Twin Boundaries-Induced Centrosymmetric Breaking of Hollow CaTiO3 Nanocuboids for Piezocatalytic Hydrogen Evolution.

Piezocatalysis, a transformative mechanochemical energy conversion technique, has received considerable attention over the past decade for its role in processes such as hydrogen evolution from water. Despite notable progress in the field, challenges remain, particularly in the areas of limited piezocatalysis efficiency and limited availability of materials requiring a non-centrosymmetric structure. Here, a pioneering contribution is presented by elucidating the piezocatalytic properties of hollow CaTiO3 nanocuboids, a centrosymmetric material with a nominally nonpolar state. Remarkably, CaTiO3 nanocuboids exhibit an impressive hydrogen production rate of 3.44 mmol g-1 h-1 under ultrasonic vibrations, surpassing the performance of the well-established piezocatalyst BaTiO3 (2.23 mmol g-1 h-1). In contrast, commercial CaTiO3 nanoparticles do not exhibit piezocatalytic performance. The exceptional performance of hollow CaTiO3 nanocuboids is attributed to the abundance presence of twin boundaries on the {110} facet within its crystal structure, which can impart significant polarization strength to CaTiO3. Extending the investigation to other centrosymmetric materials, such as SrZrO3 and BaZrO3, the experimental results also demonstrate their commendable properties for piezocatalytic hydrogen production from water. This research underscores the significant potential of centrosymmetric materials in piezocatalysis.

Jingfang granules protects against intracerebral hemorrhage by inhibiting neuroinflammation and protecting blood-brain barrier damage.

Intracerebral hemorrhage (ICH) can induce intensive oxidative stress, neuroinflammation, and brain cell apoptosis. However, conventional methods for ICH treatment have many disadvantages. There is an urgent need for alternative, effective therapies with minimal side effects. Pharmacodynamics experiment, molecular docking, network pharmacology, and metabolomics were adopted to investigate the treatment and its mechanism of Jingfang Granules (JFG) in ICH. In this study, we investigated the therapeutic effects of JFG on ICH using behavioral, brain water content and Magnetic resonance imaging experiments. However, the key active component and targets of JFG remain unknown. Here we verified that JFG was beneficial to improve brain injury after ICH. A network pharmacology analysis revealed that the anti-inflammatory effect of JFG is predominantly mediated by its activation of the phosphatidylinositol 3-kinase (PI3K)/AKT pathway through Luteolin, (+)-Anomalin and Phaseol and their targeting of AKT1, tumor necrosis factorα (TNF-α), and interleukin-1ß (IL-1ß). Molecular docking analyses revealed an average affinity of -8.633 kcal/mol, indicating a binding strength of less than -5 kcal/mol. Metabolomic analysis showed that JFG exerted its therapeutic effect on ICH by regulating metabolic pathways, such as the metabolism of taurine and hypotaurine, biosynthesis of valine, leucine, and isoleucine. In conclusion, we demonstrated that JFG attenuated neuroinflammation and BBB injury subsequent to ICH by activating the PI3K/Akt signaling pathway.

Tannin-Assisted Synthesis of Nanocomposites Loaded with Silver Nanoparticles and Their Multifunctional Applications.

Nanocomposites have been widely used in many important areas due to their particular physical/chemical properties; however, just though a simple technology, endowing multiple functions into a single nanomaterial for realizing their multifunctional applications is still a challenge. Here, we report a robust method for the facile synthesis of Ag-based multifunctional nanocomposites via using tannin-coated phenol-formaldehyde resin nanospheres (TA-PFRN) as silver nanoparticle (Ag NP) carriers. The thickness of the tannin coating is readily tuned from 50 to 320 nm by regulating the concentration of tannin added. Under the optimal conditions, the TA-PFRN has a 23.8 wt % of Ag NPs loading capacity with only 17.2 nm Ag NP layers. Consequently, the novel TA-PFRN@Ag nanocomposites possess multiple functions and integrated characteristics. As catalysts, the catalytic efficiency of TA-PFRN@Ag is nearly 6 times higher than that of the PFRN@Ag. As highly effective free radical initiators, TA-PFRN@Ag nanocomposites can trigger ultrafast acrylic acid (AA)/acrylamide (AM) polymerization at room temperature (in only a few minutes). As nano-reinforced fillers, the addition of 0.04 wt % nanocomposites can improve the tensile strength of PVA film from 60 to 153.2 MPa. In addition, the nanocomposites can also serve as antibacterial agents, efficiently inhibiting the growth of Escherichia coli (E. coli) and Staphylococcus aureus (S. aureus); as antiultraviolet agents, the presence of TA-PFRN@Ag nanocomposites endows the film/hydrogel materials excellent ultraviolet (UV) shielding. This work provides a novel strategy for the green synthesis of Ag-based multifunctional nanocomposites that show promising applications in catalysis, nanomaterials, and biomedicine.

Reveal the inequality hidden in industry land use by integrating domestic trade and the industry efficiency.

