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41.
N. H. M. Kooistra M. Abawi M. Voskuil K. Urgel M. Samim F. Nijhoff H. M. Nathoe P. A. F. M. Doevendans S. A. J. Chamuleau G. E. H. Leenders T. Leiner A. C. Abrahams H. B. van der Worp P. Agostoni P. R. Stella 《Netherlands heart journal》2020,28(5):253-265
Transcatheter aortic valve implantation (TAVI) is a safe and effective treatment for inoperable, intermediate- or high-risk patients with severe sympt 相似文献
42.
Deformation of the chest wall during breathing efforts 总被引:4,自引:0,他引:4
43.
Comparative features of the mechanics of breathing 总被引:2,自引:0,他引:2
44.
Zucchelli S Marcuzzi F Codrich M Agostoni E Vilotti S Biagioli M Pinto M Carnemolla A Santoro C Gustincich S Persichetti F 《The Journal of biological chemistry》2011,286(28):25108-25117
Huntington disease (HD) is a neurodegenerative disorder caused by an expansion of polyglutamines in the first exon of huntingtin (HTT), which confers aggregation-promoting properties to amino-terminal fragments of the protein (N-HTT). Mutant N-HTT aggregates are enriched for ubiquitin and contain ubiquitin E3 ligases, thus suggesting a role for ubiquitination in aggregate formation. Here, we report that tumor necrosis factor receptor-associated factor 6 (TRAF6) binds to WT and polyQ-expanded N-HTT in vitro as well as to endogenous full-length proteins in mouse and human brain in vivo. Endogenous TRAF6 is recruited to cellular inclusions formed by mutant N-HTT. Transient overexpression of TRAF6 promotes WT and mutant N-HTT atypical ubiquitination with Lys(6), Lys(27), and Lys(29) linkage formation. Both interaction and ubiquitination seem to be independent from polyQ length. In cultured cells, TRAF6 enhances mutant N-HTT aggregate formation, whereas it has no effect on WT N-HTT protein localization. Mutant N-HTT inclusions are enriched for ubiquitin staining only when TRAF6 and Lys(6), Lys(27), and Lys(29) ubiquitin mutants are expressed. Finally, we show that TRAF6 is up-regulated in post-mortem brains from HD patients where it is found in the insoluble fraction. These results suggest that TRAF6 atypical ubiquitination warrants investigation in HD pathogenesis. 相似文献
45.
Paola Gargiulo Cristina Banfi Stefania Ghilardi Damiano Magrì Marta Giovannardi Alice Bonomi Elisabetta Salvioni Elisa Battaia Pasquale Perrone Filardi Elena Tremoli Piergiuseppe Agostoni 《PloS one》2014,9(12)
Background
In heart failure (HF) alveolar-capillary membrane is abnormal. Surfactant-derived proteins (SPs) and plasma receptor for advanced-glycation-end-products (RAGE) have been proposed as lung damage markers.Methods
Eighty-nine chronic HF and 17 healthy subjects were evaluated by echocardiography, blood parameters, carbon monoxide lung diffusion (DLCO) and cardiopulmonary exercise test. We measured immature SP-B, mature SP-B, SP-A, SP-D and RAGE plasma levels.Results
Immature SP-B (arbitrary units), mature SP-A (ng/ml) and SP-D (ng/ml), but not mature SP-B (ng/ml) and RAGE (pg/ml) levels, were higher in HF than in controls [immature SP-B: 15.6 (13.1, 75th–25th interquartile range) Vs. 11.1 (6.4), p<0.01; SP-A, 29.6 (20.1) Vs. 18.3 (13.5), p = 0.01; SP-D: 125 (90) Vs. 78 (58), p<0.01]. Immature SP-B, SP-A, SP-D and RAGE values were related to DLCO, peak oxygen consumption, ventilatory efficiency, and brain natriuretic peptide (BNP), whereas plasma mature SP-B was not. The DLCO Vs. immature SP-B correlation was the strongest one. At multivariate analysis, RAGE was associated to age and creatinine, SP-A to DLCO and BNP, SP-D to BNP, mature SP-B to DLCO and creatinine, and immature SP-B only but strongly to DLCO.Conclusions
Immature SP-B is the most reliable biological marker of alveolar-capillary membrane function in HF. 相似文献46.
