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KV Thomas 《Biofouling》2013,29(1):73-86
Antifouling paint booster biocides are a group of organic compounds added to antifouling paints to improve their efficacy. They have become prevalent since the requirement for alternative antifouling paints formulations for small boats (< 25 m). This need followed a ban on the use of triorganotin biocides in antifouling paints for small boats, in the late 1980's. Worldwide, around eighteen compounds are currently used as antifouling biocides, viz. benzmethylamide, chlorothalonil, copper pyrithione, dichlofluanid, diuron, fluorofolpet, Irgarol 1051, Sea‐Nine 211, Mancozeb, Polyphase, pyridine‐triphenyl‐borane, TCMS (2,3,5,6‐tetrachloro‐4‐methylsulfonyl) pyridine, TCMTB [2‐(thiocyanomethylthio)benzothia‐zole], Thiram, tolyfluanid, zinc pyrithione (ZPT), ziram and Zineb. Any booster biocide released into the environment is subjected to a complex set of processes. These processes include transport mechanisms, transformation, degradation, cross media partitioning, and bioaccumulation. This paper reviews the fate and behaviour data currently available in the public domain concerning antifouling paint booster biocides. 相似文献
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Background
The function of proteins is a direct consequence of their three-dimensional structure. The structural classification of proteins describes the ways of folding patterns all proteins could adopt. Although, the protein folds were described in many ways the functional properties of individual folds were not studied.Results
We have analyzed two β-barrel folds generally adopted by small proteins to be looking similar but have different topology. On the basis of the topology they could be divided into two different folds named SH3-fold and OB-fold. There was no sequence homology between any of the proteins considered. The sequence diversity and loop variability was found to be important for various binding functions.Conclusions
The function of Oligonucleotide/oligosaccharide-binding (OB) fold proteins was restricted to either DNA/RNA binding or sugar binding whereas the Src homology 3 (SH3) domain like proteins bind to a variety of ligands through loop modulations. A question was raised whether the evolution of these two folds was through DNA shuffling. 相似文献4.
Kimberly Pelak Kevin V. Shianna Dongliang Ge Jessica M. Maia Mingfu Zhu Jason P. Smith Elizabeth T. Cirulli Jacques Fellay Samuel P. Dickson Curtis E. Gumbs Erin L. Heinzen Anna C. Need Elizabeth K. Ruzzo Abanish Singh C. Ryan Campbell Linda K. Hong Katharina A. Lornsen Alexander M. McKenzie Nara L. M. Sobreira Julie E. Hoover-Fong Joshua D. Milner Ruth Ottman Barton F. Haynes James J. Goedert David B. Goldstein 《PLoS genetics》2010,6(9)
We present the analysis of twenty human genomes to evaluate the prospects for identifying rare functional variants that contribute to a phenotype of interest. We sequenced at high coverage ten “case” genomes from individuals with severe hemophilia A and ten “control” genomes. We summarize the number of genetic variants emerging from a study of this magnitude, and provide a proof of concept for the identification of rare and highly-penetrant functional variants by confirming that the cause of hemophilia A is easily recognizable in this data set. We also show that the number of novel single nucleotide variants (SNVs) discovered per genome seems to stabilize at about 144,000 new variants per genome, after the first 15 individuals have been sequenced. Finally, we find that, on average, each genome carries 165 homozygous protein-truncating or stop loss variants in genes representing a diverse set of pathways. 相似文献
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Basavegowdanadoddi Marinaik Chandranaik Sonnahallipura Munivenkatappa Byregowda Mudalagiri Dasappagupta Venkatesha Kantharajapura Ramanna Ramesha Poojappa Nandini Poorvi Reddy Thushara Bindu KV Beechagondahalli Papanna Shivashankar Byadarahalli Puttaswamy Shankar Methuku Sobha Rani 《European Journal of Wildlife Research》2018,64(1):4