Although industrial land accounts for a low percentage of the land surface, it can significantly affect the development of the economy and the environment. Unbalanced development makes industry efficiency differ vastly across China. Industry products embodied in domestic trade link the indirect use of industry inputs and outputs. Regional inequality needs to be more scientifically checked by comprehensively considering both trade and the efficiency, which may be determined by diverse indices. Accordingly, this study examined industrial land use among provinces and the efficiency, identified the embodied land, developed approaches to ascertain how industrial land use would change without domestic trade, and revealed the inequalities in industrial land by considering the trade. Results found that provinces along China's coastline usually have a highly industrialised area, and the developed regions usually have high efficiency. Guangdong, Henan, Jiangsu, Shanghai, Shandong, Liaoning, Anhui, Hebei, and Heilongjiang have high values in both industrial land serving external provinces and the reverse use in external provinces. Through domestic trade, China saved a total of 462 km2 of land to be converted into industrial land, which is mainly due to developed regions providing industrial land use to undeveloped regions with low efficiency. The inequality analysis shows that most provinces were in a moderate state. Heilongjiang, Gansu, and Guangxi have obvious disadvantages. Some suggestions have been made for harmonious industry development and enhanced efficiency, such as the implementation of efficiency and price-based land use policies, industry and energy structure optimisation, technological improvement, and appropriate compensation.

The driving factors of corporate carbon emissions: an application of the LASSO model with survey data.

Corporate carbon performance is a key driver of achieving corporate sustainability. The identification of factors that influence corporate carbon emissions is fundamental to promoting carbon performance. Based on the carbon disclosure project (CDP) database, we integrate the least absolute shrinkage and selection operator (LASSO) regression model and the fixed effects model to identify the determinants of carbon emissions. Furthermore, we rank determining factors according to their importance. We find that Capx enters the models under all carbon contexts. For Scope 1 and Scope 2, financial-level factors play a greater role. For Scope 3, corporate internal incentive policies and emission reduction behaviors are important. Different from absolute carbon emissions, for relative carbon emissions, the financial-level factors' debt-paying ability is a vital reference indicator for the impact of corporate carbon emissions.

The NLRP3 inflammasome is involved in resident intruder paradigm-induced aggressive behaviors in mice.

Background: Aggressive behaviors are one of the most important negative behaviors that seriously endangers human health. Also, the central para-inflammation of microglia triggered by stress can affect neurological function, plasticity, and behavior. NLRP3 integrates stress-related signals and is a key driver of this neural para-inflammation. However, it is unclear whether the NLRP3 inflammasome is implicated in the development of aggressive behaviors. Methods: First, aggressive behavior model mice were established using the resident intruder paradigm. Then, aggressive behaviors were determined with open-field tests (OFT), elevated plus-maze (EPM), and aggressive behavior tests (AT). Moreover, the expression of P2X7R and NLRP3 inflammasome complexes were assessed by immunofluorescence and Western blot. The levels of NLRP3 and inflammatory cytokines were evaluated using enzyme-linked immunosorbent assay (ELISA) kits. Finally, nerve plasticity damage was observed by immunofluorescence, transmission electron microscope, and BrdU staining. Results: Overall, the resident intruder paradigm induced aggressive behaviors, activated the hippocampal P2X7R and NLRP3 inflammasome, and promoted the release of proinflammatory cytokines IL-1ß in mice. Moreover, NLRP3 knockdown, administration of P2X7R antagonist (A804598), and IL-1ß blocker (IL-1Ra) prevented NLRP3 inflammasome-driven inflammatory responses and ameliorated resident intruder paradigm-induced aggressive behaviors. Also, the resident intruder paradigm promoted the activation of mouse microglia, damaging synapses in the hippocampus, and suppressing hippocampal regeneration in mice. Besides, NLRP3 knockdown, administration of A804598, and IL-1Ra inhibited the activation of microglia, improved synaptic damage, and restored hippocampal regeneration. Conclusion: The NLRP3 inflammasome-driven inflammatory response contributed to resident intruder paradigm-induced aggressive behavior, which might be related to neuroplasticity. Therefore, the NLRP3 inflammasome can be a potential target to treat aggressive behavior-related mental illnesses.

Carbon deficit checks in high resolution and compensation under regional inequity.

Carbon compensation is an effective way of reducing carbon emissions. However, previous studies in this field have been limited and have not examined high-precision scientific carbon compensation under regional inequity. The present study examined initial carbon compensation in the grid and developed a new equitable carbon compensation model. Additionally, it modified the carbon compensation value for each province and analysed how land-use change affected carbon compensation. The results show that, after the modification, the entire carbon deficit reached 17.34 × 108 t C in 2015, representing a decrease of 14% compared with the initial carbon deficit. The area with negative carbon deficit values accounted for 36% of the whole area, concentrated mainly in the south, southwest and northwest. Without modification, the initial carbon compensation reached 537 × 108 USD, and only Yunnan, Sichuan and Hainan provinces being eligible to receive compensation. The final modified carbon compensation was approximately 20% of the initial values, and 11 provinces were eligible to obtain compensation. The other provinces responsible for paying the carbon compensation costs were typically concentrated in Central and Eastern China. Land-use changes in 2015 led to increases in the initial carbon compensation and modified carbon compensation of 3.74 × 108 and 0.13 × 108 USD, respectively. The per-unit land-use change caused greater increases in carbon emissions in China's big cities and the provinces in Central and East China. Some policies, such as macro-control by the central government, diversified forms and patterns of compensation, and auxiliary measures should be formulated/proposed.

