Performance evaluation of vehicular networks in urban environments

With the development of all kinds of science and technology nowadays, people are paying more attention to the various aspects of smart cities, especially vehicular networks. Based on the increase in traffic demand, people's dependence on vehicles is also growing gradually, which leads to an intelligent social transportation system being crucial. However, inevitably, there will always be some unexpected car accidents in the urban traffic environment. In this paper, we would mainly focus on the performance evaluation of vehicular networks with a car accident in the urban centre of Barcelona. And we will start from different angles for a multi-dimensional analysis of the impact of different vehicles and environmental factors on urban traffic. In this project, the performance of the vehicular network in the Eixample district would be evaluated from the following four perspectives:1. The configuration of the vehicles 2. The nominal road speed around accident 3. The transmission range 4. The rebroadcasting scheme of the accident message. Through the data analysis of the packet delay, the percentage of warned vehicles, and the warning distance respectively, to explore the impact of diverse factors on the vehicle network and find a better scheme to improve the intelligent transportation system (ITS) in the urban environment

Genome‐Wide Association Study for Nine Plant Architecture Traits in Sorghum

Sorghum [ (L) Moench], an important grain and forage crop, is receiving significant attention as a lignocellulosic feedstock because of its water-use efficiency and high biomass yield potential. Because of the advancement of genotyping and sequencing technologies, genome-wide association study (GWAS) has become a routinely used method to investigate the genetic mechanisms underlying natural phenotypic variation. In this study, we performed a GWAS for nine grain and biomass-related plant architecture traits to determine their overall genetic architecture and the specific association of allelic variants in gibberellin (GA) biosynthesis and signaling genes with these phenotypes. A total of 101 single-nucleotide polymorphism (SNP) representative regions were associated with at least one of the nine traits, and two of the significant markers correspond to GA candidate genes, () and (), affecting plant height and seed number, respectively. The resolution of a previously reported quantitative trait loci (QTL) for leaf angle on chromosome 7 was increased to a 1.67 Mb region containing seven candidate genes with good prospects for further investigation. This study provides new knowledge of the association of GA genes with plant architecture traits and the genomic regions controlling variation in leaf angle, stem circumference, internode number, tiller number, seed number, panicle exsertion, and panicle length. The GA gene affecting seed number variation () and the genomic region on chromosome 7 associated with variation in leaf angle are also important outcomes of this study and represent the foundation of future validation studies needed to apply this knowledge in breeding programs

The association between fetal-stage exposure to the China famine and risk of diabetes mellitus in adulthood: results from the China health and retirement longitudinal study

Abstract Background The associations of famine exposure with diabetes risk in adulthood are still unclear. This study aimed to explore the association between famine exposure in early life and risk of diabetes in adulthood. Methods A total of 4138 subjects were selected from the data of the China Health and Retirement Longitudinal Study (CHARLS) 2011–2012. Diabetes was diagnosed as fasting plasma glucose (FPG) ≥7.0 mmol/L, glycated haemoglobin (HbA1C) > 6.5%, or self-reported diabetes. Birthdates of subjects were used to categorize famine exposure groups. The association of fetal-stage famine exposure with diabetes risk in adults was assessed using logistics regression model. Results The prevalence of diabetes in the non-exposed, fetal-stage exposed, infant-stage exposed, and preschool-stage exposed groups were 9.0, 13.6, 12.7 and 10.8%, respectively. Compared with the age-balanced control group, the fetal-stage exposed group was associated with the elevated risk of diabetes in later life after adjusting for covariates (OR = 1.37; 95%CI: 1.09–1.72; P = 0.008). Stratified analysis showed that the association between prenatal famine exposure and diabetes risk in adulthood was comparable between severely affected areas and less severely affected areas (P for interaction =0.153). Conclusions Famine exposure in fetal stages was associated with the elevated diabetes risk in adults, which could be the critical periods for relative intervention

Src is required for mechanical stretch-induced cardiomyocyte hypertrophy through angiotensin II type 1 receptor-dependent β-arrestin2 pathways.

Angiotensin II (AngII) type 1 receptor (AT1-R) can be activated by mechanical stress (MS) without the involvement of AngII during the development of cardiomyocyte hypertrophy, in which G protein-independent pathways are critically involved. Although β-arrestin2-biased signaling has been speculated, little is known about how AT1-R/β-arrestin2 leads to ERK1/2 activation. Here, we present a novel mechanism by which Src kinase mediates AT1-R/β-arrestin2-dependent ERK1/2 phosphorylation in response to MS. Differing from stimulation by AngII, MS-triggered ERK1/2 phosphorylation is neither suppressed by overexpression of RGS4 (the negative regulator of the G-protein coupling signal) nor by inhibition of Gαq downstream protein kinase C (PKC) with GF109203X. The release of inositol 1,4,5-triphosphate (IP3) is increased by AngII but not by MS. These results collectively suggest that MS-induced ERK1/2 activation through AT1-R might be independent of G-protein coupling. Moreover, either knockdown of β-arrestin2 or overexpression of a dominant negative mutant of β-arrestin2 prevents MS-induced activation of ERK1/2. We further identifies a relationship between Src, a non-receptor tyrosine kinase and β-arrestin2 using analyses of co-immunoprecipitation and immunofluorescence after MS stimulation. Furthermore, MS-, but not AngII-induced ERK1/2 phosphorylation is attenuated by Src inhibition, which also significantly improves pressure overload-induced cardiac hypertrophy and dysfunction in mice lacking AngII. Finally, MS-induced Src activation and hypertrophic response are abolished by candesartan but not by valsartan whereas AngII-induced responses can be abrogated by both blockers. Our results suggest that Src plays a critical role in MS-induced cardiomyocyte hypertrophy through β-arrestin2-associated angiotensin II type 1 receptor signaling

