No abstract

A mammalian-like melanopsin (Opn4m) has been found in all major vertebrate classes except reptile. Since the pupillary light reflex (PLR) of the fresh water turtle takes between 5 and 10 min to achieve maximum constriction, and since photosensitive retinal ganglion cells (ipRGCs) in mammals use Opn4m to control their slow sustained pupil responses, we hypothesized that a Opn4m homolog exists in the retina of the turtle. To identify its presence, retinal tissue was dissected from seven turtles, and total RNA extracted. Reverse transcriptase-polymerase chain reactions (RT-PCRs) were carried out to amplify gene sequences using primers targeting the highly conserved core region of Opn4m, and PCR products were analyzed by gel electrophoresis and sequenced. Sequences derived from a 1004-bp PCR product were compared to those stored in GenBank by the basic local alignment search tool (BLAST) algorithm and returned significant matches to several Opn4ms from other vertebrates including chicken. Quantitative real-time PCR (qPCR) was also carried out to compare expression levels of Opn4m in different tissues. The normalized expression level of Opn4m in the retina was higher in comparison to other tissue types: iris, liver, lung, and skeletal muscle. The results suggest that Opn4m exists in the retina of the turtle and provides a possible explanation for the presence of a slow PLR. The turtle is likely to be a useful model for further understanding the photoreceptive mechanisms in the retina which control the dynamics of the PLR.

Surveys of almost 1,500 members of three professional societies that do risk analysis (e.g. environmental economics, epidemiology, exposure assessment, industrial hygiene, toxicology) found that 3 in 10 respondents had observed a biased research design, 2 in 10 had observed plagiarism, and 1 in 10 observed data fabrication or falsification. Respondents with many years in risk analysis, business consultants, and industrial hygienists reported the greatest prevalence of misconduct. These respondents perceived poor science, economic implications of the research, and lack of training in ethics as causes of misconduct. They supported the teaching of ethics but the vast majority did not support government auditing of their work.

This study analyzed the luminance and color emmetropization response in chicks treated with the nonselective parasympathetic antagonist atropine and the sympathetic β-receptor blocker timolol. Chicks were binocularly exposed (8hr/day) for four days to one of three illumination conditions: 2 Hz sinusoidal luminance flicker, 2 Hz sinusoidal blue/yellow color flicker, or steady light (mean 680 lux). Atropine experiments involved monocular daily injections of either 20 μl of atropine (18 nmol) or 20 μl of phosphate-buffered saline. Timolol experiments involved monocular daily applications of 2 drops of 0.5% timolol or 2 drops of distilled H2O. Changes in the experimental eye were compared with those in the fellow eye after correction for the effects of saline/water treatments. Atropine caused a reduction in axial length with both luminance flicker (−0.078 ± 0.021 mm) and color flicker (−0.054 ± 0.017 mm), and a reduction in vitreous chamber depth with luminance flicker (−0.095 ± 0.023 mm), evoking a hyperopic shift in refraction (3.40 ± 1.77 D). Timolol produced an increase in axial length with luminance flicker (0.045 ± 0.030 mm) and a myopic shift in refraction (−4.07 ± 0.92 D), while color flicker caused a significant decrease in axial length (−0.046 ± 0.017 mm) that was associated with choroidal thinning (−0.046 ± 0.015 mm). The opposing effects on growth and refraction seen with atropine and timolol suggest a balancing mechanism between the parasympathetic and β-receptor mediated sympathetic system through stimulation of the retina with luminance and color contrast.

No abstract