Evolutionary biology - Geography and skin colour

Nature (Impact Factor: 42.35). 06/2005; 435(7040):283-4. DOI: 10.1038/435283a
Source: PubMed

ABSTRACT Human skin comes in many different shades. Recent studies of geographical differences in skin colour open up the subject scientifically by offering sophisticated accounts of the basis of this variation.

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    ABSTRACT: The diversity of notation permeating the publications on signal processing suggests the need for some consolidation and standardization. We advocate here the array theory and notation of Tait as a standardizing framework for a smooth transition from the vector-matrix era to the array domain and array processing era. A duality between array domain and matrix domain operations blends the flexibility and power of the array domain with the compactness and overview attributes of matrix expressions. The notation facilitates tractability through the super- and subscript patterns for the indices and the range set of the indices. We introduce fundamentals from Tait's work with some consolidation and exemplify notation and manipulations. The relevance for signal processing is demonstrated more fully in a companion paper [8].
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    ABSTRACT: To investigate the association of combined MTHFR C677T and A1298C gene polymorphisms with congenital heart diseases (CHD) in Egyptian children and their mothers and to determine their effect on homocysteine level in these children. MTHFR C677T and A1298C polymorphisms were genotyped in 160 Egyptian children (80 patients with CHD and 80 healthy controls) and their mothers using polymerase chain reaction restriction fragment length polymorphism (PCR-RFLP), while, homocysteine (Hcy) level was measured optically by enzymatic method. We found that MTHFR 677 TT genotype, T allele and 1298 CC genotype, C allele were associated with 2.61, 2.0, 2.91and 1.99 fold increased risk of CHD in Egyptian children respectively. Furthermore, the frequencies of MTHFR 1298AC, CC genotypes and C allele significantly increased in mothers with CHD affected children. The homocysteine levels were significantly increased in MTHFR 677 TT and 1298 CC genotypes in children with CHD. Our study demonstrated an association of MTHFR A1298C polymorphisms with CHD in Egyptian children and their mothers, while, MTHFR C677T polymorphisms were significantly associated with the risk of CHD in the children only. An association between combined MTHFR A1298C and C677T polymorphisms and CHD was recorded in the children and their mothers. Also, homocysteine levels were significantly increased with both MTHFR 677 TT and 1298 CC genotypes in Egyptian children with CHD.
    Gene 08/2013; DOI:10.1016/j.gene.2013.07.053 · 2.08 Impact Factor
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    ABSTRACT: Tyrosinase, the rate-limiting enzyme required for melanin production, has often been targeted to develop active brightening/lightening materials for skin care products. Since unexpected depigmentation of the skin characterized by diverse symptoms was reported in some subjects who used a tyrosinase-competitive inhibiting quasi-drug, rhododendrol, its mechanism of action has been investigated using more than a dozen melanocyte cell lines derived from donors of different ethnic backgrounds. Parallel to the observation of rhododendrol-induced melanocyte damage at a certain threshold of tyrosinase activity, treatment with a tyrosinase-specific siRNA was shown to dramatically rescue the rhododendrol-induced melanocyte cytotoxicity. Additionally, hydroxyl-rhododendrol was detected only in melanocytes with higher tyrosinase activity by liquid chromatography-tandem mass spectrometry whereas no relationship between an increase in reactive oxygen species levels in melanocytes and their tolerance to rhododendrol was found. Consistently, when an equivalent amount of hydroxyl-rhododendrol was administered, cell growth was almost equally suppressed even in melanocytes with lower tyrosinase activity. Taken together, these data suggest that the generation of a tyrosinase-catalyzed hydroxyl-metabolite is one of the causes for the decreased melanocyte viability causedby rhododendrol.
    Journal of Dermatological Science 10/2014; 76(1). DOI:10.1016/j.jdermsci.2014.07.001 · 3.34 Impact Factor