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Life-cycle assessment is crucial for evaluating materials’ environmental impact and guiding the development of low-carbon and sustainable buildings. However, conventional LCA methods often overlook critical impacts during the operation and maintenance stage. To address this gap, this study proposes an improved framework using four composite indicators to enable systematic evaluation of six wall materials across China’s five climate zones. Using a university teaching building in the Hot Summer and Cold Winter Zone as a case study, this study quantitatively analyzed the economic viability and carbon reduction potential of each material. Results indicate that lower thermal conductivity does not necessarily imply superior economic and carbon reduction performance. Factors including the material carbon emission factor, cost, and thermal properties, must be comprehensively considered. Buffering materials also exhibit climate dependency—WPM and BWPM (moisture-buffering plastering mortars) perform better in hot–humid zones than temperate zones. All five buffer materials reduce operational energy consumption; WPM and BWPM stand out with 15.7% and 16.7% life-cycle cost savings and 17.3% and 18.0% carbon emission reductions, respectively. This study addresses the limitations of traditional LCC/LCA and provides theoretical and practical support for scientific material selection and low-carbon building design.

By a circular increment step load and unload method, a set of rheological experiments were performed to study the creep properties of amphibolite and the deformation data of instantaneous elasticity, instantaneous plasticity, viscoplasticity and viscoelasticity could be obtained. The results showed that: the creep threshold of amphibolite(σs1) was 25.46MPa; whenσs1s2 , the proportion of plastic deformation in the total deformation was very small and the value of creep deformation always tended to a stable value; whenσ>σs2, the rock samples failed rapidly and had no obvious creep. According to the creep and failure properties of amphibolite, the generalized Kelvin creep model was acted in series with the Mohr-Coulomb criterion and a modified generalized Kelvin creep model was built and the corresponding visco-elasto-plastic constitutive relationships were deduced. The modified model could simulate visco-elasto-plastic deviatoric behavior and elasto-plastic volumetric behavior. The model parameters of amphibolite were fitted according to the data of rheological test. The testing curves were coincident well with the theoretic curves by comparison which showed the creep properties and the plastic flow of hard rock could be well simulated by the generalized Kelvin creep model.

HighlightsMechanistic understandings of metal-free carbon thermocatalysis and electrocatalysis from the viewpoint of model method are summarized.Active sites and reaction mechanisms are discussed with a focus on in-situ techniques and 2D structure–activity relationships.The real contribution of each alien species, defect and edge configuration to catalytic reactions are systematically highlighted at a molecular level.Metal-free carbon, as the most representative heterogeneous metal-free catalysts, have received considerable interests in electro- and thermo-catalytic reactions due to their impressive performance and sustainability. Over the past decade, well-designed carbon catalysts with tunable structures and heteroatom groups coupled with various characterization techniques have proposed numerous reaction mechanisms. However, active sites, key intermediate species, precise structure–activity relationships and dynamic evolution processes of carbon catalysts are still rife with controversies due to the monotony and limitation of used experimental methods. In this Review, we summarize the extensive efforts on model catalysts since the 2000s, particularly in the past decade, to overcome the influences of material and structure limitations in metal-free carbon catalysis. Using both nanomolecule model and bulk model, the real contribution of each alien species, defect and edge configuration to a series of fundamentally important reactions, such as thermocatalytic reactions, electrocatalytic reactions, were systematically studied. Combined with in situ techniques, isotope labeling and size control, the detailed reaction mechanisms, the precise 2D structure–activity relationships and the rate-determining steps were revealed at a molecular level. Furthermore, the outlook of model carbon catalysis has also been proposed in this work.