We report the molecular epidemiology of highly pathogenic avian influenza (HPAI) virus involved in an outbreak causing death in free-ranging wild birds at Mysore, Karnataka state of India. The virus was typed as HPAI A(H5N8) by conventional and TaqMan probe based real-time PCR assays. Six isolates of HPAI virus were recovered in 9-day-old embryonated chicken eggs. Haemagglutinin gene-based phylogeny of virus isolates showed >?99.9% nucleotide sequence identity with HPAI A(H5N8) isolates from migratory birds and domestic poultry from China and Korea indicating either these wild birds have routed their migration through Korea and/or eastern China or these dead birds must have directly or indirectly contacted with wild birds migrating from Eastern China and/or Korean regions. The study emphasises the role of migratory wild birds in spread of HPAI across the globe. 相似文献
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Nicole M. Walley Boris Julg Samuel P. Dickson Jacques Fellay Dongliang Ge Bruce D. Walker Mary Carrington Myron S. Cohen Paul I.W. de Bakker David B. Goldstein Kevin V. Shianna Barton F. Haynes Norman L. Letvin Andrew J. McMichael Nelson L. Michael Amy C. Weintrob 《Cell host & microbe》2009,5(5):408-410
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Sreekumar G. Pillai Dongliang Ge Guohua Zhu Xiangyang Kong Kevin V. Shianna Anna C. Need Sheng Feng Craig P. Hersh Per Bakke Amund Gulsvik Andreas Ruppert Karin C. Ldrup Carlsen Allen Roses Wayne Anderson ICGN Investigators Stephen I. Rennard David A. Lomas Edwin K. Silverman David B. Goldstein 《PLoS genetics》2009,5(3)
There is considerable variability in the susceptibility of smokers to develop chronic obstructive pulmonary disease (COPD). The only known genetic risk factor is severe deficiency of α1-antitrypsin, which is present in 1–2% of individuals with COPD. We conducted a genome-wide association study (GWAS) in a homogenous case-control cohort from Bergen, Norway (823 COPD cases and 810 smoking controls) and evaluated the top 100 single nucleotide polymorphisms (SNPs) in the family-based International COPD Genetics Network (ICGN; 1891 Caucasian individuals from 606 pedigrees) study. The polymorphisms that showed replication were further evaluated in 389 subjects from the US National Emphysema Treatment Trial (NETT) and 472 controls from the Normative Aging Study (NAS) and then in a fourth cohort of 949 individuals from 127 extended pedigrees from the Boston Early-Onset COPD population. Logistic regression models with adjustments of covariates were used to analyze the case-control populations. Family-based association analyses were conducted for a diagnosis of COPD and lung function in the family populations. Two SNPs at the α-nicotinic acetylcholine receptor (CHRNA 3/5) locus were identified in the genome-wide association study. They showed unambiguous replication in the ICGN family-based analysis and in the NETT case-control analysis with combined p-values of 1.48×10−10, (rs8034191) and 5.74×10−10 (rs1051730). Furthermore, these SNPs were significantly associated with lung function in both the ICGN and Boston Early-Onset COPD populations. The C allele of the rs8034191 SNP was estimated to have a population attributable risk for COPD of 12.2%. The association of hedgehog interacting protein (HHIP) locus on chromosome 4 was also consistently replicated, but did not reach genome-wide significance levels. Genome-wide significant association of the HHIP locus with lung function was identified in the Framingham Heart study (Wilk et al., companion article in this issue of PLoS Genetics; doi:10.1371/journal.pgen.1000429). The CHRNA 3/5 and the HHIP loci make a significant contribution to the risk of COPD. CHRNA3/5 is the same locus that has been implicated in the risk of lung cancer. 相似文献
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Elizabeth T Cirulli Abanish Singh Kevin V Shianna Dongliang Ge Jason P Smith Jessica M Maia Erin L Heinzen James J Goedert David B Goldstein the Center for HIV/AIDS Vaccine Immunology 《Genome biology》2010,11(5):R57