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Article: Recent Progress in the Synthesis of 4-Arylcoumarins

Moskvina, V. S / Khilya, V. P

Chemistry of natural compounds. 2019 May, v. 55, no. 3

2019

Abstract: Current approaches to the synthesis of 4-arylcoumarins (neoflavones) are reviewed. This is an important group of O-containing natural flavonoids that are widely used not only to prepare natural and synthetic neoflavone analogs but also to design compound ...

Abstract	Current approaches to the synthesis of 4-arylcoumarins (neoflavones) are reviewed. This is an important group of O-containing natural flavonoids that are widely used not only to prepare natural and synthetic neoflavone analogs but also to design compound libraries based on 4-arylcoumarins for biological activity studies. The use of new transition-metal catalysts and unconventional activation methods for cyclization of the coumarin system, arylation of activated coumarins, and direct arylation of unactivated coumarins are discussed.
Keywords	arylation ; bioactive properties ; catalysts ; coumarin ; flavonoids
Language	English
Dates of publication	2019-05
Size	p. 401-427.
Publishing place	Springer US
Document type	Article
ZDB-ID	213866-9
ISSN	0009-3130
ISSN	0009-3130
DOI	10.1007/s10600-019-02705-8
Database	NAL-Catalogue (AGRICOLA)

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Article: Amino-Acid Derivatives of Pyranocoumarins

Krasylov, I. V / Moskvina, V. S / Shilin, S. V / Khilya, V. P

Chemistry of natural compounds. 2020 Sept., v. 56, no. 5

2020

Abstract: A methodology for synthesizing amino-acid derivatives of pyranocoumarins in three steps using pyranocoumarin oximes as starting compounds was developed. A series of pyranocoumarins containing the amino acids glycine, alanine, phenylalanine, methionine, ... ...

Abstract	A methodology for synthesizing amino-acid derivatives of pyranocoumarins in three steps using pyranocoumarin oximes as starting compounds was developed. A series of pyranocoumarins containing the amino acids glycine, alanine, phenylalanine, methionine, leucine, and β-alanine in their structures could be prepared using the activated ester method.
Keywords	alanine ; chemistry ; leucine ; methionine ; oximes ; phenylalanine
Language	English
Dates of publication	2020-09
Size	p. 832-836.
Publishing place	Springer US
Document type	Article
Note	NAL-AP-2-clean
ZDB-ID	213866-9
ISSN	0009-3130
ISSN	0009-3130
DOI	10.1007/s10600-020-03163-3
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Article ; Online: Synthesis and Recyclization of Methylenebisflavonoids Based on Heterocyclic Analogs of Umbelliferone and Formononetin

Glibov, E. K. / Gorbulenko, N. V. / Moskvina, V. S. / Suprun, A. V. / Shablykina, O. V. / Shokol, T. V. / Khilya, V. P.

Chem Nat Compd. 2022 July, v. 58, no. 4 p.617-622

2022

Abstract: The methylenebisflavonoids 7-hydroxy-3-hetaryl-8-(4-oxo-4H-3-chromenylmethyl)-4H-4-chromenones and 7-hydroxy-3-hetaryl-8-(4-oxo-4H-3-chromenylmethyl)-2H-2-chromenones were synthesized via the reaction of 7-hydroxy-8-dialkylaminomethyl-3-hetarylcoumarins ... ...

Abstract	The methylenebisflavonoids 7-hydroxy-3-hetaryl-8-(4-oxo-4H-3-chromenylmethyl)-4H-4-chromenones and 7-hydroxy-3-hetaryl-8-(4-oxo-4H-3-chromenylmethyl)-2H-2-chromenones were synthesized via the reaction of 7-hydroxy-8-dialkylaminomethyl-3-hetarylcoumarins and chromones with 3-(dimethylamino)-1-(2-hydroxyphenyl)prop-2-en-1-one. Recyclization of 3-(1,3-benzthiazol-2-yl)-7-hydroxy-8-(4-oxo-4H-3-chromenylmethyl)-2H-2-chromenone through the action of N,N- and N,O-binucleophiles produced new 3-benzthiazolylcoumarin derivatives modified by pyrazole, isoxazole, and pyrimidine heterocycles.
Keywords	chemistry ; formononetin ; umbelliferones
Language	English
Dates of publication	2022-07
Size	p. 617-622.
Publishing place	Springer US
Document type	Article ; Online
ZDB-ID	213866-9
ISSN	0009-3130
ISSN	0009-3130
DOI	10.1007/s10600-022-03755-1
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Article: Detailed analysis of the relative power of direct and indirect association studies and the implications for their interpretation.

