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See detailHypo- et hypertension intracrânienne bénigne
DELVAUX, Valérie ULg; DIOH, Alioune ULg; Schoenen, Jean ULg

in Revue Médicale de Liège (1999), 54(8), 671-676

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See detailHypo- et hypertension intracrâniennes bénignes
DELVAUX, Valérie ULg; DIOH, Alioune ULg; Schoenen, Jean ULg

in Ahead in neurology (1999), 3(1), 10-15

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See detailHypocalcémie induite chez le sujet pagétique par la calcitonine salmine nasale. Effets des anticorps anti-calcitonine salmine
Reginster, Jean-Yves ULg; Almer, S.; Gaspar, S et al

in Revue du Rhumatisme et des Maladies Osteo-Articulaires (1989), 56(7), 563-7

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See detailHypochlorous acid activates NF-kappaB transcription factor in T lymphocytes
Schoonbroodt, Sonia; Legrand-Poels, Sylvie ULg; Best-Belpomme, Martin et al

in Biochemical Journal (1997)

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See detailHypochlorous Acid, a Major Oxidant Produced by Activated Neutrophils, Has Low Effect on Two Pyridobenzazepine Derivatives, Jl 3 and Jl 13
Liégeois, Jean-François ULg; Zahid, N.; Bruhwyler, J. et al

in Archiv der Pharmazie (2000), 333(2-3), 63-7

JL 13 (5-(4-methylpiperazin-1-yl)-8-chloro-pyrido[2,3-b]- [1,5]benzoxazepine fumarate) and JL 3 (10-(4-methylpiperazin-1- yl)pyrido[4,3-b][1,4]benzothiazepine), two pyridobenzazepine derivatives ... [more ▼]

JL 13 (5-(4-methylpiperazin-1-yl)-8-chloro-pyrido[2,3-b]- [1,5]benzoxazepine fumarate) and JL 3 (10-(4-methylpiperazin-1- yl)pyrido[4,3-b][1,4]benzothiazepine), two pyridobenzazepine derivatives structurally related to clozapine, were selected for further development. Due to their structural similarity to clozapine, they are haunted by the spectre of clozapine-induced agranulocytosis. In a previous study, JL 13 was shown to be less sensitive to oxidation than clozapine. In the present paper, using an in vitro procedure, we report the effect of hypochlorous acid (HOCl), a major in vivo oxidant, on both drugs. It appears that the oxidations of JL 3 and JL 13, unlike clozapine, are very slow and little secondary product is formed. Moreover, in contrast to clozapine, the products that were formed are not reactive and thus do not react with glutathione or N-acetylcysteine. Thus, if, as postulated for clozapine, drug-induced agranulocytosis is due to a reactive metabolite formed by neutrophils or their precursors, JL 3 and JL 13 would not be expected to cause the same adverse reaction. [less ▲]

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See detailL'hypochondroplasie: dystrophie héréditaire
Reginster, Jean-Yves ULg; FOIDART-DESSALLE, Marguerite ULg; Leroy, C et al

in Revue Médicale de Liège (1986), 61

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See detailHypochromic mature erythrocytes: a specific marker of iron deficiency
Bovy, Christophe ULg; Beguin, Yves ULg; Gothot, André ULg et al

in Acta Clinica Belgica (2003), 58-3(4), 325

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See detailHypocortisolism induces chronic respiratory failure
PIRLET, Charles ULg; BECK, Emmanuel ULg; SCHEEN, André ULg et al

in Respiratory Medicine (2011), 4(3), 107-108

Hypocortisolism is an uncommon condition. Its association with myopathy and respiratoryfailure has only rarely been described. We report the case of a 52 year-old woman presenting with progressive ... [more ▼]

Hypocortisolism is an uncommon condition. Its association with myopathy and respiratoryfailure has only rarely been described. We report the case of a 52 year-old woman presenting with progressive dyspnoea. Work-up revealed a severe restrictive syndrome with hypoxaemia. Further investigations showed hypocortisolism of pituitary origin. Response to hydrocortisone allowed us to conclude to an unusual case of hypocortisolic myopathy affecting the respiratory muscles. [less ▲]

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See detailHypodermose bovine dans le Nord-Est algérien : prévalence et intensité d'infestation
Benakhla, A.; Lonneux, J. F.; Mekroud, A. et al

in Veterinary Research (1999), 30

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See detailHypofractionation in retinoblastoma: an increased risk of retinopathy.
Coucke, Philippe ULg; Mirimanoff, R-O; Schmid, C et al

in Radiotherapy & Oncology (1993), 28

Forty-four eyes in 38 children were treated between 1963 and 1991 by external radiotherapy for retinoblastoma. Treatment modalities varied widely during this period; in addition to radiotherapy there was ... [more ▼]

