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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
3.
Unilateral epidural analgesia occurring in a parturient three times in successive pregnancies is reported. Possible causes are reviewed, and clinical and radiological evidence in support of the most likely explanation are presented. 相似文献
4.
N-acetyl-L-aspartate and other amino acid metabolites in Alzheimer's disease brain: a preliminary proton nuclear magnetic resonance study. 总被引:1,自引:0,他引:1
We used proton nuclear magnetic resonance spectroscopy in this preliminary study of perchloric acid extracts of 12 Alzheimer's disease (AD) and five control brain samples to measure the relative levels of taurine, aspartate, glutamine, glutamate, gamma-aminobutyric acid (GABA), and the putative neuronal marker, N-acetyl-L-aspartate (NAA). We found no significant changes in taurine, aspartate, or glutamine. NAA was lower in AD compared with control, and this decrease correlated with the number of senile plaques and neurofibrillary tangles in adjacent tissue sections. GABA levels also were lower in AD brain. Glutamate levels were greater in AD than control and showed a close, inverse correlation with NAA levels. These findings suggest that the decrease in NAA reflects neuronal loss and that remaining neurons could be exposed to a relative excess of glutamate and a relative lack of GABA. If present in the neurotransmitter pool, this imbalance could result in neurotoxic cell damage. This hypothesis is further supported by in vitro and in vivo phosphorus 31 nuclear magnetic resonance findings. 相似文献
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6.
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
7.
8.
PDGF AA as mediator in nicotine-dependent carcinogenesis 总被引:1,自引:0,他引:1
Rakowicz-Szulczynska Eva M.; McIntosh David G.; Perry Michael; Smith McClure L. 《Carcinogenesis》1996,17(9):1813-1818
Effect of nicotine on PDGF AA and PDGF BB interaction with cervicalcancer SiHa cells was tested. [125I]PDGF AA was internalizedby cells and accumulated in the cytoplasm and nucleus (chromatin).In the absence of nicotine, maximal accumulation of [125I]PDGFAA inside the cells occurred after 1 day of incubation, whichwas followed by a progressive degradation of the growth factorduring the next 2, 3 and 5 days of cell exposure. In the presenceof 0.001 or 0.01% nicotine, accumulation of [125I]PDGF AA wasslightly higher than in the absence of nicotine, and maximalaccumulation occurred after 2 days of incubation. In the presenceof 0.1% nicotine, maximal accumulation occurred after 5 daysof incubation and was 20 and 14 times higher in the cytoplasmand chromatin, respectively. Nicotine-postponed degradationand increased nuclear accumulation of PDGF AA resulted in activationof RNA synthesis and cell proliferation. PDGF BB, which wasnot internalized by cells did not respond to nicotine treatment.The proposed mechanism of nicotine-PDGF AA co-carcinogenesismay involve inhibition of growth factor degradation at the lysosomallevel and an increased chromatin accumulation of the non-degradedPDGF. 相似文献
9.
10.
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.
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