An evaluation model for city-scale construction and demolition waste management effectiveness: A case study in China.

The growing generation of construction and demolition waste (CDW) has emerged as a prominent challenge on global environmental agendas. However, the effectiveness of CDW management (CDWM) strategies varies among cities. Existing literature predominantly evaluates the effectiveness of CDWM at the project level, offering a localized perspective that fails to capture a city's comprehensive CDWM profile. This localized focus has certain limitations. To fill this gap in city-scale evaluations, this study introduces a novel model for assessing CDWM effectiveness at the municipal level. An empirical investigation was conducted across 11 cities within the Guangdong-Hong Kong-Macao Greater Bay Area (GBA) to operationalize this model. The model defines five distinct levels of CDWM effectiveness. Findings indicate that Hong Kong consistently achieves the highest level (level I), while the majority of cities fall within levels III and IV. This pattern suggests that CDWM effectiveness in the GBA is moderately developed, with uneven progress in CDW management outcomes and supporting systems. Essentially, there is a lack of synchronous development of CDWM results and guarantee systems. The proposed evaluation model enriches existing CDWM research field and offers a framework that may inform future studies in other countries.

Investigation of spatial association network features of construction waste in major Chinese urban agglomeration.

The illegal dumping of construction waste (CW) poses an increasingly serious environmental pollution problem with the accelerated rate of urbanization. As CW disposal capacity struggles to match municipal needs, some CW is being diverted to higher resource endowment cities rather than recycled. To address this situation, it is necessary to obtain reliable information on the characteristics and evolution of CW generation networks in China. This study combines a modified gravity model with Social Network Analysis (SNA) to analyze the spatial association networks of CW generation in four Chinese urban agglomerations between 2000 and 2020. Results reveal the evolution characteristics of the CW generation network, including increasing density and correlation and decreasing network efficiency. Furthermore, the Quality Assurance Procedure (QAP) indicates that urbanization level and population size are positively correlated with CW generations, whereas distance plays a negative role, but resources are insignificant for network formation. The findings provide insight into current patterns of waste distribution and a theoretical basis for government policy formulation in the future.

LncRNA FGD5-AS1 potentiates autophagy-associated doxorubicin resistance by regulating the miR-154-5p/WNT5A axis in osteosarcoma.

Osteosarcoma is prevalent in children and adolescent. The oncogenic function of long-chain noncoding RNA (lncRNA) FGD5 antisense RNA 1 (FGD5-AS1) has been reported. However, the function of FGD5-AS1 in doxorubicin-resistance in osteosarcoma remains to be illucidated. Quantitative real-time PCR (qRT-PCR) and western blot analysis (WB) were used to measure the expression of FGD5-AS1, miR-154-5p, WNT5A and autophagy proteins. MTT assay was used to assess cell viability and transwell assay was performed to evaluate migration. A nude mouse xenograft model was developed to verify the function of FGD5-AS1 in vivo. FGD5-AS1 was upregulated in doxorubicin-resistant (DXR) osteosarcoma cells. Knockdown of FGD5-AS1 suppressed osteosarcoma cell proliferation, migration, and autophagy. FGD5-AS1 upregulated WNT5A expression via sponging miR-154-5p. Furthermore, FGD5-AS1 enhanced osteosarcoma cell chemotherapy resistance through upregulation of WNT5A by inhibiting miR-154-5p. Suppression of FGD5-AS1 significantly suppressed tumor growth in nude mice. FGD5-AS1 may promote chemoresistance through WNT5A-induced autophagy by sponging miR-154-5p in osteosarcoma cells.

Blockchain technology-based sustainable management research: the status quo and a general framework for future application.

The problems of data leakage and unreliable information transfer in the management process make sustainability management an inevitable need for future development. Globally, there is increasing attention paid to blockchain technology and particularly its application in addressing sustainable management issues, both from academia and industry. Aiming to deepen the understanding of how blockchain technology could deal with sustainable management issues across different disciplines, this paper investigates the latest research on the application of blockchain technology in sustainable management published from 2017 to 2021. It is found that there is a drastic surge of publications in the recent 2 years. The analysis focuses on authors' origins, the collaboration network of the keywords, countries, and research topics covered. The application of blockchain technology in five key sectors of sustainable management, encompassing energy management, construction management, supply chain management, environmental management, and e-government management, is selected for further analysis detail. Also, a general framework for applying blockchain technology is proposed for broadening its use and dealing with sustainable management issues. The findings show that the identified 108 publications are distributed in 75 different journals, and scholars from China, the UK, and the USA have been working closely in BT-based sustainable management research. Blockchain technology is just emerging in sustainable management, and there is a great potential for applying blockchain technology to improve sustainable management performance and, more importantly, to provide solutions to quite a few long-lasting problems in these sectors. Opportunities for future research are also presented and discussed.

