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Aim: To explore the relationship between proinflammatory diet, habitual salt intake and the onset of type 2 diabetes. Methods: This prospective study was conducted among 171 094 UK Biobank participants who completed at least one 24‐h dietary questionnaire and were free of diabetes at baseline. Participants were followed up until 1 March 2023 for type 2 diabetes incidence, with diagnosis information obtained from linked medical records. An Energy‐adjusted Diet Inflammatory Index (E‐DII) was calculated based on 28 food parameters. Habitual salt intake was determined through the self‐reported frequency of adding salt to foods. The associations between E‐DII, habitual salt intake and type 2 diabetes incidence were tested by the Cox proportional hazard regression model. Results: Over a median follow‐up period of 13.5 years, 6216 cases of type 2 diabetes were documented. Compared with participants with a low E‐DII (indicative of an anti‐inflammatory diet), participants with a high E‐DII (indicative of a proinflammatory diet) had an 18% heightened risk of developing type 2 diabetes. The association between E‐DII and type 2 diabetes tends to be linear after adjustment for major confounders. Participants with a proinflammatory diet and always adding salt to foods had the highest risk of type 2 diabetes incidence (hazard ratio 1.60, 95% confidence interval 1.32‐1.94). Conclusions: Our findings indicate that a proinflammatory diet and higher habitual salt intake were associated with an increased risk of type 2 diabetes. These results support the public health promotion of an anti‐inflammatory diet and reducing salt intake to prevent the onset of type 2 diabetes. [ABSTRACT FROM AUTHOR]

Background Patients with type 2 diabetes (T2D) may disproportionately suffer the adverse cardiovascular effects of air pollution, but relevant evidence on microvascular outcome is lacking. We aimed to examine the association between air pollution exposure and the risk of microvascular complications among patients with T2D. Methods This prospective study included 17 995 participants with T2D who were free of macro- and micro-vascular complications at baseline from the UK Biobank. Annual average concentrations of particulate matter (PM) with diameters <2.5 μm (PM2.5), <10 μm (PM10), nitrogen dioxide (NO2) and nitrogen oxides (NOx) were assessed using land use regression models. Cox proportional hazards regression was used to estimate the associations of air pollution exposure with incident diabetic microvascular complications. The joint effects of the air pollutant mixture were examined using quantile-based g-computation in a survival setting. Results In single-pollutant models, the adjusted hazard ratios (95% confidence intervals) for composite diabetic microvascular complications per interquartile range increase in PM2.5, PM10, NO2 and NOx were 1.09 (1.04–1.14), 1.06 (1.01–1.11), 1.07 (1.02–1.12) and 1.04 (1.00–1.08), respectively. Similar significant results were found for diabetic nephropathy and diabetic neuropathy, but not for diabetic retinopathy. The associations of certain air pollutants with composite microvascular complications and diabetic nephropathy were present even at concentrations below the World Health Organization limit values. Multi-pollutant analyses demonstrated that PM2.5 contributed most to the elevated risk associated with the air pollutant mixture. In addition, we found no interactions between air pollution and metabolic risk factor control on the risk of diabetic microvascular complications. Conclusions Long-term individual and joint exposure to PM2.5, PM10, NO2 and NOx, even at low levels, was associated with an increased risk of diabetic microvascular complications, with PM2.5 potentially being the main contributor. [ABSTRACT FROM AUTHOR]