Background Ovarian cancer (OC) is the most lethal malignant gynecological tumor type for which limited therapeutic targets and drugs are available. Enhanced mitochondrial oxidative phosphorylation (OXPHOS), which enables cell growth, migration, and cancer stem cell maintenance, is a critical driver of disease progression and a potential intervention target of OC. However, the current OXPHOS intervention strategy mainly suppresses the activity of the electron transport chain directly and cannot effectively distinguish normal tissues from cancer tissues, resulting in serious side effects and limited efficacy. Methods We screened natural product libraries to investigate potential anti-OC drugs that target OXPHOS. Additionally, LC-MS, qRT-PCR, western-blot, clonogenic assay, Immunohistochemistry, wound scratch assay, and xenograft model was applied to evaluate the anti-tumor mechanism of small molecules obtained by screening in OC. Results Gossypol acetic acid (GAA), a widely used gynecological medicine, was screened out from the drug library with the function of suppressing OXPHOS and OC progression by targeting the leucine-rich pentatricopeptide repeat containing (LRPPRC) protein. Mechanically, LRPPRC promotes the synthesis of OXPHOS subunits by binding to RNAs encoded by mitochondrial DNA. GAA binds to LRPPRC directly and induces LRPPRC rapid degradation in a ubiquitin-independent manner. LRPPRC was overexpressed in OC, which is highly correlated with the poor outcomes of OC and could promote the malignant phenotype of OC cells in vitro and in vivo. GAA management inhibits cell growth, clonal formation, and cancer stem cell maintenance in vitro, and suppresses subcutaneous graft tumor growth in vivo. Conclusions Our study identified a therapeutic target and provided a corresponding inhibitor for OXPHOS-based OC therapy. GAA inhibits OC progression by suppressing OXPHOS complex synthesis via targeting LRPPRC protein, supporting its potential utility as a natural therapeutic agent for ovarian cancer.

The edible fungus industry is one of the pillar industries in the Yunnan–Guizhou Plateau, China. The expansion of the planting scale has led to the release of various mushroom residues, such as mushroom feet, and other wastes, which are not treated adequately, resulting in environmental pollution. This study investigated the ability of black soldier fly ( Hermetia illucens L .) larvae (BSFL) to degrade mushroom waste. Moreover, this study analyzed changes in the intestinal bacterial community and gene expression of BSFL after feeding on mushroom waste. Under identical feeding conditions, the remaining amount of mushroom waste in Pleurotus ostreatus treatment group was reduced by 18.66%, whereas that in Flammulina velutipes treatment group was increased by 31.08%. Regarding gut microbial diversity, compared with wheat bran-treated control group, Dysgonomonas , Providencia , Enterococcus , Pseudochrobactrum , Actinomyces , Morganella , Ochrobactrum , Raoultella , and Ignatzschineria were the most abundant bacteria in the midgut of BSFL in F. velutipes treatment group. Furthermore, Dysgonomonas , Campylobacter , Providencia , Ignatzschineria , Actinomyces , Enterococcus , Morganella , Raoultella , and Pseudochrobactrum were the most abundant bacteria in the midgut of BSFL in P. ostreatus treatment group. Compared with wheat bran-treated control group, 501 upregulated and 285 downregulated genes were identified in F. velutipes treatment group, whereas 211 upregulated and 43 downregulated genes were identified in P. ostreatus treatment group. Using Kyoto Encyclopedia of Genes and Genomes and Gene Ontology enrichment analyses, we identified 14 differentially expressed genes (DEGs) related to amino sugar and nucleotide sugar metabolism in F. velutipes treatment group, followed by 12 DEGs related to protein digestion and absorption. Moreover, in P. ostreatus treatment group, two DEGs were detected for fructose and mannose metabolism, and two were noted for fatty acid metabolism. These results indicate that feeding on edible mushroom waste can alter the intestinal microbial community structure of BSFL; moreover, the larval intestine can generate a corresponding feedback. These changes contribute to the degradation of edible mushroom waste by BSFL and provide a reference for treating edible mushroom waste using BSFL.

