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排序方式: 共有2103条查询结果,搜索用时 15 毫秒
41.
The vasa vasorum and angioplasty 总被引:2,自引:0,他引:2
Cragg AH; Einzig S; Rysavy JA; Castaneda-Zuniga WR; Borgwardt B; Amplatz K 《Radiology》1983,148(1):75-80
Interruption of flow in the vasa vasorum may lead to medial necrosis and aneurysm formation. The purpose of this study was to determine whether angioplasty produces significant alterations in the morphology or blood flow of the vasa vasorum of the dilated artery. The morphology of the canine vasa vasorum was studied before and after angioplasty; in a separate experiment vessel wall blood flow (VWBF) in canine carotid arteries was measured after angioplasty to determine whether physiologic regulation of the blood flow was disrupted by arterial dilation. No morphologic changes could be demonstrated in the vasa vasorum of the dilated artery; however, VWBF was increased by 1194 +/- 215% (mean +/- standard error, p less than 0.01) between 90 and 120 minutes after angioplasty. VWBF in the adjacent nondilated arterial segment was also increased (720 +/- 177% between 10-30 minutes, p less than 0.01) but returned toward normal after 60 minutes. Adenosine caused a "paradoxical" decrease in VWBF (p less than 0.05) of the dilated arterial segment while causing increased VWBF (p less than 0.05) in the thoracic aorta. Angioplasty appears to produce persistent hyperemia in the dilated arterial wall. A paradoxical response to adenosine suggests that vasa vasorum in the dilated arterial segment are maximally vasodilated. This may be due to mechanical disruption of vasomotor tone or to release of vasoactive substances. 相似文献
42.
Objective: To identify factors that influence a woman's decision to breast-feed.
Methodology: Five hundred and fifty-six women were recruited from the maternity wards of two Perth hospitals. Data were collected from a self-administered questionnaire completed by participants prior to discharge. Logistic regression analysis was used to determine factors influencing the initiation of breast-feeding.
Results: At discharge from hospital 83.8% of women were breast-feeding, including 6% who were giving complementary formula feeds. After controlling for potentially confounding demographic and biomedical factors, the father's reported preference for breast-feeding was found to be the most important factor influencing a woman's decision to breast-feed (OR 10.18).
Conclusion: Fathers participate in and influence the choice of infant feeding method and should be included in breast-feeding discussions. 相似文献
Methodology: Five hundred and fifty-six women were recruited from the maternity wards of two Perth hospitals. Data were collected from a self-administered questionnaire completed by participants prior to discharge. Logistic regression analysis was used to determine factors influencing the initiation of breast-feeding.
Results: At discharge from hospital 83.8% of women were breast-feeding, including 6% who were giving complementary formula feeds. After controlling for potentially confounding demographic and biomedical factors, the father's reported preference for breast-feeding was found to be the most important factor influencing a woman's decision to breast-feed (OR 10.18).
Conclusion: Fathers participate in and influence the choice of infant feeding method and should be included in breast-feeding discussions. 相似文献
43.
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45.
