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Previous observational studies have reported potential associations among attention-deficit/hyperactivity disorder (ADHD), obesity, and diabetes (including type 1 and type 2 diabetes mellitus [T1DM/T2DM]). However, whether the association between ADHD and diabetes is mediated by obesity is unknown.
With two-sample Mendelian randomization, we analysed the causal effect of ADHD on T1DM and T2DM and six obesity-related traits [including body mass index, waist circumference (WC), hip circumference, waist-to-hip ratio (WHR), body fat percentage and basal metabolic rate] and the causal effect of these obesity-related traits on T1DM/T2DM. Finally, with multivariable Mendelian randomization, we explored and quantified the possible mediation effects of obesity-related traits on the causal effect of ADHD on T1DM/T2DM.
Our results showed that ADHD increased the risk of T2DM by 14% [odds ratio (OR) = 1.140, 95% confidence interval (CI) = 1.005–1.293] but with no evidence of an effect on T1DM (OR = 0.916, 95% CI = 0.735–1.141, P = 0.433.). In addition, ADHD had a 6.1% increased causal effect on high WC (OR = 1.061, 95% CI = 1.024–1.099, P = 0.001) and an 8.2% increased causal effect on high WHR (OR = 1.082, 95% CI = 1.035–1.131, P = 0.001). In addition, a causal effect of genetically predicted high WC (OR = 1.870, 95% CI = 1.594–2.192, P < 0.001) on a higher risk of T2DM was found. In further analysis, WC mediated approximately 26.75% (95% CI = 24.20%–29.30%) of the causal association between ADHD and T2DM.
WC mediates a substantial proportion of the causal effect of ADHD on the risk of T2DM, which indicated that the risk of T2DM induced by ADHD could be indirectly reduced by controlling WC as a main risk factor.
Coastal eutrophication and hypoxia remain a persistent environmental crisis despite the great efforts to reduce nutrient loading and mitigate associated environmental damages. Symptoms of this crisis have appeared to spread rapidly, reaching developing countries in Asia with emergences in Southern America and Africa. The pace of changes and the underlying drivers remain not so clear. To address the gap, we review the up-to-date status and mechanisms of eutrophication and hypoxia in global coastal oceans, upon which we examine the trajectories of changes over the 40 years or longer in six model coastal systems with varying socio-economic development statuses and different levels and histories of eutrophication. Although these coastal systems share common features of eutrophication, site-specific characteristics are also substantial, depending on the regional environmental setting and level of social-economic development along with policy implementation and management. Nevertheless, ecosystem recovery generally needs greater reduction in pressures compared to that initiated degradation and becomes less feasible to achieve past norms with a longer time anthropogenic pressures on the ecosystems. While the qualitative causality between drivers and consequences is well established, quantitative attribution of these drivers to eutrophication and hypoxia remains difficult especially when we consider the social economic drivers because the changes in coastal ecosystems are subject to multiple influences and the cause–effect relationship is often non-linear. Such relationships are further complicated by climate changes that have been accelerating over the past few decades. The knowledge gaps that limit our quantitative and mechanistic understanding of the human-coastal ocean nexus are identified, which is essential for science-based policy making. Recognizing lessons from past management practices, we advocate for a better, more efficient indexing system of coastal eutrophication and an advanced regional earth system modeling framework with optimal modules of human dimensions to facilitate the development and evaluation of effective policy and restoration actions.
Cable is the most important bearing structure of the cable-stayed bridges. Its safety has been of crucial public concern. Traditional manual cable inspection method has many defects such as low inspection efficiency, poor reliability and hazardous working environment. In this paper, a new wirelessly controlled cable-climbing robot enabling safe and convenient inspection of stay cables is proposed. The designed robot is composed of two modules, joined by four turnbuckles to form a closed structure that clasps the cable. The robot is controlled wirelessly by a ground-based station, and a DC power is supplied via an onboard lithium battery. The climbing principle and mechanical structure of this robot are introduced. The static model of the robot during obstacle negotiation is established. The relationships of the driving force and resistance with obstacle height to determine the obstacle-negotiation capability of the robot are obtained. The effects of cable diameter, cable inclination and preload force on obstacle climbing ability of the robot are also analyzed. The experiments verify that the robot could climb random inclined cables and overcome an obstacle of 2.42 mm in height with a mass of 5 kg payload.
The present study aimed to investigate the responses of broilers with different hatching weights (HW) to dietary methionine (Met). A total of 192 1-d-old Arbor Acres broiler chicks with different HW (heavy: 48·3 (sem 0·1) g and light: 41·7 (sem 0·1) g) were allocated to a 2 (HW) × 2 (Met) factorial arrangement with six replicates of eight chicks. Control starter (1–21 d) and finisher (22–42 d) diets contained 0·50 and 0·43 % Met, respectively. Corresponding values for a high-Met treatment were 0·60 and 0·53 %. Light chicks had poorer (P< 0·05) growth performance and breast muscle weight and lower (P< 0·05) insulin-like growth factor-I (IGF-I) concentration and mRNA level in breast muscle than heavy chicks when both were fed the control diets. High-Met diets improved performance and promoted breast muscle growth and IGF-I concentration in light chicks (P< 0·05). Increased IGF-I and target of rapamycin (TOR) mRNA levels as well as decreased eIF4E-binding protein 1 (4EBP1), atrogin-1 and forkhead box O 4 (FOXO4) mRNA levels were induced by high-Met diets in light chicks (P< 0·05). In conclusion, the Met requirement of broilers might depend on their HW and Met levels used in the control diets in the present study were adequate for heavy chicks but inadequate for light chicks, resulting in poorer performance and breast muscle growth, which were improved by increasing dietary Met supply presumably through alterations in IGF-I synthesis and gene expression of the TOR/4EBP1 and FOXO4/atrogin-1 pathway.
The anti-inflammatory effects of two esters of α-tocopherol (α-TOH), all-rac-α-TOH acetate (dl-α-TOA) and RRR-α-TOH succinate (d-α-TOS), on broilers repeatedly challenged with lipopolysaccharide (LPS) were investigated. Three hundred and twenty 1-d-old broiler chicks were allotted into four treatment groups and fed on a control diet (30 mg/kg dl-α-TOA) or diets containing 10, 30, 50 mg/kg d-α-TOS. Half of the birds from each treatment group were challenged with 0·9 % NaCl solution or LPS (250 μg/kg body weight) at 16, 18 and 20 d of age. The results indicated that the pretreatment of birds with 50 mg/kg d-α-TOS markedly reduced serum PGE2 secretion and increased the concentrations of serum or hepatic α-TOH. When LPS-challenged birds were pretreated with 30 or 50 mg/kg d-α-TOS, the increases of plasma and splenic concentrations of interferon-γ, IL-1β, IL-2, IL-6, IL-4 and IL-10 were dramatically attenuated. Also, a significant decrease of hepatic reactive oxygen species (ROS) and hepatic or splenic phosphokinase C (PKC) activities was found in birds pretreated with 30 or 50 mg/kg d-α-TOS. Furthermore, d-α-TOS inhibited the activation of NF-κB by preventing the degradation of inhibitory-κBα. In conclusion, D-α-TOS is able to prevent LPS-induced inflammation response in vivo. The beneficial effect may depend on suppressing the secretion of various plasma and splenic inflammatory mediators through inhibiting NF-κB activation and by blocking ROS signalling, in which PKC may play an assistant role.
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