Correcting the chromatic anisometropia of red-green glasses and its effect on stereoaccuracy

Negative effects on stereoaccuracy induced by commonly used red-green filters have been a subject of recent investigation1. This study was designed to determine if correcting, with lenses, the chromatic anisometropia induced by these red-green filters could increase the accuracy of stereopsis. The lens power difference needed to correct the chromatic anisometropia was found to be 0.37°, divided between the two eyes. In the control condition the subjects viewed the Randot Circle Stereotest with only the required polarizing glasses. One of the remaining two test conditions used the polarizers in combination with red-green filters, while for the other condition the chromatic anisometropia from the red-green filters was corrected with appropriate lenses. The amount of light transmitted by the filters was kept constant. The chromatic anisometropia correction over the red-green filters significantly reduced stereopsis errors induced by the red-green filters alone (21%, p \u3c 0.05). However, the correction only partially restored stereopsis to control values. A mild anisometropic correction added to the red-green glasses could help improve stereopsis in most individuals

Arrhythmias and Sudden Death among Older Children and Young Adults Following Tetralogy of F allot Repair in the Current Era: Are Previously Reported Risk Factors Still Applicable?

Background Young adult patients (pts) with repaired tetralogy of F allot ( TOF ) remain at risk for arrhythmias ( A r) and sudden cardiac death ( SCD ). Based on past studies with earlier pt subsets, A r/ SCD events were associated with right ventricular ( RV ) systolic pressures >60 mm Hg, outflow tract gradients >20 mm Hg, and QRS duration >180 ms. However, there are limited recent studies to evaluate these risk factors in the current patient generation. Methods Patients with TOF followed over the past 50 years were grouped by presence of any arrhythmias (group 1), absence of arrhythmias (group 2), and presence of SCD or significant ventricular arrhythmias (group 3) and correlated with current pt age, gender, age at repair, repair types, echocardiogram, cardiac magnetic resonance imaging, electrocardiogram/ H olter, hemodynamics, and electrophysiology findings. Results Of 109 pts, 52 were male aged 17–58 years. Of these, 59 (54%) had A r, two of whom had SCD . These 59 pts were chronologically older at the time of analysis, with repair at an older age and wider QRS duration (78–240, mean 158 ms) when compared with those without A r. However, there was no correlation with surgical era, surgical repair, gender, RV pressure >60 mm Hg, right ventricular outflow tract gradient >20 mm Hg, or RV end‐diastolic volume on CMRI . Conclusions A r/ SCD risk continues to correlate with repair age and advancing pt age. QRS duration is longer in these patients but at a shorter interval (mean 158 ms) and less RV pressure (mean 43 mm Hg) than previously reported. In the current TOF patient generation, neither surgical era, type of repair, RV outflow gradient nor RV volume correlate with A r/ SCD . Electrophysiologic testing to verify and identify arrhythmias remains clinically effective.Peer Reviewedhttp://deepblue.lib.umich.edu/bitstream/2027.42/108615/1/chd12153.pd

Accountability and Transparency of Entrepreneurial Journalism: Unresolved ethical issues in crowdfunded journalism projects

Crowdfunding is a new business model in which journalists rely—and depend—on (micro-) payments by a large number of supporters to finance their reporting. In this form of entrepreneurial journalism the roles of publisher, fundraiser and journalist often overlap. This raises questions about conflicts of interest, accountability and transparency. The article presents the results of selected case studies in four different European countries—Germany (Krautreporter), Italy (Occhidellaguerra), the United Kingdom (Contributoria) and the Netherlands (De Correspondent)—as well as one US example (Kickstarter). The study used a two-step methodological approach: first a content analysis of the websites and the Twitter accounts with regard to practices of media accountability, transparency and user participation was undertaken. The aim was to investigate how far ethical challenges in crowdfunded entrepreneurial journalism are accounted for. Second, we present findings from semi-structured interviews with journalists from each crowdfunding. The study provides evidence about the ethical issues in this area, particularly in relation to production transparency and responsiveness. The study also shows that in some cases of crowdfunding (platforms), accountability is outsourced and implemented only through the audience participation

