a practical tool to implement hospital-based syndromic surveillance: SCM

Background: syndromic surveillance has been widely used for the early warning of infectious disease outbreaks, especially in mass gatherings, but the collection of electronic data on symptoms in hospitals is one of the fundamental challenges that must be overcome during operating a syndromic surveillance system. The objective of our study is to describe and evaluate the implementation of a symptom-clicking-module (SCM) as a part of the enhanced hospital-based syndromic surveillance during the 41st World Exposition in Shanghai, China, 2010.Methods: the SCM, including 25 targeted symptoms, was embedded in the sentinels’ Hospital Information Systems (HIS). The clinicians used SCM to record these information of all the visiting patients, and data were collated and transmitted automatically in daily batches. The symptoms were categorized into seven targeted syndromes using pre-defined criteria, and statistical algorithms were applied to detect temporal aberrations in the data series.Results: SCM was deployed successfully in each sentinel hospital and was operated during the 184-day surveillance period. A total of 1,730,797 patient encounters were recorded by SCM, and 6.1 % (105,352 visits) met the criteria of the seven targeted syndromes. Acute respiratory and gastrointestinal syndromes were reported most frequently, accounted for 92.1 % of reports in all syndromes, and the aggregated time-series presented an obvious day-of-week variation over the study period. In total, 191 aberration signals were triggered, and none of them were identified as outbreaks after verification and field investigation.Conclusions: SCM has acted as a practical tool for recording symptoms in the hospital-based enhanced syndromic surveillance system during the 41st World Exposition in Shanghai, in the context of without a preexisting electronic tool to collect syndromic data in the HIS of the sentinel hospitals

Tailoring the surface of perovskite through in situ growth of Ru/RuO2 nanoparticles as robust symmetrical electrodes for reversible solid oxide cells

Although numerous perovskite oxides can enhance the electrochemical activity via exsolved metallic nanoparticles on the surface, most of them can only be applied as catalysts in a reducing atmosphere. These nanoparticles cause serious performance degradation in oxidizing conditions due to the formation of low-conductive metal oxides. This poses a big challenge to the design of highly active catalysts of electrochemical devices, especially for symmetrical solid oxide cells. Herein, based on the strategy of exsolved metallic nanoparticles in A-site deficient perovskite, a unique and simple method is demonstrated for the synthesis of Ru/RuO2 nanoparticles on the surface of perovskite oxide via in situ growth. The electrode material (La0.75Sr0.25)0.9Cr0.5Mn0.45Ru0.05O3−δ (LSCMR) is designed through careful choice of composition and the core idea is to make use of the exsolved nanoparticles concept applied for the first time at both hydrogen electrode and oxygen electrode for symmetrical solid oxide cells. Inspired by exsolved Ru and RuO2, the surface-decorated LSCMR exhibits significantly enhanced electrochemical activity for both H2 and O2, respectively, accompanied by high redox long-term stability. Moreover, simple, low-cost, and environmental-friendly synthesis of Ru/RuO2 nanoparticles on the substrate of typical perovskites is realized with this in situ growth approach

Temperature fluctuation and acute myocardial infarction in Beijing: an extended analysis of temperature ranges and differences

PurposeFew studies examined the relationship between temperature fluctuation metrics and acute myocardial infarction (AMI) hospitalizations within a single cohort. We aimed to expand knowledge on two basic measures: temperature range and difference.MethodsWe conducted a time-series analysis on the correlations between temperature range (TR), daily mean temperature differences (DTDmean), and daily mean-maximum/minimum temperature differences (TDmax/min) and AMI hospitalizations, using data between 2013 and 2016 in Beijing, China. The effects of TRn and DTDmeann over n-day intervals were compared, respectively. Subgroup analysis by age and sex was performed.ResultsA total of 81,029 AMI hospitalizations were included. TR1, TDmax, and TDmin were associated with AMI in J-shaped patterns. DTDmean1 was related to AMI in a U-shaped pattern. These correlations weakened for TR and DTDmean with longer exposure intervals. Extremely low (1st percentile) and high (5°C) DTDmean1 generated cumulative relative risk (CRR) of 2.73 (95% CI: 1.56–4.79) and 2.15 (95% CI: 1.54–3.01). Extremely high TR1, TDmax, and TDmin (99th percentile) correlated with CRR of 2.00 (95% CI: 1.73–2.85), 1.71 (95% CI: 1.40–2.09), and 2.73 (95% CI: 2.04–3.66), respectively. Those aged 20–64 had higher risks with large TR1, TDmax, and TDmin, while older individuals were more affected by negative DTDmean1. DTDmean1 was associated with a higher AMI risk in females.ConclusionTemperature fluctuations were linked to increased AMI hospitalizations, with low-temperature extremes having a more pronounced effect. Females and the older adult were more susceptible to daily mean temperature variations, while younger individuals were more affected by larger temperature ranges

Fenofibrate Inhibits Cytochrome P450 Epoxygenase 2C Activity to Suppress Pathological Ocular Angiogenesis