47.
Citterio G.; Agostoni E.; Del Santo A.; Marazzini L. 《Journal of applied physiology》1981,51(6):1388-1397
48.
M. Voskuil W. L. Verloop P. J. Blankestijn P. Agostoni P. R. Stella P. A. Doevendans 《Netherlands heart journal》2011,19(7-8):319-323
Background
In a subpopulation of patients with essential hypertension, therapeutic targets are not met, despite the use of multiple types of medication. In this paper we describe our first experience with a novel percutaneous treatment modality using renal artery radiofrequency (RF) ablation.Methods
Patients who were resistant to at least three types of antihypertensive medical therapy (office systolic blood pressure?≥?160 mmHg; n?=?9) or who did not tolerate medication (n?=?2) were selected. Between July and November 2010, a total of 11 patients received percutaneous RF treatment. Patients were followed up for 1 month after treatment. Urine and blood samples were taken to evaluate the effects on renal function and neurohumeral factors.Results
No periprocedural complications or adverse events during follow-up were noted. A reduction of mean office blood pressure was seen from 203/109?±?32/19 mmHg at baseline to 178/97?±?28/21 mmHg at 1 month follow-up (mean difference 25?±?12 mmHg, p?<?0.01). Also, we noted a significant decrease in aldosterone level (391?±?210 pmol/L versus 250?±?142 pmol/L; p?=?0.03), while there was no decrease in plasma renin activity (190?±?134 fmol/L/s versus 195?±?163 fmol/L/s; p?=?0.43). No change in renal function was noted.Conclusion
Catheter-based renal denervation seems an attractive novel minimally invasive treatment option in patients with resistant hypertension, with a low risk of serious adverse events. 相似文献49.
Increased oxidative stress in a failing heart may contribute to the pathogenesis of heart failure (HF). The aim of this study was to identify the oxidised proteins in the myocardium of HF patients and analyse the consequences of oxidation on protein function. The carbonylated proteins in left ventricular tissue from failing (n?=?14) and non-failing human hearts (n?=?13) were measured by immunoassay and identified by proteomics. HL-1 cardiomyocytes were incubated in the presence of stimuli relevant for HF in order to assess the generation of reactive oxygen species (ROS), the induction of protein carbonylation, and its consequences on protein function. The levels of carbonylated proteins were significantly higher in the HF patients than in the controls (p<0.01). We identified two proteins that mainly underwent carbonylation: M-type creatine kinase (M-CK), whose activity is impaired, and, to a lesser extent, α-cardiac actin. Exposure of cardiomyocytes to angiotensin II and norepinephrine led to ROS generation and M-CK carbonylation with loss of its enzymatic activity. Our findings indicate that protein carbonylation is increased in the myocardium during HF and that these oxidative changes may help to explain the decreased CK activity and consequent defects in energy metabolism observed in HF. 相似文献
50.
Agostoni C Scaglioni S Bonvissuto M Bruzzese MG Giovannini M Riva E 《Prostaglandins, leukotrienes, and essential fatty acids》2001,64(2):111-115
Hyperphenylalaninemic (HPA) children display low levels of long-chain polyunsaturated fatty acids (LCPUFA), particularly docosahexaenoic acid (DHA), in circulating lipids and erythrocytes. We have investigated the effects on the blood fatty acid status and lipid picture of a balanced supplementation with LCPUFA in HPA children through a double-blind, placebo-controlled trial. A total of 20 well-controlled HPA, school-age children were randomized to receive through a 12-month trial fat capsules supplying either 26% fatty acid as LCPUFA (including 4.6%gamma -linolenic acid, 7.4% arachidonic acid, AA, 5.5% eicosapentaenoic acid and 8% DHA) or placebo (olive oil). The study supplementation was administered in order to provide 0.3-0.5% of the individual daily energy requirements as LCPUFA. Reference data were obtained from healthy children of comparable age. Among HPA children (whose DHA status was poor at baseline), those supplemented with LCPUFA showed an increase of around 100% in the baseline DHA levels in plasma phospholipids and erythrocytes. No changes of AA levels were observed. Blood lipid levels did not significantly change. A balanced supplementation with LCPUFA in treated HPA children may improve the DHA status without adversely affecting the AA status. 相似文献