Genetic defects of GDF6 in the zebrafish out of sight mutant and in human eye developmental anomalies

Contains fulltext : 88522.pdf (publisher's version ) (Open Access)BACKGROUND: The size of the vertebrate eye and the retina is likely to be controlled at several stages of embryogenesis by mechanisms that affect cell cycle length as well as cell survival. A mutation in the zebrafish out of sight (out) locus results in a particularly severe reduction of eye size. The goal of this study is to characterize the outm233 mutant, and to determine whether mutations in the out gene cause microphthalmia in humans. RESULTS: In this study, we show that the severe reduction of eye size in the outm233 mutant is caused by a mutation in the zebrafish gdf6a gene. Despite the small eye size, the overall retinal architecture appears largely intact, and immunohistochemical studies confirm that all major cell types are present in outm233 retinae. Subtle cell fate and patterning changes are present predominantly in amacrine interneurons. Acridine orange and TUNEL staining reveal that the levels of apoptosis are abnormally high in outm233 mutant eyes during early neurogenesis. Mutation analysis of the GDF6 gene in 200 patients with microphthalmia revealed amino acid substitutions in four of them. In two patients additional skeletal defects were observed. CONCLUSIONS: This study confirms the essential role of GDF6 in the regulation of vertebrate eye size. The reduced eye size in the zebrafish outm233 mutant is likely to be caused by a transient wave of apoptosis at the onset of neurogenesis. Amino acid substitutions in GDF6 were detected in 4 (2%) of 200 patients with microphthalmia. In two patients different skeletal defects were also observed, suggesting pleitrophic effects of GDF6 variants. Parents carrying these variants are asymptomatic, suggesting that GDF6 sequence alterations are likely to contribute to the phenotype, but are not the sole cause of the disease. Variable expressivity and penetrance suggest a complex non-Mendelian inheritance pattern where other genetic factors may influence the outcome of the phenotype

Supercoiling of an excised genomic island represses effector gene expression to prevent activation of host resistance

The plant pathogen Pseudomonas syringae pv. phaseolicola, which causes halo blight disease of beans, contains a 106kb genomic island PPHGI-1. PPHGI-1 carries a gene, avrPphB, which encodes an effector protein that triggers a resistance response in certain bean cultivars. Previous studies have shown that when PPHGI-1 is excised from the bacterial chromosome avrPphB is down regulated and therefore the pathogen avoids triggering the host’s defence mechanism. Here we investigate whether the down regulation of avrPphB is caused by supercoiling of PPHGI-1. We also investigate the effect of a PPHGI-1 encoded type 1A topoisomerase, TopB3, on island stability and the bacterial pathogenicity in the plant. Supercoiling inhibitors significantly increased the expression of avrPphB but did not affect the excision of PPHGI-1. An insertional mutant of topB3 displayed an increase in avrPphB expression and an increase in PPHGI-1 excision as well as reduced population growth in resistant and susceptible cultivars of bean. These results suggest an important role for topoisomerases in the maintenance and stability of a bacterial encoded genomic island and demonstrate that supercoiling is involved in the down regulation of an effector gene once the island has been excised, allowing the pathogen to prevent further activation of the host defence response

