Annals of Human Genetics (6)
Recherches Économiques de Louvain/ Louvain Economic Review (1)
Mössbauerite, Fe6 3+O4(OH)8[CO3]·3H2O, the fully oxidized 'green rust' mineral from Mont Saint-Michel Bay, France
J.-M. R. Génin, S. J. Mills, A. G. Christy, O. Guérin, A. J. Herbillon, E. Kuzmann, G. Ona-Nguema, C. Ruby, C. Upadhyay
Journal: Mineralogical Magazine / Volume 78 / Issue 2 / April 2014
The new mineral mössbauerite (IMA2012−049), Fe6 3+O4(OH)8[CO3]·3H2O, is a member of the fougèrite group of the hydrotalcite supergroup. Thus, it has a layered double hydroxide-type structure, in which brucite-like layers [Fe6 3+O4(OH)8]2+ are intercalated with CO3 2− anions and water molecules. Mössbauerite is the fully oxidized analogue of fougèrite and trébeurdenite, related to them chemically by the exchange of (Fe3+O2−) with (Fe2+OH−). Mössbauerite, intimately intergrown with trébeurdenite, was discovered in intertidal gleys from Mont Saint-Michel Bay, France, along with quartz, feldspars and clay minerals. Mössbauerite is formed by the oxidation of the other members of the fougèrite group. Like them, it occurs as μm-scale platelets in gleys with restricted access to atmospheric O and decomposes rapidly when exposed to air. Identification and characterization of these minerals has relied on an electrochemical study of synthetic analogues and Mössbauer spectroscopy, which inspired the name of the new mineral.
Unlike fougèrite and trébeurdenite, which are blue-green, pure synthetic mössbauerite is orange in colour. Detailed optical and other physical properties could not be determined because of the small platelet size and instability. The hardness is probably 2−3, by analogy with other members of the supergroup and the density, calculated from unit-cell parameters, is 2.950 g/cm3. Synchrotron X-ray data indicate that the natural material is a nanoscale intergrowth of 2T and 3T polytypes; the latter probably has the 3T7 stacking sequence. The corresponding maximum possible space group symmetries are P m1 and P3m1. Unit-cell parameters for the 3T cell are a = 3.032(7) Å, c = 22.258(4) = 367.420 Å and Z = ½.
Mössbauer spectroscopy at 78 K indicates that two distinct Fe3+ environments exist in a 2:1 ratio. These are interpreted to be ordered within each layer, but without the development of a threedimensional superlattice. Mössbauerite undergoes gradual magnetic ordering at 70−80 K to a ferromagnetic state, below which it splits into three sextets S 1m, S 2m and S 3m, as measured at 15 K, and shows the same intensity ratio ½:⅙:⅓ as the three doublets for fougèrite D 1f, D 2f, D 3f in the paramagnetic state at 78 K. This suggests that there is also short-range coupling of interlayer carbonate anions with respect to the octahedral layers and that the 2D long-range order of carbonates in interlayers remains unchanged.
Accurate power approximations for χ2-tests in case-control association studies of complex disease genes
M. R. JACKSON, E. GENIN, M. KNAPP, J. L. ESCARY
Journal: Annals of Human Genetics / Volume 66 / Issue 4 / July 2002
Published online by Cambridge University Press: 21 October 2002, pp. 307-321
A popular method for the analysis of case-control association studies is to compare the frequencies of the alleles between cases and controls by means of Pearson's χ2-statistic. Here, an approach for computing the power of this test is presented, which by computer simulation is shown to be more reliable than a previously published power approximation. Since the test based on Pearson's χ2- statistic can be anti-conservative if there is an excess of homozygotes for the susceptibility allele in the general population, it has been proposed to analyze case-control association studies by means of a trend test based on genotypes instead of alleles. We present an accurate power approximation for the trend test. The power approximations are implemented in an available computer program 'GenOdyPower', which in addition has an option to determine the empirical power of these tests by simulations.
Missing data in haplotype analysis: a study on the MILC method
C. BOURGAIN, E. GENIN, C. OBER, F. CLERGET-DARPOUX
Journal: Annals of Human Genetics / Volume 66 / Issue 1 / January 2002
Published online by Cambridge University Press: 25 April 2002, pp. 99-108
Print publication: January 2002
Given the enormous progress in the knowledge of the human genome, genetic markers are now available throughout the genome. Haplotype analysis, allowing the simultaneous use of information from several markers, has thus become increasingly popular. However, we often face the problem of missing data and of haplotype identification. We have proposed a haplotype based method for the genetic study of multifactorial diseases in founder populations, the MILC method (Bourgain et al. 2000). MILC is based on the contrast of identity length between haplotypes transmitted to affected offspring and haplotypes non-transmitted. In this study, the impact of different strategies, regarding missing data, on the MILC method are evaluated. A real situation is considered where data are derived from a genome screen for asthma susceptibility alleles in the Hutterites. Results are illustrated on this asthma data set.
