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We aim to create a feasible quantitative method to calculate the energy efficiency of building designs that are carbon-neutral and to develop a workable way of calculating energy efficiency in buildings that achieve carbon neutrality and the system for such a building’s design energy efficiency function. This paper first clarifies the idea of the design energy efficiency function for a carbon-neutral building over its whole life cycle. Subsequently, through the efficient analysis of carbon-neutral design dimension measures, this paper summarizes and integrates the mature theories of various disciplines, puts forward the energy efficiency function model of carbon-neutral design background, propulsion, and coverage, and implements the energy efficiency function model of carbon-neutral design in the whole life cycle of buildings. The index value of a building’s carbon emission factor is established based on the carbon accounting factor published by the Intergovernmental Panel on Climate Change, and a carbon neutrality energy efficiency model for buildings over the duration of their whole life cycle is constructed. The results were as follows. 1. Technology energy efficiency is far better than scale energy efficiency and comprehensive energy efficiency. 2. The better the energy efficiency value inside the building stage, the less consumption and the higher the production. 3. Construction is when technical energy is used the least. This paper refers to a systematic design method that makes the level of building carbon neutrality design technologically advanced with the aid of all types of big data related to the building life cycle and various innovative design theories in order to fully represent the fundamental level, development potential, and the effectiveness of choosing the strategy of building carbon neutrality.

The proliferation and migration of vascular smooth muscle cells (VSMCs) are fundamental hallmarks of vasculopathy. Transforming growth factor β-activated kinase-1 (TAK1) plays a crucial role in mediating cellular functions, including autophagy, which has been recently linked to the regulation of VSMC functions and the development of vasculopathy. This study aims to better dissect how TAK1 controls VSMC proliferation and migration.A rat model of graft arteriosclerosis was employed to explore the influence of TAK1 signaling activation on VSMC proliferation, migration, autophagy, and neointima formation in vivo. Knockdown and pharmacological inhibition of TAK1 were utilized in cultured VSMCs to investigate the mechanisms underlying the progression of VSMC proliferation and migration.Increased phosphorylation of TAK1 (Thr-184/Thr-187) was examined in SMα-actin positive cells in the medial and neointimal lesions of aortic allografts. Lentivirus-mediated Tak1 shRNA transfection of aortic allografts robustly suppressed neointimal formation and lumen stenosis, as well as autophagy and cell proliferative responses. In cultured PDGF-BB-incubated VSMCs, genetic and pharmacological inhibition of TAK1 markedly attenuated autophagy activation, and blocked the progression of cell cycle, proliferation, and migration responses.Activation of TAK1 in VSMCs in the setting of aortic transplantation is an early and critical event in VSMC proliferation and migration, as well as neointima formation, because it controls autophagy activation, constituting a potential molecular mechanism and target for preventing transplant vasculopathy.

Background Nuclear respiratory factor 1 (NRF1) is a transcription factor that participates in several kinds of tumor, but its role in hepatocellular carcinoma (HCC) remains elusive. This study aims to explore the role of NRF1 in HCC progression and investigate the underlying mechanisms. Methods HCC transcriptome sequencing data from TCGA was analysed. Functional role of NRF1 on HCC cells was explored by gain- and loss-of-function experiments including CCK8, colony formation assay, flow cytometry analysis, transwell assay, wound-healing assay and xenograft tumor model. Western blot, qRT-PCR, chromatin immunoprecipitation (ChIP) and dual luciferase reporter assay were utilized to investigate the underlying mechanisms. Results NRF1 was overexpressed and hyperactive in HCC tissue and cell lines and high expression of NRF1 indicated unfavorable prognosis of HCC patients. NRF1 promoted proliferation, migration and invasion of HCC cells both in vitro and in vivo. Mechanistically, NRF1 activated ERK1/2-CREB signaling pathway by transactivating lysophosphatidylcholine acyltransferase 1 (LPCAT1), thus promoting cell cycle progression and epithelial mesenchymal transition (EMT) of HCC cells. Meanwhile, LPCAT1 upregulated the expression of NRF1 by activating ERK1/2-CREB signaling pathway, forming a positive feedback loop. Conclusions NRF1 is overexpressed in HCC and promotes HCC progression through NRF1-LPCAT1-ERK1/2-CREB positive feedback loop. NRF1 is a promising therapeutic target for HCC patients.

