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The traditional data envelopment analysis (DEA) model usually ignores the influence of external environmental factors and random interference. This can easily lead to deviations in efficiency estimates. In order to solve this problem, a three-stage DEA model was used to better reflect the carbon emission efficiency of Chinese construction industry (CEECI) (2006–2017) from the perspective of non-management factors. The internal influencing factors of CEECI are analyzed by the Tobit model, which provides a more accurate basis for formulating policies. It is found that the CEECI is significantly affected by the GDP, the level of industrialization, the degree of opening-up, technological innovation, and energy structure. After excluding environmental factors and random interference, the average CEECI increased by 16%. The resulting calculations are noteworthy in three aspects. First, there are significant regional differences in the CEECI. Both the multi-polarization phenomenon of CEECI and regional differences also reduced gradually over time. Second, the CEECI can be decomposed into pure carbon emission efficiency (PCEE) and scale efficiency (SE), which is mainly caused by SE. Excluding external environmental factors and random interference will have a specific impact on the CEECI. All the 30 provinces are divided into four categories to analyze the reasons and solutions of the differences in the CEECI in provinces. Third, many factors had inhibitory effects on the CEECI, PCEE, and SE; these included energy structure optimization, labor force number, total power of construct ion equipment, and construction intensity in the construction industry. Nevertheless, the development level of the construction industry did have a significant positive effect.

Nonalcoholic steatohepatitis (NASH), the advanced stage of nonalcoholic fatty liver disease (NAFLD), is emerging as a leading cause of progressive liver fibrosis and end-stage liver disease. Liver macrophages, mainly composed of Kupffer cells (KCs) and monocyte-derived macrophages (MoMFs), play a vital role in NASH progression and regression. Recent advances suggest that cell-cell communication is a fundamental feature of hepatic microenvironment. The reprogramming of cell-cell signaling between macrophages and surrounding cells contributes to the pathogenesis of NASH. In this review, we summarize the current knowledge of NASH regarding the composition of liver macrophages and their communication with surrounding cells, which are composed of hepatocytes, hepatic stellate cells (HSCs), liver sinusoidal endothelial cells (LSECs) and other immune cells. We also discuss the potential therapeutic strategies based on the level of macrophages.

Oral lichen planus (OLP) is a localized autoimmune disease of the oral mucosa, with an incidence of up to 2%. Although corticosteroids are the first-line treatment, they cause several adverse effects. Quercetin, a naturally occurring compound, has fewer side-effects and provides long-term benefits. Besides, it has powerful anti‑inflammatory activities. Here, we combined network pharmacology with experimental verification to predict and verify the key targets of quercetin against OLP. First, 66 quercetin-OLP common targets were analyzed from various databases. The protein–protein interaction (PPI) network was constructed. Topology analysis and MCODE cluster analysis of common targets were conducted to identify 12 key targets including TP53, IL-6 and IFN-γ and their connections. Gene functions and key signaling pathways, including reactive oxygen species metabolism, IL-17 pathway and AGE-RAGE pathway, were enriched by Gene Ontology (GO) and Kyoto Encyclopedia of Genes and Genomes (KEGG) analysis. Then, in vitro experiments showed that quercetin interfered with Th1/Th2 balance by acting on IL-6 and IFN-γ to modulate the immune system in treating OLP. Quercetin considerably affected the apoptosis and migration of T lymphocytes in OLP patients. Our study reveals the potential therapeutic targets and signaling pathways of quercetin associated with OLP, and establishes the groundwork for future clinical applications.

The whole-grain, hulled Tartary buckwheat flour (HTBF) with outstanding bioactive functions was prepared, and the effects of partial substitution ratios (0, 30%, 51% and 70%) of wheat flour with HTBF on the characteristics of TB noodles (TBNs) were investigated, mainly including the cooking characteristics, sensory analysis, internal structure, bioactive components, and in vitro starch digestibility. With an increasing replacement level of HTBF, the water absorption index of the noodles decreased, whereas the cooking loss increased. A sensory analysis indicated that there were no off-flavors in all TBN samples. The scanning electron microscope images presented that the wheat noodles, 30% TBNs and 70% TBNs had dense and uniform cross sections. Meanwhile, the deepest color, V-type complexes, and lowest crystallinity (13.26%) could be observed in the 70% TBNs. A HTBF substitution increased the rutin content and the total phenolic and flavonoid contents in the TBNs, and higher values were found in the 70% TBNs. Furthermore, the lowest rapidly digestible starch content (16%) and highest resistant starch content (66%) were obtained in the 70% TBNs. Results demonstrated that HTBF could be successfully applied to make TBNs, and a 70% substitution level was suggested. This study provides consumers with a good option in the realm of special noodle-type products.