The genetics and neuropathology of frontotemporal lobar degeneration

Frontotemporal lobar degeneration (FTLD) is a heterogeneous group of disorders characterized by disturbances of behavior and personality and different types of language impairment with or without concomitant features of motor neuron disease or parkinsonism. FTLD is characterized by atrophy of the frontal and anterior temporal brain lobes. Detailed neuropathological studies have elicited proteinopathies defined by inclusions of hyperphosphorylated microtubule-associated protein tau, TAR DNA-binding protein TDP-43, fused-in-sarcoma or yet unidentified proteins in affected brain regions. Rather than the type of proteinopathy, the site of neurodegeneration correlates relatively well with the clinical presentation of FTLD. Molecular genetic studies identified five disease genes, of which the gene encoding the tau protein (MAPT), the growth factor precursor gene granulin (GRN), and C9orf72 with unknown function are most frequently mutated. Rare mutations were also identified in the genes encoding valosin-containing protein (VCP) and charged multivesicular body protein 2B (CHMP2B). These genes are good markers to distinguish underlying neuropathological phenotypes. Due to the complex landscape of FTLD diseases, combined characterization of clinical, imaging, biological and genetic biomarkers is essential to establish a detailed diagnosis. Although major progress has been made in FTLD research in recent years, further studies are needed to completely map out and correlate the clinical, pathological and genetic entities, and to understand the underlying disease mechanisms. In this review, we summarize the current state of the rapidly progressing field of genetic, neuropathological and clinical research of this intriguing condition

A large genome-wide association study of age-related macular degeneration highlights contributions of rare and common variants.

This is the author accepted manuscript. The final version is available from Nature Publishing Group via http://dx.doi.org/10.1038/ng.3448Advanced age-related macular degeneration (AMD) is the leading cause of blindness in the elderly, with limited therapeutic options. Here we report on a study of >12 million variants, including 163,714 directly genotyped, mostly rare, protein-altering variants. Analyzing 16,144 patients and 17,832 controls, we identify 52 independently associated common and rare variants (P < 5 × 10(-8)) distributed across 34 loci. Although wet and dry AMD subtypes exhibit predominantly shared genetics, we identify the first genetic association signal specific to wet AMD, near MMP9 (difference P value = 4.1 × 10(-10)). Very rare coding variants (frequency <0.1%) in CFH, CFI and TIMP3 suggest causal roles for these genes, as does a splice variant in SLC16A8. Our results support the hypothesis that rare coding variants can pinpoint causal genes within known genetic loci and illustrate that applying the approach systematically to detect new loci requires extremely large sample sizes.We thank all participants of all the studies included for enabling this research by their participation in these studies. Computer resources for this project have been provided by the high-performance computing centers of the University of Michigan and the University of Regensburg. Group-specific acknowledgments can be found in the Supplementary Note. The Center for Inherited Diseases Research (CIDR) Program contract number is HHSN268201200008I. This and the main consortium work were predominantly funded by 1X01HG006934-01 to G.R.A. and R01 EY022310 to J.L.H

An analysis of Naval officers serving on joint duty: the impact of the 1986 Goldwater-Nichols Act

The purpose of this thesis is to examine trends in the quality of officers assigned to joint duty and analyze the effect of joint assignments on an officer's career. This study examines officers appearing before the 1988-1994 Commander and Captain promotion boards. Results of cross tabulations indicate qualitative differences between officers receiving the JS2 before and after 1 October 1989. Officers receiving the JS2 after 1 October 1989 demonstrated significantly higher performance (as measured by fitness report data) than officers receiving a JS2 prior to 1 October 1989. Officers receiving the JS5 were of higher quality than average, regardless of the date of the AQD. This study also examines the effects of joint duty on an officer's likelihood of promotion, and compares the results across four warfare communities: SWO, SUB, PILOT, and NFO. The results indicate that SWOs and NFOs receiving a JS2 designator prior to 1989 have a lower probability of promotion to Commander. Conversely, SWOs receiving a JS2 designator after 1 October 1989 have a significantly higher probability of promotion to Commander. The effect of a JS2 on promotion to Captain is largely statistically insignificant. The effect of a JS5 on promotion to Commander is positive for SWOs appearing before the 1990-94 promotion boards and NFOs appearing before the 1988-90 promotion boards. The effect of a JS5 on promotion to Captain is positive for SWOs appearing before the 1988-90 promotion boards, and for Pilots appearing before all Captain promotion boards.http://archive.org/details/annalysisofnaval1094532173NAU.S. Navy (U.S.N.) authorApproved for public release; distribution is unlimited