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Stephan Francke Karine Clement Christian Dina Hiroshi Inoue Philip Behn Vincent Vatin Arnaud Basdevant Bernard Guy-Grand M. Alan Permutt Philippe Froguel J. Hager 《Human genetics》1997,100(5-6):491-496
Family studies have shown that in some populations up to 75% of the variation of body mass index can be explained by genetic
factors. However, in humans, no major obesity gene has been identified to date. In contrast, there are a number of genetically
well defined animal models for obesity. In two of those models (ob/ob and db/db), defects in the same pathway are responsible
for obesity. Recently, some evidence has been found for the OB gene also being involved in human obesity. In this study we
investigated the potential role of the OB receptor (OBR) in the etiology of massive obesity in humans using familial linkage
analyses and case-control association studies. The typing of two microsatellite markers (D1S198 and D1S209), flanking the
OBR gene, in 256 sib pairs showed no evidence for linkage with obesity. In order to be able to detect small gene effects,
association studies with a 3′-UTR insertion/deletion polymorphism were carried out. The results of these analyses remained
non-significant (χ2 = 3.442, P = 0.18). However, subjects heterozygous for the insertion/deletion polymorphism showed a slight trend towards lower insulin
values 30 min after an oral glucose load compared to homozygous individuals (P = 0.02). In summary, our results do not support a major role of the human OBR gene in the development of morbid obesity in
our population.
Received: 4 December 1996 / Accepted: 25 June 1997 相似文献
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Although systematic, quantitative assessment of environmental health risks is a staple of regulatory decision-making, complaints regarding its perceived failures and shortcomings are an intrinsic feature of the policy landscape. In this article, we (a) catalog the classic criticisms of conventional health risk assessment, (b) create a typology that orders the critiques according to their focus on either input errors or output biases, and (c) identify selected allegations that fall within each category. We also note that the risk assessment–risk management paradigm has evolved over the past several decades, partially in accordance with the general direction and spirit of these classic critiques. The debate continues today along familiar lines invoking the traditional critiques and rebuttals outlined here. 相似文献
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Koichi Inoue Akiko Yamaguchi Megumi Wada Yoshihiro Yoshimura Tsunehisa Makino Hiroyuki Nakazawa 《Journal of chromatography. B, Analytical technologies in the biomedical and life sciences》2001,765(2):3469-126
Due to the ubiquity of epoxy resin compounds and their potential role in increasing the risk for reproductive dysfunction and cancer, the need for an assessment of human exposure is urgent. Therefore, we developed a method for measuring bisphenol A (BPA) and bisphenol A diglycidyl ether (BADGE) metabolites in human blood samples using high-performance liquid chromatography–electrospray ionization mass spectrometry (LC–MS). Human blood samples were processed using enzymatic deconjugation of the glucuronides followed by a novel sample preparation procedure using a solid-phase-cartridge column. This selective analytical method permits rapid detection of the metabolites, free BPA and a hydrolysis product of BADGE (BADGE-4OH) with detection limits in the low nanogram per milliliter range (0.1 ng ml−1 of BPA and 0.5 ng ml−1 of BADGE-4OH). The sample extraction was achieved by Oasis HLB column on gradient elution. The recoveries of BPA and BADGE-4OH added to human plasma samples were above 70.0% with a standard deviation of less than 5.0%. This selective, sensitive and accurate method will assist in elucidating potential associations between human exposure to epoxy-based compounds and adverse health effects. 相似文献
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Ruxandra Ion L. Telvi Jean-Louis Chaussain Jacques Patrick Barbet Manoel Nunes Anne Safar Marie-Odile Réthoré Marc Fellous Ken McElreavey 《Human genetics》1998,102(2):151-156
In 46,XY individuals, testes are determined by the activity of the SRY gene (sex-determining region Y), located on the short arm of the Ychromosome. The other genetic components of the cascade
that leads to testis formation are unknown and may be located on the Xchromosome or on the autosomes. Evidence for the existence
of several loci associated with failure of male sexual development is indicated by reports of 46,XY gonadal dysgenesis associated
with structural abnormalities of the Xchromosome or of autosomes (chromosomes9, 10, 11 and 17). In this report, we describe
the investigation of a child presenting with multiple congenital abnormalities, mental retardation and partial testicular
failure. The patient had a homogeneous de novo 46,XY,inv dup(9)(pter→p24.1::p21.1 →p23.3::p24.1→qter) chromosome complement.
No deletion was found by either cytogenetic or molecular analysis. The SRY gene and DSS region showed no abnormalities. Southern blotting dosage analysis with 9p probes and fluorescent in situ hybridisation data
indicated that the distal breakpoint of the duplicated fragment was located at 9p24.1, proximal to the SNF2 gene. We therefore suggest that a gene involved in normal testicular development and/or maintenance is present at this position
on chromosome 9.
Received: 20 January 1997 / Accepted: 5 November 1997 相似文献
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