Comparison of green building policies and regulations between central and local governments of China: Analysis based on text similarity

The development of green buildings, as the focus of the construction field, is an inevitable choice to achieve the goal of carbon peaking and carbon neutralization. From the perspective of text similarity, this paper conducts a comparative study on the 14th Five-Year Plan for Building Energy Conservation and Green Building Development issued by the Ministry of Housing and Urban-Rural Development of the PRC in 2022 and sixteen local regulations on green buildings at provincial levels. The results show that: First, promoting energy-saving and green transformation of existing public buildings, promoting new green construction methods, strengthening green building management system construction and other contents, have the highest similarity value, indicating that these three contents have the highest overall notices in the legislation formulation level of green buildings in different regions; Second, the legal texts formulated by Tianjin and Shanghai are more in line with the requirements of the 14th Five-Year Plan than those of other provinces, showing the forward-looking nature of local legislation; Lastly, through data analysis, it is found that the average similarities of the three deployments of green buildings have small differences, but there are large differences between regions. Jiangxi, Qinghai and Guangdong have some outstanding contents, forming regional characteristics according to local conditions, showing the differences of local legal texts. Since the Plan is the latest national guidance, it requires local regulations to refine and implement the contents of the Plan. Based on the comprehensive comparative analysis of the text, it is recommended that all localities should check and fill gaps according to the Plan, improve the key task systems, and use local standards to build legal guarantee tailored to local conditions

Synthesis and Catalytic Performance of Ni/SiO 2

A series of Ni/SiO2 catalysts with different Ni content were prepared by sol-gel method for application in the synthesis of 2-methyltetrahydrofuran (2-MTHF) by hydrogenation of 2-methylfuran (2-MF). The catalyst structure was investigated by X-ray diffraction (XRD), transmission electron microscopy (TEM), X-ray photoelectron spectroscopy (XPS), and temperature programmed reduction (TPR). It is found that structures and catalytic performance of the catalysts were highly affected by the Ni content. The catalyst with a 25% Ni content had an appropriate size of the Ni species and larger BET surface area and produced a higher 2-MF conversion with enhanced selectivity in 2-MTHF

Ginsenoside Rd attenuates myocardial ischemia/reperfusion injury via Akt/GSK-3β signaling and inhibition of the mitochondria-dependent apoptotic pathway.

Evidence suggests Ginsenoside Rd (GSRd), a biologically active extract from the medical plant Panax Ginseng, exerts antioxidant effect, decreasing reactive oxygen species (ROS) formation. Current study determined the effect of GSRd on myocardial ischemia/reperfusion (MI/R) injury (a pathological condition where ROS production is significantly increased) and investigated the underlying mechanisms. The current study utilized an in vivo rat model of MI/R injury and an in vitro neonatal rat cardiomyocyte (NRC) model of simulated ischemia/reperfusion (SI/R) injury. Infarct size was measured by Evans blue/TTC double staining. NRC injury was determined by MTT and lactate dehydrogenase (LDH) leakage assay. ROS accumulation and apoptosis were assessed by flow cytometry. Mitochondrial membrane potential (MMP) was determined by 5, 5\u27, 6, 6\u27-tetrachloro-1, 1\u27, 3, 3\u27-tetrathylbenzimidazol carbocyanine iodide (JC-1). Cytosolic translocation of mitochondrial cytochrome c and expression of caspase-9, caspase-3, Bcl-2 family proteins, and phosphorylated Akt and GSK-3β were determined by western blot. Pretreatment with GSRd (50 mg/kg) significantly augmented rat cardiac function, as evidenced by increased left ventricular ejection fraction (LVEF) and ±dP/dt. GSRd reduced myocardial infarct size, apoptotic cell death, and blood creatine kinase/lactate dehydrogenase levels after MI/R. In NRCs, GSRd (10 µM) inhibited SI/R-induced ROS generation (

Hybrid Dynamic Pricing Model for Transport PPP Projects during the Residual Concession Period

Public–Private-Partnerships (PPPs) have been adopted worldwide to deliver infrastructure projects and/or provide public services. Having a reasonable concession price (operation and transfer) in place is pivotal for sustaining a win-win relationship between governments and private sectors. However, historical data have shown that the concession price of PPPs when transfer is less than satisfactory due to the changing attribute of pricing parameters, causing substantial loss of residual value (RV). Nevertheless, a rational and systematic pricing model for PPPs, especially transport PPPs, is not yet available. To this end, a hybrid dynamic pricing model for transport PPPs during the residual concession period underpinned by the case-based reasoning technique is proposed. Furthermore, using a case study of the Western Harbor Crossing tunnel in Hong Kong, the proposed model is validated to be able to account for the dynamic pricing parameters and calculate a reasonable and accurate residual concession price. The contributions of this study are twofold: (1) it highlights that a reasonable concession price beyond the operation period is significant in maintaining RV; and (2) it provides a hybrid dynamic pricing model for governments and private sectors to calibrate the current less-than-satisfactory residual concession price

Adiponectin inhibits tumor necrosis factor-α-induced vascular inflammatory response via caveolin-mediated ceramidase recruitment and activation.

