Enzymatic dyeing and functional finishing of textile fibres with ferulic acid

The catalyzed polymerization of ferulic acid (FA) by laccase from Rhus vernicifera has been studied, and its polymeric products are used for the dyeing and functional finishing of silk, wool, nylon, viscose and cotton fabrics by two methods, namely simultaneous enzymatic polymerization of FA and dyeing at 50 oC (one-step method), and enzymatic polymerization of FA at 50 oC followed by dyeing at 90 oC (two-step method). The analyses of UV-Visible and FTIR spectra show the formation of yellow poly(ferulic acid) (PFA) in which FA units are mainly linked together with C–C bonds. The colouration of PFA on fabrics occurs due to physical adsorption, and not because of interaction of covalent bond between PFA and fibres. The enzymatically dyed fabrics display yellow to orange colour hues, and pale to moderate colour depth, depending on fibre species and dyeing methods. The dyed fabrics show excellent rub fastness and staining fastness during washing, relatively weak light fastness and colour change fastness during washing; the two-step method shows better wash fastness ratings for colour change. The enzymatic dyeing of FA provides fabrics with multifunctional properties of antioxidant activity, UV-protection and deodorization

Detecting susceptibility genes for rheumatoid arthritis based on a novel sliding-window approach

With the recent rapid improvements in high-throughout genotyping techniques, researchers are facing a very challenging task of large-scale genetic association analysis, especially at the whole-genome level, without an optimal solution. In this study, we propose a new approach for genetic association analysis based on a variable-sized sliding-window framework. This approach employs principal component analysis to find the optimal window size. Using the bisection algorithm in window size searching, the proposed method tackles the exhaustive computation problem. It is more efficient and effective than currently available approaches. We conduct the genome-wide association study in Genetic Analysis Workshop 16 (GAW16) Problem 1 data using the proposed method. Our method successfully identified several susceptibility genes that have been reported by other researchers and additional candidate genes for follow-up studies

Human Mitochondrial tRNA Mutations in Maternally Inherited Deafness

AbstractMutations in mitochondrial tRNA genes have been shown to be associated with maternally inherited syndromic and non-syndromic deafness. Among those, mutations such as tRNALeu(UUR)3243A>G associated with syndromic deafness are often present in heteroplasmy, and the non-syndromic deafness-associated tRNA mutations including tRNASer(UCN)7445A>G are often in homoplasmy or in high levels of heteroplasmy. These tRNA mutations are the primary factors underlying the development of hearing loss. However, other tRNA mutations such as tRNAThr15927G>A and tRNASer(UCN)7444G>A are insufficient to produce a deafness phenotype, but always act in synergy with the primary mitochondrial DNA mutations, and can modulate their phenotypic manifestation. These tRNA mutations may alter the structure and function of the corresponding mitochondrial tRNAs and cause failures in tRNAs metabolism. Thereby, the impairment of mitochondrial protein synthesis and subsequent defects in respiration caused by these tRNA mutations, results in mitochondrial dysfunctions and eventually leads to the development of hearing loss. Here, we summarized the deafness-associated mitochondrial tRNA mutations and discussed the pathophysiology of these mitochondrial tRNA mutations, and we hope these data will provide a foundation for the early diagnosis, management, and treatment of maternally inherited deafness

PLA2G6-Associated Neurodegeneration (PLAN): Review of Clinical Phenotypes and Genotypes

Phospholipase A2 group VI (PLA2G6)-associated neurodegeneration (PLAN) includes a series of neurodegenerative diseases that result from the mutations in PLA2G6. PLAN has genetic and clinical heterogeneity, with different mutation sites, mutation types and ethnicities and its clinical phenotype is different. The clinical phenotypes and genotypes of PLAN are closely intertwined and vary widely. PLA2G6 encodes a group of VIA calcium-independent phospholipase A2 proteins (iPLA2β), an enzyme involved in lipid metabolism. According to the age of onset and progressive clinical features, PLAN can be classified into the following subtypes: infantile neuroaxonal dystrophy (INAD), atypical neuroaxonal dystrophy (ANAD) and parkinsonian syndrome which contains adult onset dystonia parkinsonism (DP) and autosomal recessive early-onset parkinsonism (AREP). In this review, we present an overview of PLA2G6-associated neurodegeneration in the context of current research