Abril N; Luque-Romero FL; Prieto-Alamo MJ; Rafferty JA; Margison GP; Pueyo C 《Carcinogenesis》1997,18(10):1883-1888
Here we confirm and extend our previous studies demonstrating that the
mutagenic potency of 1,2-dibromoethane (DBE) and dibromomethane (DBM) is
markedly enhanced (not prevented) in bacteria expressing the O6-
alkylguanine-DNA alkyltransferase (ATase) encoded by the Escherichia coli
ogt gene. We demonstrate that, in close parallel with mutagenesis, the Ogt
ATase sensitizes the bacteria to the lethal effects of these carcinogens,
suggesting that one or more of the potentially mutagenic lesions induced by
DBE and DBM in the presence of Ogt has additional lethal capacity. We
further demonstrate that the sensitization to both lethality and
mutagenesis by DBE and DBM is a property shared by other DNA
alkyltransferases. This objective was accomplished by quantifying the
induction of mutations and lethal events in ogt- ada- E. coli expressing an
exogenous bacterial or mammalian ATase from a multicopy plasmid. Mammalian
recombinant ATases enhanced the lethal and mutagenic actions of DBE and
suppressed the lack of sensitivity of the vector- transformed bacteria to
DBM. In most cases the order of effectiveness of the ATases ranked: murine
> human > Ogt > rat. Further comparisons included the full-length
Ada ATase from E. coli and a truncated Ada version (T-ada) that retains the
O6-methylguanine binding domain of the protein. The full-length Ada ATase
was effective in enhancing the lethality but not the mutagenicity induced
by DBE and DBM. The T-ada ATase provided less sensitization than Ada to
lethality by DBE, but of the three bacterial ATases T-ada yielded the
highest sensitization to mutagenesis by this compound. T-ada and Ada ATases
were in general less effective than the mammalian versions, with the
exception of the rat recombinant ATase. The effectiveness of the different
mammalian and bacterial ATases in promoting the deleterious actions of
dibromoalkanes was compared with the effectiveness of these proteins in
suppressing the lethal and mutagenic effects induced by
N-nitroso-N-methylurea. The ability to sensitize E. coli to the lethal and
mutagenic effects of DBE and DBM seems restricted to DNA alkyltransferase,
since overexpression of thioredoxin (Trx) or glutaredoxin (Grx1) in ogt-
ada- cells showed no effect, in spite of the reported potential of
bioactive dihaloethane- derived species to alkylate Trx.
相似文献
46.
Dibenzo[a,l]pyrene-induced DNA adduction, tumorigenicity, and Ki-ras oncogene mutations in strain A/J mouse lung 总被引:1,自引:0,他引:1
Prahalad AK; Ross JA; Nelson GB; Roop BC; King LC; Nesnow S; Mass MJ 《Carcinogenesis》1997,18(10):1955-1963
Dibenzo[a,l]pyrene (DB[a,l]P), an environmental polycyclic aromatic
hydrocarbon, is the most potent carcinogen ever tested in mouse skin and
rat mammary gland. In this study, DB[a,l]P was examined for DNA adduction,
tumorigenicity, and induction of Ki-ras oncogene mutations in tumor DNA in
strain A/J mouse lung. Groups of mice received a single i.p. injection of
0.3, 1.5, 3.0, or 6.0 mg/kg DB[a,l]P in tricaprylin. Following treatment,
DNA adducts were measured at times between 1 and 28 days, while tumors were
counted at 250 days and analyzed for the occurrence of point mutations in
codons 12 and 61 of the Ki-ras oncogene. DB[a,l]P in strain A/J mouse lung
induced six major and four minor DNA adducts. Maximal levels of adduction
occurred between 5 and 10 days after injection followed by a gradual
decrease. DB[a,l]P-DNA adducts in lung tissue were derived from both anti-
and syn-11,12- dihydroxy-13,14-epoxy-
11,12,13,14-tetrahydrodibenzo[a,l]pyrene (DB[a,l]PDE) and both
deoxyadenosine (dAdo) and deoxyguanosine (dGuo) residues in DNA as revealed
by cochromatography. The major adduct was identified as a product of the
reaction of an anti-DB[a,l]PDE with dAdo in DNA. DB[a,l]P induced
significant numbers of lung adenomas in a dose- dependent manner, with the
highest dose (6.0 mg/kg) yielding 16.1 adenomas/mouse. In
tricaprylin-treated control animals, there were 0.67 adenomas/mouse. Based
on the administered dose, DB[a,l]P was more active than other environmental
carcinogens including benzo[a]pyrene. As a function of time-integrated DNA
adduct levels, DB[a,l]P induced lung adenomas with about the same potency
as other PAHs, suggesting that the adducts formed by DB[a,l]P are similar
in carcinogenic potency to other PAHs in the strain A/J mouse lung model.
Analysis of the Ki- ras mutation spectrum in DB[a,l]P-induced lung tumors
revealed the predominant mutations to be G-->T transversions in the
first base of codon 12, A-->G transitions in the second base of codon
12, and A-->T transversions in the second or third base of codon 61,
concordant with the DNA adduct profile.
