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排序方式: 共有244条查询结果,搜索用时 15 毫秒
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64.
Lisa M. Torres Bocena Konopnika Liliana N. Berti‐Mattera Carole Liedtke Andrea Romani 《Alcoholism, clinical and experimental research》2010,34(9):1659-1669
Background: Rats chronically fed ethanol for 3 weeks presented a marked decreased in total hepatic Mg2+ content and required approximately 12 days to restore Mg2+ homeostasis upon ethanol withdrawal. This study was aimed at investigating the mechanisms responsible for the EtOH‐induced delay. Methods: Hepatocytes from rats fed ethanol for 3 weeks (Lieber‐De Carli diet—chronic model), rats re‐fed a control diet for varying periods of time following ethanol withdrawal, and age‐matched control rats fed a liquid or a pellet diet were used. As acute models, hepatocytes from control animals or HepG2 cells were exposed to varying doses of ethanol in vitro for 8 minutes. Results: Hepatocytes from ethanol‐fed rats presented a marked inhibition of Mg2+ accumulation and a defective translocation of PKCε to the cell membrane. Upon ethanol withdrawal, 12 days were necessary for PKCε translocation and Mg2+ accumulation to return to normal levels. Exposure of control hepatocytes or HepG2 cells to a dose of ethanol as low as 0.01% for 8 minutes was already sufficient to inhibit Mg2+ accumulation and PKCε translocation for more than 60 minutes. Also in this model, recovery of Mg2+ accumulation was associated with restoration of PKCε translocation. The use of specific antisense in HepG2 cells confirmed the involvement of PKCε in modulating Mg2+ accumulation. Conclusions: Translocation of PKCε isoform to the hepatocyte membrane is essential for Mg2+ accumulation to occur. Both acute and chronic ethanol administrations inhibit Mg2+ accumulation by specifically altering PKCε translocation to the cell membrane. 相似文献
65.
AB Houston MJ Brodie MR Moore GG Thompson JB Stephenson 《Archives of disease in childhood》1977,52(8):646-650
A 9-year-old boy with mental deterioration and epilepsy suffered an acute attack of hereditary coproporphyria associated with worsening of seizure control. Leucocyte coproporphyrinogen oxidase activity was undetectable in the patient during this attack, and was reduced in his mother, a latent case. The complex relationship between porphyria, epilepsy, and anticonvulsant drugs is discussed. 相似文献
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Artyom Sedrakyan Viola Vaccarino John A. Elefteriades Jennifer A. Mattera Zhenqiu Lin Sarah A. Roumanis Harlan M. Krumholz 《Quality of life research》2006,15(7):1153-1160
Background: The decision to replace or repair mitral valves is often a difficult decision, and outcomes from the patients’ perspective
should guide decision-making. We investigated whether the change in health related quality of life (HRQOL) after mitral valve
surgery is different after valve repairs compared with replacements.Methods: We prospectively studied 25 patients with mitral valve replacement and 45 patients with valve repairs performed in 1998–99.
We measured HRQOL at baseline and at 18 months using the Medical Outcomes Trust Short Form 36-item Health Survey (SF-36) questionnaire.
We compared mean HRQOL scores of the groups with age-adjusted U.S. population scores. We used analysis of covariance to determine
a change in HRQOL within groups (repair or replacement) and if the change in HRQOL was different between the groups.Results: We found few differences between the groups, with more men and simultaneous coronary artery bypass graft surgery in the
valve repair group and more prior operation in the valve replacement group. HRQOL improved after surgery in most domains,
and was comparable to age-adjusted U.S. norms in the valve repair group. In the multivariable analysis, mitral valve repair
recipients reported higher social functioning compared with patients who received valve replacement (p = 0.04). We did not find other statistically significant differences. However, the adjusted improvements in the component
scales of physical functioning (PCS) and mental functioning (MCS) were substantial in the valve repair group (mean changes:
PCS = 6.8, p = 0.003; MCS = 8.1, p = 0.014) and less pronounced in the replacement group (mean changes: PCS = 3.6, p = 0.09; MCS = 4.3, fsp = 0.16).Conclusions: While many considerations influence the decision to repair or replace mitral valves, these findings suggest that repair
may be better from the health status perspective. Further studies are necessary to validate this finding. 相似文献
68.
Adamson PB Vanoli E Mattera GG Germany R Gagnol JP Carminati P Schwartz PJ 《Journal of cardiovascular pharmacology》2003,42(2):169-173
Inotropic agents for acute decompensated heart failure are associated with a lack of efficacy or increased mortality. New compounds are needed to support patients with acute exacerbations of heart failure. This study examined the hemodynamic effects of a new inotropic agent (PST-2744) in dogs with chronic ischemic heart failure. Eight mongrel dogs at low risk for postmyocardial infarction (MI) sudden death entered the protocol. Dogs were studied after ischemic left ventricular dysfunction was induced by repeated injections of latex microspheres into the circumflex artery until the ejection fraction reached 35%. Hemodynamic parameters were measured at baseline and peak drug effect (PST-2744 5 microg.kg-1.min-1). In 5 animals, PST-2744 effects were compared with dobutamine. Heart rates, PR intervals and QT intervals were unchanged following PST-2744 administration. PST-2744 increased contractility (+dP/dt) by 56% from 1881 +/- 282 mm Hg/s to 2939 +/- 734 mm Hg/s (P < 0.01). The inotropic effect of PST-2744 was equal to that produced by 5-microg.kg-1.min-1 dobutamine (56% increase in +dP/dt), but peak heart rates were significantly higher with dobutamine (129 +/- 24 bpm PST-2744 versus 160 +/- 6 bpm 5-microg.kg-1.min-1 dobutamine, P < 0.002). No arrhythmias or conduction delays were seen with either compound. PST-2744 is an effective inotropic agent without positive chronotropic effect in subjects with stable moderate left ventricular dysfunction. 相似文献
69.
