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Background: Atrial fibrillation (AF) is associated with increased risk of ischemic stroke. In Canada, the contemporary burden of AF-related stroke is incompletely characterized. Our objective was to determine temporal trends in hospital admissions and in-hospital mortality for AF-related stroke in Canada from 2007 to 2015. Methods: We conducted a retrospective cohort study using Canadian national administrative data to identify admissions to hospital for stroke with comorbid AF between 2007 and 2015. We analyzed temporal trends in age- and sex-standardized proportion of admissions with comorbid AF and associated in-hospital mortality. Results: There were 222,100 admissions to hospital for ischemic (182,990) or hemorrhagic (39,110) stroke. The age-sex adjusted proportion of ischemic stroke admissions with comorbid AF increased from 16.2% to 20.5% (p for trend = 0.02) between 2007 and 2015, and was stable among hemorrhagic stroke. In-hospital mortality for ischemic stroke with comorbid AF decreased from 21.6% to 15.0% (p for trend = 0.001). Conclusions: Rates of hospital admission for ischemic stroke with comorbid AF have increased, while associated in-hospital mortality has decreased. These results identify AF as an important continued focus for stroke prevention. Our findings provide insight into current trends and highlight the need for continued focus on AF-related stroke.
Faster eating rates are associated with increased energy intake, but little is known about the relationship between children’s eating rate, food intake and adiposity. We examined whether children who eat faster consume more energy and whether this is associated with higher weight status and adiposity. We hypothesised that eating rate mediates the relationship between child weight and ad libitum energy intake. Children (n 386) from the Growing Up in Singapore Towards Healthy Outcomes cohort participated in a video-recorded ad libitum lunch at 4·5 years to measure acute energy intake. Videos were coded for three eating-behaviours (bites, chews and swallows) to derive a measure of eating rate (g/min). BMI and anthropometric indices of adiposity were measured. A subset of children underwent MRI scanning (n 153) to measure abdominal subcutaneous and visceral adiposity. Children above/below the median eating rate were categorised as slower and faster eaters, and compared across body composition measures. There was a strong positive relationship between eating rate and energy intake (r 0·61, P<0·001) and a positive linear relationship between eating rate and children’s BMI status. Faster eaters consumed 75 % more energy content than slower eating children (Δ548 kJ (Δ131 kcal); 95 % CI 107·6, 154·4, P<0·001), and had higher whole-body (P<0·05) and subcutaneous abdominal adiposity (Δ118·3 cc; 95 % CI 24·0, 212·7, P=0·014). Mediation analysis showed that eating rate mediates the link between child weight and energy intake during a meal (b 13·59; 95 % CI 7·48, 21·83). Children who ate faster had higher energy intake, and this was associated with increased BMI z-score and adiposity.
Background: The pathophysiology of subarachnoid hemorrhage (SAH) is complex and includes disruption of the blood-brain barrier (BBB). We freshly isolated BBB endothelial cells (BECs) by 2 distinct methods after experimental SAH and then interrogated their gene expression profiles with the goal of uncovering new therapeutic targets. Methods: SAH was induced using the prechiasmatic blood injection mouse model. BBB permeability studies were performed by administering intraperitoneal cadaverine dye injections at 24h and 48h. BECs were isolated either by sequential magnetic-based sorting for CD45-CD31+ cells or by fluorescence-activated cell sorting (FACS) for Tie2+Pdgfrb- cells. Total RNA was extracted and analyzed using Affymetrix Mouse Gene 2.0 ST Arrays. Results: BBB impairment occurred at 24h and resolved by 48h after SAH. Analysis of gene expression patterns in BECs at 24h reveal clustering of SAH and sham samples. We identified 707 (2.8%) significant differentially-expressed genes (403 upregulated, 304 downregulated) out of 24,865 interrogated probe sets. Many significantly upregulated genes were involved in inflammatory pathways. These microarray results were validated with real-time polymerase chain reaction (RT-PCR). Conclusions: This study is the first to investigate in an unbiased manner, whole genome expression profiling of freshly-isolated BECs in an SAH animal model, yielding targets for novel therapeutic intervention.
Background: Blood breakdown products such as bilirubin and bilirubin oxidation products damage cortex and white matter after intracerebral hemorrhage(ICH). Here, we tested whether albumin can antagonize axonal damage caused by bilirubin. Methods: The effect of albumin on white matter injury was investigated using brain slices in vitro. After CD-1 mice brain slices were cut using a vibratome, they were incubated in one of five solutions: artificial cerebral spinal fluid (ACSF), bilirubin ACSF, bilirubin and albumin ACSF, bilirubin ACSF that had albumin added 1 hour(h) later, and bilirubin and denatured albumin ACSF. All solutions were continuously aerated with 95% O2 and 5% CO2. Subsequently, electrophysiological recordings of axonal response to electrical stimulation were performed 8h after incubation of brain slices. Results: Bilirubin treatment profoundly damaged both myelinated and unmeylinated axons in brain slices, but had a greater effect on myelinated axons. Unmyelinated axons were found to be more susceptible to damage from denatured albumin. Albumin treatment at 0 h and 1 h significantly diminished bilirubin toxicity for both myelinated and unmyelinated axons, with 1 h delayed albumin treatment conferring greater neuroprotection. Conclusions: These results implicate the role of albumin in preventing bilirubin-induced axonal damage following ICH and its potential therapeutic value for hemorrhagic stroke.