Moskvina, V / O'Donovan, M C

Human heredity

2007 Volume 64, Issue 1, Page(s) 63–73

Abstract: Objectives: Genetic association studies are usually based upon restricted sets of 'tag' markers selected to represent the total sequence variation. Tag selection is often determined by some threshold for the r(2) coefficients of linkage disequilibrium ( ... ...

Abstract	Objectives: Genetic association studies are usually based upon restricted sets of 'tag' markers selected to represent the total sequence variation. Tag selection is often determined by some threshold for the r(2) coefficients of linkage disequilibrium (LD) between tag and untyped markers, it being widely assumed that power to detect an effect at the untyped sites is retained by typing the tag marker in a sample scaled by the inverse of the selected threshold (1/r(2)). However, unless only a single causal variant occurs at a locus, it has been shown [Eur J Hum Genet 2006;14:426-437] that significant power loss can occur if this principle is applied. We sought to investigate whether unexpected loss of power might be an exceptional case or more general concern. In the absence of detailed knowledge about the genetic architecture at complex disease loci, we developed a mathematical approach to test all possible situations. Methods: We derived mathematical formulae allowing the calculation of all possible odds ratios (OR) at a tag marker locus given the effect size that would be observed by typing a second locus and the r(2) between the two loci. For a range of allele frequencies, r(2) between loci, and strengths of association at the causal locus (OR from 0.5 to 2) that we consider realistic for complex disease loci, we next determined the sample sizes that would be necessary to give equivalent power to detect association by genotyping tag and causal loci and compared these with the sample sizes predicted by applying 1/r(2). Results: Under most of the hypothetical scenarios we examined, the calculated sample sizes required to maintain power by typing markers that tag the causal locus at even moderately high r(2) (0.8) were greater than that calculated by applying 1/r(2). Even in populations with apparently similar measurements of allele frequency, LD structure, and effect size at the susceptibility allele, the required sample size to detect association with a tag marker can vary substantially. We also show that in apparently similar populations, associations to either allele at the tag site are possible. Conclusions: Indirect tests of association are less powered than sizes predicted by applying 1/r(2) in the majority of hypothetical scenarios we examined. Our findings pertain even for what we consider likely to be larger than average effect sizes in complex diseases (OR = 1.5-2) and even for moderately high r(2) values between the markers. Until a substantial number of disease genes have been identified through methods that are not based on tagging, and therefore biased towards those situations most favourable to tagging, it is impossible to know how the true scenarios are distributed across the range of possible scenarios. Nevertheless, while association designs based upon tag marker selection by necessity are the tool of choice for de novo gene discovery, our data suggest power to initially detect association may often be less than assumed. Moreover, our data suggest that to avoid genuine findings being subsequently discarded by unpredictable losses of power, follow up studies in other samples should be based upon more detailed analyses of the gene rather than simply on the tag SNPs showing association in the discovery study.
MeSH term(s)	Gene Frequency ; Genetic Markers ; Genetic Predisposition to Disease ; Genetic Techniques ; Genetics, Medical ; Haplotypes ; Humans ; Linkage Disequilibrium ; Mathematics ; Models, Statistical ; Polymorphism, Single Nucleotide ; Sample Size
Chemical Substances	Genetic Markers
Language	English
Publishing date	2007
Publishing country	Switzerland
Document type	Journal Article
ZDB-ID	2424-7
ISSN	1423-0062 ; 0001-5652
ISSN (online)	1423-0062
ISSN	0001-5652
DOI	10.1159/000101424
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Article ; Online: On multiple-testing correction in genome-wide association studies.

Moskvina, Valentina / Schmidt, Karl Michael

Genetic epidemiology

2008 Volume 32, Issue 6, Page(s) 567–573

Abstract: The interpretation of the results of large association studies encompassing much or all of the human genome faces the fundamental statistical problem that a correspondingly large number of single nucleotide polymorphisms markers will be spuriously ... ...

