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排序方式: 共有635条查询结果,搜索用时 15 毫秒
1.
Golli M; Van Nhieu JT; Mathieu D; Zafrani ES; Cherqui D; Dhumeaux D; Vasile N; Rahmouni A 《Radiology》1994,190(3):741
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Regulation of calcium release from mouse calvariae by glycosaminoglycans and known modulators of bone resorption has been examined. Anticoagulant and nonanticoagulant fragments of heparin were combined with parathyroid hormone (PTH) and interleukin-1, beta (IL1), and calcium release from radiolabeled bone was determined. Three heparin fragments, dextran and dextran sulfate, when tested alone, released similar amounts of calcium as did native heparin alone. Suboptimal concentrations of PTH combined with heparin fragments of varying amounts of anticoagulant activity released similar amounts of calcium as did native heparin. When dextran or dextran sulfate was combined with PTH, the amount of calcium released was significantly greater than dextran or dextran sulfate alone but not from PTH when tested alone. Heparin, in combination with 0.1 mu/ml IL1, stimulated significant calcium release compared to heparin but not to IL1 tested alone. There was no significant difference in calcium release when hyaluronic acid in combination with 0.1 U/ml IL1 was compared to the amount of calcium released by either agent alone. Two of the heparin fragments combined with 0.1 U/ml IL1 significantly inhibited calcium release compared to IL1 alone. In combination with 1.0 U/ml of IL1, heparin and hyaluronic acid inhibited calcium release compared to IL1 alone but this inhibition was not significant. The heparin fragments, combined with 1.0 U/ml IL1, had decreasing inhibitory activity as the degree of anticoagulant activity decreased. A comparison of glycosaminoglycan-modulated calcium release in mouse calvariae to that release in mouse radii/ulnae revealed consistently greater percentages of calcium release from calvariae.(ABSTRACT TRUNCATED AT 250 WORDS) 相似文献
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Inhibition of 2-nitropropane-induced rat liver DNA and RNA damage by benzyl selenocyanate 总被引:5,自引:2,他引:3
We observed that pretreatment of male F344 rats with benzyl selenocyanate,
a versatile organoselenium chemopreventive agent in several animal model
systems, decreases the levels of DNA and RNA modifications produced in the
liver by the hepatocarcinogen 2- nitropropane. To clarify the mechanisms
involved, we pretreated male F344 rats with either benzyl selenocyanate,
its sulfur analog benzyl thiocyanate, phenobarbital or cobalt
protoporphyrin IX; the latter is a depletor of P450. We then determined (1)
the ability of liver microsomes to denitrify 2-nitropropane, (2) effects on
2-nitropropane- induced liver DNA and RNA modifications and (3) amount of
nitrate excreted in rat urine following administration of the carcinogen.
Pretreatment with benzyl selenocyanate or phenobarbital increased the
denitrification activity of liver microsomes by 217 and 765%, respectively,
increased liver P4502B1 by 31- and 435-fold, respectively, decreased the
levels of 2-nitropropane-induced modifications in liver DNA (29-70% and
17-30%, respectively) and RNA (67-85% and 30-50%, respectively), and
increased the 24-h urinary excretion of nitrate by 157 and 209%,
respectively. Pretreatment with benzyl thiocyanate had no significant
effect on any of these parameters. Pretreatment with cobalt protoporphyrin
IX decreased liver P4502B 1 by 87%, decreased the denitrification activity
of liver microsomes by 76%, decreased the 24 h urinary excretion of nitrate
by 88.5%, but increased the extent of 2-nitropropane-induced liver nucleic
acid modifications by 17-67%. These results indicate that the metabolic
sequence from 2-nitropropane to the reactive species causing DNA and RNA
modifications does not involve the removal of the nitro group. Moreover,
they suggest that benzyl selenocyanate inhibits 2-NP-induced liver nucleic
acid modifications in part by increasing its detoxication through induction
of denitrification, although it is evident that other mechanisms must also
be involved.