Objective: Prediabetes and lifestyle factors have been associated with the risks of multiple adverse outcomes, but the effect of a healthy lifestyle on prediabetes‐related complications remains unknown. We aimed to investigate whether the risks of multiple adverse outcomes including incident type 2 diabetes mellitus (T2DM), cardiovascular disease (CVD), and chronic kidney disease (CKD) among individuals with prediabetes can be offset by a broad combination of healthy lifestyle factors. Methods: This prospective study used data from the UK Biobank cohort. An overall lifestyle score ranging from 0 to 6 was created with 1 point for each of the 6 healthy lifestyle factors: no current smoking, moderate alcohol consumption, regular physical activity, healthy diet, no overweight or obese, and adequate sleep duration. T2DM, CVD, and CKD were ascertained during a median follow‐up of 14 years. Cox proportional hazard regression models were used to estimate the associations. Sensitivity analyses were performed to test the robustness of the results. Results: We included 202,993 participants without T2DM, CVD, and CKD at baseline (mean age 55.5 years [SD 8.1]; 54.7% were women). Among these participants, 6,745, 16,961, and 6,260 participants eventually developed T2DM, CVD, and CKD, respectively. Compared with the participants with normoglycaemia, those with prediabetes showed a higher risk of these adverse outcomes. In addition, those prediabetic participants with a lifestyle score of 0‐1 had a significantly higher risk of T2DM (hazard ratio [HR] 16.73, 95% CI 14.24, 19.65), CVD (HR 1.96, 95% CI 1.74, 2.21), and CKD (HR 1.92, 95% CI 1.58, 2.34) compared with those with no prediabetes and a score of 5–6. Moreover, among the participants with prediabetes, the HRs for T2DM, CVD, and CKD comparing a lifestyle score of 5–6 versus 0‐1 decreased to 0.43 (95% CI 0.36, 0.51), 0.52 (95% CI 0.44, 0.62), and 0.60 (95% CI 0.46, 0.79), respectively. Conclusions: Combined healthy lifestyle factors were associated with a significantly lower risk of multiple adverse outcomes, including T2DM, CVD, and CKD. This indicates that prioritising multifactorial approaches to behavioural lifestyle modification is crucial for preventing and postponing the development of complications related to prediabetes. [ABSTRACT FROM AUTHOR]

Aims: To estimate the association between long‐term changes in frailty and the risk of incident type 2 diabetes (T2DM) and to evaluate the effect of preventing the worsening of frailty on the risk of T2DM. Methods: We included 348 205 participants free of baseline T2DM and with frailty phenotype (FP) data from the UK Biobank; among them, 36 175 had at least one follow‐up assessment. According to their FP score, participants were grouped into nonfrailty, prefrailty and frailty groups. Frailty assessed at baseline and at follow‐up was used to derive the trajectory of frailty (ΔFP). Cox regression models were used to estimate hazard ratios (HRs) and 95% confidence intervals (CIs). Results: Compared with those in the nonfrailty group at baseline, the HRs of T2DM for the prefrailty and frailty groups were 1.38 (95% CI 1.33–1.43) and 1.69 (95% CI 1.59–1.79), respectively (both p < 0.001), in the multivariable‐adjusted model. During a median follow‐up of 5.4 years after the final assessment, data for 472 T2DM patients were recorded. A 1‐point increase in the final FP was associated with a 25% (95% CI 1.14–1.38; p < 0.001) increased risk of T2DM. For the trajectory of frailty, each 0.5‐point/year increase in ΔFP was associated with a 52% (95% CI 1.18–1.97; p < 0.001) greater risk of T2DM, independent of the FP score at baseline. Compared with those that remained in the nonfrailty group, the greatest risk of T2DM over time was prefrailty aggravation (HR 3.03, 95% CI 2.00–4.58; p < 0.001). Using the frailty index did not materially change the results. Conclusions: Long‐term changes in frailty were associated with the risk of incident T2DM, irrespective of baseline frailty status. Preventing the worsening of frailty may reduce T2DM risk. [ABSTRACT FROM AUTHOR]