RATIONALE: Anti-inflammatory and vascular protective actions of adiponectin are well recognized. However, many fundamental questions remain unanswered. OBJECTIVE: The current study attempted to identify the adiponectin receptor subtype responsible for adiponectin\u27s vascular protective action and investigate the role of ceramidase activation in adiponectin anti-inflammatory signaling. METHODS AND RESULTS: Adiponectin significantly reduced tumor necrosis factor (TNF)α-induced intercellular adhesion molecule-1 expression and attenuated TNFα-induced oxidative/nitrative stress in human umbilical vein endothelial cells. These anti-inflammatory actions were virtually abolished by adiponectin receptor 1 (AdipoR1-), but not AdipoR2-, knockdown (KD). Treatment with adiponectin significantly increased neutral ceramidase (nCDase) activity (3.7-fold; P87% of adiponectin-induced nCDase activation was lost. Whereas adiponectin treatment failed to inhibit TNFα-induced intercellular adhesion molecule-1 expression, treatment with sphingosine-1-phosphate or SEW (sphingosine-1-phosphate receptor agonist) remained effective in Cav1-KD cells. AdipoR1 and Cav1 colocalized and coprecipitated in human umbilical vein endothelial cells. Adiponectin treatment did not affect this interaction. There is weak basal Cav1/nCDase interaction, which significantly increased after adiponectin treatment. Knockout of AdipoR1 or Cav1 abolished the inhibitory effect of adiponectin on leukocyte rolling and adhesion in vivo. CONCLUSIONS: These results demonstrate for the first time that adiponectin inhibits TNFα-induced inflammatory response via Cav1-mediated ceramidase recruitment and activation in an AdipoR1-dependent fashion

C1q/tumor necrosis factor-related protein-3, a newly identified adipokine, is a novel antiapoptotic, proangiogenic, and cardioprotective molecule in the ischemic mouse heart.

BACKGROUND: Obesity and diabetes mellitus adversely affect postischemic heart remodeling via incompletely understood mechanisms. C1q/tumor necrosis factor-related protein-3 (CTRP3) is a newly identified adipokine exerting beneficial metabolic regulation, similar to adiponectin. The aim of the present study was to determine whether CTRP3 may regulate postischemic cardiac remodeling and cardiac dysfunction, and, if so, to elucidate the underlying mechanisms. METHODS AND RESULTS: Male adult mice were subjected to myocardial infarction (MI) via left anterior descending coronary artery occlusion. Both the effect of MI on endogenous CTRP3 expression/production and the effect of exogenous CTRP3 (adenovirus or recombinant CTRP3) replenishment on MI injury were investigated. MI significantly inhibited adipocyte CTRP3 expression and reduced the plasma CTRP3 level, reaching a nadir 3 days after MI. CTRP3 replenishment improved survival rate (P CONCLUSION: CTRP3 is a novel antiapoptotic, proangiogenic, and cardioprotective adipokine, the expression of which is significantly inhibited after MI

Pre-treatment Resting-State Functional MR Imaging Predicts the Long-Term Clinical Outcome After Short-Term Paroxtine Treatment in Post-traumatic Stress Disorder

Background: The chronic phase of post-traumatic stress disorder (PTSD) and the limited effectiveness of existing treatments creates the need for the development of potential biomarkers to predict response to antidepressant medication at an early stage. However, findings at present focus on acute therapeutic effect without following-up the long-term clinical outcome of PTSD. So far, studies predicting the long-term clinical outcome of short-term treatment based on both pre-treatment and post-treatment functional MRI in PTSD remains limited.Methods: Twenty-two PTSD patients were scanned using resting-state functional MRI (rs-fMRI) before and after 12 weeks of treatment with paroxetine. Twenty patients were followed up using the same psychopathological assessments 2 years after they underwent the second MRI scan. Based on clinical outcome, the follow-up patients were divided into those with remitted PTSD or persistent PTSD. Amplitude of low-frequency fluctuations (ALFF) and degree centrality (DC) derived from pre-treatment and post-treatment rs-fMRI were used as classification features in a support vector machine (SVM) classifier.Results: Prediction of long-term clinical outcome by combined ALFF and DC features derived from pre-treatment rs-fMRI yielded an accuracy rate of 72.5% (p < 0.005). The most informative voxels for outcome prediction were mainly located in the precuneus, superior temporal area, insula, dorsal medial prefrontal cortex, frontal orbital cortex, supplementary motor area, lingual gyrus, and cerebellum. Long-term outcome could not be successfully classified by post-treatment imaging features with accuracy rates <50%.Conclusions: Combined information from ALFF and DC from rs-fMRI data before treatment could predict the long-term clinical outcome of PTSD, which is critical for defining potential biomarkers to customize PTSD treatment and improve the prognosis

Reduced cardioprotective action of adiponectin in high-fat diet-induced type II diabetic mice and its underlying mechanisms.