Studies have suggested that maternal PUFA status during pregnancy may influence early childhood allergic diseases, although findings are inconsistent. We examined the relationship between maternal PUFA status and risk of allergic diseases in early childhood in an Asian cohort. Maternal plasma samples from the Growing Up in Singapore Towards Healthy Outcomes mother–offspring cohort were assayed at 26–28 weeks of gestation for relative abundance of PUFA. Offspring (n 960) were followed up from 3 weeks to 18 months of age, and clinical outcomes of potential allergic diseases (rhinitis, eczema and wheezing) were assessed by repeated questionnaires. Skin prick testing (SPT) was also performed at the age of 18 months. Any allergic disease with positive SPT was defined as having any one of the clinical outcomes plus a positive SPT. The prevalence of a positive SPT, rhinitis, eczema, wheezing and any allergic disease with positive SPT was 14·1 % (103/728), 26·5 % (214/808), 17·6 % (147/833), 10·9 % (94/859) and 9·4 % (62/657), respectively. After adjustment for confounders, maternal total n-3, n-6 PUFA status and the n-6:n-3 PUFA ratio were not significantly associated with offspring rhinitis, eczema, wheezing, a positive SPT and having any allergic disease with positive SPT in the offspring (P>0·01 for all). A weak trend of higher maternal n-3 PUFA being associated with higher risk of allergic diseases with positive SPT in offspring was observed. These findings do not support the hypothesis that the risk of early childhood allergic diseases is modified by variation in maternal n-3 and n-6 PUFA status during pregnancy in an Asian population.
Early life environments interact with genotype to determine stable phenotypic outcomes. Here we examined the influence of a variant in the brain-derived neurotropic factor (BDNF) gene (Val66Met), which underlies synaptic plasticity throughout the central nervous system, on the degree to which antenatal maternal anxiety associated with neonatal DNA methylation. We also examined the association between neonatal DNA methylation and brain substructure volume, as a function of BDNF genotype. Infant, but not maternal, BDNF genotype dramatically influences the association of antenatal anxiety on the epigenome at birth as well as that between the epigenome and neonatal brain structure. There was a greater impact of antenatal maternal anxiety on the DNA methylation of infants with the methionine (Met)/Met compared to both Met/valine (Val) and Val/Val genotypes. There were significantly more cytosine–phosphate–guanine sites where methylation levels covaried with right amygdala volume among Met/Met compared with both Met/Val and Val/Val carriers. In contrast, more cytosine–phosphate–guanine sites covaried with left hippocampus volume in Val/Val infants compared with infants of the Met/Val or Met/Met genotype. Thus, antenatal Maternal Anxiety × BDNF Val66Met Polymorphism interactions at the level of the epigenome are reflected differently in the structure of the amygdala and the hippocampus. These findings suggest that BDNF genotype regulates the sensitivity of the methylome to early environment and that differential susceptibility to specific environmental conditions may be both tissue and function specific.
Substituting used tyres for anthracite in the EAF in France and in
Belgium is reported. First trials have been carried out in Lorraine in
1997 in the frame of a partnership between Usinor (now Arcelor
Mittal), Michelin and Ademe. The substitution process has been
eventually implemented by LME in cooperation with Aliapur over the
years 2002-2003. Industeel Belgium got started on substitution in
2004. To day, both steel plants have achieved stable operation, with
a regular load of 8 to 12 kg used tyres per ton of steel, thus allowing
significant and sustainable savings on anthracite.
Twin designs, comparing correlations in monozygotic (MZ) versus dizygotic (DZ) twins, have an extensive history. One major confounder in such studies is that MZ twins may share postnatal environmental influences more so than do DZ twins. To avoid such confounding, twins separated at or soon after birth have been studied, but their scarcity often makes this approach impractical. Another method has been to measure the degree of contact twins have maintained over time, and adjust the observed correlations. Here, we remove confounding by utilizing the discrepancy between biological and self-perceived zygosity to separate environmental from genetic sources of twin similarity. We analyzed dietary patterns and physiologic traits in 350 female twin pairs of the 1988 Kaiser Permanente Twin Registry. Among twin pairs, 175 were MZ by self-report and genetic testing (MZC), 136 were DZ by self-report and genetic testing (DZC), 30 were MZ by genetic testing but not by self-report (MZW), and 9 were DZ by genetic testing but not by self-report (DZW) but were excluded due to small sample size. For healthy food patterns, MZC and MZW intraclass correlations were similar and greater than for DZC, yielding positive and significant heritability estimates. For unhealthy food patterns, the MZC, MZW and DZC correlations were similar with no significant heritability. For physiologic traits, MZC and MZW correlations were similar and higher than those for DZC, indicating significant heritability, except for insulin for which MZW and DZC were similar and which showed modest heritability. Twins of mistaken zygosity (TOMZ) provides a useful approach to robust determination of heritability.
New emissions regulations will increase the need for compact, inexpensive sensors for monitoring and control of automotive exhaust gas pollutants. Species of interest include hydrocarbons, carbon monoxide, and oxides of nitrogen (NOx). The current work is directed towards the development of fast, high sensitivity electrochemical NOx sensors for automotive diesel applications. We have investigated potentiometric NO sensors with good sensitivity and fast response when operated in 10% O2. The sensors consist of yttria-stabilized zirconia substrates attached with NiCr2O4 sensing electrodes and Pt reference electrodes. A composite NiCr2O4:Rh sensing electrode is shown to give significantly faster response than NiCr2O4 alone. The exact role of the Rh in enhancing the response speed is not clear at present. However, the Rh appears to accumulate at the contacts between the NiCr2O4 particles and may enhance the inter-particle electronic conduction. Ongoing testing of these sensors is being performed to elucidate the sensing mechanisms and to quantify cross sensitivity to, for example, NO2.