Background: Type 2 diabetes (T2D) is associated with an increased risk of premature death. Whether multifactorial risk factor modification could attenuate T2D-related excess risk of death is unclear. We aimed to examine the association of risk factor target achievement with mortality and life expectancy among patients with T2D, compared with individuals without diabetes. Methods: In this longitudinal cohort study, we included 316 995 participants (14 162 with T2D and 302 833 without T2D) free from cardiovascular disease (CVD) or cancer at baseline between 2006 and 2010 from the UK Biobank. Participants with T2D were categorised according to the number of risk factors within target range (non-smoking, being physically active, healthy diet, guideline-recommended levels of glycated haemoglobin, body mass index, blood pressure, and total cholesterol). Survival models were applied to calculate hazard ratios (HRs) for mortality and predict life expectancy differences. Results: Over a median follow-up of 13.8 (IQR 13.1–14.4) years, deaths occurred among 2105 (14.9%) participants with T2D and 18 505 (6.1%) participants without T2D. Compared with participants without T2D (death rate per 1000 person-years 4.51 [95% CI 4.44 to 4.57]), the risk of all-cause mortality among those with T2D decreased stepwise with an increasing number of risk factors within target range (0–1 risk factor target achieved: absolute rate difference per 1000 person-years 7.34 [4.91 to 9.78], HR 2.70 [2.25 to 3.25]; 6–7 risk factors target achieved: absolute rate difference per 1000 person-years 0.68 [-0.62 to 1.99], HR 1.16 [0.93 to 1.43]). A similar pattern was observed for CVD and cancer mortality. The association between risk factors target achievement and all-cause mortality was more prominent among participants younger than 60 years than those 60 years or older (P for interaction = 0.012). At age 50 years, participants with T2D who had 0–1 and 6–7 risk factors within target range had an average 7.67 (95% CI 6.15 to 9.19) and 0.99 (-0.59 to 2.56) reduced years of life expectancy, respectively, compared with those without T2D. Conclusions: Individuals with T2D who achieved multiple risk factor targets had no significant excess mortality risk or reduction in life expectancy than those without diabetes. Early interventions aiming to promote risk factor modification could translate into improved long-term survival for patients with T2D. [ABSTRACT FROM AUTHOR]

Background and Aims Atrial fibrillation (AF) is the most common sustained arrhythmia in adults. Investigations of risk factor profiles for AF according to age and genetic risk groups are essential to promote individualized strategies for the prevention and control of AF. Methods A total of 409 661 participants (mean age, 56 years; 46% men) free of AF at baseline and with complete information about risk factors were included from the UK Biobank cohort. The hazard ratios and population-attributable risk (PAR) percentages of incident AF associated with 23 risk factors were examined, including 3 social factors, 7 health behaviours, 6 cardiometabolic factors, 6 clinical comorbidities, and the genetic risk score (GRS), across 3 age groups (40–49, 50–59, and 60–69 years) and 3 genetic risk groups (low, moderate, and high GRS). Results After a follow-up of 5 027 587 person-years, 23 847 participants developed AF. Most cardiometabolic factors and clinical comorbidities showed a significant interaction with age, whereby the associations were generally strengthened in younger groups (P interaction <.002). However, only low LDL cholesterol, renal dysfunction, and cardiovascular disease showed a significant interaction with genetic risk, and the associations with these factors were stronger in lower genetic risk groups (P interaction <.002). Cardiometabolic factors consistently accounted for the largest number of incident AF cases across all age groups (PAR: 36.2%–38.9%) and genetic risk groups (34.0%–41.9%), with hypertension and overweight/obesity being the two leading modifiable factors. Health behaviours (PAR: 11.5% vs. 8.7%) and genetic risk factors (19.1% vs. 14.3%) contributed to more AF cases in the 40–49 years group than in the 60–69 years group, while the contribution of clinical comorbidities remained relatively stable across different age groups. The AF risk attributable to overall cardiometabolic factors (PAR: 41.9% in the low genetic risk group and 34.0% in the high genetic risk group) and clinical comorbidities (24.7% and 15.9%) decreased with increasing genetic risk. The impact of social factors on AF was relatively low across the groups by age and genetic risk. Conclusions This study provided comprehensive information about age- and genetic predisposition-related risk factor profiles for AF in a cohort of UK adults. Prioritizing risk factors according to age and genetic risk stratifications may help to achieve precise and efficient prevention of AF. [ABSTRACT FROM AUTHOR]

This article discusses a study that examines the association between frailty, genetic predisposition, and incident atrial fibrillation (AF). The study is based on data from the UK Biobank and includes 368,862 participants. The results show that frail individuals have a higher risk of developing AF compared to non-frail individuals. There is also a significant interaction between frailty status and genetic risk, with participants at high genetic risk and frailty having the highest risk of AF. The study suggests that frailty could be a novel risk factor for AF and may be incorporated into the evaluation of AF risk. However, the study has limitations, including the inability to establish causality and potential confounding factors. Further research is needed to replicate the findings in other populations. [Extracted from the article]

