scholarly journals Blue eyes, brittle bones

2021 ◽  
Vol 50 (6) ◽  
pp. 377-378
Author(s):  
Adam Morton
Keyword(s):  
Bone ◽  
2019 ◽  
Vol 127 ◽  
pp. 646-655 ◽  
Author(s):  
Yi Liu ◽  
Jianhai Wang ◽  
Shuo Liu ◽  
Mingjie Kuang ◽  
Yaqing Jing ◽  
...  

2021 ◽  
Vol 10 (7) ◽  
pp. 1444
Author(s):  
William Myles ◽  
Catherine Dunlop ◽  
Sally A. McFadden

Myopia will affect half the global population by 2050 and is a leading cause of vision impairment. High-dose atropine slows myopia progression but with undesirable side-effects. Low-dose atropine is an alternative. We report the effects of 0.01% or 0.005% atropine eye drops on myopia progression in 13 Australian children aged between 2 and 18 years and observed for 2 years without and up to 5 years (mean 2.8 years) with treatment. Prior to treatment, myopia progression was either ‘slow’ (more positive than −0.5D/year; mean −0.19D/year) or ‘fast’ (more negative than −0.5D/year; mean −1.01D/year). Atropine reduced myopic progression rates (slow: −0.07D/year, fast: −0.25D/year, combined: before: −0.74, during: −0.18D/year, p = 0.03). Rebound occurred in 3/4 eyes that ceased atropine. Atropine halved axial growth in the ‘Slow’ group relative to an age-matched model of untreated myopes (0.098 vs. 0.196mm/year, p < 0.001) but was double that in emmetropes (0.051mm/year, p < 0.01). Atropine did not slow axial growth in ‘fast’ progressors compared to the age-matched untreated myope model (0.265 vs. 0.245mm/year, p = 0.754, Power = 0.8). Adverse effects (69% of patients) included dilated pupils (6/13) more common in children with blue eyes (5/7, p = 0.04). Low-dose atropine could not remove initial myopia offsets suggesting treatment should commence in at-risk children as young as possible.


1985 ◽  
Vol 61 ◽  
Author(s):  
K. Nassau

ABSTRACTAll but two of the fifteen physical and chemical mechanisms which are necessary to explain all the varied causes of color apply in one way or another to glass. These fifteen causes of color derive from a variety of physical and chemical mechanisms and are summarized in five groups with concentration on those mechanisms that apply to glass and the related glazes and enamels. Vibrations and simple excitations explain the colors of incandescence (e.g. flames, hot glass), gas excitations (neon tube, aurora), and vibrations and rotations (blue ice, water, glasses based on water). Ligand field effect colors are seen in transition metal compounds (turquoise, chrome oxide green, glasses based on copper sulfate) and impurities (ruby, emerald, many doped glasses). Molecular orbitals explain the colors of organic compounds (indigo, chlorophyll, organic glasses) and charge transfer compounds (blue sapphire, lapis lazuli, “beer-bottle” brown and chromate glasses). Energy bands are involved in the colors of metals and alloys (gold, brass, glassy metals), of semiconductors (cadmium yellow, vermillion, chalcogenide glasses), doped semiconductors (blue and yellow diamond), and color centers (amethyst, topaz, irradiated glass). Geometrical and physical optics are involved in the colors derived from dispersive refraction (rainbow, green flash, glass prism spectrum), scattering (blue sky, blue eyes, red sunset, ruby gold and opal glasses), interference (soap bubbles, iridescent beetles, cracks in glasses, interference filters), and diffraction (the corona aureole, diffraction grating spectrum).


PEDIATRICS ◽  
1962 ◽  
Vol 29 (5) ◽  
pp. 714-728
Author(s):  
H. Ghadimi ◽  
M. W. Partington ◽  
A. Hunter

A 3-year-old girl with fair hair and blue eyes came under observation because of speech retardation. The patient was given a phenylalanine-free diet, since persistently positive urine tests with ferric chloride and reagent strips (Phenistix) were strongly suggestive of phenylketonuria. On further investigation she was found to be suffering from a totally different and not heretofore recognized condition, the salient features of which were an abnormally high concentration of histidine in the blood and an excessive output of histidine in the urine. The child's sister, one year older, presented the same metabolic anomaly. In each case both the concentration of histidine in plasma and the daily output were directly related to the amount of protein in the diet; but even at their lowest levels they greatly exceeded those of normal children of the same age. An oral load of histidine was followed by an increase of histidine in plasma much higher and more prolonged than that observed in controls, and by the excretion of a much larger fraction of the ingested dose. The urine of each sister contained not only excessive amounts of histidine but also notable quantities of imidazole-pyruvic, imidazole-acetic, and imidazole-lactic acid, histidine derivatives of which normal urine contains only traces. It is concluded that in the two sisters the normally predominant pathway of histidine catabolism, which leads through urocanic acid to glutamic acid, was partially or completely blocked. Since, even after histidine loading, the urines never contained detectable amounts of urocanic acid, the block must precede the formation of that substance. The condition presented is therefore due primarily to a deficiency or total lack of histidine-alpha-deaminase; the enzyme which converts histidine to urocanic acid. As a result of this defect histidine is forced to take the alternative but less efficient pathway which begins with its transamination to imidazole-pyruvic acid. This substance is the one responsible for positive reactions in the ferric chloride and Phenistix tests. All urine specimens examined, whether from the patient or from normal controls, contained considerable quantities of an unidentifiable imidazole compound ("X"), which does not appear to have been previously reported. The existence of this substance may call for some modification of current concepts of histidine metabolism in man.


2011 ◽  
Vol 27 (6) ◽  
pp. 609-613 ◽  
Author(s):  
Enrico Di Stasio ◽  
Daria Maggi ◽  
Enzo Berardesca ◽  
Georgiana Clare Marulli ◽  
Carla Bizzarri ◽  
...  

Science ◽  
1933 ◽  
Vol 77 (1990) ◽  
pp. 191-192
Author(s):  
Vilhjalmur Stefansson
Keyword(s):  

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