[Representations of object animacy and real-world size in the ventral visual pathway].

How the brain perceives objects and classifies perceived objects is one of the important goals of visual cognitive neuroscience. Previous research has shown that when we see objects, the brain's ventral visual pathway recognizes and classifies them, leading to different ways of interacting with them. In this paper, we summarize the latest research progress of the ventral visual pathway related to the visual classification of objects. From the perspective of the neural representation of objects and its underlying mechanisms in the visual cortex, we summarize the current research status of the two important organizational dimensions of object animacy and real-world size, provide new insights, and point out the direction of further research.

[Retracted] Oncolytic adenovirus­mediated mda­7/IL­24 expression suppresses osteosarcoma growth and enhances sensitivity to doxorubicin.

Following the publication of this paper, it was drawn to the Editors' attention by a concerned reader that the western blot assay data shown in Figs. 1B, 5A, 6A and C were strikingly similar to data appearing in different form in other articles by different authors. Owing to the fact that the contentious data in the above article were already under consideration for publication prior to its submission to Molecular Medicine Reports, the Editor has decided that this paper should be retracted from the Journal. After having been in contact with the authors, they agreed with the decision to retract the paper. The Editor apologizes to the readership for any inconvenience caused. [the original article was published in Molecular Medicine Reports 12: 6358­6364, 2015; DOI: 10.3892/mmr.2015.4180].

Oncogenic role of early growth response-1 in liver cancer through the regulation of the microRNA-675/sestrin 3 and the Wnt/ß-catenin signaling pathway.

Early growth response-1 (EGR1) is a multi-domain protein and an immediate early transcription factor that is induced during liver injury and controls the expression of a variety of genes implicated in metabolism, cell proliferation, and tumorigenesis. Liver cancer (LC) is a highly malignant disease with high mortality worldwide. This study focused on the function of EGR1 in LC development and the mechanism of action. Two LC-related datasets GSE101728 and GSE138178 downloaded from the Gene Expression Omnibus (GEO) database were used for identification of key genes involved in cancer progression. A microarray analysis was conducted to identify differentially expressed microRNAs (miRNAs) after EGR1 knockdown. The target gene of miR-675 was identified by integrated analysis. EGR1 and miR-675 were highly expressed, whereas sestrin 3 (SESN3) was poorly expressed in LC tissues and cells. High EGR1 expression was associated with poor liver function and disease severity in patients with LC. Knockdown of EGR1 weakened proliferation and invasiveness of LC cells. EGR1 bound to the miR-675 promoter and increased its transcription, and miR-675 bound to SESN3 mRNA to induce its downregulation. miR-675 upregulation promoted the malignance of LC cells, but further upregulation of SESN3 reduced invasiveness of cells. SESN3 was enriched in the Wnt/ß-catenin signaling. EGR1 and miR-675 activated the Wnt/ß-catenin through downregulating SESN3. This study demonstrated that EGR1 promotes the malignant behaviors of LC cells through mediating the miRNA-675/SESN3/Wnt/ß-catenin axis.

[Retracted] MicroRNA­154 functions as a tumor suppressor in osteosarcoma by targeting Wnt5a.

Following the publication of this paper, it was drawn to the Editors' attention by a concerned reader that the western blotting data featured in Fig. 5B and C, and also in Fig. 6B, were strikingly similar to data appearing in different form in other articles by different authors at different research institutes. Owing to the fact that the contentious data in the above article were already under consideration for publication, or had already been published, elsewhere prior to its submission to Oncology Reports, the Editor has decided that this paper should be retracted from the Journal. After having been in contact with the authors, they agreed with the decision to retract the paper. The Editor apologizes to the readership for any inconvenience caused. [the original article was published in Oncology Reports 35: 1851­1858, 2016; DOI: 10.3892/or.2015.4495].

A text mining-based thematic model for analyzing construction and demolition waste management studies.

