The Emergence of Commercial Scale Offshore Wind: Progress Made and Challenges Ahead

This Article examines the offshore wind development process from leasing and permitting to electric power supply and interconnection. Willing developers may divide the process into three discrete, but not necessarily sequential, endeavors. First, the developer must secure a viable purchaser or market for the output. “Offshore wind energy” is a more complex commercial product than one might envision—it includes the actual electric energy produced, the electric generating capacity that is available to serve load, and both the environmental and clean energy attributes of wind energy. The environmental and clean energy attributes may have an economic and regulatory value separate from, or in addition to, the value of the electric energy itself. These separate complexities give rise to several questions: What are the available markets for actual offshore wind energy? How does a developer find a buyer (off-taker) for the offshore wind electric output? How are the markets for the actual energy and the environmental attributes, normally embodied in a “renewable energy certificate” (REC), combined or otherwise related? How much control can individual states exercise over the decisions of an individual utility or other purchasers of offshore wind energy and RECs (or each of them separately)? If the average cost to the developer of electric energy generation from offshore wind per kilowatt-hour (kWh) is substantially higher than the average cost of energy in the onshore markets, what features of state regulation or policy facilitate the sale? Second, the developer must secure, or acquire by sale or assignment, appropriate offshore sites for development of the physical resource. Most available offshore wind resources are located in the OCS and will be under federal control for leasing. Developers must secure OCS leases either through successful bids in the initial offering or through a later acquisition or assignment from winning bidders. Offshore wind development requires large areas within which to erect the number of turbines needed, as well as a gathering system of cables and substations, to collect and deliver the output of all the turbines via transmission lines to interconnections with the existing mainland grid. The developer also must obtain rights-of-way to lay cable for its gathering and transmission facilities—on the OCS and across state submerged lands and coastal areas. In the alternative, a new offshore wind transmission system may be built by a third party to connect with multiple wind farms and deliver energy to an onshore point of interconnection. These leasing and project configuration scenarios present many questions. If the offshore wind developer and the transmission facility developer are separate entities, how much coordination is required? What is the appropriate scope of environmental impact studies needed in connection with the OCS leasing process? What are the mechanics for acquiring the necessary property rights and leases between winning bidders and other interested developers? Third, the offshore wind developer, alone or with a third-party transmission developer, must be concerned about the interconnection of the offshore cable to the onshore transmission grid. Most onshore transmission and distribution grids were planned, constructed and operated on the assumption that electricity consumers on the coast are the end of the delivery line. While transmission grids are somewhat more robust at these isolated coastal locations—particularly when large nuclear and fossil generation exists at water’s edge—these more robust coastal grid systems are limited and may be neither geographically nor electrically proximate to offshore wind generation locations. With advances in turbine technology and the overall economics of offshore wind farm development most proposed commercial-scale projects are likely to have generation capacity in the hundreds of megawatts (MWs). Typically, interconnection of offshore wind and related transmission delivery facilities require not only reconfiguration and enlargement of the receiving onshore transmission grid to accept the input of such electric capacity at water’s edge, but also delivery to load centers that may be located a substantial distance inland. Owners of the onshore grid may not be the same as the utility purchaser or other off-taker of the offshore electric energy. The complexities of onshore interconnection raise vexing questions, such as: (i) how to reconfigure and enlarge the grid to interconnect with offshore generation, accept the energy output, and deliver to load centers; and (ii) who should bear the costs of that reconfiguration and enlargement. This Article is intended to provide a helpful roadmap or guidance for major issues in three principal areas—securing a viable purchaser, siting the offshore development farm, and onshore interconnection of the offshore cable. To date, most offshore wind development efforts in the United States occur off the Northeast and Mid-Atlantic coast. This Article highlights the emerging federal-state dynamic in the development of offshore wind generation and illuminates several key uncertainties developers face today

Cognitive function in a middle aged cohort is related to higher quality dietary pattern 5 and 25 years earlier: The cardia study

Preserving cognitive function is an important public health issue. We investigated whether dietary pattern associates with cognitive function in middle-age

Is telomere length socially patterned? Evidence from the West of Scotland Twenty-07 study