Aims: To investigate whether the association between sleep patterns and cardiovascular disease (CVD) risk differs according to glucose tolerance status. Materials and Methods: This prospective study included 358,805 participants initially free of CVD from the UK Biobank. We created a sleep score based on five sleep factors (sleep duration, chronotype, insomnia, snoring, and daytime sleepiness) with one point for each unhealthy factor. Cox proportional hazards models were used to examine the association between sleep and incident CVD, including coronary heart disease (CHD) and stroke, according to normal glucose tolerance (NGT), prediabetes, and diabetes. Results: During a median follow‐up of 12.4 years, 29,663 incident CVD events were documented. There was a significant interaction between sleep score and glucose tolerance status on CVD (P for interaction = 0.002). Each 1 point increment in sleep score was associated with a 7% (95% confidence interval 6%–9%), 11% (8%–14%), and 13% (9%–17%) higher risk of CVD among participants with NGT, prediabetes, and diabetes, respectively. Similar interaction patterns were observed for CHD and stroke. Among the individual sleep factors, sleep duration and insomnia significantly interacted with glucose tolerance status on CVD outcomes (all P for interaction <0.05). All five unhealthy sleep factors accounted for 14.2% (8.7%–19.8%), 19.5% (7.4%–31.0%), and 25.1% (9.7%–39.3%) of incident CVD cases among participants with NGT, prediabetes, and diabetes, respectively. Conclusions: The CVD risk associated with a poor sleep pattern was exacerbated across glucose intolerance status. Our findings emphasise the importance of integrating sleep management into a lifestyle modification programme, particularly in people with prediabetes or diabetes. [ABSTRACT FROM AUTHOR]

While blockchain technologies are gaining momentum within supply chains, academic understanding of concrete, real-life design and implementation is still lagging, hence offering very limited insights into the true implications of blockchain technology on supply chains. This paper reports a two-year design science research (DSR) study of a smart contract initiative piloted by a consortium in the UK's construction sector. We seek answers to the research question, 'How should a blockchain enabled supply chain be designed?' Guided by the theory of business model, we explore how a group of supply chain actors collectively designs and pilots a blockchain solution that addresses the supply chain transparency and provenance problem. Our research is one of the very few longitudinal empirical studies to offer in-depth evidence about how blockchain is deployed in complex multi-tier supply chain networks. In compliance with DSR research paradigm, we make contributions at three levels: designing and instantiating the blockchain architect and proving its utility in addressing the target problem; developing a set of design principles as a mid-range theory that can be applied and tested in different blockchain supply chain contexts; and refining and extending the kernel theory of business value at supply chain network level. [ABSTRACT FROM AUTHOR]

Aims: To evaluate the association of cardiovascular health (CVH), measured by Life's Essential 8 score, with the risk of premature mortality and to determine the patterns of CVH‐related differences in life expectancy among people with and without type 2 diabetes (T2D). Materials and Methods: This prospective study included 309,789 participants (age 56.6 ± 8.1 years; 46% men) enroled in the UK Biobank. The Life's Essential 8 composite measure consists of four health behaviours (diet, physical activity, nicotine exposure, and sleep) and four health factors (BMI, non‐HDL cholesterol, blood glucose, and blood pressure), and the maximum CVH score was 100 points. CVH was categorised into low, moderate, and high groups. Premature death was defined as death before the age of 75. Cox proportional hazard ratios (HRs) with 95% confidence intervals (CIs) were calculated, and life expectancy was estimated. Results: During a median follow‐up of 12.7 years, 13,683 cases of premature death were documented. Compared to participants with low CVH, the multivariable HRs (95% CIs) of premature death were 0.59 (0.56–0.62) and 0.42 (0.39–0.45) for the moderate and high CVH groups, respectively. This association was stronger in participants with T2D compared with those without T2D. At the age of 50 years, compared to low CVH groups, high CVH was associated with a gain of 9.79 (9.70–9.87) and 5.58 (5.48–5.67) additional life years for men with and without T2D, respectively. The corresponding life gain for women with and without T2D was 24.21 (24.13–24.27) and 10.18 (10.10–10.27), respectively. Conclusions: Maintaining an ideal Life's Essential 8 score may provide more benefits for people with T2D than for those without T2D, including a lower risk of premature death and an increased lifespan. [ABSTRACT FROM AUTHOR]

