Spatial-temporal differences and convergence analysis of residential building carbon emission efficiency in China.

Data indicate that carbon dioxide emissions from residential buildings in China constitute 60% of the country's total, making carbon reduction efforts in residential construction crucial for achieving dual carbon goals. From the perspective of eight major economic regions, this paper selects energy consumption, per capita residential area, and residential population as input indicators, per capita disposable income as the output indicator, and carbon dioxide emissions as the undesired output indicator. It employs the super-efficiency model based on the directional distance (super-DDF) function and the Malmquist-Luenberger (ML) index to measure the static and dynamic carbon emission efficiencies of residential buildings (RBCEE) during their operational phase from 2010 to 2020. After analyzing the differences and equity in RBCEE among regions using the Theil index and Gini coefficient, the σ-convergence, absolute ß-convergence, and conditional ß-convergence methods are utilized to explore the changing trends of RBCEE across the eight major economic regions. Results show that the static RBCEE in China is at a medium level; dynamic efficiency has improved across all eight regions, though at varying rates; overall, RBCEE exhibits poor equity and significant differences, with intra-group differences being a major cause. In terms of convergence, all eight economic regions display significant absolute ß-convergence and conditional ß-convergence. Finally, based on the research findings, this paper proposes corresponding emission reduction recommendations for the eight major economic regions.

RNAi silencing of c-Myc inhibits cell migration, invasion, and proliferation in HepG2 human hepatocellular carcinoma cell line: c-Myc silencing in hepatocellular carcinoma cell.

BACKGROUND: Hepatocellular carcinoma (HCC) is the most common type of liver cancer. Although much is known about both the cellular changes that lead to HCC and the etiological agents responsible for the majority of HCC cases, the molecule pathogenesis of HCC is still not well understood. We aimed to determine the effect of c-Myc gene expression on the proliferative, invasive, and migrative capabilities of hepatocellular carcinoma HepG2 cells. METHODS: A plasmid- based polymerase III promoter system was used to deliver and express short interfering RNA targeting c-Myc to reduce its expression in HepG2 cells. Western blot analysis was used to measure the protein level of c-Myc in HepG2 cells. The effects of c-Myc silencing on the invasion, motility, and proliferation of HepG2 cells were assessed using a Transwell chamber cell migration assay system and a growth curve assay, respectively. RESULTS: The data showed that plasmids expressing siRNA against c-Myc significantly decreased its expression in HepG2 cells by up to 85%. Importantly, pSilencer-c-Myc transfected cells showed a significantly reduced potential in migration, invasion, and proliferation. CONCLUSION: C-Myc plays an important role in the development of hepatocellular carcinoma. The data show that down-regulating the c-Myc protein level in HepG2 cells by RNAi could significantly inhibit migration, invasion and proliferation of HepG2 cells. Thus, c-Myc might be a potential therapeutic target for hepatocellular carcinoma.

Effect of combined treatment with recombinant interleukin-2 and allicin on pancreatic cancer.

This study aimed to evaluate the efficacy of combined treatment with recombinant interleukin-2 (rIL-2) and allicin on pancreatic cancer and explore the potential immunological mechanism. A total of 60 C57/BL6 nude mice pancreatic cancer xenograft models were randomized into four groups of 15 mice per group: control group, allicin treatment group, rIL-2 treatment group, combined treatment with allicin and rIL-2 group. Mice in each group were treated with saline, rIL-2, allicin, or combination of rIL-2 and allicin by weekly i.v injection for four weeks. After four weeks of treatment, eyeballs of the mice were extracted and blood was drawn, percentages of CD4+T, CD8+T and NK cell were analyzed by FACS, IFN-γ level was detected by ELISA. One mouse in each group was sacrificed to measure the weight and volume of the tumor and prepared to the paraffin section of tumor tissue. Apoptosis of the tumor cells was analyzed by TUNEL and FACS. Other mice continued to receive treatment, survival period were compared between each group. We observed a significant suppression of xenograft growth and a significant prolonged survival time in the combined treatment with allicin and rIL-2 group (P < 0.05). The most amount of apoptotic cells were observed in the combined therapy group (P < 0.05). The percentages of CD4+T, CD8+T and NK cell and serum IFN-γ level increased significantly in the combined treatment group compared with other groups (P < 0.05). Combined treatment with allicin and rIL-2 resulted in suppression of tumor growth and prolonged survival time possibly through activation of CD4+T, CD8+T and NK cell.

