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The role of dialysis in contrast-induc ed nephropathy: doubts and certainties.: J Cardiovasc Med (Hagerstown), Vol. 8, No. 8. (August 2007), pp. 549-557.Over past years, there has been a progressive increase in percutaneous endovascular procedures in patients with chronic renal disease, owing to the high incidence of vascular disease, particularly coronary artery disease, in this population. The use of contrast media may further worsen renal function in such patients, in some cases even accelerating the progression towards end-stage renal failure, and may increase patient morbidity and mortality. In this review, we discuss the role of dialysis in preventing contrast-induc ed nephropathy as well as present indications to its use in patients already on dialysis treatment undergoing diagnostic or therapeutic procedures with contrast medium injection.

Source: J Cardiovasc Med (Hagerstown), Vol. 8, No. 8. (August 2007), pp. 549-557.
Mapping common regulatory variants to human haplotypes: Hum. Mol. Genet., Vol. 14, No. 24. (15 December 2005), pp. 3963-3971.Inte r-individual variation in gene expression has proven to be in part governed by genetic determinants, which may be trans- or cis-acting. The underlying cause of cis-acting regulatory variation has been identified in only a handful of the hundreds of genes shown to display differential allelic expression. In this report, we describe a systematic effort to map common cis-acting variants in 64 genes, using association methods in HapMap samples. We identified 16 loci (25%), each of which harbors common haplotypes that affect total expression of a gene, and a further 17 loci (27%) with evidence of haplotypes affecting relative allelic expression in heterozygote samples. Our survey suggests that detailed mapping of allele-specifi c in vivo expression will provide a rich source of regulatory SNPs or haplotypes that should be given high priority in association studies of human phenotypes. 10.1093/hmg/dd i420

Source: Hum. Mol. Genet., Vol. 14, No. 24. (15 December 2005), pp. 3963-3971.
Analysis of allelic differential expression in human white blood cells: Genome Res., Vol. 16, No. 3. (1 March 2006), pp. 331-339.Alleli c variation of gene expression is common in humans, and is of interest because of its potential contribution to variation in heritable traits. To identify human genes with allelic expression differences, we genotype DNA and examine mRNA isolated from the white blood cells of 12 unrelated individuals using oligonucleotid e arrays containing 8406 exonic SNPs. Of the exonic SNPs, 1983, located in 1389 genes, are both expressed in the white blood cells and heterozygous in at least one of the 12 individuals, and thus can be examined for differential allelic expression. Of the 1389 genes, 731 (53%) show allele expression differences in at least one individual. To gain insight into the regulatory mechanisms governing allelic expression differences, we analyze a set of 60 genes containing exonic SNPs that are heterozygous in three or more samples, and for which all heterozygotes display differential expression. We find three patterns of allelic expression, suggesting different underlying regulatory mechanisms. Exonic SNPs in three of the 60 genes are monoallelicall y expressed in the human white blood cells, and when examined in families show expression of only the maternal copy, consistent with regulation by imprinting. Approximately one-third of the genes have the same allele expressed more highly in all heterozygotes, suggesting that their regulation is predominantly influenced by cis-elements in strong linkage disequilibrium with the assayed exonic SNP. The remaining two-thirds of the genes have different alleles expressed more highly in different heterozygotes, suggesting that their expression differences are influenced by factors not in strong linkage disequilibrium with the assayed exonic SNP. 10.1101/gr.455 9106

Source: Genome Res., Vol. 16, No. 3. (1 March 2006), pp. 331-339.
Allele-specifi c gene expression differences in humans.: Hum Mol Genet, Vol. 13 Spec No 2 (1 October 2004)In the last decade, the search for the genetic origins of phenotypic variation has expanded beyond the non-synonymous variants which alter the amino acid sequence of the encoded protein, and many examples of sequence variants which alter gene expression have been found. Recently, using both traditional and novel technologies, a number of surveys have been carried out to examine the frequency with which cis-acting sequence variants or other cis-acting effects, alter gene expression either in vitro or in vivo. Microarray data have shown that the expression of many genes varies markedly between individuals and allele-specifi c expression studies have shown that the source of much of this variation appears to be cis-acting effects. A significant proportion of the variation may originate in gene promoter regions and a large number of sequence variants which have functional effect in vitro have been found. The evidence suggests that given a large enough population, most, if not all genes may have allele-specifi c expression differences in at least some individuals and finding the genetic origins of each of these and linking the former to a possible phenotype must be a major long term goal of the biomedical community.

Source: Hum Mol Genet, Vol. 13 Spec No 2 (1 October 2004)
Efficient peptide-MHC-I binding prediction for alleles with few known binders: Bioinformatics , Vol. 24, No. 3. (1 February 2008), pp. 358-366.Motiva tion: In silico methods for the prediction of antigenic peptides binding to MHC class I molecules play an increasingly important role in the identification of T-cell epitopes. Statistical and machine learning methods in particular are widely used to score candidate binders based on their similarity with known binders and non-binders. The genes coding for the MHC molecules, however, are highly polymorphic, and statistical methods have difficulties building models for alleles with few known binders. In this context, recent work has demonstrated the utility of leveraging information across alleles to improve the performance of the prediction. Results: We design a support vector machine algorithm that is able to learn peptideMHC-I binding models for many alleles simultaneously , by sharing binding information across alleles. The sharing of information is controlled by a user-defined measure of similarity between alleles. We show that this similarity can be defined in terms of supertypes, or more directly by comparing key residues known to play a role in the peptideMHC binding. We illustrate the potential of this approach on various benchmark experiments where it outperforms other state-of-the-a rt methods. Availability: The method is implemented on a web server: http://cbio.en smp.fr/kiss. All data and codes are freely and publicly available from the authors. Contact: laurent.jacob@ ensmp.fr Supplementary information: Supplementary data are available at Bioinformatics online. 10.1093/bioinf ormatics/btm61 1

