[Coordinated Control of Carbon Emission Reduction and Air Quality Improvement in the Industrial Sector in Hunan Province].

Climate warming and air pollution are the main environmental problems in China. This study used China's Carbon Accounting Database, energy economic model, and air quality model to analyze the potential carbon emission peaking path and synergistic air quality improvement gain in the industrial sector in Hunan Province. Based on China's Carbon Accounting Database and the local industry/energy statistical yearbooks in Hunan, the total CO2 emissions in Hunan Province in 2019 were 310.6 Mt, of which the industrial sector accounted for over 70% of the emissions, mainly from the production and supply of electricity, steam, and heat; the production of non-metallic minerals; and the smelting and pressing of ferrous metals. Three potential industrial carbon emission peaking scenarios were analyzed using the LEAP energy economic model, including the business-as-usual scenario (peaking by 2030), moderate emission reduction scenario (peaking by 2028), and aggressive emission reduction scenario (peaking by 2025), by employing different economic growth rates, energy technology progress, and energy structures of the industrial sector. Furthermore, by combining the anthropogenic air pollutant emission inventory and the regional air quality model WRF-Chem, we analyzed the air quality improvement associated with various carbon emission peak paths. The results showed that the annual mean concentrations of major air pollutants had decreased in the three scenarios, especially in the Chang-Zhu-Tan Region. The aggressive emission reduction scenario was the most effective scenario, followed by the moderate emission reduction scenario and the business-as-usual scenario. Manufacturing was the sector with the most significant synergistic effect of pollution and carbon reduction. When carbon emission peaks were achieved, the annual average concentrations of PM2.5 and PM10 in Hunan Province could be synergistically reduced by 0.6-1.8 µg·m-3 and 1.8-8.9 µg·m-3, respectively. Our findings offer important insights into carbon emission peaking and can provide useful information for potential mitigation actions.

[Quantification of renal medullary perfusion with contrast-enhanced ultrasound: an experimental study].

OBJECTIVE: To quantitatively evaluate the effects of dopamine (DA) and noradrenaline (NE) on renal medullary perfusion and the differences in perfusion in the outer and inner medulla using contrast-enhanced ultrasound. METHODS AND RESULTS: Contrast-enhanced ultrasound was performed in 10 dogs with simultaneous renal artery flow (RAF) measurement at the baseline level and during application of 3 different doses of DA and NE. During treatment with the 3 doses of DA, the changes of ultrasound-derived parameters (A, beta and A*beta) in the medulla were similar to the changes in the cortex. As compared with the baseline level, the ratios between the cortex and medulla exhibited no significant difference in A, beta and A*beta during DA treatment (P>0.05). No significant difference in ultrasound-derived medullar parameters was noted in dogs with NE treatment from the baseline level (P>0.05). However, a progressive decrease in the ratios of A, beta and A*beta between the cortex and medulla was noted during NE treatment in comparison with the baseline level (P<0.05). The velocity (beta) and perfusion (A*beta) of blood flow in the medulla decreased progressively from the outer medulla to the inner medulla at baseline (P<0.05), while the blood volume (A) remained unchanged (P<0.05). CONCLUSIONS: The changes of blood flow in both the cortex and medulla are identical during DA treatment but different in the presence of NE. The progressive decrease in perfusion from the outer medulla to the inner medulla is attributed to the decrease in the velocity of blood flow.

Knockdown of the HDAC1 promotes the directed differentiation of bone mesenchymal stem cells into cardiomyocytes.

Failure of the directed differentiation of the transplanted stem cells into cardiomyocytes is still a major challenge of cardiac regeneration therapy. Our recent study has demonstrated that the expression of histone deacetylase 1 (HDAC1) is decreased in bone mesenchymal stem cells (BMSCs) during their differentiation into cardiomyocytes. However, the potential roles of HDAC1 in cardiac cell differentiation of BMSCs, as well as the mechanisms involved are still unclear. In current study, the expression of HDAC1 in cultured rat BMSCs is knocked down by lentiviral vectors expressing HDAC1-RNAi. The directed differentiation of BMSCs into cardiomyocytes is evaluated by the expression levels of cardiomyocyte-related genes such as GATA-binding protein 4 (GATA-4), Nirenberg, Kim gene 2 homeobox 5 (Nkx2.5), cardiac troponin T (CTnT), myosin heavy chain (MHC), and connexin-43. Compared with that in control BMSCs, the expression of these cardiomyocyte-related genes is significantly increased in these HDAC1 deficient stem cells. The results suggest that HDAC1 is involved in the cardiomyocyte differentiation of BMSCs. Knockdown of the HDAC1 may promote the directed differentiation of BMSCs into cardiomyocytes.