Diabetes exacerbates ischemic heart disease morbidity and mortality via incompletely understood mechanisms. Although adiponectin (APN) reduces myocardial ischemia/reperfusion (MI/R) injury in nondiabetic animals, whether APN\u27s cardioprotective actions are altered in diabetes, a pathologic condition with endogenously reduced APN, has never been investigated. High-fat diet (HD)-induced diabetic mice and normal diet (ND) controls were subjected to MI via coronary artery ligation, and given vehicle or APN globular domain (gAPN, 2 μg/g) 10 min before reperfusion. Compared to ND mice (where gAPN exerted pronounced cardioprotection), HD mice manifested greater MI/R injury, and a tripled gAPN dose was requisite to achieve cardioprotective extent seen in ND mice (i.e., infarct size, apoptosis, and cardiac function). APN reduces MI/R injury via AMP-activated protein kinase (AMPK)-dependent metabolic regulation and AMPK-independent antioxidative/antinitrative pathways. Compared to ND, HD mice manifested significantly blunted gAPN-induced AMPK activation, basally and after MI/R (p\u3c0.05). Although both low- and high-dose gAPN equally attenuated MI/R-induced oxidative stress (i.e., NADPH oxidase expression and superoxide production) and nitrative stress (i.e., inducible nitric oxide synthase expression, nitric oxide production, and peroxynitrite formation) in ND mice, only high-dose gAPN efficaciously did so in HD mice. We demonstrate for the first time that HD-induced diabetes diminished both AMPK-dependent and AMPK-independent APN cardioprotection, suggesting an unreported diabetic heart APN resistance

Synthesis and Catalytic Performance of Ni/SiO 2 for Hydrogenation of 2-Methylfuran to 2-Methyltetrahydrofuran

A series of Ni/SiO 2 catalysts with different Ni content were prepared by sol-gel method for application in the synthesis of 2-methyltetrahydrofuran (2-MTHF) by hydrogenation of 2-methylfuran (2-MF). The catalyst structure was investigated by Xray diffraction (XRD), transmission electron microscopy (TEM), X-ray photoelectron spectroscopy (XPS), and temperature programmed reduction (TPR). It is found that structures and catalytic performance of the catalysts were highly affected by the Ni content. The catalyst with a 25% Ni content had an appropriate size of the Ni species and larger BET surface area and produced a higher 2-MF conversion with enhanced selectivity in 2-MTHF

High-expression of the innate-immune related gene UNC93B1 predicts inferior outcomes in acute myeloid leukemia

Acute myeloid leukemia (AML) is a heterogeneous hematological malignancy with dismal prognosis. Identification of better biomarkers remained a priority to improve established stratification and guide therapeutic decisions. Therefore, we extracted the RNA sequence data and clinical characteristics of AML from The Cancer Genome Atlas (TCGA) and Genotype-Tissue Expression database (GTEx) to identify the key factors for prognosis. We found UNC93B1 was highly expressed in AML patients and significantly linked to poor clinical features (p < 0.05). We further validated the high expression of UNC93B1 in another independent AML cohort from GEO datasets (p < 0.001) and performed quantitative PCR of patient samples to confirm the overexpression of UNC93B1 in AML (p < 0.005). Moreover, we discovered high level of UNC93B1 was an independent prognostic factor for poorer outcome both in univariate analysis and multivariate regression (p < 0.001). Then we built a nomogram model based on UNC93B1 expression, age, FAB subtype and cytogenetic risk, the concordance index of which for predicting overall survival was 0.729 (p < 0.001). Time-dependent ROC analysis for predicting survival outcome at different time points by UNC93B1 showed the cumulative 2-year survival rate was 43.7%, and 5-year survival rate was 21.9%. The differentially expressed genes (DEGs) between two groups divided by UNC93B1 expression level were enriched in innate immune signaling and metabolic process pathway. Protein–protein interaction (PPI) network indicated four hub genes (S100A9, CCR1, MRC1 and CD1C) interacted with UNC93B1, three of which were also significantly linked to inferior outcome. Furthermore, we discovered high UNC93B1 tended to be infiltrated by innate immune cells, including Macrophages, Dendritic cells, Neutrophils, Eosinophils, and NK CD56dim cells. We also found UNC93B1 had a significantly positive correlation with CD14, CD68 and almost all Toll-like receptors. Finally, we revealed negatively correlated expression of UNC93B1 and BCL2 in AML and conjectured that high-UNC93B1 monocytic AML is more resistant to venetoclax. And we found high MCL-1 expression compensated for BCL-2 loss, thus, we proposed MCL-1 inhibitor might overcome the resistance of venetoclax in AML. Altogether, our findings demonstrated the utility of UNC93B1 as a powerful poor prognostic predictor and alternative therapeutic target