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11.
Ghosh D; Stewart DR; Nayak NR; Lasley BL; Overstreet JW; Hendrickx AG; Sengupta J 《Human reproduction (Oxford, England)》1997,12(5):914-920
The present study was undertaken to assess the temporal association between
the profiles of serum concentrations of oestradiol-17beta, progesterone,
chorionic gonadotrophin (CG) and relaxin in pregnancies established
naturally, and after embryo transfer, as well as in failed pregnancies in
rhesus monkeys. In naturally mated cycles (group 1) a conception rate of
75% was obtained. In group 1, the mean day of CG detection in serum was
11.5 +/- 1.9 day post-ovulation, and for relaxin, 9.0 +/- 2.5 day
post-ovulation. In group 2, embryo transfer to synchronous, non-mated
surrogate recipients was performed; seven embryo transfer cycles yielded
three pregnancies which were allowed to continue to term and normal infants
were delivered. In embryo transfer cycles the mean day of CG detection was
14.8 +/- 1.8 day post- ovulation, and for relaxin, 11.4 +/- 2.6 day
post-ovulation. A delay of about 3 days was observed in the appearance in
circulation of CG (P < 0.05) and also of relaxin (P < 0.05) between
natural mated and embryo transfer conception cycles. Significant
differences (P < 0.05 for progesterone and P < 0.03 for oestradiol)
were obtained for the areas under the curves for progesterone and
oestradiol between days 12 and 16 in conception cycles compared with failed
pregnancies. These data provide the first observation of the normal
hormonal signals associated with maternal recognition of transferred
embryos during the peri- implantation period, and suggest that the use of
such an experimental primate embryo transfer model may help to elucidate
components of maternal and embryonic signal-response mechanisms during
embryo implantation.
相似文献
12.
Linkage of the MHC to familial multiple sclerosis suggests genetic heterogeneity. The Multiple Sclerosis Genetics Group 总被引:5,自引:0,他引:5
Haines JL; Terwedow HA; Burgess K; Pericak-Vance MA; Rimmler JB; Martin ER; Oksenberg JR; Lincoln R; Zhang DY; Banatao DR; Gatto N; Goodkin DE; Hauser SL 《Human molecular genetics》1998,7(8):1229-1234
Multiple sclerosis (MS) is a demyelinating autoimmune disease of the
central nervous system. While its etiology is not well understood, genetic
factors are clearly involved. Until recently, most genetic studies in MS
have been association studies using the case-control design testing
specific candidate genes and studying only sporadic cases. The only
consistently replicated finding has been an association with the HLA-DR2
allele within the major histocompatibility complex (MHC) on chromosome 6.
Using the genetic linkage design, however, evidence for and against linkage
of the MHC to MS has been found, fostering suggestions that sporadic and
familial MS have different etiologies. Most recently, two of four genomic
screens demonstrated linkage to the MHC, although specific allelic
associations were not tested. Here, a dataset of 98 multiplex families was
studied to test for an association to the HLA-DR2 allele in familial MS and
to determine if genetic linkage to the MHC was due solely to such an
association. Three highly polymorphic markers (HLA-DR, D6S273 and TNFbeta)
in the MHC demonstrated strong genetic linkage (parametric lod scores of
4.60, 2.20 and 1.24, respectively) and a specific association with the
HLA-DR2 allele was confirmed (TDT; P < 0.001). Stratifying the results
by HLA-DR2 status showed that the linkage results were limited to families
segregating HLA-DR2 alleles. These results demonstrate that genetic linkage
to the MHC can be explained by the HLA-DR2 allelic association. They also
indicate that sporadic and familial MS share a common genetic
susceptibility. In addition, preliminary calculations suggest that the MHC
explains between 17 and 62% of the genetic etiology of MS. This
heterogeneity is also supported by the minority of families showing no
linkage or association with loci within the MHC.
相似文献
13.
The intercellular adhesion molecule (ICAM) family of proteins 总被引:8,自引:0,他引:8
Macromolecular adhesive associations between cells are important for transmitting spatial and temporal information that is
critical for immune system function. One such group of proteins, the intercellular adhesion molecules (ICAMs), has grown as
newly identified members are revealed. In addition, the functions of the ICAMs, in general, have begun to be better understood,
including intracellular signaling events. This information has led to the design of novel therapeutic agents that may prove
effective in a variety of disease states. 相似文献
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18.
Sequence comparison of human and yeast telomeres identifies structurally distinct subtelomeric domains 总被引:6,自引:2,他引:6
Flint J; Bates GP; Clark K; Dorman A; Willingham D; Roe BA; Micklem G; Higgs DR; Louis EJ 《Human molecular genetics》1997,6(8):1305-1313
We have sequenced and compared DNA from the ends of three human
chromosomes: 4p, 16p and 22q. In all cases the pro-terminal regions are
subdivided by degenerate (TTAGGG)n repeats into distal and proximal sub-
domains with entirely different patterns of homology to other chromosome
ends. The distal regions contain numerous, short (<2 kb) segments of
interrupted homology to many other human telomeric regions. The proximal
regions show much longer (approximately 10-40 kb) uninterrupted homology to
a few chromosome ends. A comparison of all yeast subtelomeric regions
indicates that they too are subdivided by degenerate TTAGGG repeats into
distal and proximal sub-domains with similarly different patterns of
identity to other non-homologous chromosome ends. Sequence comparisons
indicate that the distal and proximal sub-domains do not interact with each
other and that they interact quite differently with the corresponding
regions on other, non- homologous, chromosomes. These findings suggest that
the degenerate TTAGGG repeats identify a previously unrecognized,
evolutionarily conserved boundary between remarkably different subtelomeric
domains.
相似文献
19.
ATRX encodes a novel member of the SNF2 family of proteins: mutations point to a common mechanism underlying the ATR-X syndrome 总被引:11,自引:3,他引:11
Picketts DJ; Higgs DR; Bachoo S; Blake DJ; Quarrell OW; Gibbons RJ 《Human molecular genetics》1996,5(12):1899-1907
It was shown recently that mutations of the ATRX gene give rise to a
severe, X-linked form of syndromal mental retardation associated with alpha
thalassaemia (ATR-X syndrome). In this study, we have characterised the
full-length cDNA and predicted structure of the ATRX protein. Comparative
analysis shows that it is an entirely new member of the SNF2 subgroup of a
superfamily of proteins with similar ATPase and helicase domains. ATRX
probably acts as a regulator of gene expression. Definition of its genomic
structure enabled us to identify four novel splicing defects by screening
52 affected individuals. Correlation between these and previously
identified mutations with variations in the ATR-X phenotype provides
insights into the pathophysiology of this disease and the normal role of
the ATRX protein in vivo.
相似文献
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