Over the years, numerous studies have been conducted to investigate construction and demolition waste (CDW) management problems. However, the massive amount of literature brings challenges to scholars because it is difficult and time-consuming to manually identify research emphasis from the literature. Therefore, a method that can informationize literature collection and automatically detect insights from the identified literature is worthy of exploration. This paper attempts to present a comprehensive thematic model by combining Latent Dirichlet Allocation, word2vec, and community detection algorithm on python to detect insights from CDW management literature. Based on the database of Web of Science, 641 articles published between 2000 and 2019 are retrieved and used as the sample for analysis. The comprehensive thematic results reveal a four-domain knowledge map in CDW management research, which covers (1) introducing current situation of CDW management, (2) quantifying CDW generation, (3) assessing CDW and by-products, and (4) facilitating waste diversion. Future research directions in CDW management research have also been discussed. The results prove that the comprehensive thematic model is useful in mining insights from CDW management literature.

TRPV1 activation mitigates hypoxic injury in mouse cardiomyocytes by inducing autophagy through the AMPK signaling pathway.

Autophagy is a highly conserved self-protection mechanism that plays a crucial role in cardiovascular diseases. Cardiomyocyte hypoxic injury promotes oxidative stress and pathological alterations in the heart, although the interplay between these effects remains elusive. The transient receptor potential vanilloid 1 (TRPV1) ion channel is a nonselective cation channel that is activated in response to a variety of exogenous and endogenous physical and chemical stimuli. Here, we investigated the effects and mechanisms of action of TRPV1 on autophagy in hypoxic cardiomyocytes. In this study, primary cardiomyocytes isolated from C57 mice were subjected to hypoxic stress, and their expression of TRPV1 and adenosine 5'-monophosphate-activated protein kinase (AMPK) was regulated. The autophagy flux was assessed by Western blotting and immunofluorescence staining, and the cell viability was determined through Cell counting kit-8 assay and Lactate dehydrogenase assays. In addition, the calcium influx after the upregulation of TRPV1 expression in cardiomyocytes was examined. The results showed that the number of autophagosomes in cardiomyocytes was higher under hypoxic stress and that the blockade of autophagy flux aggravated hypoxic damage to cardiomyocytes. Moreover, the expression of TRPV1 was induced under hypoxic stress, and its upregulation by capsaicin improved the autophagy flux and protected cardiomyocytes from hypoxic damage, whereas the silencing of TRPV1 significantly attenuated autophagy. Our observations also revealed that AMPK signaling was activated and involved in TRPV1-induced autophagy in cardiomyocytes under hypoxic stress. Overall, this study demonstrates that TRPV1 activation mitigates hypoxic injury in cardiomyocytes by improving autophagy flux through the AMPK signaling pathway and highlights TRPV1 as a novel therapeutic target for the treatment of hypoxic cardiac disease.

Long noncoding RNA LINC00958 accelerates the proliferation and matrix degradation of the nucleus pulposus by regulating miR-203/SMAD3.

Emerging evidence suggests that long noncoding RNAs (lncRNAs) play important roles in the development of intervertebral disc degeneration (IDD). LncRNA LINC00958 has recently been shown to play crucial roles in the development of tumors. However, the role of LINC00958 in IDD remains unclear. We showed that the expression of lncRNA LINC00958 was upregulated in degenerative NP samples, and LINC00958 expression increased gradually along with the grade of exacerbation of disc degeneration. Ectopic expression of LINC00958 promoted nucleus pulposus (NP) cell proliferation, inhibited aggrecan and Col II expression and promoted MMP-2 and MMP-13 expression. In addition, we showed that miR-203 expression was downregulated in degenerative NP samples, and miR-203 expression reduced gradually along with the grade of exacerbation of disc degeneration. Moreover, we demonstrated that the expression of miR-203 was inversely related with LINC00958 expression in NP samples. Ectopic expression of miR-203 inhibited NP cell growth and inhibited ECM degradation. Furthermore, we showed that ectopic expression of miR-203 suppressed the luciferase activity of the wild-type LINC00958 3'-UTR but not the mutant LINC00958 3'-UTR. Elevated expression of LINC00958 inhibited the expression of miR-203 and promoted the expression of SMAD3. In addition, we demonstrated that lncRNA LINC00958 exerted its function by targeting miR-203 in the NP cells. These data suggested that dysregulated lncRNA LINC00958 expression might play an important role in the development of IDD.

Microtubule-associated protein 4 phosphorylation regulates epidermal keratinocyte migration and proliferation.

