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Bruha R Vitek L Marecek Z Pospisilova L Nevsimalova S Martasek P Petrtyl J Urbanek P Jiraskova A Malikova I Haluzik M Ferenci P 《Journal of inherited metabolic disease》2012,35(3):541-548
Background &; Aims
Wilson disease (WD) is an inherited disorder of copper disposition caused by an ATP7B transporter gene mutation, leading to copper accumulation in predisposed tissues. In addition to a genetic predisposition, other factors are likely to contribute to its clinical manifestation. The aim of the study was to assess whether oxidative stress affects the phenotypic manifestation of WD.Methods
In 56 patients with WD (29 men; 26 with the hepatic form, 22 with the neurologic form, and eight asymptomatic; mean age 38.5?±?12 years), total serum antioxidant capacity (TAC) and inflammatory parameters (hs-CRP, IL-1??, IL-2, IL-6, IL-10, and TNF-??) were analyzed and related to the clinical manifestation, and mutations of the ATP7B gene. The control group for the TAC and inflammatory parameters consisted of 50 age- and gender-matched healthy individuals.Results
WD patients had a significantly lower TAC (p?0.00001), lower IL-10 levels (p?=?0.039), as well as both higher IL-1?? (p?=?0.019) and IL-6 (p?=?0.005) levels compared to the control subjects. TNF-??, hs-CRP, and IL-2 did not differ from the controls. Patients with the neurological form of WD had a significantly lower TAC than those with the hepatic form (p?0.001). In addition, the lower TAC was associated with the severity of the neurological symptoms (p?=?0.02). No relationship between the inflammatory parameters and clinical symptoms was found.Conclusions
Data from our study suggest that the increased oxidative stress contributes significantly to the clinical manifestation of WD; as a lower TAC is associated with the neurological symptoms in WD patients. 相似文献94.
Fath-Ordoubadi F Barac Y Abergel E Danzi GB Kerner A Nikolsky E Halabi M Mamas M El-Omar M Fraser D Roguin A 《The American journal of cardiology》2012,110(5):636-642
Women have a higher risk of adverse outcomes after percutaneous coronary intervention (PCI) than men. However, in acute coronary syndrome (ACS), long-term outcomes after contemporary PCI with drug-eluting stent (DES) have not been fully investigated. We aimed to test the impact of gender on outcomes in patients with ACS after PCI with DES. We analyzed all patients with ACS from the prospective NOBORI-2 trial who underwent PCI with a Nobori DES from 2008 through 2009 in 125 centers worldwide. End points of the study were target lesion failure, cardiac death, myocardial infarction (MI), and clinically driven target lesion revascularization, and major adverse cardiac events (composite of cardiac death, MI, and target vessel revascularization) at 1 year and yearly up to 5 years. There were 1,640 patients with ACS, 1,268 men (77%) and 372 women (23%). Compared to men, women were 5 years older and more frequently had co-morbidities such as diabetes mellitus and hypertension. There were no gender differences for cardiac death (1.3% vs 2.7%), MI (2.1% vs 3.2%), or target lesion revascularization (2.6% vs 3.8%) at 1 year after the procedure for men and women, respectively. The trend was the same at 2 years (cardiac death 2.0% vs 2.3%, MI 2.5% vs 3.5%, target lesion revascularization 3.2% vs 4.6%). Target lesion failure rates were 4.5% and 5.9% at 1 year and 5.7% and 7.3% at 2 years in men and women, respectively (p = NS). Multivariate analysis, which included age, hypertension, diabetes mellitus, and number of diseased vessels, showed that gender was not a predictor for outcome. There were no differences in bleeding or stent thrombosis rates. Relief from anginal symptoms was similar. The same rate of adherence to dual antiplatelet therapy was observed and reached 73% at 1 year and 31% at 2 years after the ACS event and PCI. In conclusion, although women had worse baseline characteristics, no differences in outcomes were observed between men and women treated for ACS with contemporary DES. 相似文献
95.
Lansky AJ Brar SS Yaqub M Sood P Applegate RJ Lazar D Jankovic I Hermiller JB Koo K Sudhir K Stone GW 《The American journal of cardiology》2012,110(1):21-29
Routine angiographic follow-up after bare-metal stent implantation has been associated with an increase in coronary revascularization. The impact of angiographic follow-up after drug-eluting stent placement remains poorly characterized. The prospective, randomized, single-blinded SPIRIT III trial assigned patients to the everolimus-eluting stent or the paclitaxel-eluting stent (PES). Major adverse cardiovascular events (cardiac death, myocardial infarction, and ischemia-driven target lesion revascularization [ID-TLR]) at 3 years were assessed by angiographic versus clinical-only follow-up at 8 months ± 28 days and a landmark survival analysis from 9 months to 3 years. Of 1,002 patients, 564 patients were assigned to angiographic follow-up at 8 months ± 28 days and 438 patients underwent clinical follow-up alone. Three-year major adverse cardiovascular event rates were 10.6% in the angiographic group and 12.0% in the clinical follow-up group (p = 0.64). Ischemia-driven revascularization increased twofold at 9 months, but no difference was noted in ID-TLR for either device. Non-ID-TLR was significantly higher in patients in the angiographic group (4.5% vs 1.0%, p = 0.002), a difference resulting from PES (9.1% vs 0.7%, p = 0.0007) rather than everolimus-eluting stent (2.2% vs 1.1%, p = 0.36) treatment. The landmark analysis showed no significant differences between the angiographic and clinical follow-up groups from 9 months to 3 years of major clinical outcomes. In conclusion, routine angiographic follow-up in SPIRIT III did not increase rates of ID-TLR compared to clinical follow-up alone. Despite higher nonischemia-driven revascularization rates with angiographic follow-up of patients with PESs, none of the safety end points were adversely affected. 相似文献
96.