Molecular mechanisms underlying the tumorigenesis of a highly malignant cancer, cholangiocarcinoma (CCA), are still obscure. In our study, the CCA expression profile data were acquired from The Cancer Genome Atlas (TCGA) database, and differentially expressed genes (DEGs) in the TCGA-Cholangiocarcinoma (TCGA-CHOL) data set were utilized to construct a co-expression network via weighted gene co-expression network analysis (WGCNA). The blue gene module associated with the histopathologic grade of CCA was screened. Then, five candidate hub genes were screened by combining the co-expression network with protein–protein interaction (PPI) network. After progression and survival analyses, bloom syndrome helicase (BLM) was ultimately identified as a real hub gene. Moreover, the receiver operating characteristic (ROC) curve analysis suggested that BLM had a favorable diagnostic and predictive recurrence value for CCA. The gene set enrichment analysis (GSEA) results for a single hub gene revealed the importance of cell cycle-related pathways in the CCA progression and prognosis. Furthermore, we detected the BLM expression in vitro, and the results demonstrated that the expression level of BLM was much higher in the CCA tissues and cells relative to adjacent non-tumor samples and normal bile duct epithelial cells. Additionally, after further silencing the BLM expression by small interfering RNA (siRNA), the proliferation and migration ability of CCA cells were all inhibited, and the cell cycle was arrested. Altogether, a real hub gene (BLM) and cell cycle-related pathways were identified in the present study, and the gene BLM may be involved in the CCA progression and could act as a reliable biomarker for potential diagnosis and prognostic evaluation.

Background Liver cancer is one of the most common malignancies worldwide. HCC (hepatocellular carcinoma) is the predominant pathological type of liver cancer, accounting for approximately 75–85 % of all liver cancers. Lipid metabolic reprogramming has emerged as an important feature of HCC. However, the influence of lipid metabolism-related gene expression in HCC patient prognosis remains unknown. In this study, we performed a comprehensive analysis of HCC gene expression data from TCGA (The Cancer Genome Atlas) to acquire further insight into the role of lipid metabolism-related genes in HCC patient prognosis. Methods We analyzed the mRNA expression profiles of 424 HCC patients from the TCGA database. GSEA(Gene Set Enrichment Analysis) was performed to identify lipid metabolism-related gene sets associated with HCC. We performed univariate Cox regression and LASSO(least absolute shrinkage and selection operator) regression analyses to identify genes with prognostic value and develop a prognostic model, which was tested in a validation cohort. We performed Kaplan-Meier survival and ROC (receiver operating characteristic) analyses to evaluate the performance of the model. Results We identified three lipid metabolism-related genes (ME1, MED10, MED22) with prognostic value in HCC and used them to calculate a risk score for each HCC patient. High-risk HCC patients exhibited a significantly lower survival rate than low-risk patients. Multivariate Cox regression analysis revealed that the 3-gene signature was an independent prognostic factor in HCC. Furthermore, the signature provided a highly accurate prediction of HCC patient prognosis. Conclusions We identified three lipid-metabolism-related genes that are upregulated in HCC tissues and established a 3-gene signature-based risk model that can accurately predict HCC patient prognosis. Our findings support the strong links between lipid metabolism and HCC and may facilitate the development of new metabolism-targeted treatment approaches for HCC.