Oxidative Stress and 4-hydroxy-2-nonenal (4-HNE): Implications in the Pathogenesis and Treatment of Aging-related Diseases.

Oxidative stress plays an important role in the development of aging-related diseases by accelerating the lipid peroxidation of polyunsaturated fatty acids in the cell membrane, resulting in the production of aldehydes, such as malondialdehyde and 4-hydroxy-2-nonenal (4-HNE) and other toxic substances. The compound 4-HNE forms adducts with DNA or proteins, disrupting many cell signaling pathways including the regulation of apoptosis signal transduction pathways. The binding of proteins to 4-HNE (4-HNE-protein) acts as an important marker of lipid peroxidation, and its increasing concentration in brain tissues and fluids because of aging, ultimately gives rise to some hallmark disorders, such as neurodegenerative diseases (Alzheimer's and Parkinson's diseases), ophthalmic diseases (dry eye, macular degeneration), hearing loss, and cancer. This review aims to describe the physiological origin of 4-HNE, elucidate its toxicity in aging-related diseases, and discuss the detoxifying effect of aldehyde dehydrogenase and glutathione in 4-HNE-driven aging-related diseases.

Research progress of natural products for the treatment of ischemic stroke.

Stroke is a leading cause of death and disability world-widely. The incidence rate of stroke has been increasing due to the aging population and lifestyle changes. At present, the only drug approved by the US Food and Drug Administration (FDA) for the treatment of ischemic stroke is tissue plasminogen activator (t-PA), but its clinical application is greatly limited because of its narrow time window and bleeding risk. Natural products have a long history of being used in traditional medicine with good safety, making them an important resource for the development of new drugs. Indeed, some natural products can target a variety of pathophysiological processes related to stroke, including oxidative stress, inflammation and neuronal apoptosis. Therefore, the development of high-efficiency, low-toxicity, safe and cheap active substances from natural products is of great significance for improving the treatment alternatives of patients with stroke. This article reviews the neuroprotective effects of 33 natural compounds by searching recent related literature. Among them, puerarin, pinocembrin, quercetin, epigallocatechin-3-gallate (EGCG), and resveratrol have great potential in the clinical treatment of ischemic stroke. This review will provide a powerful reference for screening natural compounds with potential clinical application value in ischemic stroke or synthesizing new neuroprotective agents with natural compounds as lead compounds.

Targeting NLRP3 Inflammasome in Translational Treatment of Nervous System Diseases: An Update.

Neuroinflammatory response is the immune response mechanism of the innate immune system of the central nervous system. Both primary and secondary injury can activate neuroinflammatory response. Among them, the nucleotide-binding oligomerization domain-like receptor protein 3 (NLRP3) inflammasome plays a key role in the inflammatory response of the central system. Inflammasome is a type of pattern recognition receptor, a cytoplasmic polyprotein complex composed of members of the Nod-like receptor (NLR) family and members of the pyrin and HIN domain (PYHIN) family, which can be affected by a variety of pathogen-related molecular patterns or damage-related molecular patterns are activated. As one of the research hotspots in the field of medical research in recent years, there are increasing researches on immune function abnormalities in the onset of neurological diseases such as depression, AD, ischemic brain injury and cerebral infarction, the NLRP3 inflammasome causes the activated caspase-1 to cleave pre-interleukin-1ß and pre-interleukin-18 into mature interleukin-1ß and interleukin-18, in turn, a large number of inflammatory factors are produced, which participate in the occurrence and development of the above-mentioned diseases. Targeted inhibition of the activation of inflammasomes can reduce the inflammatory response, promote the survival of nerve cells, and achieve neuroprotective effects. This article reviews NLRP3 inflammasome's role in neurological diseases and related regulatory mechanisms, which providing references for future research in this field.

Brain-derived Neurotrophic Factor and Its Applications through Nanosystem Delivery.

Brain-derived neurotrophic factor (BDNF) is a protein that performs a neurotrophic function. BDNF and its receptors are widely expressed in the nervous system and can promote the growth of neurons and the formation of neuronal synapses in the brain. Studies have shown that a lack of BDNF can lead to impairment of memory and cognitive functions, indicating that BDNF plays an important role in mental illness and neurodegenerative diseases. The combination of stem cells and BDNF-releasing nanomaterials holds great promise in regenerative medicine, especially in the treatment of neurological diseases. For example, Alzheimer's disease, depression, Parkinson's disease, spinal cord injury, etc. The combination of stem cell/pharmacologically active carrier and BDNF-nano/hydrogel provided a useful new type of local delivery tool for the treatment of the nervous system and other diseases. It can not only provide BDNF but also stem cells. These studies will provide a scientific basis for the development and application of BDNF in the future.