Baričević M Ratkaj I Mladinić M Zelježić D Kraljević SP Lončar B Stipetić MM 《Clinical oral investigations》2012,16(1):325-331
Given long-term effect on oral tissues due to contact with dental appliances, the biocompatibility studies of casting alloys
are of great importance. It has been previously documented that metal dental appliances, due to corrosion, might induce genotoxic
and mutagenic effects in cells. Therefore, the aim of presented study was to examine the genotoxicity of two dental casting
alloys (Co-Cr-Mo and Ni-Cr) commonly used in fixed and removable prosthodontic appliances that are in contact with the oral
epithelium for 5 years or more. For that purpose, 55 age-matched subjects were included in the study; 30 wearers of prosthodontic
appliances and 25 controls. Buccal cells of oral mucosa were collected and processed for further analysis. The cell viability
has been assessed by trypan blue exclusion test, while genotoxic effect of metal ions on DNA in oral mucosa cells was studied
by use of alkaline comet assay. Results have shown significantly higher comet assay parameters (tail length and percentage
DNA in the tail) in the group wearing metal appliances. Both subjects with Co-Cr-Mo alloy and Ni-Cr alloy showed significantly
higher comet assay parameters when compared with controls. It has been confirmed that metal ions released by the two base
metal dental casting alloys examined in this study, might be responsible for DNA damage of oral mucosa cells. Therefore, the
results of this study emphasize the importance of the in vivo evaluation of dental materials with respect to their genotoxicity,
which is of major importance to ensure long-term biocompatibility. 相似文献
97.
Porrata LF Ristow K Habermann TM Witzig TE Colgan JP Inwards DJ Ansell SM Micallef IN Johnston PB Nowakowski GS Thompson C Markovic SN 《British journal of haematology》2012,157(3):321-330
The pathological background in nodular lymphocyte predominant Hodgkin lymphoma (NLPHL) consists of lymphocytes and histocytes. This study analysed the peripheral blood absolute lymphocyte count/absolute monocyte count ratio at diagnosis (ALC/AMC-DX) on the impact of survival in NLPHL. One hundred and three consecutive NLPHL patients that were followed at Mayo Clinic from 1974 to 2010 were included in the study. Receiver operating characteristic and area under the curve were used for ALC/AMC-DX cut-off value analysis and proportional-hazards models were used to compare survival based on the ALC/AMC-DX ratio. With a median follow-up of 8·9 years (range: 0·3-31 years), an ALC/AMC-DX ≥2·1 was the best cut-off value for survival with an area under the curve of 0·82, a sensitivity of 70% and specificity of 84%. After adjusting for the International Prognostic Score (IPS), ALC/AMC-DX remained an independent prognostic factor for overall survival [Hazard Ratio (HR), 0·33, 95% confidence interval (CI), 0·15-0·71%, P < 0·004]; lymphoma-specific survival (HR, 0·05; 95%CI, 0·01-0·68%, P < 0·002); progression-free survival (HR, 0·30; 95%CI, 0·14-0·60%, P < 0·006), and time to progression (HR, 0·06, 95%CI, 0·04-0·30%, P < 0·004). ALC/AMC-DX is a low cost, already standarized, biomarker to predict clinical outcomes in NLPHL. 相似文献
98.
Carnevale D Mascio G D'Andrea I Fardella V Bell RD Branchi I Pallante F Zlokovic B Yan SS Lembo G 《Hypertension》2012,60(1):188-197
Although epidemiological data associate hypertension with a strong predisposition to develop Alzheimer disease, no mechanistic explanation exists so far. We developed a model of hypertension, obtained by transverse aortic constriction, leading to alterations typical of Alzheimer disease, such as amyloid plaques, neuroinflammation, blood-brain barrier dysfunction, and cognitive impairment, shown here for the first time. The aim of this work was to investigate the mechanisms involved in Alzheimer disease of hypertensive mice. We focused on receptor for advanced glycation end products (RAGE) that critically regulates Aβ transport at the blood-brain barrier and could be influenced by vascular factors. The hypertensive challenge had an early and sustained effect on RAGE upregulation in brain vessels of the cortex and hippocampus. Interestingly, RAGE inhibition protected from hypertension-induced Alzheimer pathology, as showed by rescue from cognitive impairment and parenchymal Aβ deposition. The increased RAGE expression in transverse aortic coarctation mice was induced by increased circulating advanced glycation end products and sustained by their later deposition in brain vessels. Interestingly, a daily treatment with an advanced glycation end product inhibitor or antioxidant prevented the development of Alzheimer traits. So far, Alzheimer pathology in experimental animal models has been recognized using only transgenic mice overexpressing amyloid precursor. This is the first study demonstrating that a chronic vascular insult can activate brain vascular RAGE, favoring parenchymal Aβ deposition and the onset of cognitive deterioration. Overall we demonstrate that RAGE activation in brain vessels is a crucial pathogenetic event in hypertension-induced Alzheimer disease, suggesting that inhibiting this target can limit the onset of vascular-related Alzheimer disease. 相似文献
99.