Objective— Vascular smooth muscle cells (VSMCs) phenotype modulation is critical for the resolution of vascular injury. Genetic and pharmacological inhibition of PI3Kγ (phosphoinositide 3-kinase γ) exerts anti-inflammatory and protective effects in multiple cardiovascular diseases. This study investigated the role of PI3Kγ and its downstream effector molecules in the regulation of VSMC phenotypic modulation and neointimal formation in response to vascular injury. Approach and Results— Increased expression of PI3Kγ was found in injured vessel wall as well in cultured, serum-activated wild-type VSMCs, accompanied by a reduction in the expression of calponin and SM22α, 2 differentiation markers of VSMCs. However, the injury-induced downregulation of calponin and SM22α was profoundly attenuated in PI3Kγ −/− mice. Pharmacological inhibition and short hairpin RNA knockdown of PI3Kγ (PI3Kγ-KD) markedly attenuated YAP (Yes-associated protein) expression and CREB (cyclic AMP-response element binding protein) activation but improved the downregulation of differentiation genes in cultured VSMCs accompanied by reduced cell proliferation and migration. Mechanistically, activated CREB upregulated YAP transcriptional expression through binding to its promoter. Ectopic expression of YAP strikingly repressed the expression of differentiation genes even in PI3Kγ-KD VSMCs. Moreover, established carotid artery ligation and chimeric mice models demonstrate that deletion of PI3Kγ in naïve PI3Kγ −/− mice as well as in chimeric mice lacking PI3Kγ either in bone marrow or vascular wall significantly reduced neointimal formation after injury. Conclusions— PI3Kγ controls phenotypic modulation of VSMCs by regulating transcription factor CREB activation and YAP expression. Modulating PI3Kγ signaling on local vascular wall may represent a new therapeutic approach to treat proliferative vascular disease.

Background Transplant arteriosclerosis (TA) remains the major cause of chronic graft failure in solid organ transplantation. The phenotypic modulation of vascular smooth muscle cells (VSMCs) is a key event for the initiation and progression of neointimal formation and TA. This study aims to explore the role and underlying mechanism of phosphoinositide 3-kinases γ (PI3Kγ) in VSMC phenotypic modulation and TA. Methods The rat model of aortic transplantation was established to detect PI3Kγ expression and its role in neointimal formation and vascular remodeling in vivo. PI3Kγ shRNA transfection was employed to knockdown PI3Kγ gene. Aortic VSMCs was cultured and treated with TNF-α to explore the role and molecular mechanism of PI3Kγ in VSMC phenotypic modulation. Findings Activated PI3Kγ/p-Akt signaling was observed in aortic allografts and in TNF-α-treated VSMCs. Lentivirus-mediated shRNA transfection effectively inhibited PI3Kγ expression in medial VSMCs while restoring the expression of VSMC contractile genes, associated with impaired neointimal formation in aortic allografts. In cultured VSMCs, PI3Kγ blockade with pharmacological inhibitor or genetic knockdown markedly abrogated TNF-α-induced downregulation of VSMC contractile genes and increase in cellular proliferation and migration. Moreover, SOX9 located in nucleus competitively inhibited the interaction of Myocardin and SRF, while PI3Kγ inhibition robustly reduced SOX9 expression and its nuclear translocation and repaired the Myocardin/SRF association. Interpretation These results suggest that PI3Kγ plays a critical role in VSMC phenotypic modulation via a SOX9-dependent mechanism. Therefore, PI3Kγ in VSMCs may represent a promising therapeutic target for the treatment of TA. Fund National Natural Science Foundation of China.

We designed the image-enabled EHR sharing solution (i-EHR) for cross-enterprise and cross-domain with SOA architecture and combined the grid-based image management and distribution capability, which are compliant with IHE XDS-I/XCA integration profiles. We selected one districts with four hospitals and two hospital groups as image sharing pilot testing bed. Our approach presented in this presentation uses peer-to-peer mode to share and exchange image data cross enterprise PACSs and domains, which provides single point of services to local systems so it is easy to integrate with different vendor's PACS and easy to deploy to different hospitals to implement the i-EHR.

There are many Web-based image accessing technologies used in medical imaging area, such as component-based (ActiveX Control) thick client Web display, Zerofootprint thin client Web viewer (or called server side processing Web viewer), Flash Rich Internet Application(RIA) ,or HTML5 based Web display. Different Web display methods have different peformance in different network environment. In this presenation, we give an evaluation on two developed Web based image display systems. The first one is used for thin client Web display. It works between a PACS Web server with WADO interface and thin client. The PACS Web server provides JPEG format images to HTML pages. The second one is for thick client Web display. It works between a PACS Web server with WADO interface and thick client running in browsers containing ActiveX control, Flash RIA program or HTML5 scripts. The PACS Web server provides native DICOM format images or JPIP stream for theses clients.