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Peer Reviewed
See detailLes myopathies subcliniques constituent-elles une cause d’intolérance à l’effort ?
Van Erck, Emmanuelle; Lekeux, Pierre ULg

in 36èmes Journées AVEF (2008)

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See detailMyopia, redistribution and pensions
Pestieau, Pierre ULg; Cremer, H.

in European Economic Review (2011), 55

This paper reviews a number of recent contributions that study pension design with myopic individuals. Its objective is to explore how the presence of more or less myopic individuals affects pension ... [more ▼]

This paper reviews a number of recent contributions that study pension design with myopic individuals. Its objective is to explore how the presence of more or less myopic individuals affects pension design when individuals differ also in productivity. This double heterogeneity gives rise to an interesting interplay between paternalistic and redistributive considerations, which is at the heart of most of the results that are presented. The main part of the paper is devoted to the issue of pension design when myopic individual do not save ‘‘enough’’ for their retirement because their ‘‘myopicself’’ (with a high discount rate) emerges when labor supply and savings decisions are made. Some extensions and variations are considered in the second part. In particular we deal with situations where labor disutility or preferences for consumption are subject to ‘‘habit formation’’and where sin goods have a detrimental effect on second period health. Myopic individuals tend to underestimate the effects of both habit formation and sinful consumption, which complicates public policy. [less ▲]

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See detailMyopia, redistribution and pensions
Pestieau, Pierre ULg

Scientific conference (2009, June 18)

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See detailMyopia, redistribution and pensions
Pestieau, Pierre ULg

Conference (2009, June 15)

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See detailMyopia, redistribution and pensions
Pestieau, Pierre ULg

Scientific conference (2009, December 18)

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See detailMyopia, regrets, and risky behaviors
Pestieau, Pierre ULg; Pontiere, Gregory

in International Tax and Public Finance (2012), 19

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See detailMyorelaxant effects of 2-alkyl-substituted 2H-pyrido[4,3-e]-1,2,4-thiadiazine 1,1-dioxides
Pirotte, Bernard ULg; De Tullio, Pascal ULg; Ouedraogo, R. et al

Poster (1996, September)

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See detailMyosite focale sur atteinte radiculaire S1
Kaux, Jean-François ULg

Conference (2007, March 19)

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See detailLa myosite orbitaire chez l'enfant; Diagnostic et traitement
Legrand, B.; Misson, Jean-Paul ULg

in Comptes Rendus de la Société Belge de Neurologie Infantile (1985)

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Peer Reviewed
See detailLa myosite ossifiante traumatique
WANG, François-Charles ULg; Laurent, Luc; CRIELAARD, Jean-Michel ULg

Conference (1991)

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See detailLa myosite ossifiante traumatique
Laurent, L.; Wang, François-Charles ULg; Crielaard, Jean-Michel ULg

in Revue Médicale de Liège (1990), 45(7), 321-30

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See detail« Myosite » focale de la loge antéro-externe de la jambe : à propos d’un cas
TOMASELLA, Marco ULg; CRIELAARD, Jean-Michel ULg; WANG, François-Charles ULg

in Neurophysiologie Clinique = Clinical Neurophysiology (2004)

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See detailMyositis During Borrelia Burgdorferi Infection (Lyme Disease)
Schoenen, Jean ULg; Sianard-Gainko, J.; Carpentier, M. et al

in Journal of Neurology, Neurosurgery & Psychiatry (1989), 52(8), 1002-5

During the second stage of an illness caused by Borrelia burgdorferi, a young woman developed a myopathic syndrome characterised by severe muscular pains, incapacitating weakness of the proximal limb and ... [more ▼]

During the second stage of an illness caused by Borrelia burgdorferi, a young woman developed a myopathic syndrome characterised by severe muscular pains, incapacitating weakness of the proximal limb and the neck, as well as the bulbar muscles and elevated serum CK levels. Muscle biopsy revealed a non-inflammatory necrotising myopathy. B. burgdorferi infection was confirmed by a considerable rise of specific IgG antibodies. A course of high dose steroids alleviated the myalgias, but paresis began to improve only after treatment with antibiotics. Our observations confirm that B burgdorferi can cause, through an undertermined mechanism, a necrotising myopathy, in addition to the wide spectrum of already known neurological complications. [less ▲]

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See detailMyostatin gene deletion prevents glucocorticoid-induced muscle atrophy
Gilson, H.; Schakman, O.; Combaret, L. et al

in Endocrinology (2007), 148(1), 452-460

Glucocorticoids mediate muscle atrophy in many catabolic states. Myostatin expression, a negative regulator of muscle growth, is increased by glucocorticoids and myostatin overexpression is associated ... [more ▼]

Glucocorticoids mediate muscle atrophy in many catabolic states. Myostatin expression, a negative regulator of muscle growth, is increased by glucocorticoids and myostatin overexpression is associated with lower muscle mass. This suggests that myostatin is required for the catabolic effects of glucocorticoids. We therefore investigated whether myostatin gene disruption could prevent muscle atrophy caused by glucocorticoids. Male myostatin knockout (KO) and wild-type mice were subjected to dexamethasone treatment (1 mg/kg.d for 10 d or 5 mg/kg.d for 4 d). In wild-type mice, daily administration of low-dose dexamethasone for 10 d resulted in muscle atrophy (tibialis anterior: -15%; gastrocnemius: -13%; P < 0.01) due to 15% decrease in the muscle fiber cross-sectional area (1621 +/- 31 vs. 1918 +/- 64 mu m(2), P < 0.01). In KO mice, there was no reduction of muscle mass nor fiber cross-sectional area after dexamethasone treatment. Muscle atrophy after 4d of high-dose dexamethasone was associated with increased mRNA of enzymes involved in proteolytic pathways (atrogin-1, muscle ring finger 1, and cathepsin L) and increased chymotrypsin-like proteasomal activity. In contrast, the mRNA of these enzymes and the proteasomal activity were not significantly affected by dexamethasone in KO mice. Muscle IGF-I mRNA was paradoxically decreased in KO mice (-35%, P < 0.05); this was associated with a potentially compensatory increase of IGF-II expression in both saline and dexamethasone-treated KO mice (2-fold, P < 0.01). In conclusion, our results show that myostatin deletion prevents muscle atrophy in glucocorticoid-treated mice, by blunting the glucocorticoid-induced enhanced proteolysis, and suggest an important role of myostatin in muscle atrophy caused by glucocorticoids. [less ▲]

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See detailMyotis bechsteini en Corse
Libois, Roland ULg; Vranken, Martin

in Mammalia (1981), 45(3), 380-381

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See detailMyotis daubentoni; Nyctalus leisleri; Pipistrellus pipistrellus
Libois, Roland ULg

in Fayard, Armand (Ed.) Atlas des mammifères sauvages de France (1983)

Detailed reference viewed: 6 (1 ULg)