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1.
2.
De Leo V; Morgante G; Lanzetta D; D'Antona D; Bertieri RS 《Human reproduction (Oxford, England)》1997,12(2):357-360
We report the results of administration of danazol after suspension of
gonadotrophin-releasing hormone analogue (GnRHa) therapy for uterine
myomas. A total of 21 women with uterine myomas was treated with 100 mg
danazol for 6 months after GnRHa therapy. Uterine volume and endocrine
status were monitored monthly by ultrasound and assay of plasma
gonadotrophins, oestradiol and progesterone. The results show a rebound of
uterine volume about 30% less than in controls at the end of danazol
therapy. Menstrual cyclicity returned after 65 +/- 3 days in 16 subjects
and five patients remained amenorrhoeic. Hormone assays confirmed renewed
ovarian function in the women whose menstrual periods returned. Bone
mineral content was substantially reduced during GnRHa treatment but
improved significantly during danazol therapy even in the women who
remained amenorrhoeic. These results show the utility of danazol in
prolonging the therapeutic effects of GnRHa. The mechanism by which danazol
inhibits rebound of uterine volume may be due to its antiprogesterone
effects on uterine myomas.
相似文献
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4.
The authors report the clinical and laboratory findings of a patient who had severe immune hemolytic anemia due to hydrochlorothiazide (HCTZ). In this case, the HCTZ antibody reacted not only with other thiazide and thiazide-like drugs, but also with a chemically unrelated diuretic, ethacrynic acid. These results indicate that HCTZ antibody activity is not restricted solely to the thiazides and imply that therapy with any of the reactive drugs would be contraindicated for this patient. The serologic screening for drug reactivity may be useful for selecting alternative therapy for patients with drug-induced immune hemolytic anemia. 相似文献
5.
6.
Targeted gene disruption of murine CD7 总被引:2,自引:0,他引:2
CD7 is a 40 kDa type I transmembrane glycoprotein member of the Ig
superfamily. CD7 is a marker of mature human T cells and NK cells, and is
expressed early in their development. Cross-linking CD7 positively
modulates T cell and NK cell activity as measured by calcium fluxes,
expression of adhesion molecules, cytokine secretion and proliferation. CD7
associates directly with phosphoinositol 3'-kinase, and CD7 ligation
induces production of D-3 phosphoinositides and tyrosine phosphorylation.
Severe combined immunodeficiency has been associated with a lack of
lymphocyte surface CD7. The CD7 ligand is unknown. The murine CD7 homolog
is encoded by a single gene on chromosome 11. In order to characterize the
role of CD7 in lymphocyte development and function we have eliminated the
CD7 gene by targeted disruption. CD7- deficient mice display normal
histology of thymus and spleen, normal lymphocyte populations in primary
and secondary lymphoid tissues, and normal serum Ig levels. Specific
antibody responses after immunization with T-dependent and T-independent
antigens are equivalent in wild-type and CD7 knockout mice. CD7-deficient
lymphocytes respond normally to T cell mitogenic and allogeneic stimuli,
and display normal NK cell cytotoxicity.
相似文献
7.
Androgen receptor YAC transgenic mice carrying CAG 45 alleles show trinucleotide repeat instability 总被引:1,自引:15,他引:1
La Spada AR; Peterson KR; Meadows SA; McClain ME; Jeng G; Chmelar RS; Haugen HA; Chen K; Singer MJ; Moore D; Trask BJ; Fischbeck KH; Clegg CH; McKnight GS 《Human molecular genetics》1998,7(6):959-967
X-linked spinal and bulbar muscular atrophy (SBMA) is caused by a CAG
repeat expansion in the first exon of the androgen receptor (AR) gene.