Chimeric antigen receptor (CAR) T-cell therapy (CAR-T therapy) has demonstrated significant efficacy in the ZUMA-2 study. After regulatory approvals, several clinical trials and real-world studies on CAR-T therapy for relapsed or refractory mantle cell lymphoma (R/R MCL) were conducted. However, data on clinical safety and efficacy are inconsistent. In this study, we aimed to conduct a systematic analysis of the effectiveness and safety of CAR-T therapy across a wider and more representative cohort of patients with R/R MCL. We performed a systematic review and meta-analysis of studies on patients with R/R MCL who received CAR-T cell therapy. Data were extracted and consolidated, with primary focus on the evaluation of safety and efficacy outcome measures. This study has not been registered with PROSPERO. This meta-analysis identified and included 16 studies with 984 patients. The pooled estimate for overall response rate (ORR) was 89%; complete remission (CR) rate was 74%. The 6-month and 12-month progression-free survival (PFS) rates were 69% and 53%, respectively, while the overall survival (OS) rates were 80% and 69%, respectively. Cytokine release syndrome (CRS) of grade 3 or higher was observed in 8% of patients, whereas neurotoxicity of grade 3 or higher was observed in 22% of patients. The risk of bias was assessed as low in 9 studies and moderate in 7 studies. CAR-T therapy exhibited promising efficacy and manageable adverse reactions in patients with R/R MCL.

Aim Repeated exposure to ketamine during the neonatal period in mice leads to cognitive impairments in adulthood. These impairments are likely caused by synaptic plasticity and excitability damage. We investigated the precise role of brain‐derived neurotrophic factor (BDNF) in the cognitive impairments induced by repeated ketamine exposure during the neonatal period. Methods We evaluated the cognitive function of mice using the Morris water maze test and novel object recognition test. Western blotting and immunofluorescence were used to detect the protein levels of BDNF. Western blotting, Golgi‐Cox staining, transmission electron microscopy, and long‐term potentiation (LTP) recordings were used to assess synaptic plasticity in the hippocampus. The excitability of neurons was evaluated using c‐Fos. In the intervention experiment, pAdeno‐CaMKIIα‐BDNF‐mNeuronGreen was injected into the hippocampal CA1 region of mice to increase the level of BDNF. The excitability of neurons was enhanced using a chemogenetic approach. Results Our findings suggest that cognitive impairments in mice repeatedly exposed to ketamine during the neonatal period are associated with downregulated BDNF protein level, synaptic plasticity damage, and decreased excitability of glutamatergic neurons in the hippocampal CA1 region. Furthermore, the specific upregulation of BDNF in glutamatergic neurons of the hippocampal CA1 region and the enhancement of excitability can improve impaired synaptic plasticity and cognitive function in mice. Conclusion BDNF downregulation mediates synaptic plasticity and excitability damage, leading to cognitive impairments in adulthood following repeated ketamine exposure during the neonatal period. This study illustrates the role of BDNF in cognitive dysfunction in adult mice that results from repeated ketamine exposure during development. After neonatal mice were anesthetized with ketamine multiple times, the level of BDNF in glutamatergic neurons in the CA1 area of the hippocampus was reduced, resulting in impaired neuronal synaptic plasticity and decreased neuronal excitability, ultimately leading to cognitive dysfunction in adulthood.