Both cell migration and proliferation are indispensable parts of reepithelialization during skin wound healing, which is a complex process for which the underlying molecular mechanisms are largely unknown. Here, we identify a novel role for microtubule-associated protein 4 (MAP4), a cytosolic microtubule-binding protein that regulates microtubule dynamics through phosphorylation modification, as a critical regulator of epidermal wound repair. We showed that MAP4 phosphorylation was induced in skin wounds. In an aberrant phosphorylated MAP4 mouse model, hyperphosphorylation of MAP4 (S737 and S760) accelerated keratinocyte migration and proliferation and skin wound healing. Data from both primary cultured keratinocytes and HaCaT cells in vitro revealed the same results. The promigration and proproliferation effects of MAP4 phosphorylation depended on microtubule rearrangement and could be abolished by MAP4 dephosphorylation. We also identified p38/MAPK as an upstream regulator of MAP4 phosphorylation in keratinocytes. Our findings provide new insights into the molecular mechanisms underlying wound-associated keratinocyte migration and proliferation and identify potential targets for the remediation of defective wound healing.

Procurement innovation for a circular economy of construction and demolition waste: Lessons learnt from Suzhou, China.

Amidst the global trend of advocating a circular economy, various nations and regions in recent years have started to explore innovative procurement models (e.g., Public Private Partnership [PPP]) in dealing with beset issues related to construction and demolition (C&D) waste. However, PPP is suffering from problems such as 'long negotiation time', 'lack of transparency', and 'uneven risk and return allocation', which in turn lead to 'ineffective delivery' and 'poor value for money'. Using a case study, this paper reports some lessons learnt from innovative practices of procuring C&D management services in Suzhou, China. It is discovered that the public and private sectors, without prior knowledge, are operating based on a general concession framework instead of negotiating a clear-cut agreement from the outset. Several key arrangements, such as price, concession period, and strategic operations, are based on relational contract-type of agreements, which are found particularly innovative for shortening the negotiation time, fostering the trust between the relevant parties, dealing with emerging ad hoc problems, and allowing sustainable development of the circular economy. To make such PPP work, it is critical to devise institutions to prevent corruption and opportunistic behaviors. This research provides useful references to developing a circular economy. Although they focus on C&D waste management, the research findings can be applied to other public procurement settings, such as municipal solid waste management service.

Author Correction: Involvement of autophagy in hypoxia-BNIP3 signaling to promote epidermal keratinocyte migration.

Following publication of the original article, it has come to our attention that the Materials and Methods section of the paper was missing. This is because this section was accidentally omitted from the final version of the manuscript when it was submitted to production. Both the PDF and HTML versions of the article have been updated with the missing section and references. As a result, the references at the end of article have been renumbered as well. We apologize for this inconvenience.

Involvement of autophagy in hypoxia-BNIP3 signaling to promote epidermal keratinocyte migration.

BNIP3 is an atypical BH3-only member of the Bcl-2 family with pro-death, pro-autophagic, and cytoprotective functions, depending on the type of stress and cellular context. Recently, we demonstrated that BNIP3 stimulates the migration of epidermal keratinocytes under hypoxia. In the present study found that autophagy and BNIP3 expression were concomitantly elevated in the migrating epidermis during wound healing in a hypoxia-dependent manner. Inhibition of autophagy through lysosome-specific chemicals (CQ and BafA1) or Atg5-targeted small-interfering RNAs greatly attenuated the hypoxia-induced cell migration, and knockdown of BNIP3 in keratinocytes significantly suppressed hypoxia-induced autophagy activation and cell migration, suggesting a positive role of BNIP3-induced autophagy in keratinocyte migration. Furthermore, these results indicated that the accumulation of reactive oxygen species (ROS) by hypoxia triggered the activation of p38 and JNK mitogen-activated protein kinase (MAPK) in human immortalized keratinocyte HaCaT cells. In turn, activated p38 and JNK MAPK mediated the activation of BNIP3-induced autophagy and the enhancement of keratinocyte migration. These data revealed a previously unknown mechanism that BNIP3-induced autophagy occurs through hypoxia-induced ROS-mediated p38 and JNK MAPK activation and supports the migration of epidermal keratinocytes during wound healing.

Impacts of Lean Construction on Safety Systems: A System Dynamics Approach.