Lower socioeconomic status (SES) is strongly associated with an increased risk of morbidity and premature mortality, but it is not known if the same is true for telomere length, a marker often used to assess biological ageing. The West of Scotland Twenty-07 Study was used to investigate this and consists of three cohorts aged approximately 35 (N = 775), 55 (N = 866) and 75 years (N = 544) at the time of telomere length measurement. Four sets of measurements of SES were investigated: those collected contemporaneously with telomere length assessment, educational markers, SES in childhood and SES over the preceding twenty years. We found mixed evidence for an association between SES and telomere length. In 35-year-olds, many of the education and childhood SES measures were associated with telomere length, i.e. those in poorer circumstances had shorter telomeres, as was intergenerational social mobility, but not accumulated disadvantage. A crude estimate showed that, at the same chronological age, social renters, for example, were nine years (biologically) older than home owners. No consistent associations were apparent in those aged 55 or 75. There is evidence of an association between SES and telomere length, but only in younger adults and most strongly using education and childhood SES measures. These results may reflect that childhood is a sensitive period for telomere attrition. The cohort differences are possibly the result of survival bias suppressing the SES-telomere association; cohort effects with regard different experiences of SES; or telomere possibly being a less effective marker of biological ageing at older ages

Cardiovascular Health through Young Adulthood and Cognitive Functioning in Midlife

To examine the association between overall cardiovascular health as recently defined by the American Heart Association in young adulthood to middle-age and cognitive function in midlife. Overall ideal cardiovascular health incorporates 7 metrics, including the avoidance of overweight or obesity, a healthful diet, nonsmoking, and physical activity, total cholesterol, blood pressure, and fasting glucose at goal levels

Hypoxia Due to Cardiac Arrest Induces a Time-Dependent Increase in Serum Amyloid β Levels in Humans

Amyloid β (Aβ) peptides are proteolytic products from amyloid precursor protein (APP) and are thought to play a role in Alzheimer disease (AD) pathogenesis. While much is known about molecular mechanisms underlying cerebral Aβ accumulation in familial AD, less is known about the cause(s) of brain amyloidosis in sporadic disease. Animal and postmortem studies suggest that Aβ secretion can be up-regulated in response to hypoxia. We employed a new technology (Single Molecule Arrays, SiMoA) capable of ultrasensitive protein measurements and developed a novel assay to look for changes in serum Aβ42 concentration in 25 resuscitated patients with severe hypoxia due to cardiac arrest. After a lag period of 10 or more hours, very clear serum Aβ42 elevations were observed in all patients. Elevations ranged from approximately 80% to over 70-fold, with most elevations in the range of 3–10-fold (average approximately 7-fold). The magnitude of the increase correlated with clinical outcome. These data provide the first direct evidence in living humans that ischemia acutely increases Aβ levels in blood. The results point to the possibility that hypoxia may play a role in the amyloidogenic process of AD

C-Reactive Protein and Genetic Variants and Cognitive Decline in Old Age: The PROSPER Study

Background: Plasma concentrations of C-reactive protein (CRP), a marker of chronic inflammation, have been associated with cognitive impairment in old age. However, it is unknown whether CRP is causally linked to cognitive decline. Methods and Findings: Within the Prospective Study of Pravastatin in the Elderly at Risk (PROSPER) trial, with 5680 participants with a mean age of 75 years, we examined associations of CRP levels and its genetic determinants with cognitive performance and decline over 3.2 years mean follow-up. Higher plasma CRP concentrations were associated with poorer baseline performance on the Stroop test (P = 0.001) and Letter Digit Tests (P, 0.001), but not with the immediate and delayed Picture Learning Test (PLT; both P>0.5). In the prospective analyses, higher CRP concentrations associated with increased rate of decline in the immediate PLT (P = 0.016), but not in other cognitive tests (all p>0.11). Adjustment for prevalent cardiovascular risk factors and disease did not change the baseline associations nor associations with cognitive decline during follow-up. Four haplotypes of CRP were used and, compared to the common haplotype, carrierships associated strongly with levels of CRP (all P < 0.007). In comparison to strong associations of apolipoprotein E with cognitive measures, associations of CRP haplotypes with such measures were inconsistent. Conclusion: Plasma CRP concentrations associate with cognitive performance in part through pathways independent of (risk factors for) cardiovascular disease. However, lifelong exposure to higher CRP levels does not associate with poorer cognitive performance in old age. The current data weaken the argument for a causal role of CRP in cognitive performance, but further study is warranted to draw definitive conclusions

Functional Expression of Human Adenine Nucleotide Translocase 4 in Saccharomyces Cerevisiae

The adenine nucleotide translocase (ANT) mediates the exchange of ADP and ATP across the inner mitochondrial membrane. The human genome encodes multiple ANT isoforms that are expressed in a tissue-specific manner. Recently a novel germ cell-specific member of the ANT family, ANT4 (SLC25A31) was identified. Although it is known that targeted depletion of ANT4 in mice resulted in male infertility, the functional biochemical differences between ANT4 and other somatic ANT isoforms remain undetermined. To gain insight into ANT4, we expressed human ANT4 (hANT4) in yeast mitochondria. Unlike the somatic ANT proteins, expression of hANT4 failed to complement an AAC-deficient yeast strain for growth on media requiring mitochondrial respiration. Moreover, overexpression of hANT4 from a multi-copy plasmid interfered with optimal yeast growth. However, mutation of specific amino acids of hANT4 improved yeast mitochondrial expression and supported growth of the AAC-deficient yeast on non-fermentable carbon sources. The mutations affected amino acids predicted to interact with phospholipids, suggesting the importance of lipid interactions for function of this protein. Each mutant hANT4 and the somatic hANTs exhibited similar ADP/ATP exchange kinetics. These data define common and distinct biochemical characteristics of ANT4 in comparison to ANT1, 2 and 3 providing a basis for study of its unique adaptation to germ cells