Introduction: Nonalcoholic fatty liver disease (NAFLD) and type 2 diabetes mellitus (T2DM) are both chronic multisystem diseases that cause tremendous health burdens worldwide. Previous epidemiological studies have found a bidirectional relationship between these two diseases; however, their causality remains largely unknown. We aim to examine the causal relationship between NAFLD and T2DM. Methods: The observational analysis included 2,099 participants from the SPECT-China study and 502,414 participants from the UK Biobank. Logistic regression and Cox regression models were used to examine the bidirectional association between NAFLD and T2DM. Two-sample Mendelian randomization (MR) analyses were conducted to investigate the causal effects of the two diseases using summary statistics of genome-wide association studies from the UK Biobank for T2DM and the FinnGen study for NAFLD. Results: During the follow-up, 129 T2DM cases and 263 NAFLD cases were observed in the SPECT-China study, and 30,274 T2DM cases and 4,896 NAFLD cases occurred in the UK Biobank cohort. Baseline NAFLD was associated with an increased risk of incident T2DM in both studies (SPECT-China: OR: 1.74 (95% confidence interval (CI): 1.12-2.70); UK Biobank: HR: 2.16 (95% CI: 1.82-2.56)), while baseline T2DM was associated with incident NAFLD in the UK Biobank study only (HR: 1.58). Bidirectional MR analysis showed that genetically determined NAFLD was significantly associated with an increased risk of T2DM (OR: 1.003 (95% CI: 1.002-1.004, p< 0.001)); however, there was no evidence of an association between genetically determined T2DM and NAFLD (OR: 28.1 (95% CI: 0.7-1,143.0)). Conclusions: Our study suggested the causal effect of NAFLD on T2DM development. The lack of a causal association between T2DM and NAFLD warrants further verification. [ABSTRACT FROM AUTHOR]

Background and Aim: Non‐alcoholic fatty liver disease (NAFLD) is associated with incident type 2 diabetes; however, the extent to which NAFLD may confer its risk remains uncertain, especially in Europeans. Emerging evidence suggests that sleep behaviors are linked to NAFLD and diabetes. We aimed to measure whether sleep behaviors modified the association between NAFLD and incident type 2 diabetes. Methods: This prospective cohort study included 365 339 participants without type 2 diabetes at baseline in UK Biobank data. Five sleep behaviors, including sleep duration, insomnia, snoring, chronotype, and daytime sleepiness, were collected from the questionnaire. Overall sleep patterns were created by summing the five scores. Liver steatosis was based on the fatty liver index. Results: During a median follow up of 11.0 years, we documented 8774 patients with incident type 2 diabetes. NAFLD was significantly associated with increased diabetes risk. Sleeping 7–8 h/day, no insomnia, no self‐reported snoring, and no frequent daytime sleepiness were independently associated with incident type 2 diabetes, with a 20%, 18%, 16%, and 31% lower risk, respectively. About 33.8% and 33.5% of type 2 diabetes events in this cohort could be attributed to NAFLD and poor sleep pattern, respectively. Participants with NAFLD and poor sleep pattern showed the highest risk of type 2 diabetes (relative risk 3.17, 95% confidence interval 2.80, 3.59). Sleep pattern (healthy, intermediate, and poor) did not significantly modify the association between NAFLD and type 2 diabetes. However, when studying separately, we found a significant interaction between NAFLD and insomnia on the risk of incident type 2 diabetes (P for interaction = 0.003). Conclusion: In this large prospective study, both NAFLD and some sleep behaviors were risk factors for type 2 diabetes. Although overall sleep pattern did not modify the association between NAFLD and type 2 diabetes, certain sleep behavior, especially insomnia, showed the modification effect. [ABSTRACT FROM AUTHOR]