Search for multifactorial disease susceptibility genes in founder populations
C. BOURGAIN, E. GENIN, H. QUESNEVILLE, F. CLERGET-DARPOUX
Journal: Annals of Human Genetics / Volume 64 / Issue 3 / May 2000
The current challenge in biomedical research is to detect genetic risk factors involved in common complex diseases. The power to detect their role is generally poor in populations that have been large for a long time. It has been suggested that the power may be increased by taking advantage of the specificity of founder populations; linkage disequilibrium spanning larger regions and kinship coefficients being stronger than in large populations. A new method is proposed here, the Maximum Identity Length Contrast (MILC) which, in contrast with other existing methods, does not make the assumption of unique ancestry for the genetic risk factors. It is thus appropriate for a search for common genetic risk factors for complex diseases. Statistical properties of the method are discussed in realistic contexts.
Tell me your HLA, I will tell you whom to marry
E. GENIN, C. OBER, G. THOMSON
Published online by Cambridge University Press: 01 July 1999, p. 358
Optimization of genome search strategies for homozygosity mapping: influence of marker spacing on power and threshold criteria for identification of candidate regions
E. GÉNIN, A. A. TODOROV, F. CLERGET-DARPOUX
Journal: Annals of Human Genetics / Volume 62 / Issue 5 / September 1998
Published online by Cambridge University Press: 01 September 1998, pp. 419-429
Mapping of genes involved in rare recessive diseases is usually difficult because of the lack of families with more than one affected progeny. The problem may be avoided by using inbred affected individuals and the strategy of homozygosity mapping.
In practice, the use of homozygosity mapping in a genome-wide scan requires that a set of markers regularly spaced and spanning the whole genome are tested. Investigators are then faced to the problem of choosing the spacing of markers.
To help solve this problem, we give some useful clues by computing (1) the expected length of the region of identity by descent around the disease locus, (2) the distribution, given the spacing of markers, of the number of affected individuals expected not to be homozygous at the marker closest to the disease locus and, (3) the expected type-one error. We show that even if the markers are very closely spaced, it is not unlikely that some affected individuals in the sample will not be homozygous at the marker closest to the disease locus. Excluding a region by the criterion that all affected individuals in the sample are not homozygous may then dramatically increase the rate of false negatives. We thus propose to relax the criterion to declare a region candidate, based on the sample size and the spacing of markers.
Information provided by pairs of distantly affected relatives to search for genes involved in rare autosomal dominant diseases
E. GÉNIN, G. BELLIS, F. CLERGET-DARPOUX
When dominant mutations of different genes may lead to the same disease, it is often difficult to detect in a particular patient which gene is involved. A strategy is to make genealogical extensions to find affected relatives that should have inherited the same mutation. In particular, for diseases with late age of onset or short survival time, only poor information may be obtained from close relatives of probands and it can be particularly efficient to make genealogical extensions to detect pairs of distantly related affected individuals. Such a pair of affecteds may provide information concerning the region of the genome where the mutated gene should map. Two situations may be encountered depending on whether or not prior information on the location of mutated genes involved in the disease are available. If we already know, from previous linkage studies, that a gene located in a given region R of the genome may be involved in the disease, the problem is then to confirm that it is indeed a mutation of this gene that is involved in the affected pair. Once the implication of a gene in region R has been confirmed the affected pair of relatives may give information to restrict the length of this region R. In this paper we discuss these two points by deriving analytically first the lod score expected and second the expected reduction of the length of the region where the mutation is suspected to map as a function of the number of meioses between the two affected individuals and of the polymorphism of the markers available in the region.
Les prêts hypothécaires en Belgique et leur destination
E. Genin
Journal: Recherches Économiques de Louvain/ Louvain Economic Review / Volume 4 / Issue 2 / February 1933
Il semble permis de fixer, avec une certaine approximation, la dette hypothécaire de la Belgique. Le montant des prêts est révélé par le droit d'inscription perçu au profit du Trésor au moment même où se prend l'inscription au bureau des hypothèques. L'annuité hypothécaire étant connue, le volume de la dette hypothécaire existante à ce jour s'obtient en multipliant cette annuité par un nombre d'années correspondant à la vie normale des prêts.