Global regulation of alternative splicing during myogenic differentiation

Recent genome-wide analyses have elucidated the extent of alternative splicing (AS) in mammals, often focusing on comparisons of splice isoforms between differentiated tissues. However, regulated splicing changes are likely to be important in biological transitions such as cellular differentiation, or response to environmental stimuli. To assess the extent and significance of AS in myogenesis, we used splicing-sensitive microarray analysis of differentiating C2C12 myoblasts. We identified 95 AS events that undergo robust splicing transitions during C2C12 differentiation. More than half of the splicing transitions are conserved during differentiation of avian myoblasts, suggesting the products and timing of transitions are functionally significant. The majority of splicing transitions during C2C12 differentiation fall into four temporal patterns and were dependent on the myogenic program, suggesting that they are integral components of myogenic differentiation. Computational analyses revealed enrichment of many sequence motifs within the upstream and downstream intronic regions near the alternatively spliced regions corresponding to binding sites of splicing regulators. Western analyses demonstrated that several splicing regulators undergo dynamic changes in nuclear abundance during differentiation. These findings show that within a developmental context, AS is a highly regulated and conserved process, suggesting a major role for AS regulation in myogenic differentiation.National Institutes of Health (U.S.) (grant number R01GM076493)Ford Foundation (Predoctoral Diversity Fellowship)Baylor College of Medicine. Graduate School of Biomedical Sciences (Baylor Research Advocates for Student Scientists

Functional Implication of Dp71 in Osmoregulation and Vascular Permeability of the Retina

Functional alterations of Müller cells, the principal glia of the retina, are an early hallmark of most retina diseases and contribute to their further progression. The molecular mechanisms of these reactive Müller cell alterations, resulting in disturbed retinal homeostasis, remain largely unknown. Here we show that experimental detachment of mouse retina induces mislocation of the inwardly rectifying potassium channels (Kir4.1) and a downregulation of the water channel protein (AQP4) in Müller cells. These alterations are associated with a strong decrease of Dp71, a cytoskeleton protein responsible for the localization and the clustering of Kir4.1 and AQP4. Partial (in detached retinas) or total depletion of Dp71 in Müller cells (in Dp71-null mice) impairs the capability of volume regulation of Müller cells under osmotic stress. The abnormal swelling of Müller cells In Dp71-null mice involves the action of inflammatory mediators. Moreover, we investigated whether the alterations in Müller cells of Dp71-null mice may interfere with their regulatory effect on the blood-retina barrier. In the absence of Dp71, the retinal vascular permeability was increased as compared to the controls. Our results reveal that Dp71 is crucially implicated in the maintenance of potassium homeostasis, in transmembraneous water transport, and in the Müller cell-mediated regulation of retinal vascular permeability. Furthermore, our data provide novel insights into the mechanisms of retinal homeostasis provided by Müller cells under normal and pathological conditions

Association of anthropometry and weight change with risk of dementia and its major subtypes : A meta-analysis consisting 2.8 million adults with 57 294 cases of dementia

Uncertainty exists regarding the relation of body size and weight change with dementia risk. As populations continue to age and the global obesity epidemic shows no sign of waning, reliable quantification of such associations is important. We examined the relationship of body mass index, waist circumference, and annual percent weight change with risk of dementia and its subtypes by pooling data from 19 prospective cohort studies and four clinical trials using meta-analysis. Compared with body mass index-defined lower-normal weight (18.5-22.4 kg/m(2)), the risk of all-cause dementia was higher among underweight individuals but lower among those with upper-normal (22.5-24.9 kg/m(2)) levels. Obesity was associated with higher risk in vascular dementia. Similarly, relative to the lowest fifth of waist circumference, those in the highest fifth had nonsignificant higher vascular dementia risk. Weight loss was associated with higher all-cause dementia risk relative to weight maintenance. Weight gain was weakly associated with higher vascular dementia risk. The relationship between body size, weight change, and dementia is complex and exhibits non-linear associations depending on dementia subtype under scrutiny. Weight loss was associated with an elevated risk most likely due to reverse causality and/or pathophysiological changes in the brain, although the latter remains speculative.Peer reviewe