Objectives: Unhealthy sleep behaviors may be potential risk factors for chronic kidney disease (CKD). We aimed to examine the associations of combined sleep patterns and genetic susceptibility with incident CKD. Methods: This large-scale prospective cohort study included 370,671 participants without CKD at baseline (2006–2010) in UK Biobank data. Five sleep behaviors were made up of sleep duration, insomnia, snoring, chronotype, and daytime sleepiness according to questionnaire. Overall sleep patterns by summing the five scores were created. Weighted genetic risk score of kidney function was calculated. Incident CKD was recorded from death register, primary care, and hospital inpatient records. A subset of 41,130 individuals who participated both the initial assessment visit and follow-up visit (2012+) was also used. Results: During a median follow-up of 10.6 years (about 3.9 million person-years), we documented 6,365 patients with incident CKD. In five sleep behaviors, sleep 7–8 h/day, free of insomnia and no frequent daytime sleepiness were independently associated with incident CKD, with a 12% (95%CI 7–16), 9% (3–14), 13% (9–18) lower risk, respectively. Compared to those with a sleep score of 0–1, participants with a score of 5 had a 21% (10–31%) lower risk of CKD. 17.1% of CKD in this cohort could be attributed to total poor sleep pattern. Participants with high genetic risk and intermediate or poor sleep pattern showed the highest risk of CKD (OR = 2.58, 95%CI 2.24–2.96; OR = 2.59, 95%CI 2.02–3.32, respectively), although there was no significant interaction between sleep patterns and genetic risk categories. Among individuals who participated both the initial assessment visit and follow-up visit, we found that the association between amelioration of sleep pattern and risk of CKD was significant after fully adjustment (OR = 0.60, 95%CI 0.36–0.99), compared with group of stable sleep pattern. Conclusion: In this large prospective study, participants with a healthy sleep pattern was associated with a significant reduction of incident CKD risk no matter they had a high, intermediate, or low genetic risk. [ABSTRACT FROM AUTHOR]

Background: The fat‐to‐muscle mass ratio (FMR) might be an indicator to assess type 2 diabetes risk independent of general obesity. However, no longitudinal studies have explored the extent to which total and regional FMRs may confer risks. We aimed to measure the sex‐specific associations between FMRs of the arm, leg, trunk and whole body and incident type 2 diabetes. Methods: A total of 464 817 participants (207 286 men and 257 531 women, mean age 56.5 ± 8.2 and 56.2 ± 8.0 years old, respectively) free of diabetes at baseline were included in this prospective cohort study with UK Biobank data. Fat mass and muscle mass were estimated using a bioelectrical impedance assessment device (Tanita BC 418MA). FMR was calculated as fat mass divided by muscle mass in corresponding body parts (total body, arm, leg and trunk). Cox proportional hazard models were used to estimate the aforementioned associations among men and women. Interaction analyses were performed between FMRs and body mass index (BMI) categories (BMI < 25 kg/m2 and BMI ≥ 25 kg/m2). Results: Over the median 11.0 years (5 057 534 person‐years) of follow‐up, we documented 11 618 cases of type 2 diabetes. There was a significantly positive association between total and regional FMR and incident type 2 diabetes, even after adjusting for BMI and other covariates. Compared with other body parts, FMRs of the whole body and leg showed the strongest relationship among men and women, respectively (hazard ratio per 1 SD, 95% confidence interval: 1.67, 1.55–1.80; 1.45, 1.39–1.53). A significant interaction (P for interaction < 0.001) between BMI category and FMRs of different body parts was observed. In the stratified analysis by BMI category and tertiles of FMRs, overweight/obese individuals with a high FMR tertile tended to have the highest hazard ratio, ranging from 5.91 to 7.94 in whole body and regional areas. Conclusions: In this large prospective study, higher total and regional FMRs were associated with a higher risk of developing type 2 diabetes, independent of BMI. This association was markedly strengthened in participants with BMI ≥ 25 kg/m2. [ABSTRACT FROM AUTHOR]