Abstract	The interpretation of the results of large association studies encompassing much or all of the human genome faces the fundamental statistical problem that a correspondingly large number of single nucleotide polymorphisms markers will be spuriously flagged as significant. A common method of dealing with these false positives is to raise the significance level for the individual tests for association of each marker. Any such adjustment for multiple testing is ultimately based on a more or less precise estimate for the actual overall type I error probability. We estimate this probability for association tests for correlated markers and show that it depends in a nonlinear way on the significance level for the individual tests. This dependence of the effective number of tests is not taken into account by existing multiple-testing corrections, leading to widely overestimated results. We demonstrate a simple correction for multiple testing, which can easily be calculated from the pairwise correlation and gives far more realistic estimates for the effective number of tests than previous formulae. The calculation is considerably faster than with other methods and hence applicable on a genome-wide scale. The efficacy of our method is shown on a constructed example with highly correlated markers as well as on real data sets, including a full genome scan where a conservative estimate only 8% above the permutation estimate is obtained in about 1% of computation time. As the calculation is based on pairwise correlations between markers, it can be performed at the stage of study design using public databases.
MeSH term(s)	Genetic Markers ; Genome, Human ; Humans ; Models, Genetic ; Models, Statistical ; Polymorphism, Single Nucleotide ; Probability
Chemical Substances	Genetic Markers
Language	English
Publishing date	2008-09
Publishing country	United States
Document type	Journal Article ; Research Support, Non-U.S. Gov't
ZDB-ID	605785-8
ISSN	1098-2272 ; 0741-0395
ISSN (online)	1098-2272
ISSN	0741-0395
DOI	10.1002/gepi.20331
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Article: Susceptibility of biallelic haplotype and genotype frequencies to genotyping error.

Moskvina, Valentina / Schmidt, Karl Michael

Biometrics

2006 Volume 62, Issue 4, Page(s) 1116–1123

Abstract: With the availability of fast genotyping methods and genomic databases, the search for statistical association of single nucleotide polymorphisms with a complex trait has become an important methodology in medical genetics. However, even fairly rare ... ...

Abstract	With the availability of fast genotyping methods and genomic databases, the search for statistical association of single nucleotide polymorphisms with a complex trait has become an important methodology in medical genetics. However, even fairly rare errors occurring during the genotyping process can lead to spurious association results and decrease in statistical power. We develop a systematic approach to study how genotyping errors change the genotype distribution in a sample. The general M-marker case is reduced to that of a single-marker locus by recognizing the underlying tensor-product structure of the error matrix. Both method and general conclusions apply to the general error model; we give detailed results for allele-based errors of size depending both on the marker locus and the allele present. Multiple errors are treated in terms of the associated diffusion process on the space of genotype distributions. We find that certain genotype and haplotype distributions remain unchanged under genotyping errors, and that genotyping errors generally render the distribution more similar to the stable one. In case-control association studies, this will lead to loss of statistical power for nondifferential genotyping errors and increase in type I error for differential genotyping errors. Moreover, we show that allele-based genotyping errors do not disturb Hardy-Weinberg equilibrium in the genotype distribution. In this setting we also identify maximally affected distributions. As they correspond to situations with rare alleles and marker loci in high linkage disequilibrium, careful checking for genotyping errors is advisable when significant association based on such alleles/haplotypes is observed in association studies.
MeSH term(s)	Alleles ; Biometry ; Gene Frequency ; Genetic Markers ; Genotype ; Haplotypes ; Models, Genetic ; Models, Statistical ; Polymorphism, Single Nucleotide
Chemical Substances	Genetic Markers
Language	English
Publishing date	2006-12
Publishing country	United States
Document type	Journal Article
ZDB-ID	213543-7
ISSN	0006-341X ; 0099-4987
ISSN	0006-341X ; 0099-4987
DOI	10.1111/j.1541-0420.2006.00563.x
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Article: Individual SNP allele reconstruction from informative markers selected by a non-linear Gauss-type algorithm.

Moskvina, Valentina / Schmidt, Karl Michael

Human heredity

2006 Volume 62, Issue 2, Page(s) 97–106

Abstract: Objectives: In view of the linkage disequilibrium structure of the genome, the selection of maximally informative SNP markers is a fundamental issue in the design of association studies. Currently used selection methods rely on pairwise marker ... ...