Background Studies have shown that DAB2IP inhibits cancer progression, while HSP90AA1 promotes cancer progression. However, the specific regulatory mechanism of DAB2IP and HSP90AA1 in colorectal cancer (CRC) is not clear. Our aim is to investigate the role and mechanism of DAB2IP and HSP90AA1 in the development of CRC. Methods We used bioinformation to analyze the interaction between DAB2IP and HSP90AA1 and predict their downstream pathways. Then, a series of in vitro and in vivo experiments were conducted to reveal the role of DAB2IP and HSP90AA1 in the invasion and metastasis of colorectal cancer, and flow cytometry was used to explore their effects on apoptosis. Results Loss of DAB2IP was associated with poor prognosis of CRC. In contrast, elevated expression of HSP90AA1 was associated with the malignant behavior of CRC. The present study demonstrated a negative correlation between DAB2IP and HSP90AA1. Using bioinformatic analysis, we scanned SRP9 which was highly expressed in CRC, as a co-related gene of DAB2IP and HSP90AA1. Mechanistically, DAB2IP promoted apoptosis through HSP90AA1/SRP9/ASK1/JNK signaling axis in CRC. Conclusions These findings provide evidence that DAB2IP-based therapy may enhance the anticancer effect of HSP90AA1 inhibitors, and combined targeting of DAB2IP and HSP90AA1 may be a powerful treatment strategy to combat CRC.

Objective This study aimed to develop and validate a nomogram model for predicting 28-day mortality in patients with sepsis in the intensive care unit. Methods The health care records of 613 patients with sepsis who were hospitalized at the Affiliated Hospital of Chengde Medical University from 2022 to 2024 were retrospectively reviewed. Patients were randomly divided into training and testing sets in a 7:3 ratio. The least absolute shrinkage and selection operator regression method was used to identify potential prognostic factors for sepsis, followed by multivariate logistic regression to construct a nomogram prediction model. The predictive performance of the developed model was evaluated via receiver operating characteristic curves, decision curve analysis, and calibration curves. Results The predictive factors included the platelet distribution width to count ratio, mean platelet volume, N-terminal proB-type natriuretic peptide level, lactate level, respiratory tract infections, and diabetes. The area under the receiver operating characteristic curve for the nomogram model in the training set was 0.907, with sensitivity and specificity values of 0.846 and 0.831, respectively. The calibration curve demonstrated that the prediction results were consistent with the actual findings. Decision curve analysis revealed that the model showed robust performance in practical applications. Conclusions Platelet distribution width to count ratio, mean platelet volume, N-terminal proB-type natriuretic peptide level, lactate level, respiratory tract infection, and diabetes are closely associated with sepsis. A nomogram model based on these six variables demonstrates remarkable predictive performance and may assist clinicians in identifying high-risk patients and optimizing personalized therapy.

BackgroundThe objective of this study was to determine the risk factors and outcomes of white matter brain injury (WMBI) on magnetic resonance imaging (MRI) at term-equivalent age in infants with surgical necrotizing enterocolitis (NEC).MethodsThis retrospective study compared clinical/pathological information between infants with and those without WMBI.ResultsOut of 69 infants with surgical NEC, 17 (24.6%) had mild WMBI, 13 (18.8%) had moderate WMBI, and six (8.7%) had severe WMBI on the brain MRI. Several clinical factors (gestational age, more red blood cell (RBC) transfusions before NEC onset, pneumoperitoneum, earlier NEC onset age, postoperative ileus, acute kidney injury (AKI) by serum creatinine, postnatal steroids, hospital stay) and histopathological findings (necrosis, hemorrhage) had univariate associations with WMBI. Associations with RBC transfusion (odds ratio (OR) 23.6 [95% confidence interval (CI): 4.73–117.97]; p = 0.0001), age at NEC onset (OR 0.30 [95%CI: 0.11–0.84]; p = 0.021), necrosis (OR 0.10 [95%CI: 0.01–0.90]; p = 0.040), and bowel hemorrhage (OR 7.79 [95%CI: 2.19–27.72]; p = 0.002) persisted in multivariable association with grade 3–4 WMBI. The infants with WMBI had lower mean motor, cognitive, language scores, and higher ophthalmic morbidity at 2 years of age.ConclusionsThe WMBI was most likely associated with earlier NEC onset, higher RBC transfusions, and less necrosis and greater hemorrhage lesions on intestinal pathology in preterm infants with surgical NEC.ImpactIn preterm infants with surgical NEC, brain MRI showed injury in the white matter in 52%, gray matter in 10%, and cerebellar region in 30%.Preterm infants with severe WMBI (grade 3–4) had less necrosis and greater hemorrhagic lesions on histopathology of the bowel.Preterm infants with WMBI were more likely to have a more severe postoperative course, AKI, and longer length of hospitalization.Neuroprotective strategies to prevent brain injury in preterm infants with surgical NEC are needed with the goal of improving the neurodevelopmental outcomes.

