Paper as Object

The formulation of my thesis rests upon the proposition of paper as object. Paper, a three-dimensional plastic material, can be made to act as form as well as surface. By macerating bits of cotton or linen cloth a fine paper pulp can be produced. This paper pulp can then be cast into molds, sheets or be hand manipulated. Color, texture, thickness and strength can be controlled by the artist. It has been my concern to develop a personal image by using the material of rag paper pulp. The work in this exhibit concerns itself with exaggerated edges (deckles) which serve as a symbol of traditionally hand-made paper. The paper is cast extremely thick and thus contains many layers fused together. This is a subtle expression of one of the primary concerns of the image, that is, the image of layering. &nbsp;</p

Acanthaster planci Outbreak: Decline in Coral Health, Coral Size Structure Modification and Consequences for Obligate Decapod Assemblages

Although benthic motile invertebrate communities encompass the vast majority of coral reef diversity, their response to habitat modification has been poorly studied. A variety of benthic species, particularly decapods, provide benefits to their coral host enabling them to cope with environmental stressors, and as a result benefit the overall diversity of coral-associated species. However, little is known about how invertebrate assemblages associated with corals will be affected by global perturbations, (either directly or indirectly via their coral host) or their consequences for ecosystem resilience. Analysis of a ten year dataset reveals that the greatest perturbation at Moorea over this time was an outbreak of the corallivorous sea star Acanthaster planci from 2006 to 2009 impacting habitat health, availability and size structure of Pocillopora spp. populations and highlights a positive relationship between coral head size and survival. We then present the results of a mensurative study in 2009 conducted at the end of the perturbation (A. planci outbreak) describing how coral-decapod communities change with percent coral mortality for a selected coral species, Pocillopora eydouxi. The loss of coral tissue as a consequence of A. planci consumption led to an increase in rarefied total species diversity, but caused drastic modifications in community composition driven by a shift from coral obligate to non-obligate decapod species. Our study highlights that larger corals left with live tissue in 2009, formed a restricted habitat where coral obligate decapods, including mutualists, could subsist. We conclude that the size structure of Pocillopora populations at the time of an A. planci outbreak may greatly condition the magnitude of coral mortality as well as the persistence of local populations of obligate decapods

Design and baseline characteristics of the finerenone in reducing cardiovascular mortality and morbidity in diabetic kidney disease trial

Background: Among people with diabetes, those with kidney disease have exceptionally high rates of cardiovascular (CV) morbidity and mortality and progression of their underlying kidney disease. Finerenone is a novel, nonsteroidal, selective mineralocorticoid receptor antagonist that has shown to reduce albuminuria in type 2 diabetes (T2D) patients with chronic kidney disease (CKD) while revealing only a low risk of hyperkalemia. However, the effect of finerenone on CV and renal outcomes has not yet been investigated in long-term trials. Patients and Methods: The Finerenone in Reducing CV Mortality and Morbidity in Diabetic Kidney Disease (FIGARO-DKD) trial aims to assess the efficacy and safety of finerenone compared to placebo at reducing clinically important CV and renal outcomes in T2D patients with CKD. FIGARO-DKD is a randomized, double-blind, placebo-controlled, parallel-group, event-driven trial running in 47 countries with an expected duration of approximately 6 years. FIGARO-DKD randomized 7,437 patients with an estimated glomerular filtration rate >= 25 mL/min/1.73 m(2) and albuminuria (urinary albumin-to-creatinine ratio >= 30 to <= 5,000 mg/g). The study has at least 90% power to detect a 20% reduction in the risk of the primary outcome (overall two-sided significance level alpha = 0.05), the composite of time to first occurrence of CV death, nonfatal myocardial infarction, nonfatal stroke, or hospitalization for heart failure. Conclusions: FIGARO-DKD will determine whether an optimally treated cohort of T2D patients with CKD at high risk of CV and renal events will experience cardiorenal benefits with the addition of finerenone to their treatment regimen. Trial Registration: EudraCT number: 2015-000950-39; ClinicalTrials.gov identifier: NCT02545049

Discovery and functional prioritization of Parkinson's disease candidate genes from large-scale whole exome sequencing.