Abstract	Objectives: In view of the linkage disequilibrium structure of the genome, the selection of maximally informative SNP markers is a fundamental issue in the design of association studies. Currently used selection methods rely on pairwise marker correlation or informativity measures for subsets of markers. Nevertheless, the selected markers do not provide a completely satisfactory description of the individual remaining markers. The number of tag markers can be further reduced by using haplotypic information, but then the results of association analysis are difficult to interpret. Methods and results: We propose a non-linear Gauss-type algorithm selecting a subset of markers which is optimal with respect to the informativity measures and allows an explicit reconstruction of all other known markers, thus permitting direct inference of allelic association. The selection is based on the haplotype distribution in the population, but can be adapted to work with unphased genotypes directly. Conclusions: The proposed algorithm provides a rational methodology of informative marker selection, allowing for control and optimisation of information content and full marker reconstruction. Moreover, the reconstruction step can also be applied to tag markers selected using a different method at the stage of study design, identifying those markers which cannot be uniquely recovered from the chosen tags.
MeSH term(s)	Algorithms ; Alleles ; Case-Control Studies ; Genetic Markers ; Haplotypes/genetics ; Humans ; Nonlinear Dynamics ; Normal Distribution ; Polymorphism, Single Nucleotide
Chemical Substances	Genetic Markers
Language	English
Publishing date	2006
Publishing country	Switzerland
Document type	Comparative Study ; Journal Article
ZDB-ID	2424-7
ISSN	1423-0062 ; 0001-5652
ISSN (online)	1423-0062
ISSN	0001-5652
DOI	10.1159/000096097
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Article: Design of case-controls studies with unscreened controls.

Moskvina, V / Holmans, P / Schmidt, K M / Craddock, N

Annals of human genetics

2005 Volume 69, Issue Pt 5, Page(s) 566–576

Abstract: Traditionally in genetic case-control studies controls have been screened to exclude subjects with a personal history of illness. This control group has the advantage of optimal power to detect loci involved in illness, but requires more work and may ... ...

Abstract	Traditionally in genetic case-control studies controls have been screened to exclude subjects with a personal history of illness. This control group has the advantage of optimal power to detect loci involved in illness, but requires more work and may incur substantial cost in recruitment. An alternative approach to screening is to use unscreened controls sampled from the general population. Such controls are generally plentiful and inexpensive, but in general there is a risk that some may have the same disease as the cases, which will reduce power to detect associations. We have quantified the extent of this power loss, and produced mathematical formulae for the number of unscreened controls necessary to achieve the same power as a fixed sample of screened controls. The effect of using unscreened controls will also depend on the ratio of the number of screened controls to cases specified in the original study design, and this is also investigated. We have also investigated the cost-benefits of the screened and unscreened approaches, according to variation in the relative costs of sampling screened and unscreened controls, together with genotyping costs. We have, thus, identified the range of situations in which using unscreened controls is a cost-effective alternative to the screened control method and could be considered when designing a study. In many of the typical, real-world situations in complex genetics, the use of unscreened controls is potentially cost-effective and can, in general, be considered for disorders with population prevalence Kp < 0.2. With the steady reduction in genotyping costs and the availability of common sets of "population controls" this design is likely to become increasingly cost effective.
MeSH term(s)	Alleles ; Case-Control Studies ; Gene Frequency ; Genetic Predisposition to Disease ; Genetic Techniques ; Genotype ; Humans ; Kinetics ; Mass Screening ; Models, Genetic ; Models, Statistical ; Models, Theoretical ; Odds Ratio ; Phenotype ; Research Design ; Risk
Language	English
Publishing date	2005-09
Publishing country	England
Document type	Journal Article ; Research Support, Non-U.S. Gov't
ZDB-ID	333-5
ISSN	1469-1809 ; 0003-4800
ISSN (online)	1469-1809
ISSN	0003-4800
DOI	10.1111/j.1529-8817.2005.00175.x
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Article: Susceptibility of Biallelic Haplotype and Genotype Frequencies to Genotyping Error

Moskvina, Valentina / Schmidt, Karl Michael

Biometrics journal of the International Biometrics Society.. 2006 Dec., v. 62, no. 4

2006

Abstract	With the availability of fast genotyping methods and genomic databases, the search for statistical association of single nucleotide polymorphisms with a complex trait has become an important methodology in medical genetics. However, even fairly rare errors occurring during the genotyping process can lead to spurious association results and decrease in statistical power. We develop a systematic approach to study how genotyping errors change the genotype distribution in a sample. The general M‐marker case is reduced to that of a single‐marker locus by recognizing the underlying tensor‐product structure of the error matrix. Both method and general conclusions apply to the general error model; we give detailed results for allele‐based errors of size depending both on the marker locus and the allele present. Multiple errors are treated in terms of the associated diffusion process on the space of genotype distributions. We find that certain genotype and haplotype distributions remain unchanged under genotyping errors, and that genotyping errors generally render the distribution more similar to the stable one. In case–control association studies, this will lead to loss of statistical power for nondifferential genotyping errors and increase in type I error for differential genotyping errors. Moreover, we show that allele‐based genotyping errors do not disturb Hardy–Weinberg equilibrium in the genotype distribution. In this setting we also identify maximally affected distributions. As they correspond to situations with rare alleles and marker loci in high linkage disequilibrium, careful checking for genotyping errors is advisable when significant association based on such alleles/haplotypes is observed in association studies.
Keywords	alleles ; biometry ; gene banks ; genomics ; genotyping ; haplotypes ; linkage disequilibrium ; loci ; models ; single nucleotide polymorphism
Language	English
Dates of publication	2006-12
Size	p. 1116-1123.
Publishing place	Blackwell Publishing Inc
Document type	Article
ZDB-ID	213543-7
ISSN	0099-4987 ; 0006-341X
ISSN	0099-4987 ; 0006-341X
DOI	10.1111/j.1541-0420.2006.00563.x
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Article: Detailed Analysis of the Relative Power of Direct and Indirect Association Studies and the Implications for Their Interpretation