Avian leukosis virus subgroup J (ALV‐J) was isolated in meat‐type breeder chickens for the first time in 1988 in the United Kingdom. Due to the application of an eradication program, there were fewer reports related to myelocytomatosis or ALV‐J in China after 2013. However, there was another breakout almost simultaneously in six provinces of China in February 2018. On‐site, 15‐ to 20‐week‐old broiler breeder chickens showed depression, paralysis and weight loss. Mortality for certain flocks reached 15%. Sick chickens showed numerous yellow–white neoplasms growing in the sternum, rib and lumbar vertebra and had hepatic and renal metastasis. Histopathological observation showed all neoplasms were myelocytomas, and there were massive myelocyte‐like tumour cells in the liver, kidney and bone marrow. To explore the aetiology of this re‐outbreak of myelocytomatosis in China, we collected tumour‐bearing chickens and isolated six strains of ALV‐J (GM0209‐1 to ‐6). Phylogenetic analysis of gp85 and gp37 showed GM0209 strains were clearly distinct from the prototype strain of ADOL‐7501, HPRS‐103 and NX0101, and there was a mutation, R176G, in the conserved region between hr1 and hr2 regions of gp85, which was not found in other 44 ALV‐J strains. The 3′UTR nucleotide sequences of GM0209 isolates showed there was a signature deletion of 11 nt that was also present in 3′UTR sequences of SCDY1 and NHH, two isolates that have a reported association with haemangioma, indicating this deletion could not determine the tumour type induced by ALV‐J. Although the eradication program of ALV‐J has been successfully applied in China, the outbreak of ALV‐J still occurred, and the virus strain spread quickly. Thus, the biocharacteristics and pathogenesis of mutational ALV‐J should be further studied. [ABSTRACT FROM AUTHOR]

Purpose - The purpose of this paper is to investigate empirically how information and communication technologies (ICT) can contribute to reduction of CO[sub 2] emissions in road freight transport and to identify opportunities for further improvements. Design/methodology/approach - This research adopts a multiple case study approach with three leading UK grocery retailers as exemplars of fast-moving consumer goods retailers, conducted using multiple data collection techniques including interviews, system demonstrations, onsite observations and the use of archive information. Findings - ICT solutions have a direct positive impact on CO[sub 2] emissions reduction but opportunities to further reduce CO[sub 2] emissions are perceived as lying beyond retailers' own distribution networks. These opportunities are not fully utilised due to the complexities of collaborative ICT provisions and retailers' reluctance to share information with competitors. Research limitations/implications - A limitation of the study is that it is exploratory and only three cases were examined. Even though these three retailers represent over 60 per cent of the UK grocery retail sector, other retailers may deploy significantly different ICT applications. Practical implications - The research provides an overarching insight for businesses on how to leverage the existing and emerging information technologies for environmental and economic benefits. Originality/value - While sustainability issues have received increasing attention recently, the role of ICT in freight transport for CO[sub 2] emissions reduction has not been investigated in depth and its impact is largely unknown. This research advances understanding about how ICT contributes CO[sub 2] emissions reductions and provides a framework for further investigation. [ABSTRACT FROM AUTHOR]

We assessed the transportation tendency of dioxins and predict locations at high risk for dioxin pollution. A new parameter, the compartment distribution coefficient D, was created to account for the tendency of dioxins to preferentially accumulate in particular compartments. It was obtained by a model using levels of polychlorinated dibenzo-p-dioxins/dibenzofurans (PCDD/Fs) in four countries: Japan, the United States, the United Kingdom, and Australia. The comparison with the temporal and spatial variation of D indicated whether the location release or long-range transportation caused the changes. This study showed that PCDD/Fs have the greatest tendency to remain in soil among studied media. A higher D value in Australia may indicate that this location is a potential future reservoir source of dioxins. [ABSTRACT FROM AUTHOR]

