Implicit Environmental Injustice in Global Trade: Based on the MRIO Model.

To answer these questions in light of the MRIO model, this paper presents a study of environmental injustice affecting the global economy. Practical ideas and lifespan measurements are often used in studies of the embodied carbon industry. The input-output table method is an important method for industrial embodied carbon research, which can be divided into the regional input-output table method, bilateral input-output table method, and multiregional input-output table method. Bilateral and multistakeholder consultations are more accurate than regional proposals. Therefore, when studying the carbon industry implied by the two countries, the input-output table of the two countries is usually used, and the multilateral input-output table is more reliable for determining the input-output calculation. Therefore, when studying local problems, it is advisable to adopt a variety of display strategies. The results show that in 2010, the carbon content of the carbon industry was 26,593 thousand tons, down 34.6% from 17,383 thousand tons in 2011, calculated at 2%. From 2012 to 2018, the carbon content grew from 31,051 tons in 2014 to 84,248 tons in 2018, with an average annual increase rate of 18%. The experimental results show that there is a large incidence of carbon emissions in the bilateral trade between China, the United States, and Japan. The expansion of export industries is the main reason for the increase in carbon emissions between the two industries. The role of technology has narrowed this difference to some extent.

TBC1D21 is an essential factor for sperm mitochondrial sheath assembly and male fertility‡.

During spermiogenesis, the formation of the mitochondrial sheath is critical for male fertility. The molecular processes that govern the development of the mitochondrial sheath remain unknown. Whether TBC1D21 serves as a GTPase-activating protein (GAP) for GTP hydrolysis in the testis is unclear, despite recent findings indicating that it collaborates with numerous proteins to regulate the formation of the mitochondrial sheath. To thoroughly examine the property of TBC1D21 in spermiogenesis, we applied the CRISPR/Cas9 technology to generate the Tbc1d21-/- mice, Tbc1d21D125A R128K mice with mutation in the GAP catalytic residues (IxxDxxR), and Tbc1d21-3xFlag mice. Male Tbc1d21-/- mice were infertile due to the curved spermatozoa flagella. In vitro fertilization is ineffective for Tbc1d21-/- sperm, although healthy offspring were obtained by intracytoplasmic sperm injection. Electron microscopy revealed aberrant ultrastructural changes in the mitochondrial sheath. Thirty-four Rab vectors were constructed followed by co-immunoprecipitation, which identified RAB13 as a novel TBC1D21 binding protein. Interestingly, infertility was not observed in Tbc1d21D125A R128K mice harboring the catalytic residue, suggesting that TBC1D21 is not a typical GAP for Rab-GTP hydrolysis. Moreover, TBC1D21 was expressed in the sperm mitochondrial sheath in Tbc1d21-3xFlag mice. Immunoprecipitation-mass spectrometry demonstrated the interactions of TBC1D21 with ACTB, TPM3, SPATA19, and VDAC3 to regulate the architecture of the sperm midpiece. The collective findings suggest that TBC1D21 is a scaffold protein required for the organization and stabilization of the mitochondrial sheath morphology.

The ZFP541-KCTD19 complex is essential for pachytene progression by activating meiotic genes during mouse spermatogenesis.

Meiosis is essential for fertility in sexually reproducing species and this sophisticated process has been extensively studied. Notwithstanding these efforts, key factors involved in meiosis have not been fully characterized. In this study, we investigate the regulatory roles of zinc finger protein 541 (ZFP541) and its interacting protein potassium channel tetramerization domain containing 19 (KCTD19) in spermatogenesis. ZFP541 is expressed from leptotene to the round spermatid stage, while the expression of KCTD19 is initiated in pachytene. Depletion of Zfp541 or Kctd19 leads to infertility in male mice and delays progression from early to mid/late pachynema. In addition, Zfp541-/- spermatocytes show abnormal programmed DNA double-strand break repair, impaired crossover formation and resolution, and asynapsis of the XY chromosomes. ZFP541 interacts with KCTD19, histone deacetylase 1/2 (HDAC1/2), and deoxynucleotidyl transferase terminal-interacting protein 1 (DNTTIP1). Moreover, ZFP541 binds to and activates the expression of genes involved in meiosis and post-meiosis including Kctd19; in turn, KCTD19 promotes the transcriptional activation activity of ZFP541. Taken together, our studies reveal that the ZFP541/KCTD19 signaling complex, acting as a key transcription regulator, plays an indispensable role in male fertility by regulating pachytene progression.

MicroRNA-154 Targets the Wnt/ß-Catenin Signaling Pathway Following Injury to Human Vascular Endothelial Cells by Hydrogen Peroxide.