Disease-associated alleles (37-66 CAGs) change in length when transmitted
from parents to offspring, with a significantly greater tendency to shift
size when inherited paternally. As transgenic mice carrying human AR cDNAs
with 45 and 66 CAG repeats do not display repeat instability, we attempted
to model trinucleotide repeat instability by generating transgenic mice
with yeast artificial chromosomes (YACs) carrying AR CAG repeat expansions
in their genomic context. Studies of independent lines of AR YAC transgenic
mice with CAG 45 alleles reveal intergenerational instability at an overall
rate of approximately 10%. We also find that the 45 CAG repeat tracts are
significantly more unstable with maternal transmission and as the
transmitting mother ages. Of all the CAG/CTG repeat transgenic mice
produced to date the AR YAC CAG 45 mice are unstable with the smallest
trinucleotide repeat mutations, suggesting that the length threshold for
repeat instability in the mouse may be lowered by including the appropriate
flanking human DNA sequences. By sequence-tagged site content analysis and
long range mapping we determined that one unstable transgenic line has
integrated an approximately 70 kb segment of the AR locus due to
fragmentation of the AR YAC. Identification of the cis - acting elements
that permit CAG tract instability and the trans -acting factors that
modulate repeat instability in the AR YAC CAG 45 mice may provide insights
into the molecular basis of trinucleotide repeat instability in humans.
相似文献
8.
An eighth locus for autosomal dominant retinitis pigmentosa is linked to chromosome 17q 总被引:5,自引:2,他引:5
Bardienb Soraya; Ebenezer Neil; Greenberg Jacquie; Inglehearn Chris F.; Bartmann Lecia; Goliath Rene; Beighton Peter; Ramesar Rajkumar; Bhattacharya Shomi S. 《Human molecular genetics》1995,4(8):1459-1462
Retinitis pigmentosa is one of the most common causes of severevisual handicap in middle to late life. Prior to this report,seven loci had previously been mapped for the autosomal dominantform of this disorder (adRP). We now report the identificationof a novel adRP locus on chromosome 17q. To map the new locus,we performed linkage analysis with microsatellite markers ina large South African kindred. After exclusion of 13 RP candidategene loci (including rhodopsin and peripherin-RDS), we obtainedsignificant positive lod scores at zero recombination fraction( 相似文献
9.
Dou Q; Tarnuzzer RW; Williams RS; Schultz GS; Chegini N 《Molecular human reproduction》1997,3(11):1005-1014
10.
Miksch S Lumsden A Guenther UP Foernzler D Christen-Zäch S Daugherty C Ramesar RK Lebwohl M Hohl D Neldner KH Lindpaintner K Richards RI Struk B 《Human mutation》2005,26(3):235-248
Pseudoxanthoma elasticum (PXE) is a systemic heritable disorder that affects the elastic tissue in the skin, eye, and cardiovascular system. Mutations in the ABCC6 gene cause PXE. We performed a mutation screen in ABCC6 using haplotype analysis in conjunction with direct sequencing to achieve a mutation detection rate of 97%. This screen consisted of 170 PXE chromosomes in 81 families, and detected 59 distinct mutations (32 missense, eight nonsense, and six likely splice-site point mutations; one small insertion; and seven small and five large deletions). Forty-three of these mutations are novel variants, which increases the total number of PXE mutations to 121. While most mutations are rare, three nonsense mutations, a splice donor site mutation, and the large deletion comprising exons 23-29 (c.2996_4208del) were identified as relatively frequent PXE mutations at 26%, 5%, 3.5%, 3%, and 11%, respectively. Chromosomal haplotyping with two proximal and two distal polymorphic markers flanking ABCC6 demonstrated that most chromosomes that carry these relatively frequent PXE mutations have related haplotypes specific for these mutations, which suggests that these chromosomes originate from single founder mutations. The types of mutations found support loss-of-function as the molecular mechanism for the PXE phenotype. In 76 of the 81 families, the affected individuals were either homozygous for the same mutation or compound heterozygous for two mutations. In the remaining five families with one uncovered mutation, affected showed allelic compound heterozygosity for the cosegregating PXE haplotype. This demonstrates pseudo-dominance as the relevant inheritance mechanism, since disease transmission to the next generation always requires one mutant allelic variant from each parent. In contrast to other previous clinical and molecular claims, our results show evidence only for recessive PXE. This has profound consequences for the genetic counseling of families with PXE. 相似文献