BACKGROUND: Whole-exome sequencing (WES) has been successful in identifying genes that cause familial Parkinson's disease (PD). However, until now this approach has not been deployed to study large cohorts of unrelated participants. To discover rare PD susceptibility variants, we performed WES in 1148 unrelated cases and 503 control participants. Candidate genes were subsequently validated for functions relevant to PD based on parallel RNA-interference (RNAi) screens in human cell culture and Drosophila and C. elegans models. RESULTS: Assuming autosomal recessive inheritance, we identify 27 genes that have homozygous or compound heterozygous loss-of-function variants in PD cases. Definitive replication and confirmation of these findings were hindered by potential heterogeneity and by the rarity of the implicated alleles. We therefore looked for potential genetic interactions with established PD mechanisms. Following RNAi-mediated knockdown, 15 of the genes modulated mitochondrial dynamics in human neuronal cultures and four candidates enhanced α-synuclein-induced neurodegeneration in Drosophila. Based on complementary analyses in independent human datasets, five functionally validated genes-GPATCH2L, UHRF1BP1L, PTPRH, ARSB, and VPS13C-also showed evidence consistent with genetic replication. CONCLUSIONS: By integrating human genetic and functional evidence, we identify several PD susceptibility gene candidates for further investigation. Our approach highlights a powerful experimental strategy with broad applicability for future studies of disorders with complex genetic etiologies

Response of coral obligate and non-obligate decapod species to the loss of live coral tissue.

<p>White diamonds and discontinuous line = non-obligate decapod species richness <i>y</i> = −0.0012<i>x</i>²−0.0737<i>x</i>+21.739; <i>R²</i> = 0.85, N = 82, <i>p</i><0.001. Black diamonds and continuous line = coral obligate decapod species richness: <i>y</i> = −0.0013<i>x</i>²+0.1951<i>x</i>+0.5189 ; <i>R²</i> = 0.69, N = 82, <i>p</i><0.001.</p

Ordination plots representing the composition of decapod communities with the loss of coral tissue.

<p>Non-metric multidimensional scaling plots were computed using Jaccard, an incidence based metric (A) and Bray-Curtis, an abundance based metric (B). Light grey, dark grey and black dots represent non-eaten, partially eaten and dead <i>Pocillopora</i> respectively. Mean ± SE beta diversity (average distance to group centroid) is plotted below the corresponding ordination plot (C and D).</p

Proportion of coral that survived the 2006–2009 outbreak of <i>A. planci</i> for each coral size class.

<p>Survival for each size class was calculated from (the number of live and partially dead <i>Pocillopora</i> in 2008–2009)/(the number of live and partially dead <i>Pocillopora</i> in 2005–2006)×100. Counts of <i>Pocillopora</i> at the three study sites were combined. Linear regression: <i>y</i> = 6.14<i>x</i>; <i>R²</i> = 0.61, N = 11, <i>p</i> = 0.002.</p

Effect of the loss of live coral tissue on overall decapod species richness.

<p>(A) Total decapod species richness: polynomial regression, <i>y</i> = −0.0025<i>x</i>²+0.1214<i>x</i>+22.258; <i>R²</i> = 0.72, N = 82, <i>p</i><0.001. (B) Rarefied total decapod species richness: polynomial regression, <i>y</i> = −0.0012<i>x</i>²+0.0746<i>x</i>+10.352; <i>R²</i> = 0.67, N = 82, <i>p</i><0.001.</p

Effects of a recent outbreak of <i>Acanthaster planci</i> from 2006–2009 on <i>Pocillopora</i> populations.

<p>Size-class (cm²) distributions of live (white), partially dead (grey) and completely dead (black) corals (<i>Pocillopora</i> spp.) as a proportion of the total number of coral heads at each site. High resolution photographs of 60 permanent quadrats were taken at three sites in Moorea (20 quadrats/site) every two years from 2000 to 2008 at the sites Vaipahu and Haapiti and from 2001–2009 at Tiahura. Numbers in parentheses represent the total number of <i>Pocillopora</i> measured per site.</p

A Susceptibility Locus for Migraine with Aura, on Chromosome 4q24

Migraine is a complex neurovascular disorder with substantial evidence supporting a genetic contribution. Prior attempts to localize susceptibility loci for common forms of migraine have not produced conclusive evidence of linkage or association. To date, no genomewide screen for migraine has been published. We report results from a genomewide screen of 50 multigenerational, clinically well-defined Finnish families showing intergenerational transmission of migraine with aura (MA). The families were screened using 350 polymorphic microsatellite markers, with an average intermarker distance of 11 cM. Significant evidence of linkage was found between the MA phenotype and marker D4S1647 on 4q24. Using parametric two-point linkage analysis and assuming a dominant mode of inheritance, we found for this marker a maximum LOD score of 4.20 under locus homogeneity (P=.000006) or locus heterogeneity (P=.000011). Multipoint parametric (HLOD = 4.45; P=.0000058) and nonparametric (NPL(all) = 3.43; P=.0007) analyses support linkage in this region. Statistically significant linkage was not observed in any other chromosomal region