BACKGROUND Endothelial cells are involved in vascular homeostasis, and endothelial cell dysfunction is involved in the pathogenesis of cardiovascular disease. This study aimed to investigate the effects of microRNA-154 in human umbilical vein endothelial cells (HUVECs) following injury induced by hydrogen peroxide (H2O2). MATERIAL AND METHODS Cell viability and apoptosis of HUVECs treated with H2O2 were measured. The expression of microRNA-154 was detected by quantitative real-time polymerase chain reaction (qRT-PCR). Cell survival, caspase-3 activity, and the apoptosis rate were evaluated in H2O2-treated HUVECs cells after the upregulation and down-regulation of microRNA-154 expression. The interaction between microRNA-154 and Dickkopf WNT signaling pathway inhibitor 2 (DKK2) was predicted by bioinformatics analysis and was verified by luciferase reporter gene assay and Western blot. The effects of DKK2 short-interfering RNA (siRNA) on antioxidant injury in HUVECs cells were determined. RESULTS The survival rate of HUVECs exposed to H2O2 was significantly reduced and the apoptosis rate was significantly increased, and H2O2 significantly inhibited the expression of microRNA-154 in a dose-dependent manner. Overexpression of microRNA-154 increased cell survival, reduced the activity of caspase-3, and reduced cell apoptosis. Inhibition of microRNA-154 expression decreased cell survival, increased the activity of caspase-3, and promoted cell apoptosis. Luciferase reporter gene assay and Western blot showed that microRNA-154 interacted with the Wnt pathway molecule DKK2 in HUVECS. Also, DDK2 siRNA resulted in a similar protective effect on H2O2-treated HUVECs as overexpression of microRNA-154. CONCLUSIONS Oxidative injury in HUVECs was regulated by microRNA-154 targeting the Wnt/ß-catenin signaling pathway.

Risk Factors for Recurrent Carotid-Artery Stenosis Following Stenting Treatment.

BACKGROUND Carotid artery stenting (CAS) has been regarded as a reliable treatment approach for carotid artery stenosis. However, recurrent carotid artery stenosis after CAS affects long-term outcomes. In this study, we aimed to investigate the potential risk factors for carotid restenosis. MATERIAL AND METHODS We retrospectively analyzed the clinical data of patients diagnosed with carotid artery stenosis who underwent CAS implantation at our department from September 2012 to July 2015. Each included study patient was followed up with serial duplex ultrasound scanning. Kaplan-Meier estimates were used to evaluate freedom from restenosis and potential risk factors were analyzed. RESULTS There were 33 patients enrolled in our study. The mean age was 65.5±11.5 years. The technique was successfully achieved in all patients. No death or major stroke occurred after stenting. There were 2 events of minor stroke and one myocardial infarction within 30 days after stent implantation. All the patients were followed up for 3 years. Cumulative rates of freedom from recurrent stenosis at 1, 2, and 3 years were 87.4%, 74.6%, and 68.3% respectively. Cox multivariate regression analysis revealed that male sex, smoking and hyperlipidemia were independent risk factors associated with restenosis. CONCLUSIONS In this study, we identified that CAS was a reliable approach for carotid artery stenosis. Male sex, smoking, and hyperlipidemia were independent risk factors associated with restenosis. Thus, hyperlipidemia should be monitored and routine follow-up with ultrasonography are recommended especially for male patients with current or history of smoking.

Linagliptin protects rat carotid artery from balloon injury and activates the NRF2 antioxidant pathway.

Percutaneous coronary intervention (PCI) is main treatment for acute coronary syndrome (ACS). However, restenosis caused by PCI-induced injury influences the outcome of patients. Linagliptin, a dipeptidyl peptidase-4 (DPP-4) inhibitor, has been reported to ameliorate intimal hyperplasia post vascular injury. The underlying mechanisms by which linagliptin protects against balloon injury are unclear and require to be explored. Herein, Wistar rats with carotid artery balloon injury were given 1, 2 or 3 mg/kg/day linagliprin for 6 weeks. We found that linagliptin attenuated vascular injury-mediated neointima formation in rats without affecting body weight and blood glucose levels. ELISA results indicated that linagliptin significantly reduced overproduction of cytokines including tumor necrosis factor-α (TNF-α), interleukin-1ß (IL-1ß) and IL-6 post balloon injury. By detecting the level of malondialdehyde (MDA) and the activities of superoxide dismutase (SOD) and glutathione peroxidase (GSH-Px), we found that linagliptin prevented balloon injury-induced oxidative stress. Additionally, linagliptin decreased the level of Kelch ECH-associating protein 1 (KEAP1) compared with injury group. Results of Western blots and electrophoretic mobility shift assay (EMSA) demonstrated that linagliptin augmented nuclear accumulation of nuclear factor-E2-related factor 2 (NRF2) and its binding ability to target genes in rats with balloon injury. Moreover, heme oxygenase-1 (HO-1) and NAD (P) H quinine oxidoreductase 1 (NQO1), two downstream targets of NRF2, were further up-regulated after linagliptin treatment compared with injury group. In conclusion, our data suggest that linagliptin protects carotid artery from balloon injury-induced neointima formation and activates the NRF2 antioxidant pathway.