相似文献
47.
Nesnow S; Davis C; Nelson G; Ross JA; Allison J; Adams L; King LC 《Carcinogenesis》1997,18(10):1973-1978
C3H10T1/2CL8 (C3H10T1/2) mouse embryo fibroblasts were used to study the in
vitro carcinogenic activities of dibenzo[a,l]pyrene (DB[a,l]P) and
benzo[a]pyrene (B[a]P). The morphological transforming activities of these
rodent carcinogens were compared using replicate concentration- response
studies. In concentration ranges where both polycyclic aromatic
hydrocarbons (PAHs) were active, DB[a,l]P proved to be four to 12 times as
potent as B[a]P based on concentration. At lower concentrations DB[a,l]P
was active at 0.10 and 0.20 microM, concentrations where B[a]P was
inactive. This makes DB[a,l]P the most potent non-methylated PAH evaluated
to date in C3H10T1/2 cells. DNA adducts of DB[a,l]P in C3H10T1/2 cells were
analyzed by both TLC and TLC/HPLC 32P-postlabeling methods using
mononucleotide 3'-phosphate adduct standards derived from the reactions of
anti-DB[a,l]P-11,12-diol- 13,14-epoxide (anti-DB[a,l]PDE) and
syn-DB[a,l]P-11,12-diol-13,14- epoxide (syn-DB[a,l]PDE) with deoxyadenosine
3'-monophosphate and deoxyguanosine 3'-monophosphate. All of the DNA
adducts observed in C3H10T1/2 cells treated with DB[a,l]P were identified
as being derived from the metabolism of DB[a,l]P to its fjord region diol
epoxides through DB[a,l]P-11,12-diol. The predominant adduct was identified
as an anti-DB[a,l]PDE-deoxyadenosine adduct. Other major adducts were anti-
DB[a,l]PDE-deoxyguanosine and syn-DB[a,l]PDE-deoxyadenosine adducts with
minor amounts of syn-DB[a,l]PDE-deoxyguanosine adducts. These DNA adduct
data are consistent with similar findings of DB[a,l]PDE- deoxyadenosine
adducts in mouse skin studies and human mammary cells in culture.
相似文献
48.
Assessment of the mutagenicity of dichloroacetic acid in lacI transgenic B6C3F1 mouse liver 总被引:2,自引:0,他引:2
Dichloroacetic acid (DCA) is a chlorination byproduct found in finished
drinking water. When administered in drinking water this chemical has been
shown to produce hepatocellular adenomas and carcinomas in B6C3F1 mice over
the animal's lifetime. In this study, we investigated whether mutant
frequencies were increased in mouse liver using treatment protocols that
yielded significant tumor induction. DCA was administered continuously at
either 1.0 or 3.5 g/l in drinking water to male transgenic B6C3F1 mice
harboring the bacterial lacI gene. Groups of five or six animals were
killed at 4, 10 or 60 weeks and livers removed. At both 4 and 10 weeks of
treatment, there was no significant difference in mutant frequency between
the treated and control animals at either dose level. At 60 weeks, mice
treated with 1.0 g/l DCA showed a 1.3-fold increase in mutant frequency
over concurrent controls (P = 0.05). Mice treated with 3.5 g/l DCA for 60
weeks had a 2.3-fold increase in mutant frequency over the concurrent
controls (P = 0.002). The mutation spectrum recovered from mice treated
with 3.5 g/l DCA for 60 weeks contained G:C-->A:T transitions (32.79%)
and G:C-->T:A transversions (21.31%). In contrast, G:C-->A:T
transitions comprised 53.19% of the recovered mutants among control
animals. Although only 19.15% of mutations among the controls were at T:A
sites, 32.79% of the mutations from DCA-treated animals were at T:A sites.
This is consistent with the previous observation that the proportion of
mutations at T:A sites in codon 61 of the H-ras gene was increased in
DCA-induced liver tumors in B6C3F1 mice. The present study demonstrates
DCA-associated mutagenicity in the mouse liver under conditions in which
DCA produces hepatic tumors.
相似文献
49.
50.