Alteration in methyl-methanesulfonate-induced poly(ADP-ribosyl)ation by 2-butoxyethanol in Syrian hamster embryo cells 总被引:1,自引:0,他引:1
The effects of 2-butoxyethanol (2-BE) on poly(ADP-ribosyl)ation were
studied in Syrian hamster embryo (SHE) cells by measuring the cellular
concentrations of the polymer poly(ADP-ribose) (pADPr) and of NAD+, the
substrate of poly(ADP-ribose) polymerase (PARP). As biotransformation
pathways of ethylene glycol ethers involve NAD+-dehydrogenases, it was
hypothesized that 2-BE could reduce poly(ADP-ribosyl)ation by consuming
NAD+. As a result DNA repair could be altered, which would explain that
2-BE had been shown to potentiate the effects of clastogenic substances
such as methyl-methanesulfonate (MMS). In this study, the effects of 2- BE
on MMS-induced pADPr metabolism were analyzed. The results indicated that:
(i) 2-BE (5 mM) by itself did not influence significantly pADPr or NAD+
levels. (ii) 2-BE inhibited pADPr synthesis in MMS (0.2 mM)- pretreated
cells, without any change in NAD+ concentrations. (iii) MMS treatment,
which rapidly increased pADPr levels, also affected the
poly(ADP-ribosyl)ation system as a secondary effect by damaging cell
structures. Membrane permeabilization, which occurred at concentrations
>1 mM MMS, led to a dramatic leakage of cellular NAD+ resulting in a
strong reduction in pADPr levels. (iv) A bleomycin pulse (100 microM)
applied after MMS and/or 2-BE treatment confirmed that 2-BE reduced
poly(ADP-ribosyl)ation capacities of MMS-treated cells, though the glycol
ether had no effect alone. This study confirmed that the inhibition of
pADPr synthesis could be responsible for the synergistic effects of 2-BE
with genotoxic substances. The mechanism of this inhibition cannot be
explained by a lack of NAD+ at the concentrations of 2-BE tested.
相似文献
70.
While inhaled polycyclic aromatic hydrocarbons have long been suspected to
induce lung cancer in humans, their dosimetry has not been fully
elucidated. A key question is whether the critical exposure occurs during
absorption in the lungs, or if toxicants in the systemic circulation
contribute significantly to lung cancer risk. In particular, data are
needed to determine how the physical properties of inhalants affect local
dosimetry in the respiratory tract. Pyrene, a tobacco smoke component, was
selected for study because it has physical properties between those of
highly lipophilic benzo[a]pyrene and water- soluble nitrosamines. Aliquots
of 5 ng of pyrene dissolved in a phospholipid/ saline suspension were
instilled as a single-spray bolus in the posterior trachea of the dog just
anterior to the carina. For 3 h after instillation, blood was repeatedly
sampled from the azygous vein, which drains the mucosa around the point of
instillation, and from both sides of the systemic circulation. At 3 h
post-instillation, tissue samples were taken. Autoradiography was used to
determine the depth distribution of pyrene in the tracheal mucosa. The
concentration of pyrene-equivalent radioactivity in the azygous vein peaked
9 min after the instillation. At approximately 30 min after instillation, a
rapid early clearance phase shifted into a distinctly slower second
clearance phase. Rates of rapid clearance were, however, sufficiently slow
to indicate diffusion-limited absorption of pyrene in the trachea. This
finding was corroborated by high concentrations of pyrene in the epithelium
as determined by autoradiography. High epithelial concentration of pyrene
combined with a slow penetration into the circulating blood allowed
substantial first-pass metabolic conversion of pyrene in the tracheal
mucosa. A total of 13% of the instilled pyrene was retained in the tracheal
mucosa 3.2 h after instillation; of this, 29% was parent compound, 52% was
organic-extractable metabolites, 14% was water-soluble metabolites and 6%
(approximately 1% of the instilled amount) was covalently bound to tracheal
tissues. Results support the inference that lipophilic protoxicants,
because of slow, diffusion-limited absorption, are more likely than
water-soluble protoxicants to be bioactivated in the lining epithelium and,
in turn, induce first-pass toxicity at the site of entry. In addition,
limitations were identified in the use of systemically distributed
biomarkers of PAHs, such as urinary hydroxypyrene levels, as indicators of
the biologically effective dose in airway target cells.
相似文献