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Purpose - There has been a growing attention to building information modeling (BIM) globally due to its benefits to various stages of a building's life cycle. To facilitate the implementation of BIM in the construction industry effectively, the purpose of this paper is to gain a better understanding of the mechanism for BIM adoption by practitioners such as architects. Design/methodology/approach - A questionnaire survey of architects is conducted in Shenzhen, China. A structural equation model is built with survey data to identify the key factors affecting architects' BIM adoption in the design firms. Findings - It is found that motivation, technical defects of BIM and BIM capability are the statistically significant factors affecting architects' BIM adoption whereas management support and knowledge structure are not. Research limitations/implications - Only one architectural, engineering and construction (AEC) profession, i.e. architects were selected as research participants. In future, other professions such as construction engineers, project managers, etc. should be investigated with respect to their BIM adoption issues. Practical implications - BIM technology developers should improve the technology along the objectives of economic benefits, effectiveness and efficiency of BIM adoption. The compatibility and integration between BIM and other widely available software in the industry should also be improved. Moreover, AEC company and project managers should provide architects with opportunities of BIM training so that architects are more likely to apply BIM in future projects. Originality/value - A quantitative theoretical model, i.e. structural equation model is built to identify key factors affecting architects' BIM adoption, which takes one step further to reveal the BIM adoption mechanism in contrast to previous descriptive-oriented studies.

In meat processing, changes in the myofibrillar protein (MP) structure can affect the quality of meat products. High hydrostatic pressure (HHP) has been widely utilized to change the conformational structure (secondary, tertiary and quaternary structure) of MP so as to improve the quality of meat products. However, a systematic summary of the relationship between the conformational structure (secondary and tertiary structure) changes in MP, gel properties and product quality under HHP is lacking. Hence, this review provides a comprehensive summary of the changes in the conformational structure and gel properties of MP under HHP and discusses the mechanism based on previous studies and recent progress. The relationship between the spatial structure of MP and meat texture under HHP is also explored. Finally, we discuss considerations regarding ways to make HHP an effective strategy in future meat manufacturing.

Introduction: Graves’ disease (GD) is the most common cause of hyperthyroidism and can affect multiple systems of the body. Currently, commonly-used treatment methods for GD have a series of shortcomings. In contrast, traditional Chinese medicine has been proven to be effective in inhibiting the progression of GD and is expected to become a key direction for the development of new drugs in the future. Therefore, a network meta-analysis was performed to compare the impacts of different traditional Chinese medicines on the curative effect, thyroid-stimulating hormone (TSH), free triiodothyronine (FT3), free thyroxine (FT4), thyroglobulin antibody (TGAb), thyroid peroxidase antibody (TPOAb) and thyrotropin receptor antibody (TRAb) in patients with GD. Methods: PubMed, Embase, Cochrane Library, Web of Science, WanFang, Weipu, and CNKI were searched for the randomized controlled trials of traditional Chinese medicine on GD patients up to 19 December 2023. The quality of the included studies was evaluated regarding the risk of bias, and the data were analyzed by R software. Results: Thirty-five articles were included in the analysis, involving 2828 GD patients and traditional Chinese medicines including Bailing Capsule, Jinshuibao Capsule, Astragalus injection, Jiakangling Tablet, Jiakangling Capsule, Tripterygium Wilfordii, Sanjie Xiaoying Decoction, Prunella vulgaris (L.) Oral Liquid, P. vulgaris (L.) Granules, Xiehuo Xiaoying Recipe, Xiehuo Yangyin Powder, Yikang Pill and Yinjia Pellet. The results of network meta-analysis suggested that for GD patients, Bailing Capsule, Jiakangling Capsule, Tripterygium wilfordii, P. vulgaris (L.) Oral Liquid and Yinjia Pellet had better curative effect compared with Western medicine. Prunella vulgaris (L.) Granules and Yikang Pill could improve the TSH level. Prunella vulgaris (L.) Granules, P. vulgaris (L.) Oral Liquid and Yikang Pill could reduce FT3 level. Jiakangling Capsule, P. vulgaris (L.) Granules, P. vulgaris (L.) Oral Liquid and Yikang Pill could reduce the FT4 level. Prunella vulgaris (L.) Oral Liquid can reduce the level of TPOAb and TRAb. Besides, Yinjia Pellet was the most helpful in improving the curative effect. Yikang Pill could best improve TSH. Prunella vulgaris (L.) Granules had the best effect on reducing FT3. Prunella vulgaris (L.) Granules performed best in reducing FT4. Prunella vulgaris (L.) Oral Liquid had the most favorable effect on reducing TPOAb and TRAb. Conclusion: Based on the current research, it is safe to conclude that Chinese medicine can improve the curative effect and TSH level of patients with GD, and reduce the levels of FT3, FT4, TPOAb and TRAb. Besides, Yinjia Pellet is the most helpful in improving the curative effect. Yikang Pill can best improve TSH. Prunella vulgaris (L.) Granules have the best effect on reducing FT3. Prunella vulgaris (L.) Granules perform best in reducing FT4. Prunella vulgaris (L.) Oral Liquid has the most favorable effect on reducing TPOAb and TRAb. Systematic Review Registration: https://www.crd.york.ac.uk/PROSPERO/#recordDetails , identifier CRD42024521912.

