127 research outputs found

    Eyelid development, fusion and subsequent reopening in the mouse

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    The process of eyelid development was studied in the mouse. The critical events occur between about 15.5 d postcoitum (p.c.) and 12 d after birth, and were studied by conventional histology and by scanning electron microscopy. At about 15.5 d p.c. the cornea of the eye is clearly visible with the primitive eyelids being represented by protruding ridges of epithelium at its periphery. Over the next 24 h, eyelid development proceeds to the stage when the cornea is completely covered by the fused eyelids. Periderm cells stream in to fill the gap between the developing eyelids. Their proliferative activity is such that they produce a cellular excrescence on the outer surface of the line of fusion of the eyelids. This excrescence had almost disappeared by about 17.5 d p.c. Keratinisation is first evident at this stage on the surface of the eyelids and passes continuously from one eyelid to the other. Evidence of epidermal differentiation is more clearly seen in the newborn, where a distinctive stratum granulosum now occupies about one third of its entire thickness. Within the subjacent dermis, hair follicles are differentiating. By about 5 d after birth, a thick layer of keratin extends without interruption across the junctional region. While a noticeable surface indentation overlies the latter, a similar depression is only seen on the conjunctival surface by about 10 d after birth. Keratinisation is also observed to extend in from the epidermal surface to involve the entire region between the 2 eyelids at about this time.(ABSTRACT TRUNCATED AT 250 WORDS

    Morphometric study of the optic nerve of adult normal mice and mice heterozygous for the Small eye mutation (Sey/+)

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    The Small eye (Sey) gene, which has been mapped to chromosome 2 in the mouse, is known to cause variable malformations of the eye and nose. The effect of the gene in the heterozygous state is mainly on the eye. A combined electron microscopy and morphometric analysis of the optic nerve in adult littermates with a normal (+/+) and heterozygous mutant (Sey/+) genotype was carried out. The optic nerve could be dissected from the posterior pole of the eyeball to the optic chiasma in all the mice examined. The results of morphometric analyses carried out in this study show that the Sey gene indirectly affects the normal morphogenesis of the optic nerve in the heterozygous mutant Sey male mouse to a significant degree compared with its male normal littermate. The heterozygous mutant Sey female mouse is also affected, but not significantly so when compared with its normal female littermate. The mean nerve cross-sectional area and mean nerve fibre counts for the Sey strain are lower than those observed in other strains of mice that have been studied. The nerve fibre densities and the spectrum of nerve fibre sizes encountered are, however, similar to those seen in other strains of mice. We believe that the findings indicate that the smaller mean nerve fibre counts observed in the heterozygous mutant (Sey/+) mice compared to their normal (+/+) siblings is unlikely to have resulted from primary retinal dysgenesis, but is a consequence of the reduced size of their neural retina, and total retinal ganglion cell population

    Adaptive model-driven user interface development systems

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    Adaptive user interfaces (UIs) were introduced to address some of the usability problems that plague many software applications. Model-driven engineering formed the basis for most of the systems targeting the development of such UIs. An overview of these systems is presented and a set of criteria is established to evaluate the strengths and shortcomings of the state-of-the-art, which is categorized under architectures, techniques, and tools. A summary of the evaluation is presented in tables that visually illustrate the fulfillment of each criterion by each system. The evaluation identified several gaps in the existing art and highlighted the areas of promising improvement

    Mouse SPNS2 Functions as a Sphingosine-1-Phosphate Transporter in Vascular Endothelial Cells

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    Sphingosine-1-phosphate (S1P), a sphingolipid metabolite that is produced inside the cells, regulates a variety of physiological and pathological responses via S1P receptors (S1P1–5). Signal transduction between cells consists of three steps; the synthesis of signaling molecules, their export to the extracellular space and their recognition by receptors. An S1P concentration gradient is essential for the migration of various cell types that express S1P receptors, such as lymphocytes, pre-osteoclasts, cancer cells and endothelial cells. To maintain this concentration gradient, plasma S1P concentration must be at a higher level. However, little is known about the molecular mechanism by which S1P is supplied to extracellular environments such as blood plasma. Here, we show that SPNS2 functions as an S1P transporter in vascular endothelial cells but not in erythrocytes and platelets. Moreover, the plasma S1P concentration of SPNS2-deficient mice was reduced to approximately 60% of wild-type, and SPNS2-deficient mice were lymphopenic. Our results demonstrate that SPNS2 is the first physiological S1P transporter in mammals and is a key determinant of lymphocyte egress from the thymus
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