Optical and Infrared Spectroscopy

Contains research objectives and reports on one research project

Integration of Catalysis with Storage for the Design of Multi-Electron Photochemistry Devices for Solar Fuel

Decarbonization of the transport system and a transition to a new diversified energy system that is scalable and sustainable, requires a widespread implementation of carbon-neutral fuels. In biomimetic supramolecular nanoreactors for solar-to-fuel conversion, water-splitting catalysts can be coupled to photochemical units to form complex electrochemical nanostructures, based on a systems integration approach and guided by magnetic resonance knowledge of the operating principles of biological photosynthesis, to bridge between long-distance energy transfer on the short time scale of fluorescence, ~10−9 s, and short-distance proton-coupled electron transfer and storage on the much longer time scale of catalysis, ~10−3 s. A modular approach allows for the design of nanostructured optimized topologies with a tunneling bridge for the integration of storage with catalysis and optimization of proton chemical potentials, to mimic proton-coupled electron transfer processes in photosystem II and hydrogenase

School census autumn 2017 : 16 to 19 reports : user guide

The synthesis of a series of cobalt NHC complexes of the types [Co­(NHC)₂(CO)­(NO)] (NHC = <i>i</i>Pr₂Im (<b>2</b>), <i>n</i>Pr₂Im (<b>3</b>), Cy₂Im (<b>4</b>), Me₂Im (<b>5</b>), <i>i</i>Pr₂ImMe (<b>6</b>), Me₂ImMe (<b>7</b>), Me<i>i</i>PrIm (<b>8</b>), Me<i>t</i>BuIm (<b>9</b>); R₂Im = 1,3-dialkylimidazolin-2-ylidene) and [Co­(NHC)­(CO)₂(NO)] (NHC = <i>i</i>Pr₂Im (<b>13</b>), <i>n</i>Pr₂Im (<b>14</b>), Me₂Im (<b>15</b>), <i>i</i>Pr₂ImMe (<b>16</b>), Me₂ImMe (<b>17</b>), Me<i>i</i>PrIm (<b>18</b>), Me<i>t</i>BuIm (<b>19</b>)) from the reaction of the NHC with [Co­(CO)₃(NO)] (<b>1</b>) is reported. These complexes have been characterized using elemental analysis, IR spectroscopy, multinuclear NMR spectroscopy, and in many cases by X-ray crystallography. Bulky NHCs tend to form the mono-NHC-substituted complexes [Co­(NHC)­(CO)₂(NO)], even from the reaction with an stoichiometric excess of the NHC, as demonstrated by the synthesis of [Co­(Dipp₂Im)­(CO)₂(NO)] (<b>11</b>), [Co­(Mes₂Im)­(CO)₂(NO)] (<b>12</b>), and [Co­(^MecAAC)­(CO)₂(NO)] (<b>20</b>). For <i>t</i>Bu₂Im a preferred coordination via the NHC backbone (“abnormal” coordination at the 4-position) was observed and the complex [Co­(<i>t</i>Bu₂^aIm)­(CO)₂(NO)] (<b>10</b>) was isolated. All of these complexes are volatile, are stable upon sublimation and prolonged storage in the gas phase, and readily decompose at higher temperatures. Furthermore, DTA/TG analyses revealed that the complexes [Co­(NHC)₂(CO)­(NO)] are seemingly more stable toward thermal decomposition in comparison to the complexes [Co­(NHC)­(CO)₂(NO)]. We thus conclude that the cobalt complexes of the type [Co­(NHC)­(CO)₂(NO)] and [Co­(NHC)₂(CO)­(NO)] have potential for application as precursors in the vapor deposition of thin cobalt films

Genetic Loci Associated With Atrial Fibrillation: Relation to Left Atrial Structure in the Framingham Heart Study

Background: Atrial fibrillation (AF) results in significant morbidity and mortality. Genome‐wide association studies (GWAS) have identified genetic variants associated with AF. Whether genetic variants associated with AF are also associated with atrial structure, an intermediate phenotype for AF, has had limited investigation. We sought to investigate associations between single nucleotide polymorphisms (SNPs) and atrial structure obtained by cardiovascular imaging in the Framingham Heart Study. Methods and Results: We selected 11 SNPs that have been associated with AF in GWAS. We examined the SNPs' relations to cross‐sectional left atrial (LA) dimensions (determined by transthoracic echocardiography) and LA volume (determined by cardiovascular magnetic resonance [CMR]) employing linear regression. The total sample included 1555 participants with CMR LA volume (age 60±9 years, 53% women) and 6861 participants with echocardiographic LA diameter (age 48±13 years, 52% women) measured. We employed a significance threshold of P<0.0023 to account for multiple testing of the 11 SNPs and 2 LA measures. In a primary analysis, no SNPs were significantly related to the LA measures. Likewise, in secondary analyses excluding individuals with prevalent AF (n=77, CMR sample; n=105, echocardiography sample) no SNPs were related to LA volume or diameter. Conclusion: In a community‐based cohort, we did not identify a statistically significant association between selected SNPs associated with AF and measures of LA anatomy. Further investigations with larger longitudinally assessed samples and a broader array of SNPs may be necessary to determine the relation between genetic loci associated with AF and atrial structure