This study utilized the MIMIC-IV 3.0 database to investigate the correlation between the endothelial activation and stress index (EASIX) and the short-term (30-day) and long-term (1-year) death rates of patients with ischemic stroke (IS), thus providing insights into optimizing the risk stratification and management in clinical practice. Data from the MIMIC-IV 3.0 database were used. IS patients were identified by ICD codes. log2-EASIX scores were calculated based on admission platelet count, creatinine, and lactate dehydrogenase levels and patients were grouped into quartiles. The primary outcome was 30-day all - cause death rate, and the secondary was 1-year death rate. Multivariate Cox models, LASSO regression, Kaplan - Meier curves, restricted cubic splines, subgroup and interaction analyses were performed. R software was used for data cleaning and statistical analysis. This study enrolled 3,625 acute IS patients, stratified into four groups by log₂-EASIX quartiles (Q1: -3.24 to -0.55; Q2: -0.55, 0.17]; Q3: 0.17, 1.06]; Q4: 1.06 to 7.15). Q4 had markedly higher 30-day (32.0%) and 1-year (50.7%) mortality than Q1 (15.0%, 29.3%). Fully adjusted Cox models showed Q4 vs. Q1 had elevated 30-day (HR = 1.291, 95%CI:1.035-1.610, P = 0.024) and 1-year (HR = 1.246, 95%CI:1.059-1.467, P = 0.008) mortality risks, with a significant 1-year mortality trend (P = 0.004). RCS analysis revealed nonlinear associations between EASIX and both mortalities (all P < 0.05). Bonferroni-corrected subgroup analyses found only GCS had a modifying effect (P < 0.004). ROC analysis showed EASIX had moderate predictive value (30-day AUC = 0.7545; 1-year AUC = 0.7277). EASIX is independently linked to short- and medium-term ACM in ICU-admitted IS patients; higher EASIX correlates with increased mortality, serving as a useful risk stratification and prognosis tool. Limited to moderate-severe ICU IS cases, prospective studies are required to verify its causal mechanisms.

Background Acetyl-CoA carboxylase alpha (ACACA) is a key enzyme in fatty acid biosynthesis and a proposed therapeutic target in prostate cancer. However, its role in androgen receptor-independent prostate cancer (ARIPC), an aggressive and treatment-resistant subtype, remains unclear. This study aimed to investigate the effects of ACACA depletion on ARIPC, with a focus on inflammation and metastasis. Methods ACACA expression patterns were analyzed across multiple metastatic castration-resistant prostate cancer (mCRPC) datasets. In ARIPC cell lines, ACACA was inhibited via both shRNA and the pharmacological inhibitor TOFA. Transcriptomic, metabolomic, and single-cell RNA sequencing data were used to identify downstream changes. Inflammatory signaling was assessed by qPCR, western blotting, and immunofluorescence. Cell migration was evaluated via wound healing and transwell assays, and the metastatic potential was examined in a mouse tail vein injection model. The roles of arachidonic acid (AA), cytosolic phospholipase A2 (cPLA2), and NF-κB signaling were further tested through targeted inhibition. Results ACACA expression was reduced in ARIPC and was negatively correlated with inflammatory pathways. Its inhibition upregulated proinflammatory cytokines and chemokines, elevated AA and eicosanoid levels, and increased cPLA2 expression. Single-cell RNA sequencing confirmed NF-κB signaling enrichment in ACACA-low tumor cells. Mechanistically, elevated AA activated NF-κB signaling. ACACA depletion enhanced cell migration and metastasis, along with macrophage infiltration. Inhibiting cPLA2 or NF-κB signaling reversed these effects. Conclusions This study reveals a previously unrecognized tumor-promoting effect of ACACA depletion in ARIPC. Targeting ACACA in this context enhances inflammation and metastasis via arachidonic acid-mediated activation of NF-κB signaling. These findings highlight a context dependent, tumor-promoting role of ACACA inhibition and underscore the need for combinational strategies to avoid potential adverse outcomes in metabolic therapies. Trial registration Not applicable. Graphical Abstract

