The kinetics of growth for chemical deposition of
normalCdS
films from alkaline solutions of cadmium salts has been studied with respect to temperature of deposition and the relative concentrations of the various reactants in the solution. It has been established that the growth of the film takes place either by ion‐by‐ion condensation of Cd+2 and S−2 ions or by adsorption of colloidal particles of
normalCdS
formed in the solution, depending on the various deposition parameters and the method of preparation. The former process of growth results in thin, hard, adherent and specularly reflecting films, whereas the latter results in thick, powdery and diffusely reflecting films. Occurrence of different polymorphic phases of
normalCdS
(hexagonal and cubic) has been observed under different growth conditions. A model for growth mechanism has also been proposed.
The authors performed a meta-analysis to estimate the magnitude of polymorphism effects for the complement component C3 gene (C3) and their possible mode of action on age-related macular degeneration (AMD). The meta-analysis included 16 and 7 studies for rs2230199 and rs1047286, respectively. Data extraction and risk of bias assessments were performed in duplicate, and heterogeneity and publication bias were explored. There was moderate evidence for association between both polymorphisms and AMD in Caucasians. For rs2230199, patients with CG and GG genotypes were 1.44 (95% confidence interval (CI): 1.33, 1.56) and 1.88 (95% CI: 1.59, 2.23) times more likely to have AMD than patients with the CC genotype. For rs1047286, GA and AA genotypes had 1.27 (95% CI: 1.15, 1.41) and 1.70 (95% CI: 1.27, 2.11) times higher risk of AMD than did GG genotypes. These gene effects suggested an additive model. The population attributable risks for the GG/GC and AA/GA genotypes are approximately 5%-10%. Subgroup analysis by ethnicity indicates that these variants are very infrequent in Asians and that the observed gene effects are based largely on the high frequency within Caucasian populations. This meta-analysis supports the association between C3 and AMD and provides a robust estimate of the genetic risk.
Macular degenerations, inherited and age related, are important causes of vision loss. Human genetic studies have suggested perturbation of the complement system is important in the pathogenesis of age-related macular degeneration. The mechanisms underlying the involvement of the complement system are not understood, although complement and inflammation have been implicated in drusen formation. Drusen are an early clinical hallmark of inherited and age-related forms of macular degeneration. We studied one of the earliest stages of macular degeneration which precedes and leads to the formation of drusen, i.e. the formation of basal deposits. The studies were done using a mouse model of the inherited macular dystrophy Doyne Honeycomb Retinal Dystrophy/Malattia Leventinese (DHRD/ML) which is caused by a p.Arg345Trp mutation in EFEMP1. The hallmark of DHRD/ML is the formation of drusen at an early age, and gene targeted Efemp1(R345W/R345W) mice develop extensive basal deposits. Proteomic analyses of Bruch's membrane/choroid and Bruch's membrane in the Efemp1(R345W/R345W) mice indicate that the basal deposits comprise normal extracellular matrix (ECM) components present in abnormal amounts. The proteomic analyses also identified significant changes in proteins with immune-related function, including complement components, in the diseased tissue samples. Genetic ablation of the complement response via generation of Efemp1(R345W/R345W):C3(-/-) double-mutant mice inhibited the formation of basal deposits. The results demonstrate a critical role for the complement system in basal deposit formation, and suggest that complement-mediated recognition of abnormal ECM may participate in basal deposit formation in DHRD/ML and perhaps other macular degenerations.
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