Regulating Blood Clot Fibrin Films to Manipulate Biomaterial-Mediated Foreign Body Responses

The clinical efficacy of implanted biomaterials is often compromised by host immune recognition and subsequent foreign body responses (FBRs). During the implantation, biomaterials inevitably come into direct contact with the blood, absorbing blood protein and forming blood clot. Many studies have been carried out to regulate protein adsorption, thus manipulating FBR. However, the role of clot surface fibrin films formed by clotting shrinkage in host reactions and FBR is often ignored. Because of the principle of fibrin film formation being relevant to fibrinogen or clotting factor absorption, it is feasible to manipulate the fibrin film formation via tuning the absorption of fibrinogen and clotting factor. As biological hydroxyapatite reserved bone architecture and microporous structure, the smaller particle size may expose more microporous structures and adsorb more fibrinogen or clotting factor. Therefore, we set up 3 sizes (small, <0.2 mm; medium, 1 to 2 mm; large, 3 to 4 mm) of biological hydroxyapatite (porcine bone-derived hydroxyapatite) with different microporous structures to investigate the absorption of blood protein, the formation of clot surface fibrin films, and the subsequent FBR. We found that small group adsorbed more clotting factors because of more microporous structures and formed the thinnest and sparsest fibrin films. These thinnest and sparsest fibrin films increased inflammation and profibrosis of macrophages through a potential signaling pathway of cell adhesion–cytoskeleton–autophagy, leading to the stronger FBR. Large group adsorbed lesser clotting factors, forming the thickest and densest fibrin films, easing inflammation and profibrosis of macrophages, and finally mitigating FBR. Thus, this study deepens the understanding of the role of fibrin films in host recognition and FBR and demonstrates the feasibility of a strategy to regulate FBR by modulating fibrin films via tuning the absorption of blood proteins

Association between GLO1 variants and gestational diabetes mellitus susceptibility in a Chinese population: a preliminary study

BackgroundGlyoxalase 1 (GLO1) plays a crucial role in defending against glycation. Single nucleotide polymorphism (SNP) variants in the GLO1 gene may affect gene expression and alter enzyme activity. However, there have been limited studies evaluating the association between GLO1 and diabetes, especially gestational diabetes mellitus (GDM). Therefore, this study is the first to explore the association of GLO1 SNPs and GDM risk.MethodsThe study included a total of 500 GDM patients and 502 control subjects. The SNPscan™ genotyping assay was used to genotype rs1781735, rs4746 and rs1130534. To assess the disparities in genotype, allele, and haplotype distributions and their correlation with GDM risk, the independent sample t-test, logistic regression, and chi-square test were employed during the data processing phase. Furthermore, one-way ANOVA was conducted to determine the differences in genotype and blood glucose and methylglyoxal(MG) levels.ResultsSignificant differences were observed in prepregnancy body mass index (pre-BMI), age, systolic blood pressure (SBP), diastolic blood pressure (DBP), and parity between GDM and healthy subjects (P &lt; 0.05). After adjusting for these factors, GLO1 rs1130534 TA remained associated with an increased risk of GDM (TA vs. TT + AA: OR = 1.320; 95% CI: 1.008-1.728; P = 0.044), especially in the pre-BMI ≥ 24 subgroup (TA vs. TT + AA: OR = 2.424; 95% CI: 1.048-5.607; P = 0.039), with fasting glucose levels being significantly elevated in the TA genotype compared to the TT genotype (P &lt; 0.05). Conversely, the GLO1 rs4746 TG was associated with a decreased risk of GDM (TG vs. TT: OR = 0.740; 95% CI: 0.548-0.999; P = 0.049; TG vs. TT + GG: OR = 0.740; 95% CI: 0.548-0.998; P = 0.048). Additionally, the haplotype T-G-T of rs1781735, rs4746 and rs1130534 was associated with a decreased risk of GDM among individuals with a pre-BMI ≥ 24 (OR = 0.423; 95% CI: 0.188-0.955; P = 0.038). Furthermore, the rs1781735 GG genotype was found to be more closely related to maternal MG accumulation and neonatal weight gain (P &lt; 0.05).ConclusionOur findings suggested that GLO1 rs1130534 was associated with an increased susceptibility to GDM and higher blood glucose levels, but GLO1 rs4746 was associated with a decreased risk of GDM. The rs1781735 has been associated with the accumulation of maternal MG and subsequent weight gain in neonates

The effects of different ARBs on the cardiac function and Src expression in AGT KO mice.

<p>AGT KO mice were induced by AngII or TAC for 2 weeks with or without the pretreatment of valsartan or candesartan. (<b>A</b>) Representative M-mode tracings of AGT KO hearts stimulated by AngII (10⁻⁵ mol/L, top line) or by TAC for 2 weeks (bottom line). (<b>B</b>) Representative recording of LVAWd, LVPWd and LVEF in AGT KO mice from each group. (<b>C</b>) The expression of Src in myocardium of AGT KO mice from each group was determined. Data were presented as mean ± s.e.m. from five to eight mice. * <i>P</i><0.05 vs. AngII-treated AGT KO mice; # <i>P</i><0.05 vs. TAC-treated AGT KO mice.</p