Association Between Frailty and Atrial Fibrillation in Older Adults: The Framingham Heart Study Offspring Cohort

Background: Frailty is associated bidirectionally with cardiovascular disease. However, the relations between frailty and atrial fibrillation (AF) have not been fully elucidated. Methods and Results: Using the FHS (Framingham Heart Study) Offspring cohort, we sought to examine both the association between frailty (2005-2008) and incident AF through 2016 and the association between prevalent AF and frailty status (2011-2014). Frailty was defined using the Fried phenotype. Models adjusted for age, sex, and smoking. Cox proportional hazards models, adjusted for competing risk of death, assessed the association between prevalent frailty and incident AF. Logistic regression models assessed the association between prevalent AF and new-onset frailty. For the incident AF analysis, we included 2053 participants (56% women; mean age, 69.7+/-6.9 years). By Fried criteria, 1018 (50%) were robust, 903 (44%) were prefrail, and 132 (6%) were frail. In total, 306 incident cases of AF occurred during an average 9.2 (SD, 3.1) follow-up years. After adjustment, there was no statistically significant association between prevalent frailty status and incident AF (prefrail versus robust: hazard ratio [HR], 1.22 [95% CI, 0.95-1.55]; frail versus robust: HR, 0.92 [95% CI, 0.57-1.47]). At follow-up, there were 111 new cases of frailty. After adjustment, there was no statistically significant association between prevalent AF and new-onset frailty (odds ratio, 0.48 [95% CI, 0.17-1.36]). Conclusions: Although a bidirectional association between frailty and cardiovascular disease has been suggested, we did not find evidence of an association between frailty and AF. Our findings may be limited by sample size and should be further explored in other populations

Atrial fibrillation without comorbidities: Prevalence, incidence and prognosis (from the Framingham Heart Study)

BACKGROUND: The epidemiology of atrial fibrillation (AF) without comorbidities, known as \u27lone AF\u27, is uncertain. Although it has been considered a benign condition, we hypothesized that it confers a worse prognosis compared with a matched sample without AF. METHODS: We described the proportion of AF without comorbidities (clinical, subclinical cardiovascular disease and triggers) among the entire AF sample in Framingham Heart Study (FHS). We compared AF without comorbidities with typical AF, and age-, sex- and cohort-matched individuals without AF, using Cox proportional hazards analysis in relation to combined cardiovascular events (stroke, heart failure, myocardial infarction), and mortality. RESULTS: Of 10,311 FHS participants, 1,961 were diagnosed with incident AF, among which 173 individuals had AF without comorbidities (47% women, mean age 71+/-12 years). AF without comorbidities had a prevalence of 1.7% of the entire cohort, and an annual incidence of 0.5 per 1000 person-years. During a median follow-up of 9.7 years after initial AF, 137 individuals with AF without comorbidities (79.2%) died and 141 individuals developed cardiovascular events (81.5%). AF without comorbidities had significantly lower mortality (HR 0.67, 95%CI 0.55-0.81, P \u3c .001) and total cardiovascular events (HR 0.66, 95% CI 0.55-0.80, P \u3c .001) compared with typical AF. However, mortality (HR1.43, 95% CI 1.18-1.75, P \u3c .001) and risk of total cardiovascular events (HR 1.73, 95% CI 1.39-2.16, P \u3c .001) were higher than age-, sex-, and cohort-matched individuals without AF. CONCLUSIONS: The risk of cardiovascular outcomes and mortality among individuals with AF without comorbidities is lower than typical AF, but is significantly elevated compared with matched individuals without AF

Challenges Facing the Implementation of Pico-Hydropower Technologies

840 million people living in rural areas across the world lack access to electricity, creating a large imbalance in the development potential between urban and rural areas. Pico-hydropower offers a cost-effective way of accessing electricity, where the resource exists. This paper discusses and critically examines several challenges that remain in implementing pico-hydropower systems, such as local manufacturing, maintenance and repair of turbines, low-head solutions, dealing with variation in the water flow between seasons, the ability to deal with income generating loads and low system power and capacity factor. The solutions to many of these problems exist; several low head turbine systems are appearing on the market, and new power electronic packages are able to improve the system capacity factor. Some turbines are now being designed for local construction using design for manufacturing rules, so only basic workshop tools and process are required to build turbine systems and components, and enabling turbines to be locally repaired. Through the commercialisation and implementation of these solutions, the proliferation of pico-hydropower systems can take place providing low cost sustainable electricity for remote communities, but this requires a stronger emphasis in social awareness and policy. Three critical enabling factors for the success of pico-hydropower projects are identified through this analysis: understanding the local context, financial sustainability and stakeholder awareness