Background Autism spectrum disorder (ASD) is a neurodevelopmental disorder affecting ~ 2% of children worldwide and is characterized by repetitive, stereotypical behaviours and impaired expressive communication. Cytomegalovirus (CMV) is considered a risk factor for ASD; however, published studies are usually limited by covering too few events and have different conclusions, indicating that the relationship between CMV infection and ASD remains elusive. Methods To investigate the association between CMV infection and ASD, we conducted this 2-sample Mendelian randomization (MR) study using genome-wide association studies (GWAS) summary data from FinnGen and the IEU Open GWAS project. Results Our results showed no significant relationship between all 3 CMV infections (unspecified cytomegaloviral diseases, anti-CMV IgG levels, and maternal CMV) and ASD. Conclusions Our results indicate that CMV infection does not significantly increase ASD risk. These results show that the relationship between CMV infection and ASD remains elusive and needs to be further clarified.

Colorectal carcinoma (CRC) remains a huge challenge in clinical treatment due to tumor metastasis and recurrence. Stem cell‐like colon tumor‐repopulating cells (TRCs) are a subpopulation of cancer cells with highly tumorigenic and chemotherapy resistant properties. The core transcription factor c‐Myc is essential for maintaining cancer stem‐like cell phenotypes, yet its roles and regulatory mechanisms remain unclear in colon TRCs. We report that elevated c‐Myc protein supported formation and growth of TRC spheroids. The tumor suppressor DOC‐2/DAB2 interactive protein (DAB2IP) suppressed c‐Myc expression to inhibit TRC expansion and self‐renewal. Particularly, DAB2IP disrupted c‐Myc stability through glycogen synthase kinase 3β/protein phosphatase 2A‐B56α‐mediated phosphorylation and dephosphorylation cascade on c‐Myc protein, leading to its eventual degradation through the ubiquitin‐proteasome pathway. The expression of DAB2IP was negatively correlated with c‐Myc in CRC specimens. Overall, our results improved mechanistic insight into how DAB2IP suppressed TRC growth and self‐renewal. We reported that elevated c‐Myc protein supported formation and growth of tumor‐repopulating cell (TRC) spheroids. The tumor suppressor DOC‐2/DAB2 interactive protein (DAB2IP) suppressed c‐Myc expression to inhibit TRC expansion and self‐renewal. Particularly, DAB2IP disrupted c‐Myc stability through glycogen synthase kinase 3β/protein phosphatase 2A‐B56α‐mediated phosphorylation and dephosphorylation cascade on c‐Myc protein, leading to its eventual degradation through the ubiquitin‐proteasome pathway.

Background Cyclin-dependent kinase 16 (CDK16) is an atypical PCTAIRE kinase, and its activity is dependent on the Cyclin Y (CCNY) family. Ccnys have been reported to regulate mammary stem cell activity and mammary gland development, and CCNY has been recognized as an oncoprotein in various cancers, including breast cancer. However, it remains unclear whether CDK16 has a role in breast cancer and whether it can be used as a therapeutic target for breast cancer. Methods Publicly available breast cancer datasets analyses and Kaplan-Meier survival analyses were performed to reveal the expression and clinical relevance of atypical CDKs in breast cancer. CDK16 protein expression was further examined by immunohistochemical and immunoblot analyses of clinical samples. Cell proliferation was measured by colony formation and MTT analyses. Cell cycle and apoptosis were examined by fluorescence-activated cell sorting (FACS) analysis. Wound-healing and trans-well invasion assays were conducted to test cell migration ability. The functions of CDK16 on tumorigenesis and metastasis were evaluated by cell line-derived xenograft, patient-derived organoid/xenograft, lung metastasis and systemic metastasis mouse models. Transcriptomic analysis was performed to reveal the potential molecular mechanisms involved in the function of CDK16. Pharmacological inhibition of CDK16 was achieved by the small molecular inhibitor rebastinib to further assess the anti-tumor utility of targeting CDK16. Results CDK16 is highly expressed in breast cancer, particularly in triple-negative breast cancer (TNBC). The elevated CDK16 expression is correlated with poor outcomes in breast cancer patients. CDK16 can improve the proliferation and migration ability of TNBC cells in vitro, and promote tumor growth and metastasis of TNBC in vivo. Both genetic knockdown and pharmacological inhibition of CDK16 significantly suppress the tumor progression of TNBC. Mechanistically, CDK16 exerts its function by phosphorylating protein regulator of cytokinesis 1 (PRC1) to regulate spindle formation during mitosis. Conclusion CDK16 plays a critical role in TNBC and is a novel promising therapeutic target for TNBC.