Forty-four eyes in 38 children were treated between 1963 and 1991 by external radiotherapy for retinoblastoma. Treatment modalities varied widely during this period; in addition to radiotherapy there was chemotherapy (16/44), photocoagulation (14/44), and laser therapy or cryotherapy (14/44). Treatment technique and dose fractionation also varied widely; lateral beam technique (39/44) versus anterior or anterior/lateral beam; doses per fraction ranged from 1 to 4.5 Gy, total doses from 30 to 61.5 Gy, and overall times from 22 to 49 days. Patients were followed at 3-month intervals, and actuarial survival at 10 years was 88%, with 62% local control. Ten eyes showed clinical evidence of retinopathy. A multivariate analysis of factors associated with increased risk of retinopathy was carried out using the Cox proportional hazards model and the mixture model of Farewell. The estimated latent time was 17 months (95% confidence interval, 14-20 months). The only factors found to be significantly associated with retinopathy were total dose multiplied by dose per fraction, or total dose normalized to the equivalent total dose in 2-Gy fractions as estimated from the LQ model, and these gave equivalent descriptions. There were trends (not significant) for increased risk of retinopathy when treatments included chemotherapy or photocoagulation, and for decreased risk (also not significant) when cryotherapy was used in conjunction with radiotherapy. No significance could be attached to any of the following: number of sites per eye, Reese-Ellsworth stage, and family history. We conclude that hypofractionation carries a significant risk for retinopathy in the treatment of retinoblastoma. [less ▲]

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See detailHypofractionation in retinoblastoma: an increased risk of retinopathy.
Coucke, Philippe ULg; Schmid; Balmer et al

in Radiotherapy & Oncology (1993), 28(2), 157-161

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See detailL'hypoglycemie du patient diabetique. Recommendations of ALFEDIAM (French Language Association for the Study of Diabetes and Metabolic Diseases.
Grimaldi, A.; Slama, G.; Tubiana-Rufi, N. et al

in Diabètes & Métabolism (1997), 23(1), 100-8

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See detailHypoglycémie et hypoxie cérébrales
Battisti, Oreste ULg; Bertrand, J. M.; Langhendries, J. P.

Conference (1988)

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See detailL'hypoglycemie reactive: un phenomene critique mysterieux, insidieux, mais non dangereux.
Scheen, André ULg; Lefebvre, Pierre ULg

in Revue Médicale de Liège (2004), 59(4), 237-42

Numerous individuals complain of malaise attributed to hypoglycaemia. However, the diagnosis of hypoglycaemia is rarely documented and most often overstated. Reactive hypoglycaemia in the postprandial ... [more ▼]

Numerous individuals complain of malaise attributed to hypoglycaemia. However, the diagnosis of hypoglycaemia is rarely documented and most often overstated. Reactive hypoglycaemia in the postprandial state is rather exceptional. The diagnosis relies upon the measurement of plasma glucose concentration (< 3 mmol/l or 55 mg/dl) at the time of the malaise. Reactive hypoglycaemia is generally associated with adrenergic symptoms and, less often, with cognitive disturbances. Importantly, a plasma glucose concentration below 3 mmol/l during an oral glucose tolerance test is not sufficient to decide that the patient suffers from reactive hypoglycaemia. Treatment is based on dietary advices including frequent small split meals and limitation of carbohydrates with high glycaemic index. Acarbose, a specific inhibitor of gut alpha-glucosidase enzymes, may be helpful in case of diet failure. As compared with true reactive hypoglycaemia, a postprandial hyperadrenergic reaction without real concomitant hypoglycaemia is much more prevalent. Careful anamnesis may suspect such a diagnosis, but other diagnoses such as panic attack or vasovagal reaction should be excluded. Treatment is purely symptomatic and essentially empiric. [less ▲]

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See detailHypogonadism in a patient with a mutation in the luteinizing hormone beta-subunit gene
VALDES SOCIN, Hernan Gonzalo ULg

Master of advanced studies dissertation (2008)

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See detailHypogonadism in a Patient with a Mutation in the Luteinizing Hormone Beta-Subunit Gene
Valdes Socin, Hernan Gonzalo ULg; Salvi, R.; Daly, Adrian ULg et al

in New England Journal of Medicine [=NEJM] (2004), 351(25), 2619-2625

A 30-year-old man who presented with delayed puberty and infertility was found to have hypogonadism associated with an absence of circulating luteinizing hormone. The patient had a homozygous missense ... [more ▼]

