Analysis on solid waste emission and management in the development of Beijing City

Beijing, as a typical large city of China, is experiencing a transformational development that huge change occurs in the industrial structure and the city infrastructure. It will have an impact on the resources consumption and solid waste management of Beijing. Based on the data of city development and resources utilization in 2010-2014, this research analyzes the relationship among the different solid waste types, resources consumption and industry development on the premise of sustainable industrial structure adjustment by the methods of the material flow analysis and scenarios analysis. The results show that: firstly, Beijing city has become a typical city relying on resources consumption, with a slow growth of the waste solid emission. Secondly, construction and demolition waste has become the major solid waste in total amount, while municipal solid waste is still the major solid waste in the central urban. Thirdly, a larger reduction of solid waste landfill would be obtained by adjusting the mode of resources recycle, utilization and disposition. The potential reduction of solid waste landfill is estimated to be above 10 million tons in 2020. References [1] Jinglan Hong, Xiangzhi Li, Cui Zhaojie. Life cycle assessment of four municipal solid waste management scenarios in China [J]. Waste Management, 2010, 30: 2362-2369. [2] Dong QingZhang, Soon Keat Tan, Richard M.Gersberg. Municipal solid waste management in China: Status, problems and challenges [J]. Journal of Environmental Management, 2010, 91: 1623-1633. [3] Yan Zhao, Thomas H. Christensen, Wenjing L, et al. Environmental impact assessment of solid waste management in Beijing City, China [J]. Waste Management, 2011, 31: 793-799. [4] Lilliana Abarca Guerrero, Ger Maas, William Hogland. Solid waste management challenges for cities in developing countries [J]. Waste Management, 2013, 33: 220-231

Joint UL/DL Resource Allocation for UAV-Aided Full-Duplex NOMA Communications

This paper proposes an unmanned aerial vehicle (UAV)-aided full-duplex non-orthogonal multiple access (FD-NOMA) method to improve spectrum efficiency. Here, UAV is utilized to partially relay uplink data and achieve channel differentiation. Successive interference cancellation algorithm is used to eliminate the interference from different directions in FD-NOMA systems. Firstly, a joint optimization problem is formulated for the uplink and downlink resource allocation of transceivers and UAV relay. The receiver determination is performed using an access-priority method. Based on the results of the receiver determination, the initial power of ground users (GUs), UAV, and base station is calculated. According to the minimum sum of the uplink transmission power, the Hungarian algorithm is utilized to pair the users. Secondly, the subchannels are assigned to the paired GUs and the UAV by a message-passing algorithm. Finally, the transmission power of the GUs and the UAV is jointly fine-tuned using the proposed access control methods. Simulation results confirm that the proposed method achieves higher performance than state-of-the-art orthogonal frequency division multiple-access method in terms of spectrum efficiency, energy efficiency, and access ratio of the ground users

Identification of <em>CHIP</em> as a novel causative gene for autosomal recessive cerebellar ataxia

Autosomal recessive cerebellar ataxias are a group of neurodegenerative disorders that are characterized by complex clinical and genetic heterogeneity. Although more than 20 disease-causing genes have been identified, many patients are still currently without a molecular diagnosis. In a two-generation autosomal recessive cerebellar ataxia family, we mapped a linkage to a minimal candidate region on chromosome 16p13.3 flanked by single-nucleotide polymorphism markers rs11248850 and rs1218762. By combining the defined linkage region with the whole-exome sequencing results, we identified a homozygous mutation (c.493CT) in CHIP (NM_005861) in this family. Using Sanger sequencing, we also identified two compound heterozygous mutations (c.389AT/c.441GT; c.621C>G/c.707GC) in CHIP gene in two additional kindreds. These mutations co-segregated exactly with the disease in these families and were not observed in 500 control subjects with matched ancestry. CHIP colocalized with NR2A, a subunit of the N-methyl-D-aspartate receptor, in the cerebellum, pons, medulla oblongata, hippocampus and cerebral cortex. Wild-type, but not disease-associated mutant CHIPs promoted the degradation of NR2A, which may underlie the pathogenesis of ataxia. In conclusion, using a combination of whole-exome sequencing and linkage analysis, we identified CHIP, encoding a U-box containing ubiquitin E3 ligase, as a novel causative gene for autosomal recessive cerebellar ataxia