The peroxiredoxins (PRDXs) family plays a crucial role in balancing reactive oxygen species (ROS) levels in tumor cells. However, its potential role in prognosis and therapy response of prostate cancer (PCa) remains unknown. In this study, we utilized 2 public single-cell RNA datasets and 8 bulk-RNA datasets to investigate the clinical value of six PRDXs family members in PCa. Expression comparison, biochemical recurrence analysis, and therapy response analysis were measured. Pathway enrichments were utilized to predict the potential down-stream pathway it may involve. In vitro experiments were used to validate the function of PRDX5 in the progression of castration-resistant prostate cancer (CRPC) cell lines. Among the PRDXs family, PRDX5 was most related to the advancement of prostate cancer. A nomogram integrating the expression of PRDX5 with clinical features was developed to better predict clinical outcomes in PCa patients compared to 30 published signatures. Immunohistochemistry was used to verify that PRDX5 expression was higher in advanced levels of PCa tissue. Gene Set Enrichment Analysis (GSEA) and pathway predictive analysis revealed that the PRDX5 related genes were mainly relevant to ROS Pathway, Mitochondria-related functions, cellular respiration, and oxidative phosphorylation. In vitro cell proliferation assays, ROS determination assay, and apoptosis assay together revealed that depletion of PRDX5 induces apoptosis via ROS accumulation in CRPC cells. Moreover, the expression of PRDX5 in CRPC cells also affects the sensitivity to the ARSI therapy. This study offers new evidence for determining that the expression of PRDX5 is associated with advanced tumor grade, poor prognosis, and suboptimal response to multiple therapies in PCa within the PRDXs family. Last but not least, our study provides new insights into precision medicine in PCa and provides a reference for further research on PRDX5.

Soil aggregates, which are highly influenced by land conversion, play key roles in driving soil nutrient distribution and microbial colonization. However, the role of soil aggregates in shaping the responses of microbial community composition and multiple ecosystem functions, especially ecosystem multifunctionality (EMF), to land conversion remains poorly understood. In this study, we investigated the impact of the conversion of a longan orchard (LO) to a conventional tea plantation (CTP) and organic tea plantation (OTP) on soil EMF at the aggregate level and explored the underlying mechanism. Our results showed that EMF was significantly reduced in the conventional tea plantation, with 3.44, 1.79, and 1.24 times for large macro-, macro-, and micro-aggregates. In contrast, it was relatively preserved in the organic tea plantation. Notably, micro-aggregates with higher microbial biomass supported more EMF than larger aggregates under the land conversion conditions. The EMF associated with soil aggregates was found to be regulated by the differences in nutrient content and microbial community composition. Random forest analysis, redundancy analysis, and Pearson analysis indicated that both soil nutrient and microbial community composition within soil aggregates jointly determined EMF. This study highlights that soil aggregation influences the stratification of nutrients and microbial communities, which leads to the differing response of aggregate-related EMF to land conversion.