Neovascular eye diseases including retinopathy of prematurity, diabetic retinopathy and age-related-macular-degeneration are major causes of blindness. Fenofibrate treatment in type 2 diabetes patients reduces progression of diabetic retinopathy independent of its peroxisome proliferator-activated receptor (PPAR)α agonist lipid lowering effect. The mechanism is unknown. Fenofibrate binds to and inhibits cytochrome P450 epoxygenase (CYP)2C with higher affinity than to PPARα. CYP2C metabolizes ω-3 long-chain polyunsaturated fatty acids (LCPUFAs). While ω-3 LCPUFA products from other metabolizing pathways decrease retinal and choroidal neovascularization, CYP2C products of both ω-3 and ω-6 LCPUFAs promote angiogenesis. We hypothesized that fenofibrate inhibits retinopathy by reducing CYP2C ω-3 LCPUFA (and ω-6 LCPUFA) pro-angiogenic metabolites. Fenofibrate reduced retinal and choroidal neovascularization in PPARα-/-mice and augmented ω-3 LCPUFA protection via CYP2C inhibition. Fenofibrate suppressed retinal and choroidal neovascularization in mice overexpressing human CYP2C8 in endothelial cells and reduced plasma levels of the pro-angiogenic ω-3 LCPUFA CYP2C8 product, 19,20-epoxydocosapentaenoic acid. 19,20-epoxydocosapentaenoic acid reversed fenofibrate-induced suppression of angiogenesis ex vivo and suppression of endothelial cell functions in vitro. In summary fenofibrate suppressed retinal and choroidal neovascularization via CYP2C inhibition as well as by acting as an agonist of PPARα. Fenofibrate augmented the overall protective effects of ω-3 LCPUFAs on neovascular eye diseases

PPARα is essential for retinal lipid metabolism and neuronal survival

Background: Peroxisome proliferator activated receptor-alpha (PPARα) is a ubiquitously expressed nuclear receptor. The role of endogenous PPARα in retinal neuronal homeostasis is unknown. Retinal photoreceptors are the highest energy-consuming cells in the body, requiring abundant energy substrates. PPARα is a known regulator of lipid metabolism, and we hypothesized that it may regulate lipid use for oxidative phosphorylation in energetically demanding retinal neurons. Results: We found that endogenous PPARα is essential for the maintenance and survival of retinal neurons, with Pparα -/- mice developing retinal degeneration first detected at 8 weeks of age. Using extracellular flux analysis, we identified that PPARα mediates retinal utilization of lipids as an energy substrate, and that ablation of PPARα ultimately results in retinal bioenergetic deficiency and neurodegeneration. This may be due to PPARα regulation of lipid transporters, which facilitate the internalization of fatty acids into cell membranes and mitochondria for oxidation and ATP production. Conclusion: We identify an endogenous role for PPARα in retinal neuronal survival and lipid metabolism, and furthermore underscore the importance of fatty acid oxidation in photoreceptor survival. We also suggest PPARα as a putative therapeutic target for age-related macular degeneration, which may be due in part to decreased mitochondrial efficiency and subsequent energetic deficits. Electronic supplementary material The online version of this article (doi:10.1186/s12915-017-0451-x) contains supplementary material, which is available to authorized users

Solution-processed blue/deep blue and white phosphorescent organic light emitting diodes (PhOLEDs) hosted by a polysiloxane derivative with pendant mCP (1, 3-bis(9-carbazolyl)benzene)

The synthesis and characterization is reported of an efficient polysiloxane derivative containing the 1,3-bis(9-carbazolyl)benzene (mCP) moiety as a pendant unit on the polysiloxane backbone. In comparison with mCP, the mCP-polysiloxane hybrid (PmCPSi) has significantly improved thermal and morphological stabilities with a high decomposition temperature (Td = 523 °C) and glass transition temperature (Tg = 194 °C). The silicon–oxygen linkage of PmCPSi prevents intermolecular π-stacking and ensures a high triplet energy level (ET = 3.0 eV). Using PmCPSi as a host, blue phosphorescent organic light emitting devices (PhOLEDs) effectively confine triplet excitons, with efficient energy transfer to the guest emitter and a relatively low turn-on voltage of 5.8 V. A maximum external quantum efficiency of 9.24% and maximum current efficiency of 18.93 cd/A are obtained. These values are higher than for directly analogous poly(vinylcarbazole) (PVK) based devices (6.76%, 12.29 cd/A). Good color stability over a range of operating voltages is observed. A two-component “warm-white” device with a maximum current efficiency of 10.4 cd/A is obtained using a blend of blue and orange phosphorescent emitters as dopants in PmCPSi host. These results demonstrate that well-designed polysiloxane derivatives are highly efficient hosts suitable for low-cost solution-processed PhOLEDs

Photoreceptor glucose metabolism determines normal retinal vascular growth

Abstract The neural cells and factors determining normal vascular growth are not well defined even though vision‐threatening neovessel growth, a major cause of blindness in retinopathy of prematurity (ROP) (and diabetic retinopathy), is driven by delayed normal vascular growth. We here examined whether hyperglycemia and low adiponectin (APN) levels delayed normal retinal vascularization, driven primarily by dysregulated photoreceptor metabolism. In premature infants, low APN levels correlated with hyperglycemia and delayed retinal vascular formation. Experimentally in a neonatal mouse model of postnatal hyperglycemia modeling early ROP, hyperglycemia caused photoreceptor dysfunction and delayed neurovascular maturation associated with changes in the APN pathway; recombinant mouse APN or APN receptor agonist AdipoRon treatment normalized vascular growth. APN deficiency decreased retinal mitochondrial metabolic enzyme levels particularly in photoreceptors, suppressed retinal vascular development, and decreased photoreceptor platelet‐derived growth factor (Pdgfb). APN pathway activation reversed these effects. Blockade of mitochondrial respiration abolished AdipoRon‐induced Pdgfb increase in photoreceptors. Photoreceptor knockdown of Pdgfb delayed retinal vascular formation. Stimulation of the APN pathway might prevent hyperglycemia‐associated retinal abnormalities and suppress phase I ROP in premature infants