The Physiological Basis of Alfalfa Plant Height Establishment

Plant height plays an important role in crop yield, product quality, and cultivation management. However, the physiological mechanisms that regulate the establishment of plant height in alfalfa plants remain unclear. Herein, we measured plant height traits, leaf characteristics, photosynthetic physiology, cell wall composition, and endogenous hormone contents of tall- and short-stalked alfalfa materials at different reproductive periods. We analyzed the physiology responsible for differences in plant height. The results demonstrated that the number of internodes in tall- and short-stalked alfalfa materials tended to converge with the advancement of the fertility period. Meanwhile, the average internode length (IL) of tall-stalked materials was significantly higher than that of short-stalked materials at different fertility periods, with internode length identified as the main trait determining the differences in alfalfa plant height. Leaf characteristics, which are closely related to photosynthetic capacity, are crucial energy sources supporting the expression of plant height traits, and we found that an increase in the number of leaves contributed to a proportional increase in plant height. Additionally, a significant positive correlation was observed between plant height and leaf dry weight per plant during the branching and early flowering stages of alfalfa. The leaves of alfalfa affect plant height through photosynthesis, with the budding stage identified as the key period for efficient light energy utilization. Plant height at the budding stage showed a significant positive correlation with soluble sugar (SS) content and a significant negative correlation with intercellular CO2 concentration. Moreover, we found that alfalfa plant height was significantly correlated with the contents of indole-3-acetic acid in stem tips (SIAA), gibberellin A3 in leaves (LGA3), zeatin in stem tips (SZT), and abscisic acid in leaves (LABA). Further investigation revealed that SS, SIAA, and LGA3 contents were important physiological indicators affecting alfalfa plant height. This study provides a theoretical basis for understanding the formation of alfalfa plant height traits and for genetic improvement studies

Angiotensin II Inhibits Adipogenic Differentiation and Promotes Mature Adipocyte Browning through the Corepressor CtBP1

The mechanisms of angiotensin II (Ang II) on regulating adipogenic differentiation and function remain unknown. In this study, we focus on revealing the role of C-terminal-binding protein 1 (CtBP1) on Ang II-mediated adipogenic differentiation and mature adipocyte browning. Amounts of 3T3-L1 and CtBP1-KO 3T3-L1 were treated with Ang II for 24 h and then induced adipogenic differentiation, or cells were first induced differentiation and then treated with Ang II. The expressions of CtBP1 and adipogenic markers were checked by Western blot. Transcription of CtBP1 was assayed by Real-time RT-PCR. Lipid droplet formation and size were detected by Oil Red O. Mitochondrial content and reactive oxygenspecies (ROS) were detected by Mito-tracker and MitoSOX. Mitochondrial respiratory function was detected with the corresponding kits. Mitochondrial membrane potential (MMP) (&#8710;&Psi;m) was assayed by JC-1. The results show that Ang II promoted CtBP1 transcription and expression via AT1 receptor during 3T3-L1 adipogenic differentiation. Ang II significantly inhibited lipid droplet formation and adipogenic markers expression in 3T3-L1 differentiation, which was blocked by CtBP1 knockout. In mature 3T3-L1, Ang II treatment increased uncoupling protein-1 (UCP-1) expression and the number of lipid droplets, and also reduced lipid droplet size and single cell lipid accumulation, which was reversed by CtBP1 knockout. In addition, Ang II treatment enhanced mitochondrial numbers, ATP production, oxygen consumption rate (OCR) and ROS generation, and reduced MMP (&#8710;&Psi;m) via CtBP1 in mature 3T3-L1 adipocytes. In conclusion, this study demonstrates that CtBP1 plays a key role in the inhibitory effect of Ang II on adipogenesis. Moreover, Ang II regulates the function of mature adipocyte via CtBP1, including promoting adipocyte browning, mitochondrial respiration and ROS generation

RhoGDI1-Cdc42 Signaling Is Required for PDGF-BB-Induced Phenotypic Transformation of Vascular Smooth Muscle Cells and Neointima Formation