Downregulation of HDAC1 is involved in the cardiomyocyte differentiation from mesenchymal stem cells in a myocardial microenvironment.

Under myocardial microenvironment, bone marrow-derived mesenchymal stem cells (MSCs) can transdifferentiate into cardiomyocytes (CMs). However, the role of histone deacetylase 1 (HDAC1) in this directed differentiation process remains unclear. The current study is to determine the acetylation regulatory mechanisms that may be involved in the directed CM differentiation from MSCs. MSCs isolated from male Sprague-Dawley (SD) rats were marked with Ad-EGFP and co-cultured with CMs. Flow cytometry was used to sort EGFP-positive (EGFP+) MSCs from the co-culture system. Then, the expression of cardiac troponin T (cTnT) in these MSCs was detected by immunofluorescence assay. In addition, HDAC1 levels at different co-culture times were measured by quantitative real-time polymerase chain reaction (QT-PCR) and Western blotting. At 4 days after co-culture with CMs, the MSCs began to expression detectable levels of cTnT. The expression of HDAC1 in CMs was much lower than that in MSCs. After co-culture with CMs, the expression of HDAC1 in MSCs was significantly decreased in a time dependent manner. In addition, our recent study has also identified that knockdown of the HDAC1 could promote the directed differentiation of MSCs into CMs. The results suggest that HDAC1 has a negative correlation with cardiac cell differentiation from MSCs under a myocardial microenvironment. HDAC1 might play an important role in the directed differentiation of MSCs into CMs in heart.

[Protective effects of estrogen on mitochondria in human umbilical vascular endothelial cells].

OBJECTIVE: To investigate the protective effects of estrogen on the mitochondria in human umbilical vascular endothelial cells (HUVECs). METHODS: HUVECs were exposed to H2O2 at 250 micromol/L for 4 h with or without pretreatment with 17-estradiol (E2) and ICI182780. Complex IV activity of the cells was measured with chromometry, and 2, 7-dichlorofluorescein diacetate (DCFH-DA) was used to determine intracellular reactive oxygen species (ROS). Intracellular adenosine triphosphate (ATP) level was quantified with a luciferin- and luciferase-based assay. RESULTS: Compared to the blank control group, H2O2 caused a decrease in complex IV activity, intracellular ATP level, and the cell viability, but elevated intracellular ROS. E2 pretreatment of cells significantly attenuated these effects of H2O2 exposure. ICI182780 administered prior to E2 pretreatment antagonized the protective effects of E2 against H2O2 exposure. CONCLUSION: E2 offers mitochondrial protective effects on HUVECs, which is mediated by the estrogen receptors.

Effects of testosterone on cytokines and left ventricular remodeling following heart failure.

AIMS: To investigate the effects of testosterone treatment on cytokines, ventricular remodeling in rats with heart failure. MATERIALS AND METHODS: Sprague-Dawley male rats with heart failure were divided into testosterone (n = 22) and placebo (n = 22) group. Pseudo surgery was performed on a third group of 15 male rats as control. RESULTS: Compared with the placebo group, the testosterone group had a greater LVEF (P <0.05), a higher serum IL-10 level (P <0.05) and a lower serum TNF-alpha level (P<0.05). The expression of TNF-alpha mRNA, MMP-9 mRNA and the myocardial hydroxyproline contents in the testosterone group were also lower than in the placebo group (P<0.05). The mortality rate in the testosterone and placebo group was 31.8% and 68.2%, respectively (P <0.05). CONCLUSION: Serum testosterone levels were decreased significantly in male rats with heart failure. Testosterone treatment diminishes the imbalance between interleukin-10 and TNF-alpha, suppresses ventricular remodeling and improves cardiac function.