Lean construction has been viewed as an effective management approach for reducing the occurrence of no-value or destructive activities, such as wasting resources and safety-related accidents. However, few studies have systematically addressed how and to what extent lean construction practices influence construction safety. To bridge this gap, a conceptual model is developed and validated using a system dynamics approach. The construction system in this model comprises four sub-systems (i.e., environment system, equipment system, management system, and employee system). Data were collected from 448 projects in China. Simulations were conducted to determine the correlations between five types of lean tools and the four construction sub-systems. The results show that: (a) 5S management has significant positive impacts on the control of key locations and facilities at construction sites, and contributes to the mitigation of environmental impacts; (b) visual management can significantly improve safety compliance and safety management; (c) just-in-time management has significantly positive influences on the safety facilities layout and formulation of the safety plan; and (d) the Last Planner® System and conference management are effective in improving safety training and the implementation of the safety plan. These findings provide new insights into the use of lean construction for improving construction safety through the implementation of a targeted lean approach.

Ginsenoside Rb1 protects against spinal cord ischemia-reperfusion injury in rats by downregulating the Bax/Bcl-2 ratio and caspase-3 and p-Ask-1 levels.

The aim of this study was to confirm the effects of ginsenoside Rb1 on neural cell apoptosis in the spinal cord of rats with spinal cord ischemia-reperfusion injury (SCII) and to explore its potential mechanisms. A total of 100 healthy adult Sprague-Dawley (SD) rats were randomly divided into four groups: normal control (n = 10), sham-operated (n = 10), SCII model (n = 40), and ginsenoside Rb1-treated groups (n = 40). Basso, Beattie, Bresnahan (BBB) scale was used to examine rat hindlimb locomotor function. Nissl and Tunnel staining were used to observe neural cell injury and apoptosis, respectively, in the spinal cord of rats with SCII. Immunofluorescence staining was performed to detect the expression of Bax and Bcl-2. The levels of caspase-3 and phosphorylated Ask-1 (p-Ask-1) were detected by western blotting. Ginsenoside Rb1 prevented neural cell apoptosis in the spinal cord and improved hindlimb locomotor dysfunction of rats (P < .05). Moreover, SCII-induced upregulation of caspase-3 and p-Ask-1 levels and the Bax/Bcl-2 ratio were significantly decreased by ginsenoside Rb1 (P < .05). The protective effects of ginsenoside Rb1 on neural cells in the spinal cord of rats with SCII were mediated by the ginsenoside Rb1-induced downregulation of caspase-3 and p-Ask-1 levels and the Bax/Bcl-2 ratio.

Effects of distinct drugs on gene transcription in an osteosarcoma cell line.

Osteosarcoma (OS) is a common cancerous bone tumor which has a detrimental impact on the lives of patients and their families. The present study aimed at investigating the underlying molecular mechanism of various drug treatments pertaining to OS, including dimethyl sulfoxide (DMSO), doxorubicin (DXP), Nutlin-3, actinomycin D (ActD) and etoposide (Eto). Microarray and p53 chromatin immunoprecipitation combined with sequencing (ChIP-seq) datasets of the OS cell line U2OS treated with distinct drugs were acquired from the Gene Expression Omnibus and differentially-expressed genes (DEGs) were screened for alignment analysis. The p53-binding target genes were identified and ChIP-seq and microarray gene expression data were combined to identify directly and indirectly targeted genes. A regulatory network of p53 was constructed with the acquired data. Finally, the Database for Annotation, Visualization and Integrated Discovery was interrogated for annotation of target genes. A total of 212 p53-binding peaks were obtained in the untreated group, whereas thousands of peaks were obtained in the treated groups. In total, ~1,000 target genes were identified in each of DXP, DMSO, Eto and ActD treatment groups, whereas the Nutlin-3 treatment group identified an increased number, with 5,458 target genes obtained. Several common DEGs including MDM2, TP53I3, RRM2B, FAS and SESN1 were targeted by all the drugs with the exception of DMSO. p53 regulated various genes including EHF, HOXA10 and BHLHE40 in the Nutlin-3 treatment group, whereas p53 regulated EHF, RFX3, TRAF40 and TCF7L2 in the DXR treatment group. The results of the present study indicate that p53 was able to directly regulate target genes including MDM2, TP53I3 and RRM2B or indirectly regulate numerous further genes through several hub genes including EHF and RFX through various drug treatments in U2OS cells. Furthermore, p53 regulated distinct molecular processes in various drug treatments.