Whole Blood Gene Expression and Atrial Fibrillation: The Framingham Heart Study

Background: Atrial fibrillation (AF) involves substantial electrophysiological, structural and contractile remodeling. We hypothesize that characterizing gene expression might uncover important pathways related to AF. Methods and Results: We performed genome-wide whole blood transcriptomic profiling (Affymetrix Human Exon 1.0 ST Array) of 2446 participants (mean age 66±9 years, 55% women) from the Offspring cohort of Framingham Heart Study. The study included 177 participants with prevalent AF, 143 with incident AF during up to 7 years follow up, and 2126 participants with no AF. We identified seven genes statistically significantly up-regulated with prevalent AF. The most significant gene, PBX1 (P = 2.8×10−7), plays an important role in cardiovascular development. We integrated differential gene expression with gene-gene interaction information to identify several signaling pathways possibly involved in AF-related transcriptional regulation. We did not detect any statistically significant transcriptomic associations with incident AF. Conclusion: We examined associations of gene expression with AF in a large community-based cohort. Our study revealed several genes and signaling pathways that are potentially involved in AF-related transcriptional regulation

Genetic risk prediction of atrial fibrillation

Background—Atrial fibrillation (AF) has a substantial genetic basis. Identification of individuals at greatest AF risk could minimize the incidence of cardioembolic stroke. Methods—To determine whether genetic data can stratify risk for development of AF, we examined associations between AF genetic risk scores and incident AF in five prospective studies comprising 18,919 individuals of European ancestry. We examined associations between AF genetic risk scores and ischemic stroke in a separate study of 509 ischemic stroke cases (202 cardioembolic [40%]) and 3,028 referents. Scores were based on 11 to 719 common variants (≥5%) associated with AF at P-values ranging from &lt;1x10-3 to &lt;1x10-8 in a prior independent genetic association study. Results—Incident AF occurred in 1,032 (5.5%) individuals. AF genetic risk scores were associated with new-onset AF after adjusting for clinical risk factors. The pooled hazard ratio for incident AF for the highest versus lowest quartile of genetic risk scores ranged from 1.28 (719 variants; 95%CI, 1.13-1.46; P=1.5x10-4) to 1.67 (25 variants; 95%CI, 1.47-1.90; P=9.3x10-15). Discrimination of combined clinical and genetic risk scores varied across studies and scores (maximum C statistic, 0.629-0.811; maximum ΔC statistic from clinical score alone, 0.009-0.017). AF genetic risk was associated with stroke in age- and sex-adjusted models. For example, individuals in the highest versus lowest quartile of a 127-variant score had a 2.49-fold increased odds of cardioembolic stroke (95%CI, 1.39-4.58; P=2.7x10-3). The effect persisted after excluding individuals (n=70) with known AF (odds ratio, 2.25; 95%CI, 1.20-4.40; P=0.01). Conclusions—Comprehensive AF genetic risk scores were associated with incident AF beyond associations for clinical AF risk factors, though offered small improvements in discrimination. AF genetic risk was also associated with cardioembolic stroke in age- and sex-adjusted analyses. Efforts are warranted to determine whether AF genetic risk may improve identification of subclinical AF or help distinguish between stroke mechanisms

Lifetime risk of atrial fibrillation according to optimal, borderline, or elevated levels of risk factors: cohort study based on longitudinal data from the Framingham Heart Study

OBJECTIVE: To examine the association between risk factor burdens-categorized as optimal, borderline, or elevated-and the lifetime risk of atrial fibrillation. DESIGN: Community based cohort study. SETTING: Longitudinal data from the Framingham Heart Study. PARTICIPANTS: Individuals free of atrial fibrillation at index ages 55, 65, and 75 years were assessed. Smoking, alcohol consumption, body mass index, blood pressure, diabetes, and history of heart failure or myocardial infarction were assessed as being optimal (that is, all risk factors were optimal), borderline (presence of borderline risk factors and absence of any elevated risk factor), or elevated (presence of at least one elevated risk factor) at index age. MAIN OUTCOME MEASURE: Lifetime risk of atrial fibrillation at index age up to 95 years, accounting for the competing risk of death. RESULTS: At index age 55 years, the study sample comprised 5338 participants (2531 (47.4%) men). In this group, 247 (4.6%) had an optimal risk profile, 1415 (26.5%) had a borderline risk profile, and 3676 (68.9%) an elevated risk profile. The prevalence of elevated risk factors increased gradually when the index ages rose. For index age of 55 years, the lifetime risk of atrial fibrillation was 37.0% (95% confidence interval 34.3% to 39.6%). The lifetime risk of atrial fibrillation was 23.4% (12.8% to 34.5%) with an optimal risk profile, 33.4% (27.9% to 38.9%) with a borderline risk profile, and 38.4% (35.5% to 41.4%) with an elevated risk profile. Overall, participants with at least one elevated risk factor were associated with at least 37.8% lifetime risk of atrial fibrillation. The gradient in lifetime risk across risk factor burden was similar at index ages 65 and 75 years. CONCLUSIONS: Regardless of index ages at 55, 65, or 75 years, an optimal risk factor profile was associated with a lifetime risk of atrial fibrillation of about one in five; this risk rose to more than one in three a third in individuals with at least one elevated risk factor