diseases can regulate the development and function of the immune, metabolic, and nervous systems through dynamic bidirectional communication on the brain-gut axis. However, the specific mechanism of intestinal diseases and vascular dementia (VD) remains unclear. We designed this study especially, to further clarify the connection between VD and inflammatory bowel disease (IBD) from bioinformatics analyses.MethodsWe downloaded Gene expression profiles for VD (GSE122063) and IBD (GSE47908, GSE179285) from the Gene Expression Omnibus (GEO) database. Then individual Gene Set Enrichment Analysis (GSEA) was used to confirm the connection between the two diseases respectively. The common differentially expressed genes (coDEGs) were identified, and the STRING database together with Cytoscape software were used to construct protein-protein interaction (PPI) network and core functional modules. We identified the hub genes by using the Cytohubba plugin. Gene Ontology (GO) and Kyoto Encyclopedia of Genes and Genomes (KEGG) pathway enrichment analysis were applied to identify pathways of coDEGs and hub genes. Subsequently, receiver operating characteristic (ROC) analysis was used to identify the diagnostic ability of these hub genes, and a training dataset was used to verify the expression levels of the hub genes. An alternative single-sample gene set enrichment (ssGSEA) algorithm was used to analyze immune cell infiltration between coDEGs and immune cells. Finally, the correlation between hub genes and immune cells was analyzed.ResultsWe screened 167 coDEGs. The main articles of coDEGs enrichment analysis focused on immune function. 8 shared hub genes were identified, including PTPRC, ITGB2, CYBB, IL1B, TLR2, CASP1, IL10RA, and BTK. The functional categories of hub genes enrichment analysis were mainly involved in the regulation of immune function and neuroinflammatory response. Compared to the healthy controls, abnormal infiltration of immune cells was found in VD and IBD. We also found the correlation between 8 shared hub genes and immune cells.ConclusionsThis study suggests that IBD may be a new risk factor for VD. The 8 hub genes may predict the IBD complicated with VD. Immune-related coDEGS may be related to their association, which requires further research to prove.

The sealing performance of a bentonite barrier is highly dependent on its seepage characteristics, which are directly related to the characteristics of its pore structure. Based on scanning electron microscopy (SEM) and focused ion beam-SEM (FIB-SEM), the pore structure of bentonite was characterized at different scales. First, a reasonable gray threshold was determined through back analysis, and the image was binarized based on the threshold. In addition, binary images were used to analyze bentonite's pore structure (porosity and pore size distribution). Furthermore, the effects of different algorithms on the pore structure characterization were evaluated. Then, permeability calculations were performed based on the previous pore structure characteristics and a modified permeability prediction model. For permeability prediction based on the three-dimensional model, the effect of pore tortuosity was also considered. Finally, the accuracy of numerical calculations was verified by conducting macroscopic gas and alcohol permeability experiments. This approach provides a better understanding of the microscale mechanism of gas transport in bentonite and the importance of pore structures at different scales in determining its seepage characteristics.

BackgroundAlzheimer’s disease (AD), a common neurological disorder, has no effective treatment due to its complex pathogenesis. Disulfidptosis, a newly discovered type of cell death, seems to be closely related to the occurrence of various diseases. In this study, through bioinformatics analysis, the expression and function of disulfidptosis-related genes (DRGs) in Alzheimer’s disease were explored.MethodsDifferential analysis was performed on the gene expression matrix of AD, and the intersection of differentially expressed genes and disulfidptosis-related genes in AD was obtained. Hub genes were further screened using multiple machine learning methods, and a predictive model was constructed. Finally, 97 AD samples were divided into two subgroups based on hub genes.ResultsIn this study, a total of 22 overlapping genes were identified, and 7 hub genes were further obtained through machine learning, including MYH9, IQGAP1, ACTN4, DSTN, ACTB, MYL6, and GYS1. Furthermore, the diagnostic capability was validated using external datasets and clinical samples. Based on these genes, a predictive model was constructed, with a large area under the curve (AUC = 0.8847), and the AUCs of the two external validation datasets were also higher than 0.7, indicating the high accuracy of the predictive model. Using unsupervised clustering based on hub genes, 97 AD samples were divided into Cluster1 (n = 24) and Cluster2 (n = 73), with most hub genes expressed at higher levels in Cluster2. Immune infiltration analysis revealed that Cluster2 had a higher level of immune infiltration and immune scores.ConclusionA close association between disulfidptosis and Alzheimer’s disease was discovered in this study, and a predictive model was established to assess the risk of disulfidptosis subtype in AD patients. This study provides new perspectives for exploring biomarkers and potential therapeutic targets for Alzheimer’s disease.

Abstract Mitophagy is a highly conserved cellular process that maintains the mitochondrial quantity by eliminating dysfunctional or superfluous mitochondria through autophagy machinery. The mitochondrial outer membrane protein BNIP3L/Nix serves as a mitophagy receptor by recognizing autophagosomes. BNIP3L is initially known to clear the mitochondria during the development of reticulocytes. Recent studies indicated it also engages in a variety of physiological and pathological processes. In this review, we provide an overview of how BNIP3L induces mitophagy and discuss the biological functions of BNIP3L and its regulation at the molecular level. We further discuss current evidence indicating the involvement of BNIP3L-mediated mitophagy in human disease, particularly in cancer and neurological disorders.