The expression and regulation of DFNA5 in human hepatocellular carcinoma DFNA5 in hepatocellular carcinoma.

Hepatocellular carcinoma is a primary malignancy of hepatocytes which accounts for 80 % of all primary liver cancers. DFNA5 has been identified as a tumor suppressor gene with an important role in several frequent forms of cancers, while little is known about its role in hepatocellular carcinoma. Through comparison of the DFNA5 protein expression in hepatocellular carcinoma cells (HepG2) with human fetal lung fibroblast cells (MRC5), we found that the DFNA5 protein expression in hepatocellular carcinoma cells was significantly lower than that in normal cells. The transfection of DFNA5 gene into HepG2 cells could increase DFNA5 protein expression, which subsequently led to inhibition of cell proliferation. Underlying mechanism study revealed that decreased proliferation was due to increased apoptosis and cell cycle arrest. In view of the important role of DFNA5 gene in carcinogenesis, these findings are expected to provide new understanding on development and treatment of human hepatocellular carcinoma.

[The correlation of synuclein-γ and matrix metalloproteinase 9 in breast cancer].

OBJECTIVES: To evaluate the expression of synuclein-γ (SNCG) and metalloproteinase 9 (MMP-9) both in the invasive ductal breast cancer samples and T47D and T47D(SNCG)- cell lines, to investigate the correlation between SNCG and MMP-9. METHODS: Totally 96 invasive ductal breast cancer samples (female, mean age of (56 ± 8) years) were collected between June 2009 and June 2012. The expressions of SNCG and MMP-9 were investigated by immunohistochemistry. T47D and SNCG knock down T47D(SNCG)- cell lines were established and SNCG and MMP-9 protein expression were investigated by Western blot and gene expression by real-time PCR. RESULTS: Among 96 samples, 26 (27.1%) of them co-expressed SNCG and MMP-9, 30(31.2%) of them expressed neither SNCG nor MMP-9. The expression of SNCG was correlated with the expression of MMP-9 (r = 0.655, P = 0.000).SNCG mRNA level of T47D cell line was 13.5 fold of T47D(SNCG)- cell line and SNCG protein expression was 2.1 fold. While MMP-9 mRNA level of T47D cell line was 7.3 fold of T47D(SNCG)- cell line and MMP-9 protien expression was 1.6 fold.When SNCG was knocked down, the expression of MMP-9 decreased. CONCLUSIONS: SNCG and MMP-9 are significantly correlated with each other in breast cancer. SNCG may promote the invasion and metastasis of breast cancer mediated by up-regulating the expression of MMP-9.

Evaluation of in vivo antioxidant and immunity enhancing activities of sodium aescinate injection liquid.

Oxidative stress is involved in the development and progression of disease. Because sodium aescinate has been reported to have immunity enhancing and antioxidative effects, we investigated its activity by employing a hepatocellular carcinoma (HCC) mouse model. Sixty BALB/c mice were randomly divided into four groups, including a 1.4 mg/kg treated group (n = 15), a 2.8 mg/kg treated group (n = 15), an untreated hepatocellular carcinoma control group (n = 15) and a normal control group (n = 15). After H22 cells were cultured for one week, we collected 2 × 106 cells and injected them subcutaneously as 0.2 mL cell suspensions in sterile saline into the right shoulder region of every mouse. The animals were monitored for changes in activity, physical condition and body weight during the experiment. The next day after injection of H22 cells, animals in these test groups received one intraperitoneal injection of drug or physiological saline for 13 days. Results showed that in the sodium aescinate injection liquid (SAIL)-treated HCC mice, serum interleukin-1 beta (IL-1ß), interleukin-6 (IL-6), tumor necrosis factor-alpha (TNF-α), interferon-gamma (IFN-γ), Gamma-glutamyltransferase (γ-GT), alanine transaminase (ALT), aspartate transaminase (AST) and alkaline phosphatase (ALP) levels were significantly decreased compared with normal control mice. In addition, treatment with sodium aescinate injection liquid significantly decreased blood and liver malondialdehyde (MDA) levels, increased glutathione (GSH) levels, and antioxidant enzyme [superoxide dismutase (SOD), catalase (CAT) and glutathione peroxidase (GSH-Px)] activities in a dose-dependent manner. We conclude that sodium aescinate injection liquid can decrease oxidative injury and enhance immunity functions in HCC mice.