相似文献
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A model of corrective gene transfer in X-linked ichthyosis 总被引:5,自引:0,他引:5
Freiberg RA; Choate KA; Deng H; Alperin ES; Shapiro LJ; Khavari PA 《Human molecular genetics》1997,6(6):927-933
Single gene recessive genetic skin disorders offer attractive prototypes
for the development of therapeutic cutaneous gene delivery. We have
utilized X-linked ichthyosis (XLI), characterized by loss of function of
the steroid sulfatase arylsulfatase C (STS), to develop a model of
corrective gene delivery to human skin in vivo. A new retroviral expression
vector was produced and utilized to effect STS gene transfer to primary
keratinocytes from XLI patients. Transduction was associated with
restoration of full-length STS protein expression as well as steroid
sulfatase enzymatic activity in proportion to the number of proviral
integrations in XLI cells. Transduced and uncorrected XLI keratinocytes,
along with normal controls, were then grafted onto immunodeficient mice to
regenerate full thickness human epidermis. Unmodified XLI keratinocytes
regenerated a hyperkeratotic epidermis lacking STS expression with
defective skin barrier function, effectively recapitulating the human
disease in vivo. Transduced XLI keratinocytes from the same patients,
however, regenerated epidermis histologically indistinguishable from that
formed by keratinocytes from patients with normal skin. Transduced XLI
epidermis demonstrated STS expression in vivo by immunostaining as well as
a normalization of histologic appearance at 5 weeks post-grafting. In
addition, transduced XLI epidermis demonstrated a return of barrier
function parameters to normal. These findings demonstrate corrective gene
delivery in human XLI patient skin tissue at both molecular and functional
levels and provide a model of human cutaneous gene therapy.
相似文献
9.
A. KIJLSTRA D. W. KNUTSON M. R. DAHA L. A. VAN ES 《Scandinavian journal of immunology》1979,10(5):421-429
The in vivo behaviour of well-defined immune complexes in rats was studied using complexes derived from DNP-conjugated bovine thyroglobulin (DNP-BTG) and purified specific goat anti-DNP IgG. Both clearance and glomerular localization were mainly dependent on the nature of the antigen. Soluble immune complexes formed with DNP17-BTG were cleared faster and showed a more marked localization in the glomerular mesangium than complexes formed with DNP3.4-BTG. A slight increase in the antibody to antigen ratio seemed to facilitate mesangial localization of soluble immune complexes. Insoluble immune complexes showed temporary localization as microemboli in the lumina of glomerular and peritubular capillaries. This study thus shows that not only the size and composition of the complexes but also the nature of the antigen within the complex can influence the clearance and organ localization of circulating immune complexes. 相似文献
10.
Constitutional and mosaic large NF1 gene deletions in neurofibromatosis type 1. 总被引:7,自引:1,他引:7
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S A Rasmussen S D Colman V T Ho C R Abernathy P H Arn L Weiss C Schwartz R A Saul M R Wallace 《Journal of medical genetics》1998,35(6):468-471
A set of neurofibromatosis type 1 (NF1) patients was screened for large NF1 gene deletions by comparing patient and parent genotypes at 10 intragenic polymorphic loci. Of 67 patient/parent sets (47 new mutation patients and 20 familial cases), five (7.5%) showed loss of heterozygosity (LOH), indicative of NF1 gene deletion. These five patients did not have severe NF1 manifestations, mental retardation, or dysmorphic features, in contrast to previous reports of large NF1 deletions. All five deletions were de novo and occurred on the maternal chromosome. However, two patients showed partial LOH, consistent with somatic mosaicism for the deletion, suggesting that mosaicism may be more frequent in NF1 than previously recognised (and may have bearing on clinical severity). We suggest that large NF1 deletions (1) are not always associated with unusual clinical features, (2) tend to occur more frequently on maternal alleles, and (3) are an important mechanism for constitutional and somatic mutations in NF1 patients. 相似文献