Stroke is considered a leading cause of mortality and neurological disability, which puts a huge burden on individuals and the community. To date, effective therapy for stroke has been limited by its complex pathological mechanisms. Autophagy refers to an intracellular degrading process with the involvement of lysosomes. Autophagy plays a critical role in maintaining the homeostasis and survival of cells by eliminating damaged or non-essential cellular constituents. Increasing evidence support that autophagy protects neuronal cells from ischemic injury. However, under certain circumstances, autophagy activation induces cell death and aggravates ischemic brain injury. Diverse naturally derived compounds have been found to modulate autophagy and exert neuroprotection against stroke. In the present work, we have reviewed recent advances in naturally derived compounds that regulate autophagy and discussed their potential application in stroke treatment.

TP53-induced glycolysis and apoptosis regulator (TIGAR) alleviates oxidative stress and protects against ischemic neuronal injury by shifting glucose metabolism into the pentose phosphate pathway (PPP). However, the brain alters glucose metabolism from PPP to glycolysis during prolonged ischemia. It is still unknown whether and how TIGAR exerts the antioxidant activity and neuroprotection in prolonged ischemic brains. Here, we determined the significant upregulation of TIGAR that was proportional to the duration of ischemia. However, TIGAR failed to upregulate the NADPH level but still alleviated oxidative stress in neuronal cells with prolonged oxygen glucose-deprivation (OGD). Furthermore, inhibiting PPP activity, either by the expression of mutant TIGAR (which lacks enzymatic activity) or by silencing Glucose 6-phosphate dehydrogenase, still retained antioxidant effects and neuroprotection of TIGAR with prolonged OGD. Intriguingly, TIGAR-induced autophagy alleviated oxidative stress, contributing to neuron survival. Further experiments indicated that TIGAR-induced autophagy neutralized oxidative stress by activating Nrf2, which was cancelled by ML385 or Nrf2 knockdown. Remarkably, either Atg7 deletion or Nrf2 silencing abolished the neuroprotection of TIGAR in mice with prolonged ischemia. Taken together, we found a PPP-independent pathway in which TIGAR alleviates oxidative stress. TIGAR induces autophagy and, thus, activates Nrf2, offering sustainable antioxidant defense in brains with extended ischemia. This previously unexplored mechanism of TIGAR may serve as a critical compensation for antioxidant activity caused by the lack of glucose in ischemic stroke.

Low salinity water injection (LSWI) is considered to be more cost-effective and has less environmental impacts over conventional chemical Enhanced Oil Recovery (EOR) methods. CO2 Water-Alternating-Gas (WAG) injection is also a leading EOR flooding process. The hybrid EOR method, CO2 low salinity (LS) WAG injection, which incorporates low salinity water into CO2 WAG injection, is potentially beneficial in terms of optimizing oil recovery and decreasing operational costs. Experimental and simulation studies reveal that CO2 LSWAG injection is influenced by CO2 solubility in brine, brine salinity and composition, rock composition, WAG parameters, and wettability. However, the mechanism for increased recovery using this hybrid method is still debatable and the conditions under which CO2 LSWAG injection is effective are still uncertain. Hence, a comprehensive review of the existing literature investigating LSWI and CO2 WAG injection, and laboratory and simulation studies of CO2 LSWAG injection is essential to understand current research progress, highlight knowledge gaps and identify future research directions. With the identified research gap, a core-scale simulation study on hysteresis effect in CO2 LSWAG injection is carried out. The results indicate different changing trend in oil recovery due to the impact of salinity on hysteresis and excluding of hysteresis effect in CO2 LSWAG injection simulation and optimization might lead to significant errors.

Gas permeability, which is measured mainly through gas permeability experiments, is a critical technical index in many engineering fields. In this study, permeability is firstly calculated based on information from a digital image and an improved permeability prediction model. The calculated results are experimentally verified. Subsequently, a selfdeveloped image-processing program is used to extract feature parameters from a scanning electron microscopy image. Meanwhile, an extreme learning machine algorithm is used to input the image feature parameters obtained using the image-processing program into the extreme learning machine algorithm for machine learning. Additionally, we compare several typically used machine learning algorithms, which confirmed the reliability and accuracy of our algorithm. The best activation function can be obtained by comparing the predicted permeability using an appropriate number of neuron nodes. Experimental results show that the program can accurately identify the features of the microscopy image. Combining the program with an extreme learning machine neural network algorithmgas permeability results to be obtained with high accuracy. This method yields good predictions of permeability in certain cases and has been adapted to other geomaterials. [ABSTRACT FROM AUTHOR]

Mitophagy protects against ischemic neuronal injury by eliminating damaged mitochondria, but it is unclear how mitochondria in distal axons are cleared. We find that oxygen and glucose deprivation-reperfusion reduces mitochondrial content in both cell bodies and axons. Axonal mitochondria elimination was not abolished in Atg7fl/fl;nes-Cre neurons, suggesting the absence of direct mitophagy in axons. Instead, axonal mitochondria were enwrapped by autophagosomes in soma and axon-derived mitochondria prioritized for elimination by autophagy. Intriguingly, axonal mitochondria showed prompt loss of anterograde motility but increased retrograde movement upon reperfusion. Anchoring of axonal mitochondria by syntaphilin blocked neuronal mitophagy and aggravated injury. Conversely, induced binding of mitochondria to dynein reinforced retrograde transport and enhanced mitophagy to prevent mitochondrial dysfunction and attenuate neuronal injury. Therefore, we reveal somatic autophagy of axonal mitochondria in ischemic neurons and establish a direct link of retrograde mitochondrial movement with mitophagy. Our findings may provide a new concept for reducing ischemic neuronal injury by correcting mitochondrial motility. [ABSTRACT FROM AUTHOR]