Prospective lncRNA-miRNA-mRNA regulatory network of long non-coding RNA LINC00968 in non-small cell lung cancer A549 cells: A miRNA microarray and bioinformatics investigation.

Accumulating evidence suggests that the dysregulation of long non-coding RNAs (lncRNAs) serves vital roles in the incidence and progression of lung cancer. However, the molecular mechanisms of LINC00968, a recently identified lncRNA, remain unknown. The objective of present study was to investigate the role of a prospective lncRNA-miRNA­mRNA network regulated by LINC00968 in non-small cell lung cancer cells. Following the transfection of lentiviruses carrying LINC00968 into A549 cells, the microRNA (miRNA) expression profile of the cells in response to the overexpression of LINC00968 was detected using an miRNA microarray. Five differentially expressed miRNAs (DEMs) with LINC00968 overexpression were obtained, including miR-9-3p, miR­22-5p, miR-668-3p, miR­3675-3p and miR-4536-3p. Five target prediction algorithms and three target validation algorithms were used to obtain 1,888 prospective target genes of the five DEMs. The result of Gene Ontology analysis suggested that these five DEMs were involved in complex cellular pathways, which included intracellular transport, organelle lumen and nucleotide binding. Furthermore, analysis of Kyoto Encyclopedia of Genes and Genomes pathways indicated that the five DEMs were important regulators in the adherens junction and focal adhesion. An lncRNA-miRNA-mRNA regulatory network and a protein-protein interaction network were then constructed. Eventually, a prospective lncRNA­miRNA-mRNA regulatory network of LINC00968, three miRNAs (miR-9, miR-22 and miR-4536) and two genes (polo-like kinase 1 and exportin-1) was obtained following validation in the Cancer Genome Atlas database. These results may provide novel insights to support future research into lncRNA in lung cancer.

[Study on the self-assembly ability of expressed capsid protein of rabbit haemorrhagic disease virus that fused with foreign epitope at the N-terminus].

The RHDV capsid protein (VP60) gene was first subcloned into the transfer plasmid pBLUEBACHIS2B located downstream of a 6 * HIS tag, then the recombinant transfer plasmid DNA were cotransfected Sf 9 cells with Bac-N-Blue DNA and purified for cloned recombinant baculovirus by plaque assay. The expression of fused-VP60 gene was analyzed by SDS-PAGE and Western blot. A specific 69 kD protein band was obtained. Observed under electron micrography, the recombinant baculovirus expressed VP60 protein assembled into viruslike particles which were morphologically and antigenically similar to native RHD virus but did not package RNA. The close-to-native conformation of the VLPs was also supported by the haemagglutination test, in which recombinant VLPs, like RHDV, agglutinated human blood type O erythrocytes.

Sorbitol induces apoptosis of human colorectal cancer cells via p38 MAPK signal transduction.