Psychologic wellbeing can impact cardiovascular health. We aimed to evaluate the joint association of multiple psychologic wellbeing factors with cardiovascular diseases (CVD) and examine whether this association was modified by genetic susceptibility. In the UK Biobank, 126,255 participants free of CVD (coronary heart disease [CHD], stroke, and heart failure [HF]) at baseline, who completed a questionnaire on psychological factors, were included. The psychological wellbeing score was calculated by four factors: happiness, life satisfaction, broad depression, and neuroticism. Cox proportional hazard models were used to assess the association between the psychological wellbeing score and CVD risk. During the median follow-up of 11.5 years, 10,815 participants had newly diagnosed CVDs. Low life satisfaction, the presence of depression, and neuroticism score ≥1 were significantly associated with an increased risk of CVD in the multivariable-adjusted model. Through decreasing the psychological wellbeing score, there were significant increasing linear trends in the risk of CVD, CHD, stroke, and HF (all p for trend < 0.001). Participants with the lowest psychological wellbeing score had the highest risk for CVD (HR 1.51, 95% CI 1.42–1.61). Women were more susceptible to worse psychological wellbeing status for CVD than men (p for interaction = 0.009). The associations of the psychological wellbeing score with CVD were consistent across genetic risk (p for interaction >0.05). When considered jointly, participants exposed to high-risk psychological wellbeing and genetic status had a 2.70-fold (95% CI 2.25–3.24) risk for CHD. Joint exposure to multiple psychological wellbeing factors was associated with increased risks of incident CVD in an additive manner, regardless of genetic susceptibility. [Display omitted] • Multiple psychological wellbeing factors are associated with risk of cardiovascular diseases (CVD). • Psychological wellbeing score could be used in large populations as a combination indicator. • Lower psychologic wellbeing score is associated with increased CVD risk, regardless of genetic risk. • In CVD events, women are more vulnerable to poor psychological status than men. [ABSTRACT FROM AUTHOR]

In the process of implementing circular economy within the built environment, quantifying progress and performance towards this effort has posed a substantial challenge. In response, this paper reviews the current state of building-specific circularity indicators, creates a taxonomy, and integrates them within the Royal Institute of British Architects (RIBA) Plan of Work, a commonly employed framework within the UK's built environment. Through a systematic literature review considering both academic and grey literature, 32 building circularity indicators, developed by academia, consulting agencies, and governments, are identified. The first contribution of this study is the creation of a taxonomy of building circularity indicators, which classifies the identified indicators into 8 categories, such as basic characteristics of indicators, circularity level, and sustainability pillars. The second contribution of this study is the alignment of circularity within the stages of Plan of Work framework. It is revealed that the framework does not currently incorporate circularity, resulting in the proposal of a new Stage 8: End of Life to encompass demolition, disassembly, and deconstruction activities. Alignment of the taxonomy to Plan of Work framework provides a guide in utilization of building circularity indicators throughout the process of designing, constructing and operating building projects. • Building-specific circularity indicators are reviewed for the built environment. • A taxonomy of 32 building circularity indicators is created across eight categories. • A new Stage 8: End of Life is proposed for RIBA framework to enhance circularity. • The circularity indicators are integrated with the RIBA Plan of Work framework. • A traffic light approach is employed to guide the use of circularity indicators. [ABSTRACT FROM AUTHOR]

The prospective relation of childhood adversity with the risk of chronic kidney disease (CKD) remains unclear. We aimed to investigate the association of childhood adversity with new-onset CKD and examine the potential modifications by unhealthy lifestyle on this association. A total of 115,453 adults without prior CKD at baseline were included from UK Biobank (2006–2010). Childhood adversity was retrospectively evaluated through online Childhood Trauma Screener in 2016. Six common lifestyle factors including smoking, body mass index, sleep, diet, physical activity and alcohol consumption, were combined into an unhealthy lifestyle score. New-onset CKD was the primary outcome. The average age of participants in the study was 55.3 (SD, 7.7) years, and 39.3% of them were male. During a median follow-up duration of 14.1 years, 1905 participants developed new-onset CKD. Childhood adversity was significantly positively related with the risk of new-onset CKD in dose-response pattern. Each additional type of childhood adversity was associated with a 12% increment in the risk of developing CKD (adjusted hazard ratio (HR)1.12; 95% CI 1.08, 1.16). Among participants with high unhealthy lifestyle score, those with 4–5 types of childhood adversity increased the 1.73-fold risk of incident CKD (95% CI 1.17, 2.54) compared with those free of any childhood adversity. However, no statistically significant interaction was observed between unhealthy lifestyle and childhood adversity for new-onset CKD (P interaction = 0.734). Childhood adversity was significantly associated with an increased risk of new-onset CKD in a dose-response pattern regardless of unhealthy lifestyle. • Childhood adversity is highly prevalent and relates to poor health in late life. • Childhood adversity is a critical risk factor of new-onset CKD in adulthood. • Physical abuse was the strongest type associated with new-onset CKD. • Action of childhood adversity on incident CKD was independent of unhealthy lifestyle. [ABSTRACT FROM AUTHOR]