RhoGTPase is involved in PDGF-BB-mediated VSMC phenotypic modulation. RhoGDIs are key factors in regulating RhoGTPase activation. In the present study, we investigated the regulatory effect of RhoGDI1 on the activation of RhoGTPase in VSMC transformation and neointima formation. Western blot and co-immunoprecipitation assays showed that the PDGF receptor inhibition by crenolanib promoted RhoGDI1 polyubiquitination and degradation. Inhibition of RhoGDI1 degradation via MG132 reversed the decrease in VSMC phenotypic transformation. In addition, RhoGDI1 knockdown significantly inhibited VSMC phenotypic transformation and neointima formation in vitro and in vivo. These results suggest that PDGF-BB promotes RhoGDI1 stability via the PDGF receptor and induces the VSMC synthetic phenotype. The co-immunoprecipitation assay showed that PDGF-BB enhanced the interaction of RhoGDI1 with Cdc42 and promoted the activation of Cdc42; these enhancements were blocked by crenolanib and RhoGDI1 knockdown. Moreover, RhoGDI1 knockdown and crenolanib pretreatment prevented the localization of Cdc42 to the plasma membrane (PM) to activate and improve the accumulation of Cdc42 on endoplasmic reticulum (ER). Furthermore, Cdc42 inhibition or suppression significantly reduced VSMC phenotypic transformation and neointima formation in vitro and in vivo. This study revealed the novel mechanism by which RhoGDI1 stability promotes the RhoGDI1-Cdc42 interaction and Cdc42 activation, thereby affecting VSMC phenotypic transformation and neointima formation

Comparative Proteomic Analysis of tPVAT during Ang II Infusion

Perivascular adipose tissue (PVAT) homeostasis plays an important role in maintaining vascular function, and PVAT dysfunction may induce several pathophysiological situations. In this study, we investigated the effect and mechanism of the local angiotensin II (Ang II) on PVAT. High-throughput comparative proteomic analysis, based on TMT labeling combined with LC-MS/MS, were performed on an in vivo Ang II infusion mice model to obtain a comprehensive view of the protein ensembles associated with thoracic PVAT (tPVAT) dysfunction induced by Ang II. In total, 5037 proteins were confidently identified, of which 4984 proteins were quantified. Compared with the saline group, 145 proteins were upregulated and 146 proteins were downregulated during Ang II-induced tPVAT pathogenesis. Bioinformatics analyses revealed that the most enriched GO terms were annotated as gene silencing, monosaccharide binding, and extracellular matrix. In addition, some novel proteins, potentially associated with Ang II infusion, were identified, such as acyl-CoA carboxylase α, very long-chain acyl-CoA synthetase (ACSVL), uncoupling protein 1 (UCP1), perilipin, RAS protein-specific guanine nucleotide-releasing factor 2 (RasGRF2), and hypoxia inducible factor 1α (HIF-1α). Ang II could directly participate in the regulation of lipid metabolism, transportation, and adipocyte differentiation by affecting UCP1 and perilipin. Importantly, the key KEGG pathways were involved in fatty acid biosynthesis, FABP3-PPARα/γ, RasGRF2-ERK-HIF-1α, RasGRF2-PKC-HIF-1α, and STAT3-HIF-1α axis. The present study provided the most comprehensive proteome profile of mice tPVAT and some novel insights into Ang II-mediated tPVAT dysfunction and will be helpful for understanding the possible relationship between local RAS activation and PVAT dysfunction

Comparison of the perinatal outcomes of expected high ovarian response patients and normal ovarian response patients undergoing frozen-thawed embryo transfer in natural/small amount of HMG induced ovulation cycles