Sorbitol has been reported to have anticancer effects in several tumor models, however its effects on colorectal cancer remain elusive. In the present study, the effects of sorbitol on growth inhibition and apoptosis in the colorectal cancer HCT116 cell line were evaluated and its mechanism of action was examined. An MTT assay was utilized to determine the effect of sorbitol on HCT116 cell proliferation at different time points and variable doses. Western blot analysis was used to examine the effect of sorbitol on apoptosis-related protein expression and the p38 MAPK signaling pathway. The results revealed that sorbitol may inhibit the growth of HCT116 cells in a time- and dose-dependent manner. Following treatment with sorbitol for 3 h, western blotting demonstrated cleavage of the caspase-3 zymogen protein and a cleavage product of poly (ADP-ribose) polymerase (PARP), a known substrate of caspase-3, was also evident. During sorbitol-induced apoptosis, the mitochondrial pathway was activated by a dose-dependent increase in Bax expression and cytochrome c release, while the expression of anti-apoptotic protein Bcl-2 was significantly decreased in a dose-dependent manner. The investigation for the downstream signal pathway revealed that sorbitol-induced apoptosis was mediated by an increase in phosphorylated p38 MAPK expression. Overall, the observations from the present study imply that sorbitol causes increased levels of Bax in response to p38 MAPK signaling, which results in the initiation of the mitochondrial death cascade. Therefore, sorbitol is a promising candidate as a potential chemotherapeutic agent for the treatment of colorectal cancer HCT116 cells.

Bioinformatics method to analyze the mechanism of pancreatic cancer disorder.

Pancreatic cancer is an aggressive malignancy with a five-year mortality of 97-98% due to widespread metastatic disease. A better understanding of the molecular mechanism of pancreatic cancer is beneficial for the development of novel approaches for early detection and monitoring of pancreatic cancer. We aim to comprehensively identify the gene expression profile in pancreatic cancer and explore the molecular pathway of pancreatic cancer disorder. Using GSE15471 datasets downloaded from Gene Expression Omnibus data, we first screened the differentially expressed genes in pancreatic cancer using packages in R language. The key pathways of differentially expressed genes were investigated with the Kyoto Encyclopedia of Genes and Genomes (KEGG) pathway enrichment analysis and synergetic network construction based on weighted Jaccard index. A total of 13,211 differentially expressed genes were identified, and they were enriched in several pathways, such as mitogen-activated protein kinase (MAPK) signaling pathway, transforming growth factor (TGF)-beta signaling pathway, Janus kinase-signal transducers and activators of transcription (JAK-STAT) signaling pathway, and calcium signaling pathway, as well as cell cycle, focal adhesion, complement and coagulation cascades, and leukocyte transendothelial migration. Synergetic pathway network analysis revealed that cytokine-cytokine receptor interaction pathway, calcium signaling pathway, and focal adhesion pathway were three important pathways in the development of pancreatic cancer. The method introduced here is helpful to screen the key pathways for controlling pancreatic cancer progression and provide potential therapeutic targets in the treatment of pancreatic cancer.

[Expression of capsid gene of Chinese isolate of rabbit hemorrhagic disease virus in Pichia pastoris].

The capsid protein (VP60) gene of RHDV was subcloned into the Pichia expressin vector pPICZ B to express the VP60 protein intracellularly. The recombinant plasmid was initially transformed into a E. coli strain TOP10 F'. After verification of the construct by sequencing, the recombinant plasmid was linearized by Sac I in the 5' AOX1 region and then transformed into Pichia pastoris strain GS115 using the Pichia EasyComp Kit. After selecting and verifing for the insertion of VP60 gene in the genome, two clones of Pichia transformants were select for expression test. The recombinant clones were first inoculate with BMGY in baffled flask at 28-30 degrees C in a shaking incubator (250-300 r/min) until culture reaches an OD600 = 2-6, then resuspend the cell pellet to an OD6oo of 1.0 in BMMY medium to induce expression for 5 days by methanol at a concentration of 0.5% in a 1 liter baffled flask covered with 2 layers of sterile gauze. Collect the cell pellets and break it by acid-washed 0.5 mm glass beads. The expression of recombinant Pichia strains was detected by SDS-PAGE and Western analysis with a polyclonal serum which showed a specific protein band of 60kD. Theses results indicates that the recombinant VP60 produced in Pichia was antigenically similar to the viral polypeptide. Electron microscopic observation of the recombinant Pichia-derived protein revealed the presence of virus-like particles similar in size and appearance to native virus capsids. In the haemagglutination test, the recombinant VLPs, like the native RHDV, also agglutinated human blood type O erythrocytes and could be inhibited by the anti-RHDV polyclonal serum.