A 30-year-old man who presented with delayed puberty and infertility was found to have hypogonadism associated with an absence of circulating luteinizing hormone. The patient had a homozygous missense mutation in the gene that encodes the beta subunit of luteinizing hormone (Gly36Asp), a mutation that disrupted a vital cystine knot motif and abrogated the heterodimerization and secretion of luteinizing hormone. Treatment with human chorionic gonadotropin increased circulating testosterone, promoted virilization, and was associated with the appearance of normal spermatozoa in low concentrations. This case illustrates the important physiological role that luteinizing hormone plays in male sexual maturation and fertility. [less ▲]

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See detailHypogonadisme congénital chez un homme, associé à une LK immunoréactive normale, élévation de FSH et azoospermie
Valdes Socin, Hernan Gonzalo ULg; Chachati, Anne-Sophie ULg; De Roux, N. et al

in Annales d'Endocrinologie (2010, September), 71(5), 355

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See detailHypogonadisme génétique masculin: diagnostic et prise en charge
VALDES SOCIN, Hernan Gonzalo ULg

Scientific conference (2014, December 05)

The neuroendocrine control of reproduction in mammals is governed by a hypothalamic neural network of nearly 1500 gonadotropin-releasing hormone (GnRH) secreting neurons that modulate the activity of the ... [more ▼]

The neuroendocrine control of reproduction in mammals is governed by a hypothalamic neural network of nearly 1500 gonadotropin-releasing hormone (GnRH) secreting neurons that modulate the activity of the reproductive axis across life. Congenital Hypogonadotropic hypogonadism (HH) is a clinical syndrome that is characterized by partial or complete pubertal failure. HH may result from inadequate hypothalamic GnRH axis activation, or a failure of pituitary gonadotropin secretion/effects. In man, several genes that participate in olfactory and GnRH neuronal migration are thought to interact during the embryonic life. A growing list of mutations of these genes is responsible for congenital HH. Based on the presence or the absence of olfaction dysfunction, HH is divided in two syndromes: HH with olfactory alterations (Kallmann syndrome) and Idiopathic hypogonadotropic hypogonadism (IHH) with normal smell (normosmic IHH). Kallmann syndrome (KS) is a heterogeneous disorder affecting 1 in 5000 to 8000 males, with a 3-5 fold male excess over female. KS is associated with mutations in KAL1, FGFR1/FGF8, FGF17, IL17RD, PROK2/PROKR2, NELF, CHD7, HS6ST1 and WDR11 genes that are related to defects in neuronal migration. These reproductive and olfactory deficits include a variable non reproductive phenotype, including sensorineural deafness, coloboma, bimanual synkinesis, craniofacial abnormalities and/or renal agenesis. Interestingly, defects in PROKR2, FGFR1, FGF8, CHD7 and WDR11 genes are also associated with normosmic IHH, whereas mutations in KISS1/KISSR, TAC3/TACR3, GNRH1/GNRHR, βFSH and βLH are only present in patients with normosmic IHH. βLH mutations are responsible for Pasqualini 's Syndrome (fertile eunuch) first described in 1950 in males with eunuchoidism, hypoandrogenism and spermatogenesis in testis biopsies. Congenital primary hypogonadism include several genetic syndromes such as Klinefelter syndrome (XXY), Del Castillo syndrome (only sertoli syndrome).In this lecture, we summarize the reproductive, neurodevelopmental and genetic aspects of IHH and primary hypogonadism in human pathology. [less ▲]

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See detailHypogonadisme par déficience de LH.
Beckers, Albert ULg

in Bulletin et Mémoires de l'Académie Royale de Médecine de Belgique (2007), 162(5-6), 291-7298

A 30-year-old man was investigated for delayed puberty and infertility. These investigations showed a complete absence of circulating luteinizing hormone (LH). Genetic studies revealed a missense mutation ... [more ▼]

A 30-year-old man was investigated for delayed puberty and infertility. These investigations showed a complete absence of circulating luteinizing hormone (LH). Genetic studies revealed a missense mutation in the LHbeta gene (G36D). This mutation disrupts a vital cystine knot motif and abrogates the heterodimerization and secretion of LH. Treatment with hCG was instituted, which led to arise in testosterone and improvement in spermatogenesis. After in vitro fertilization the patient had a son who was heterozygous for the G36D mutation. A second patient with similar clinical and biological presentation has been explored. A non-frame shift deletion of 3 base-pairs was discovered at position 20 which led to the deletion of a lysine residue. The proband and his prepubescent brother were homozygotic for this mutation. These cases illustrate the important physiological role of LH in male sexual maturation and fertility. [less ▲]

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