Abstract Background Due to the high risk of complications in fresh transfer cycles among expected high ovarian response patients, most choose frozen-thawed embryo transfer (FET). There are currently few researches on whether the FET outcomes of expected high ovarian response patients with regular menstrual cycles are similar to those of normal ovarian response. Therefore, our objective was to explore and compare pregnancy outcomes and maternal and neonatal outcomes of natural FET cycles between patients with expected high ovarian response and normal ovarian response with regular menstrual cycles based on the antral follicle count (AFC). Methods This retrospective cohort study included 5082 women undergoing natural or small amount of HMG induced ovulation FET cycles at the Reproductive Center of the Third Affiliated Hospital of Zhengzhou University from January 1, 2017, to March 31, 2021. The population was divided into expected high ovarian response group and normal ovarian response group based on the AFC, and the differences in patient characteristics, clinical outcomes and perinatal outcomes between the two groups were compared. Results Regarding clinical outcomes, compared with the normal ovarian response group, patients in the expected high ovarian response group had a higher clinical pregnancy rate (57.34% vs. 48.50%) and live birth rate (48.12% vs. 38.97%). There was no difference in the early miscarriage rate or twin pregnancy rate between the groups. Multivariate logistic regression analysis suggested that the clinical pregnancy rate (adjusted OR 1.190) and live birth rate (adjusted OR 1.171) of the expected high ovarian response group were higher than those of the normal ovarian response group. In terms of maternal and infant outcomes, the incidence of very preterm delivery in the normal ovarian response group was higher than that in the expected high ovarian response group (0.86% vs. 0.16%, adjusted OR 0.131), Other maternal and infant outcomes were not significantly different. After grouping by age (< 30 y, 30–34 y, 35–39 y), there was no difference in the incidence of very preterm delivery among the age subgroups. Conclusion For patients with expected high ovarian response and regular menstrual cycles undergoing natural or small amount of HMG induced ovulation FET cycles, the clinical and perinatal outcomes are reassuring. For patients undergoing natural or small amount of HMG induced ovulation FET cycles, as age increases, perinatal care should be strengthened during pregnancy to reduce the incidence of very preterm delivery

RhoA/ROCK Pathway Activation is Regulated by AT1 Receptor and Participates in Smooth Muscle Migration and Dedifferentiation via Promoting Actin Cytoskeleton Polymerization

Background: In this study, we investigated the mechanism of Rho GTPases signaling on Ang II-mediated cell migration and dedifferentiation in human aortic vascular smooth muscle cells (HA-VSMCs) and an Ang II-infusion mouse model. Methods: Cells were pretreated with different inhibitors or Ang II. Cell migration was detected by Wound healing and Transwell assay. Mice were treated with Ad-RhoA-shRNA virus or Irbesartan or fasudil and then infused with Ang II. Results: Ang II treatment induced HA-VSMCs migration in a dose- and time-dependent manner and reduced the expression of VSMC contractile proteins. These effects were significantly suppressed by the inhibition of Ang II type 1 receptor (AT1 receptor), RhoA, and Rho-associated kinase (ROCK). Furthermore, Ang II treatment promoted the activation of RhoA and ROCK, which was reduced by AT1 receptor inhibition. Meanwhile, Ang II treatment induced F-actin polymerization, which was inhibited after ROCK inhibition. In mice, Ang II infusion increased VSMC migration into the neointima and reduced VSMC differentiation proteins levels, and these effects were shown to be dependent on AT1 receptor and RhoA/ROCK pathway. Conclusion: This study reveals a novel mechanism by which Ang II regulates RhoA/ROCK signaling and actin polymerization via AT1 receptor and then affects VSMC dedifferentiation

Chemiluminescence as a Novel Indicator for Interactions of Surfactant–Polymer Mixtures at the Surface of Layered Double Hydroxides

Chemiluminescence (CL) has been employed as a novel technique to monitor the interactions between poly­(ethylene glycol) (PEG) and sodium dodecyl benzenesulfonate (SDBS) at the surface of CO₃-layered double hydroxides (LDHs). The CL data demonstrated that the interactions of PEG and SDBS at the LDH surfaces were dependent on the SDBS concentration, the PEG molecular weight, and the PEG concentration. Furthermore, powder X-ray diffraction (XRD), zeta-potential measurements, thermogravimetric analysis (TGA), CL spectrum, and radical scavenging methods clarified the relationship between the CL intensity and the interactions of PEG with SDBS at the LDH surfaces. At low concentrations of SDBS, few interactions between PEG and SDBS took place. The aggregation of the LDH colloidal solution occurred as a result of SDBS hydrophobic tails pointed to the aqueous environment. As the concentration of SDBS increased, the PEG chains were bound onto the SDBS bilayers to reduce the electrostatic repulsion between anionic head groups of SDBS due to the structural transformation of SDBS at the surface of LDHs from monolayers to bilayers. This work would provide an attractive route to manipulate the adsorption and composition of polymer–surfactant mixtures at the particle surface by tuning the CL signals