Moskvina, V. / O’Donovan, M.C.

Human Heredity

2007 Volume 64, Issue 1, Page(s) 63–73

Abstract: Objectives: Genetic association studies are usually based upon restricted sets of ‘tag’ markers selected to represent the total sequence variation. Tag selection is often determined by some threshold for the r2 coefficients of linkage disequilibrium (LD) ...

Institution	Department of Psychological Medicine, Wales College of Medicine, Cardiff University, Cardiff, UK
Abstract	Objectives: Genetic association studies are usually based upon restricted sets of ‘tag’ markers selected to represent the total sequence variation. Tag selection is often determined by some threshold for the r2 coefficients of linkage disequilibrium (LD) between tag and untyped markers, it being widely assumed that power to detect an effect at the untyped sites is retained by typing the tag marker in a sample scaled by the inverse of the selected threshold (1/r2). However, unless only a single causal variant occurs at a locus, it has been shown [Eur J Hum Genet 2006;14:426–437] that significant power loss can occur if this principle is applied. We sought to investigate whether unexpected loss of power might be an exceptional case or more general concern. In the absence of detailed knowledge about the genetic architecture at complex disease loci, we developed a mathematical approach to test all possible situations. Methods: We derived mathematical formulae allowing the calculation of all possible odds ratios (OR) at a tag marker locus given the effect size that would be observed by typing a second locus and the r2 between the two loci. For a range of allele frequencies, r2 between loci, and strengths of association at the causal locus (OR from 0.5 to 2) that we consider realistic for complex disease loci, we next determined the sample sizes that would be necessary to give equivalent power to detect association by genotyping tag and causal loci and compared these with the sample sizes predicted by applying 1/r2Results: Under most of the hypothetical scenarios we examined, the calculated sample sizes required to maintain power by typing markers that tag the causal locus at even moderately high r2 (0.8) were greater than that calculated by applying 1/r2. Even in populations with apparently similar measurements of allele frequency, LD structure, and effect size at the susceptibility allele, the required sample size to detect association with a tag marker can vary substantially. We also show that in apparently similar populations, associations to either allele at the tag site are possible. Conclusions: Indirect tests of association are less powered than sizes predicted by applying 1/r2 in the majority of hypothetical scenarios we examined. Our findings pertain even for what we consider likely to be larger than average effect sizes in complex diseases (OR = 1.5–2) and even for moderately high r2 values between the markers. Until a substantial number of disease genes have been identified through methods that are not based on tagging, and therefore biased towards those situations most favourable to tagging, it is impossible to know how the true scenarios are distributed across the range of possible scenarios. Nevertheless, while association designs based upon tag marker selection by necessity are the tool of choice for de novo gene discovery, our data suggest power to initially detect association may often be less than assumed. Moreover, our data suggest that to avoid genuine findings being subsequently discarded by unpredictable losses of power, follow up studies in other samples should be based upon more detailed analyses of the gene rather than simply on the tag SNPs showing association in the discovery study.
Keywords	Association studies ; Power ; Tagging SNPs (tSNPs)
Language	English
Publishing date	2007-04-27
Publisher	S. Karger AG
Publishing place	Basel, Switzerland
Document type	Article
Note	Original Paper
ZDB-ID	2424-7
ISBN	978-3-8055-8314-5 ; 978-3-318-01481-5 ; 3-8055-8314-1 ; 3-318-01481-8
ISSN	1423-0062 ; 0001-5652
ISSN (online)	1423-0062
ISSN	0001-5652
DOI	10.1159/000101424
Database	Karger publisher's database

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