Source: Bioinformatics, Vol. 24, No. 3. (1 February 2008), pp. 358-366.
Allele-specifi c amplification in cancer revealed by SNP array analysis.: PLoS Comput Biol, Vol. 1, No. 6. (November 2005)Amplifica tion, deletion, and loss of heterozygosity of genomic DNA are hallmarks of cancer. In recent years a variety of studies have emerged measuring total chromosomal copy number at increasingly high resolution. Similarly, loss-of-hetero zygosity events have been finely mapped using high-throughpu t genotyping technologies. We have developed a probe-level allele-specifi c quantitation procedure that extracts both copy number and allelotype information from single nucleotide polymorphism (SNP) array data to arrive at allele-specifi c copy number across the genome. Our approach applies an expectation-ma ximization algorithm to a model derived from a novel classification of SNP array probes. This method is the first to our knowledge that is able to (a) determine the generalized genotype of aberrant samples at each SNP site (e.g., CCCCT at an amplified site), and (b) infer the copy number of each parental chromosome across the genome. With this method, we are able to determine not just where amplifications and deletions occur, but also the haplotype of the region being amplified or deleted. The merit of our model and general approach is demonstrated by very precise genotyping of normal samples, and our allele-specifi c copy number inferences are validated using PCR experiments. Applying our method to a collection of lung cancer samples, we are able to conclude that amplification is essentially monoallelic, as would be expected under the mechanisms currently believed responsible for gene amplification. This suggests that a specific parental chromosome may be targeted for amplification, whether because of germ line or somatic variation. An R software package containing the methods described in this paper is freely available at http://genome. dfci.harvard.e du/~tlaframb/P LASQ.

Source: PLoS Comput Biol, Vol. 1, No. 6. (November 2005)
The Joint Allele-Frequen cy Spectrum in Closely Related Species: Genetics, Vol. 177, No. 1. (1 September 2007), pp. 387-398.We develop the theory for computing the joint frequency spectra of alleles in two closely related species. We allow for arbitrary population growth in both species after they had a common ancestor. We focus on the case in which a single chromosome is sequenced from one of the species. We use classical diffusion theory to show that, if the ancestral species was at equilibrium under mutation and drift and a chromosome from one of the descendant species carries the derived allele, the frequency spectrum in the other species is uniform, independently of the demographic history of both species. We also predict the expected densities of segregating and fixed sites when the chromosome from the other species carries the ancestral allele. We compare the predictions of our model with the site-frequency spectra of SNPs in the four HapMap populations of humans when the nucleotide present in the Neanderthal DNA sequence is ancestral or derived, using the chimp genome as the outgroup. 10.1534/geneti cs.107.070730

Source: Genetics, Vol. 177, No. 1. (1 September 2007), pp. 387-398.
Constraints on Allele Size at Microsatellite Loci: Implications for Genetic Differentiatio n: Genetics, Vol. 143, No. 2. (1 June 1996), pp. 1021-1032.

Source: Genetics, Vol. 143, No. 2. (1 June 1996), pp. 1021-1032.
Dating the origin of the CCR5-Delta32 AIDS-resistanc e allele by the coalescence of haplotypes.: Am J Hum Genet, Vol. 62, No. 6. (June 1998), pp. 1507-1515.The CCR5-Delta32 deletion obliterates the CCR5 chemokine and the human immunodeficien cy virus (HIV)-1 coreceptor on lymphoid cells, leading to strong resistance against HIV-1 infection and AIDS. A genotype survey of 4,166 individuals revealed a cline of CCR5-Delta32 allele frequencies of 0%-14% across Eurasia, whereas the variant is absent among native African, American Indian, and East Asian ethnic groups. Haplotype analysis of 192 Caucasian chromosomes revealed strong linkage disequilibrium between CCR5 and two microsatellite loci. By use of coalescence theory to interpret modern haplotype genealogy, we estimate the origin of the CCR5-Delta32-c ontaining ancestral haplotype to be approximately 700 years ago, with an estimated range of 275-1,875 years. The geographic cline of CCR5-Delta32 frequencies and its recent emergence are consistent with a historic strong selective event (e.g. , an epidemic of a pathogen that, like HIV-1, utilizes CCR5), driving its frequency upward in ancestral Caucasian populations.

Source: Am J Hum Genet, Vol. 62, No. 6. (June 1998), pp. 1507-1515.
Simultaneous genotyping, gene-expressio n measurement, and detection of allele-specifi c expression with oligonucleotid e arrays.: Genome Res, Vol. 15, No. 2. (February 2005), pp. 284-291.Oligon ucleotide microarrays provide a high-throughpu t method for exploring genomes. In addition to their utility for gene-expressio n analysis, oligonucleotid e-expression arrays have also been used to perform genotyping on genomic DNA. Here, we show that in segregants from a cross between two unrelated strains of Saccharomyces cerevisiae, high-quality genotype data can also be obtained when mRNA is hybridized to an oligonucleotid e-expression array. We were able to identify and genotype nearly 1000 polymorphisms at an error rate close to 3% in segregants and at an error rate of 7% in diploid strains, a performance comparable to methods using genomic DNA. In addition, we demonstrate how simultaneous genotyping and gene-expressio n profiling can reveal cis-regulatory variation by screening hundreds of genes for allele-specifi c expression. With this method, we discovered 70 ORFs with evidence for preferential expression of one allele in a diploid hybrid of two S. cerevisiae strains.

Source: Genome Res, Vol. 15, No. 2. (February 2005), pp. 284-291.

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