Objective Transfer RNA-derived fragments (tRFs) are short non-coding RNA (ncRNA) sequences, ranging from 14 to 30 nucleotides, produced through the precise cleavage of precursor and mature tRNAs. While tRFs have been implicated in various diseases, including cancer, their role in lung adenocarcinoma (LUAD) remains underexplored. This study aims to investigate the impact of tRF-Val-CAC-010, a specific tRF molecule, on the phenotype of LUAD cells and its role in tumorigenesis and progression in vivo. Methods The expression level of tRF-Val-CAC-010 was quantified using quantitative real-time polymerase chain reaction (qRT-PCR). Specific inhibitors and mimics of tRF-Val-CAC-010 were synthesized for transient transfection. Cell proliferation was assessed using the Cell Counting Kit-8 (CCK-8), while cell invasion and migration were evaluated through Transwell invasion and scratch assays. Flow cytometry was utilized to analyze cell cycle and apoptosis. The in vivo effects of tRF-Val-CAC-010 on tumor growth and metastasis were determined through tumor formation and metastasis imaging experiments in nude mice. Results The expression level of tRF-Val-CAC-010 was upregulated in A549 and PC9 LUAD cells ( P  < 0.01). Suppression of tRF-Val-CAC-010 expression resulted in decreased proliferation of A549 and PC9 cells ( P  < 0.001), reduced invasion and migration of A549 ( P  < 0.05, P  < 0.001) and PC9 cells ( P  < 0.05, P  < 0.01), enhanced apoptosis in both A549 ( P  < 0.05) and PC9 cells ( P  < 0.05), and increased G2 phase cell cycle arrest in A549 cells ( P  < 0.05). In vivo, the tumor formation volume in the tRF-inhibitor group was significantly smaller than that in the model and tRF-NC groups ( P  < 0.05). The metastatic tumor flux value in the tRF-inhibitor group was also significantly lower than that in the model and tRF-NC groups ( P  < 0.05). Conclusion This study demonstrates that tRF-Val-CAC-010 promotes proliferation, migration, and invasion of LUAD cells and induces apoptosis in vitro, however, its specific effects on the cell cycle require further elucidation. Additionally, tRF-Val-CAC-010 enhances tumor formation and metastasis in vivo. Therefore, tRF-Val-CAC-010 may serve as a novel diagnostic biomarker and potential therapeutic target for LUAD.

Background. Wogonin is a plant monoflavonoid and has been reported to induce apoptosis of cancer cells and show inhibitory effect on cancer cell growth. However, the detailed and underlying molecular mechanisms are not elucidated. In this study, we investigated the molecular and biological effects of wogonin in human ovarian A2780 cancer cells. Materials and Methods. We determined the effects of wogonin on the changes of cell cycling and apoptotic responses of cells. Western blot analysis was used to measure the effects of wogonin on protein expressions. Results. Our results showed that treatment with wogonin inhibited the cancer cell proliferation, decreased the percentage of G0/G1 subpopulation, and reduced invasiveness of A2780 cells. Exposure to wogonin also resulted in downregulated protein levels of estrogen receptor alpha (ER-α), VEGF, Bcl-2, and Akt and increased expressions of Bax and p53. In addition, exposure to wogonin increased caspase-3 cleavage and induced apoptosis in A2780 cells. Our study further showed that MPP, a specific ER-α inhibitor, significantly enhanced antitumor effects of wogonin in A2780 cells. Conclusion. Our results suggest a potential clinical impact of wogonin on management of ovarian cancer.

Staphylococcus aureus colonizes the nose, throat, skin, and gastrointestinal (GI) tract of humans. GI carriage of S. aureus is difficult to eradicate and has been shown to facilitate the transmission of the bacterium among individuals. Although staphylococcal colonization of the GI tract is asymptomatic, it increases the likelihood of infection, particularly skin and soft tissue infections caused by USA300 isolates. We established a mouse model of persistent S. aureus GI colonization and characterized the impact of selected surface antigens on colonization. In competition experiments, an acapsular mutant colonized better than the parental strain Newman, whereas mutants defective in sortase A and clumping factor A showed impaired ability to colonize the GI tract. Mutants lacking protein A, clumping factor B, poly-N-acetyl glucosamine, or SdrCDE showed no defect in colonization. An S. aureus wall teichoic acid (WTA) mutant (ΔtagO) failed to colonize the mouse nose or GI tract, and the tagO and clfA mutants showed reduced adherence in vitro to intestinal epithelial cells. The tagO mutant was recovered in lower numbers than the wild type strain in the murine stomach and duodenum 1 h after inoculation. This reduced fitness correlated with the in vitro susceptibility of the tagO mutant to bile salts, proteases, and a gut-associated defensin. Newman ΔtagO showed enhanced susceptibility to autolysis, and an autolysin (atl) tagO double mutant abrogated this phenotype. However, the atl tagO mutant did not survive better in the mouse GI tract than the tagO mutant. Our results indicate that the failure of the tagO mutant to colonize the GI tract correlates with its poor adherence and susceptibility to bactericidal factors within the mouse gut, but not to enhanced activity of its major autolysin.