Generation of H11-albumin-rtTA Transgenic Mice: A Tool for Inducible Gene Expression in the Liver.

The modification of the mouse genome by site-specific gene insertion of transgenes and other genetic elements allows the study of gene function in different developmental stages and in the pathogenesis of diseases. Here, we generated a "genomic safe harbor" Hipp11 (H11) locus-specific knock-in transgenic mouse line in which the albumin promoter is used to drive the expression of the reverse tetracycline transactivator (rtTA) in the liver. The newly generated H11-albumin-rtTA transgenic mice were bred with tetracycline-operator-Histone-2B-green fluorescent protein (TetO-H2BGFP) mice to assess inducibility and tissue-specificity. Expression of the H2BGFP fusion protein was observed exclusively upon doxycycline (Dox) induction in the liver of H11-albumin-rtTA/TetO-H2BGFP double transgenic mice. To further analyze the ability of the Dox-inducible H11-albumin-rtTA mice to implement conditional DNA recombination, H11-albumin-rtTA transgenic mice were crossed with TetO-Cre and Ai14 mice to generate H11-albumin-rtTA/TetO-Cre/Ai14 triple transgenic mice. We successfully confirmed that the Cre-mediated recombination efficiency was as strong in Dox-induced H11-albumin-rtTA /TetO-Cre/Ai14 mice as in the control albumin-Cre/A14 mice. Finally, to characterize the expression-inducing effects of Dox in H11-albumin-rtTA/TetO-H2BGFP mice in detail, we examined GFP expression in embryos at different developmental stages and found that newly conceived H11-albumin-rtTA/TetO-H2BGFP embryos of Dox-treated pregnant female mice were expressing reporter GFP by E16.5. Our study demonstrates that these new H11-albumin-rtTA transgenic mice are a powerful and efficient tool for the temporally and spatially conditional manipulation of gene expression in the liver, and illustrates how genetic crosses with these new mice enable the generation of complex multi-locus transgenic animals for mechanistic studies.

Identification of differentially expressed genes in Budd­Chiari syndrome by RNA­sequencing.

Budd­Chiari syndrome (BCS) is an uncommon disease characterized by the occlusion or obstruction of hepatic venous outflow. The mechanism of BCS is still unclear and there are no accurate and effective diagnostic or therapeutic tools. In the present study, blood samples from BCS patients and healthy controls were used for RNA­sequencing. The differentially expressed genes (DEGs) in BCS patients compared with healthy controls were identified. Gene Ontology (GO) enrichment analysis, Kyoto Encyclopedia of Genes and Genomes pathway analysis and Protein­Protein Interaction (PPI) networks construction were performed for DEGs. A total of 405 DEGs including 317 upregulated and 88 downregulated DEGs were identified. The cytosol was the most significantly enriched GO term and the proteasome was also identified as significant enriched pathway. According to the PPI network of 30 DEGs (18 upregulated and 12 downregulated DEGs), synuclein α, tubulin ß­2A class IIa and zinc finger protein Gfi­1b (GFIIB) were the three most significant hub proteins. In conclusion, several DEGs including secreted protein acidic and cysteine rich, lipocalin­2, GFI1B and proteasome­associated DEGs may be associated with the pathological process of BCS. These results can provide novel clues for the pathogenesis and provide novel diagnostic and therapeutic strategies for BCS.

Epigallocatechin-3-gallate attenuates neointimal hyperplasia in a rat model of carotid artery injury by inhibition of high mobility group box 1 expression.

Epigallocatechin-3-gallate (EGCG) is a kind of polyphenol compound, called catechin, and is extracted from green tea. EGCG has a wide range of biological activities. The present study aimed to evaluate the effect of EGCG on neointimal hyperplasia in a rat model of carotid artery balloon injury and to explore the molecular mechanisms involved. Various experiments were performed to assess the effects of EGCG on thickening of neointima, expression levels of high mobility group box 1 protein (HMGB1) and receptor of advanced glycation end products (RAGE), the inflammatory response, oxidative stress and activation of nuclear factor (NF)-κB. Results demonstrated that EGCG decreased the intimal area and the ratio of intimal area/medial area compared with the balloon injury group. The expression levels of HMGB1 and RAGE induced by balloon injury were markedly inhibited by EGCG treatment. Furthermore, the inflammatory response and oxidative stress damage, which have close correlations with HMGB1, were restrained by EGCG. Finally, EGCG treatment markedly inhibited NF-κB activation. The present data provided evidence that EGCG attenuates neointimal hyperplasia in a model of carotid artery balloon injury, which indicated that EGCG may serve as a potential drug for restenosis in clinics.

