42 research outputs found

    Colour assessment outcomes – a new approach to grading the severity of color vision loss

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    INTRODUCTION: Recent studies have shown that a significant percentage of subjects with anomalous, congenital trichromacy can perform the suprathreshold, colour-related tasks encountered in many occupations with the same accuracy as normal trichromats. In the absence of detailed, occupation-specific studies, an alternative approach is to make use of new findings and the statistical outcomes of past practices that have been considered safe to produce graded, justifiable categories of colour vision that can be enforced. METHODS: We analyzed traditional color assessment outcomes and measured severity of colour vision loss using the CAD test in 1363 subjects (336 normals, 705 deutan, 319 protan and 3 tritan). The severity of colour vision loss was measured in each subject and statistical, pass / fail outcomes established for each of the most commonly used, conventional colour assessment tests and protocols. RESULTS: The correlation between the number of Ishihara (IH) test plates subjects fail and the severity of RG colour vision loss was very poor. The 38 plates IH test has high sensitivity when no errors are allowed (i.e., only 0.71% deutans and 0.63% protans pass). Protocols based on zero errors are uncommon since 18.15% of normal trichromats fail. The most common protocols employ either the 24 or the 14 plates editions with two or less errors. These protocols pass almost all normal trichromats, but the deutans and some protans that also pass (when two or less errors are allowed) can be severely deficient. This is simply because the most challenging plates have not been included in the 24 and 14 plates editions. As a result, normals no longer fail, but the deutans and protans that pass have more severe loss of colour vision since they fail less challenging plates. The severity of colour vision loss was measured in each subject and statistical, pass / fail outcomes established for each of the most commonly used, conventional colour assessment tests and protocols. DISCUSSION: Historical evidence and new findings that relate severity of loss to the effective use of colour signals in a number of tasks provide the basis for a new colour grading system based on six categories. A single colour assessment test is needed to establish the applicant’s Colour Vision category which can range from ‘supernormal’ (CV0), for the most stringent, colour-demanding tasks, to ‘severe colour deficiency’, when red / green colour vision is either absent or extremely weak (CV5)

    Arabidopsis COP1 shapes the temporal pattern of CO accumulation conferring a photoperiodic flowering response

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    The transcriptional regulator CONSTANS (CO) promotes flowering of Arabidopsis under long summer days (LDs) but not under short winter days (SDs). Post-translational regulation of CO is crucial for this response by stabilizing the protein at the end of a LD, whereas promoting its degradation throughout the night under LD and SD. We show that mutations in CONSTITUTIVE PHOTOMORPHOGENIC 1 (COP1), a component of a ubiquitin ligase, cause extreme early flowering under SDs, and that this is largely dependent on CO activity. Furthermore, transcription of the CO target gene FT is increased in cop1 mutants and decreased in plants overexpressing COP1 in phloem companion cells. COP1 and CO interact in vivo and in vitro through the C-terminal region of CO. COP1 promotes CO degradation mainly in the dark, so that in cop1 mutants CO protein but not CO mRNA abundance is dramatically increased during the night. However, in the morning CO degradation occurs independently of COP1 by a phytochrome B-dependent mechanism. Thus, COP1 contributes to day length perception by reducing the abundance of CO during the night and thereby delaying flowering under SDs

    Effects of Anacetrapib in Patients with Atherosclerotic Vascular Disease

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    BACKGROUND: Patients with atherosclerotic vascular disease remain at high risk for cardiovascular events despite effective statin-based treatment of low-density lipoprotein (LDL) cholesterol levels. The inhibition of cholesteryl ester transfer protein (CETP) by anacetrapib reduces LDL cholesterol levels and increases high-density lipoprotein (HDL) cholesterol levels. However, trials of other CETP inhibitors have shown neutral or adverse effects on cardiovascular outcomes. METHODS: We conducted a randomized, double-blind, placebo-controlled trial involving 30,449 adults with atherosclerotic vascular disease who were receiving intensive atorvastatin therapy and who had a mean LDL cholesterol level of 61 mg per deciliter (1.58 mmol per liter), a mean non-HDL cholesterol level of 92 mg per deciliter (2.38 mmol per liter), and a mean HDL cholesterol level of 40 mg per deciliter (1.03 mmol per liter). The patients were assigned to receive either 100 mg of anacetrapib once daily (15,225 patients) or matching placebo (15,224 patients). The primary outcome was the first major coronary event, a composite of coronary death, myocardial infarction, or coronary revascularization. RESULTS: During the median follow-up period of 4.1 years, the primary outcome occurred in significantly fewer patients in the anacetrapib group than in the placebo group (1640 of 15,225 patients [10.8%] vs. 1803 of 15,224 patients [11.8%]; rate ratio, 0.91; 95% confidence interval, 0.85 to 0.97; P=0.004). The relative difference in risk was similar across multiple prespecified subgroups. At the trial midpoint, the mean level of HDL cholesterol was higher by 43 mg per deciliter (1.12 mmol per liter) in the anacetrapib group than in the placebo group (a relative difference of 104%), and the mean level of non-HDL cholesterol was lower by 17 mg per deciliter (0.44 mmol per liter), a relative difference of -18%. There were no significant between-group differences in the risk of death, cancer, or other serious adverse events. CONCLUSIONS: Among patients with atherosclerotic vascular disease who were receiving intensive statin therapy, the use of anacetrapib resulted in a lower incidence of major coronary events than the use of placebo. (Funded by Merck and others; Current Controlled Trials number, ISRCTN48678192 ; ClinicalTrials.gov number, NCT01252953 ; and EudraCT number, 2010-023467-18 .)
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