Hyperactivation of fatty acid biosynthesis holds promise as a targeted therapeutic strategy in prostate cancer (PCa). However, inhibiting these enzymes could potentially promote metastatic progression in various other cancers. Herein, we found that depletion of acetyl‐CoA carboxylase 1 (encoded by ACACA), the enzyme responsible for the first and rate‐limiting step of de novo fatty acid biosynthesis, facilitated epithelial‐mesenchymal transition (EMT) and migration of PCa cells. This finding was validated in vitro through cell migration assays and in vivo using a metastatic model established by tail vein injection of ACACA‐depleted cells into BALB/c nude mice. Additionally, depletion of ACACA activated the mitogen‐activated protein kinase (MAPK)/extracellular signal‐regulated protein kinases (ERK) pathway. Inhibition of the MAPK/ERK signaling pathway reduced EMT and migration in ACACA‐depleted cells. Our study is the first to indicate targeting ACACA induces an “unexpected” escape program through activation of the MAPK/ERK signaling pathway in PCa, ultimately leading to EMT and metastasis. Therefore, we strongly recommend that the potential adverse effects of targeting ACACA or its derived therapeutic agents must be given extreme attention, especially in MAPK‐related cancers. Depletion of ACACA in prostate cancer cells inhibits the PI3K‐AKT pathway, leading to negative feedback activation of the MAPK pathway. This activation increases expression of EMT transcription factors, particularly SLUG, resulting in upregulation of mesenchymal biomarkers and down‐regulation of epithelial biomarkers. Consequently, cancer cells exhibit morphological changes and enhanced motility, promoting metastasis. These findings highlight the role of ACACA depletion in driving EMT and metastasis via MAPK pathway activation.

Acetyl-CoA carboxylase alpha (ACACA) is a key enzyme in fatty acid biosynthesis and a proposed therapeutic target in prostate cancer. However, its role in androgen receptor-independent prostate cancer (ARIPC), an aggressive and treatment-resistant subtype, remains unclear. This study aimed to investigate the effects of ACACA depletion on ARIPC, with a focus on inflammation and metastasis. ACACA expression patterns were analyzed across multiple metastatic castration-resistant prostate cancer (mCRPC) datasets. In ARIPC cell lines, ACACA was inhibited via both shRNA and the pharmacological inhibitor TOFA. Transcriptomic, metabolomic, and single-cell RNA sequencing data were used to identify downstream changes. Inflammatory signaling was assessed by qPCR, western blotting, and immunofluorescence. Cell migration was evaluated via wound healing and transwell assays, and the metastatic potential was examined in a mouse tail vein injection model. The roles of arachidonic acid (AA), cytosolic phospholipase A2 (cPLA2), and NF-κB signaling were further tested through targeted inhibition. ACACA expression was reduced in ARIPC and was negatively correlated with inflammatory pathways. Its inhibition upregulated proinflammatory cytokines and chemokines, elevated AA and eicosanoid levels, and increased cPLA2 expression. Single-cell RNA sequencing confirmed NF-κB signaling enrichment in ACACA-low tumor cells. Mechanistically, elevated AA activated NF-κB signaling. ACACA depletion enhanced cell migration and metastasis, along with macrophage infiltration. Inhibiting cPLA2 or NF-κB signaling reversed these effects. This study reveals a previously unrecognized tumor-promoting effect of ACACA depletion in ARIPC. Targeting ACACA in this context enhances inflammation and metastasis via arachidonic acid-mediated activation of NF-κB signaling. These findings highlight a context dependent, tumor-promoting role of ACACA inhibition and underscore the need for combinational strategies to avoid potential adverse outcomes in metabolic therapies.

Fatty acid metabolism (FAM) is a crucial metabolic characteristic of tumor cells, playing a role in various pathological processes during tumor development. Till now, the prognostic role of FAM-related genes of prostate cancer (PCa) is far from fully investigation. The combinations of 10 machine learning algorithms were applied in this study. A reliable signature, FAM-related gene score (FAMRGs), was developed to predict the prognosis of patients with PCa. External data sets were used to verify the accuracy and robustness of the FAMRGs. Drug sensitivity analysis was used to predict the optimal drug for high-risk PCa patients. The underlying mechanism related to FAMRGs were investigated by functional enrichment analysis. A nomogram based on FAMRGs was developed for personalized prediction of patient prognosis. A stable FAMRGs was construced and validated in 6 independent cohorts. FAMRGs accurately divided PCa patients into low and high risk group. FAMRGs showed stronger predictive ability compared with published prognostic signatures for PCa. Also, the androgen receptor signaling inhibitors (ARSI) treatment response predictive ability of FAMRGs was identified. Five drugs that were most suitable for patients in the high risk group of FAMRGs were screened. It was shown that FAMRGs involved in cell cycle-related pathways. The novel nomogram showed precisely predictive ability for the outcomes of patients with PCa. The FAMRGs can accurately predict the prognosis of PCa patients and is expected to direct the clinical treatment for PCa.