Determination of the stereoisomeric impurities of sitafloxacin by capillary electrophoresis with dual chiral additives.

Because of the bioactivity against the human topoisomerase II, the stereoisomeric impurities of sitafloxacin should be controlled in the process of manufactory. In the present work, a capillary electrophoresis (CE) method was developed and validated for simultaneous determination of three stereoisomeric impurities of sitafloxacin. The separation with high resolution not only for the separation of enantiomers, but also for the separation of diastereoisomers was achieved by using a background electrolyte composed of dual chiral selectors, namely γ-cyclodextrin (γ-CD) and Cu2+-d-phenylalanine (D-Phe) complex. The combination of two chiral selectors is indispensable to gain a high separation selectivity due to the cooperativity effect of different chiral discrimination modes: inclusion complexation (γ-CD) and ligand exchange (Cu2+-d-Phe). The concentrations of γ-CD, Cu2+ and D-Phe were found to be critical to the separation. Because two chiral selectors were involved in the enantiomer separation system, multiple factors and their interaction should be simultaneously optimized by using the response surface methodology (RSM) with a face centred central composite design (FCCD). The obtained optimized separation conditions were as follows: 15mmol/L dipotassium hydrogenphosphate solution (pH 4.5) containing 15mmol/L D-Phe, 20mmol/L CuSO4 and 20mmol/L γ-CD, separation voltage 15kV. The method was then validated and the robustness of the method was tested. Under the optimized conditions, as low as 0.1% (m/m) stereoisomeric impurities of sitafloxacin can be determined by the method.

Catheter-Directed Thrombolysis via Small Saphenous Veins for Treating Acute Deep Venous Thrombosis.

BACKGROUND There is little data comparing catheter-directed thrombolysis (CDT) via small saphenous veins vs. systematic thrombolysis on complications and efficacy in acute deep venous thrombosis patients. The aim of our study was to compare the efficacy and safety of CDT via the small saphenous veins with systematic thrombolysis for patients with acute deep venous thrombosis (DVT). MATERIAL AND METHODS Sixty-six patients with acute DVT admitted from June 2012 to December 2013 were divided into 2 groups: 27 patients received systemic thrombolysis (ST group) and 39 patients received CDT via the small saphenous veins (CDT group). The thrombolysis efficiency, limb circumference differences, and complications such as post-thrombotic syndrome (PTS) in the 2 groups were recorded. RESULTS The angiograms demonstrated that all or part of the fresh thrombus was dissolved. There was a significant difference regarding thrombolysis efficiency between the CDT group and ST group (71.26% vs. 48.26%, P=0.001). In both groups the postoperative limb circumference changes were higher compared to the preoperative values. The differences between postoperative limb circumferences on postoperative days 7 and 14 were significantly higher in the CDT group than in the ST group (all P<0.05). The incidence of postoperative PTS in the CDT group (17.9%) was significantly lower in comparison to the ST group (51.85%) during the follow-up (P=0.007). CONCLUSIONS Catheter-directed thrombolysis via the small saphenous veins is an effective, safe, and feasible approach for treating acute deep venous thrombosis.

Rho is involved in periodontal tissue remodelling with experimental tooth movement in rats.

OBJECTIVE: To characterise in vivo the close relationship between the Rho signalling pathway and periodontal tissue remodelling in experimental tooth movement in rats. MATERIALS AND METHODS: In total, 24 male Sprague Dawley rats were divided randomly into four groups. Closed-coil springs were used to create a 40-g mesial force to move the right upper first molars in anaesthetised rats. The untreated contralateral side served as a control. On days 3, 7, 10, and 14 after force application, paraffin wax-embedded sections of the dissected maxilla were prepared for immunohistochemistry to localise Rho kinase (ROCK), LIM kinase (LIMK), and its downstream effector (cofilin). The immunoreactivity of the molecules investigated in the periodontal ligament area was converted into grey-scale values. RESULTS: The expression of Rho and its signalling were detected mainly in the disto-coronal areas of the root in the periodontal ligament area of the control and loaded teeth. In contrast, ROCK-, LIMK-, and cofilin-positive cells were rare in the mesio-coronal areas. In the experimental group, the expression of ROCK, LIMK, and cofilin on the tension side (disto-coronal areas) increased significantly on days 7, 10, and 14, compared with those of untreated control teeth. CONCLUSIONS: These data suggest that Rho is involved in periodontal tissue remodelling during orthodontic tooth movement, modulating ROCK, LIMK, and cofilin activity.