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Van Laethem C Bartunek J Goethals M Nellens P Andries E Vanderheyden M 《American heart journal》2005,149(1):175-180
Background
The oxygen uptake efficiency slope (OUES) is a new submaximal parameter which objectively predicts the maximal exercise capacity in children and healthy subjects. However, the usefulness of OUES in adult patients with and without advanced heart failure remains undetermined. The present study investigates the stability and the usefulness of OUES in adult cardiac patients with and without heart failure.Methods
Forty-five patients with advanced heart failure (group A) and 35 patients with ischemic heart disease but normal left ventricular ejection fraction (group B) performed a maximal exercise test. PeakVO2 and percentage of predicted peakVO2 were markers of maximal exercise capacity, whereas OUES, ventilatory anaerobic threshold (VAT), and slope VE/VCO2 were calculated as parameters of submaximal exercise.Results
Group A patients had lower peakVO2 (P < .001), lower percentage of predicted peakVO2 (P = .001), lower VAT (P < .05), steeper slope VE/VCO2 (P < .001), and lower OUES (P < .02). Within group A, significant differences were found for VAT, slope VE/VCO2, and OUES (all P < .01) between patients with peakVO2 above and below 14 mL O2/kg/min. Of all the submaximal parameters, VAT correlated best with peakVO2 (r =.814, P < .01) followed by OUES/kg (r = .781, P < .01), and slope VE/VCO2 (r = −.492, P < .001). However, VAT could not be determined in 18 (23%) patients.Conclusions
OUES remains stable over the entire exercise duration and is significantly correlated with peakVO2 in adult cardiac patients with and without impaired LVEF. Therefore, OUES could be helpful to assess exercise performance in advanced heart failure patients unable to perform a maximal exercise test. Further studies are needed to confirm our hypothesis. 相似文献83.
Laurence Dangers Jonathan Giovannelli Gilles Mangiapan Mikael Alves Naïke Bigé Jonathan Messika Elise Morawiec Mathilde Neuville Christophe Cracco Gaëtan Béduneau Nicolas Terzi Isabelle Huet Xavier Dhalluin Nathalie Bautin Jean-Jacques Quiot Corinne Appere-de Vecchi Thomas Similowski Cécile Chenivesse 《Chest》2021,159(4):1621-1629
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Cornelia Speich Rita Wegmüller Gary M. Brittenham Christophe Zeder Colin I. Cercamondi Daniela Buhl Andrew M. Prentice Michael B. Zimmermann Diego Moretti 《British journal of haematology》2021,192(1):179-189
We report the first measurements of long‐term iron absorption and loss during iron supplementation in African children using a stable isotope of iron (57Fe). After uniform labelling of body iron with 57Fe, iron absorption is proportional to the rate of decrease in the 57Fe tracer concentration, while iron loss is proportional to the rate of decrease in the 57Fe tracer amount. Anaemic Gambian toddlers were given 2 mg 57Fe orally to equilibrate with total body iron over 8–11 months. After assignment to the positive control arm of the HIGH study, 22 toddlers consumed a micronutrient powder containing 12 mg iron for 12 weeks followed by 12 weeks without iron supplementation. Their daily iron absorption increased 3·8‐fold during the iron supplementation period compared to the control period [median (interquartile range, IQR): 1·00 (0·82; 1·28) mg/day vs. 0·26 (0·22; 0·35) mg/day; P = 0·001]. Unexpectedly, during the supplementation period, daily iron loss also increased by 3·4‐fold [0·75 (0·55; 0·87) mg/day vs. 0·22 (0·19; 0·29) mg/day; P = 0·005]. Consequently, most (~72%) of the absorbed iron was lost during supplementation. Long‐term studies of iron absorption and loss are a promising and accurate method for assessing and quantifying long‐term iron balance and may provide a reference method for evaluating iron intervention programs in vulnerable population groups. This study was registered as ISRCTN 0720906. 相似文献
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Lentiviral vector delivery of parkin prevents dopaminergic degeneration in an alpha-synuclein rat model of Parkinson's disease 总被引:5,自引:0,他引:5
Lo Bianco C Schneider BL Bauer M Sajadi A Brice A Iwatsubo T Aebischer P 《Proceedings of the National Academy of Sciences of the United States of America》2004,101(50):17510-17515
Parkinson's disease (PD) is characterized by a progressive loss of midbrain dopamine neurons and the presence of cytoplasmic inclusions called Lewy bodies. Mutations in several genes including alpha-synuclein and parkin have been linked to familial PD. The loss of parkin's E3-ligase activity leads to dopaminergic neuronal degeneration in early-onset autosomal recessive juvenile parkinsonism, suggesting a key role of parkin for dopamine neuron survival. To evaluate the potential neuroprotective role of parkin in the pathogenesis of PD, we tested whether overexpression of wild-type rat parkin could protect against the toxicity of mutated human A30P alpha-synuclein in a rat lentiviral model of PD. Animals overexpressing parkin showed significant reductions in alpha-synuclein-induced neuropathology, including preservation of tyrosine hydroxylase-positive cell bodies in the substantia nigra and sparing of tyrosine hydroxylase-positive nerve terminals in the striatum. The parkin-mediated neuroprotection was associated with an increase in hyperphosphorylated alpha-synuclein inclusions, suggesting a key role for parkin in the genesis of Lewy bodies. These results indicate that parkin gene therapy may represent a promising candidate treatment for PD. 相似文献
90.
CD95 engagement induces disseminated endothelial cell apoptosis in vivo: immunopathologic implications 总被引:6,自引:3,他引:6
Janin A Deschaumes C Daneshpouy M Estaquier J Micic-Polianski J Rajagopalan-Levasseur P Akarid K Mounier N Gluckman E Socié G Ameisen JC 《Blood》2002,99(8):2940-2947
Fas (CD95) is a death receptor involved in apoptosis induction on engagement by Fas ligand (CD95L). Although CD95L-mediated apoptosis has been proposed as a pathogenic mechanism in a wide range of diseases, including graft-versus-host disease, systemic CD95 engagement in mice by agonistic CD95-specific antibodies or by soluble multimeric CD95L (smCD95L), though lethal, has been reported to cause apoptosis only in a limited range of cell types, that is, hepatocytes, hepatic sinusoidal endothelial cells, and lymphocytes. Another member of the tumor necrosis factor (TNF)/CD95L family, TNF-alpha, induces disseminated vascular endothelial cell apoptosis, which precedes apoptosis of other cell types and lethal multiorgan failure. Here we show that systemic CD95 engagement in vivo by agonistic CD95-specific antibody or smCD95L causes rapid, extensive, and disseminated endothelial cell apoptosis throughout the body, by a mechanism that does not depend on TNF-alpha. Disseminated endothelial cell apoptosis was also the first detectable lesion in a murine model of acute tissue damage induced by systemic transfer of allogeneic lymphocytes and did not occur when allogeneic lymphocytes were from CD95L-defective mice. Both vascular and additional tissue lesions induced by agonistic CD95-specific antibody, smCD95L, or allogeneic lymphocytes were prevented by treatment with an inhibitor of caspase-8, the upstream caspase coupled to CD95 death signaling. Vascular lesions are likely to play an important role in the pathogenesis of allogeneic immune responses and of other diseases involving circulating CD95L-expressing cells or smCD95L, and the prevention of CD95-mediated death signaling in endothelial cells may have therapeutic implications in these diseases. 相似文献