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See detailLA FALSIFICATION DES MEDICAMENTS
Marini Djang'Eing'A, Roland ULg

in Forum Pharmaceutique (2012, March 16), -(-), 16

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See detailFalsification des médicaments: mythe ou réalité ?
Marini Djang'Eing'A, Roland ULg; Fillet, Marianne ULg; Vancauwenberghe, Roy et al

Conference (2013, April 24)

La santé publique est de nos jours minée par la problématique des médicaments falsifiés ou de qualité inférieure, avec plusieurs conséquences sanitaires, économiques voire professionnelles. On estime à 7 ... [more ▼]

La santé publique est de nos jours minée par la problématique des médicaments falsifiés ou de qualité inférieure, avec plusieurs conséquences sanitaires, économiques voire professionnelles. On estime à 7% la part du marché pharmaceutique mondial que représenterait ce fléau; l’Afrique, l’Asie et de nombreux pays d'Amérique latine étant les régions les plus touchées avec plus de 30% de médicaments falsifiés. D’après l'OMS, plus de 50% des médicaments achetés à partir des sites internet illégaux sont contrefaits, annihilant très fortement les chances de succès thérapeutique. Ces médicaments viennent dans la plupart des cas des pays asiatiques et de l’Eurasie. Le trafic de faux médicaments est un crime contre l'humanité qui représente environ 50 milliards de dollars par an (10-15 % de plus que le marché de la drogue). Au travers de deux leçons, la situation de la falsification des médicaments sera présentée au grand public dans le but de le sensibiliser à ce fléau. La première leçon présentera la situation en Europe avec un accent sur la Belgique. La problématique du droit à la propriété intellectuelle et de l’encadrement législatif sera abordée, ainsi que la falsification des médicaments modernes et des phytomédicaments, ces derniers étant utilisés par plus de 40% de la population en Europe et aux Etats-Unis. Dans la seconde leçon sera abordée la situation vécue en Afrique. L’approvisionnement en médicaments de qualité par le partage de l’information sera présenté ainsi que les moyens analytiques à la disposition de ce continent pour combattre ce fléau. Des membres du Département de Pharmacie de l’Université de Liège, de l’Agence Fédérale des Médicaments et des Produits de Santé ainsi que du programme QUAMED (Quality Medicines for All) feront partager leur expérience sur cette question d’une brûlante actualité.  [less ▲]

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See detailFalsos positivos de C5-carnitina elevada en cribado neonatal: A que son debidos?
Yahyaoui, Raquel; Rueda; Dayaldasani, Anita et al

in Medicina Clinica (2014)

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See detailFalstaff
Delville, Michel ULg

Conference given outside the academic context (2009)

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See detailFAM-MDR: A Flexible Family-Based Multifactor Dimensionality Reduction Technique to Detect Epistasis Using Related Individuals
Cattaert, Tom ULg; Urrea, V.; Naj, A. C. et al

in PLoS ONE (2010), 5(4), -

We propose a novel multifactor dimensionality reduction method for epistasis detection in small or extended pedigrees, FAM-MDR. It combines features of the Genome-wide Rapid Association using Mixed Model ... [more ▼]

We propose a novel multifactor dimensionality reduction method for epistasis detection in small or extended pedigrees, FAM-MDR. It combines features of the Genome-wide Rapid Association using Mixed Model And Regression approach (GRAMMAR) with Model-Based MDR (MB-MDR). We focus on continuous traits, although the method is general and can be used for outcomes of any type, including binary and censored traits. When comparing FAM-MDR with Pedigree-based Generalized MDR (PGMDR), which is a generalization of Multifactor Dimensionality Reduction (MDR) to continuous traits and related individuals, FAM-MDR was found to outperform PGMDR in terms of power, in most of the considered simulated scenarios. Additional simulations revealed that PGMDR does not appropriately deal with multiple testing and consequently gives rise to overly optimistic results. FAM-MDR adequately deals with multiple testing in epistasis screens and is in contrast rather conservative, by construction. Furthermore, simulations show that correcting for lower order (main) effects is of utmost importance when claiming epistasis. As Type 2 Diabetes Mellitus (T2DM) is a complex phenotype likely influenced by gene-gene interactions, we applied FAM-MDR to examine data on glucose area-under-the-curve (GAUC), an endophenotype of T2DM for which multiple independent genetic associations have been observed, in the Amish Family Diabetes Study (AFDS). This application reveals that FAM-MDR makes more efficient use of the available data than PGMDR and can deal with multi-generational pedigrees more easily. In conclusion, we have validated FAM-MDR and compared it to PGMDR, the current state-of-the-art MDR method for family data, using both simulations and a practical dataset. FAM-MDR is found to outperform PGMDR in that it handles the multiple testing issue more correctly, has increased power, and efficiently uses all available information. [less ▲]

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See detailFAM-MDR: a flexible method of multifactor dimensionality reduction for high-order interaction detection
Van Steen, Kristel ULg; Calle, M.; Urrea, V. et al

in Conference Abstract book (2008)

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See detailFamennian
Thorez, J; Dreesen, R; Streel, Maurice ULg

in Geologica Belgica (2006), 9(1/2), 27-45

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See detailFamennian charcoal of Belgium.
Prestianni, Cyrille ULg; Decombeix, Anne-laure; Thorez, Jacques ULg et al

in Palaeogeography, Palaeoclimatology, Palaeoecology (2010)

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See detailLe Famennien supérieur et les couches de transition Dévonien-Carbonifère dans la vallée de l'Ourthe (sud de Liege, Synclinorium de Dinant)
Bouckaert, J; Streel, Maurice ULg; Thorez, J

in Colloque sur la Stratigraphie du Carbonifère, (1971)

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See detailFamilial abdominal aortic aneurysms: collection of 233 multiplex families.
Kuivaniemi, Helena; Shibamura, Hidenori; Arthur, Claudette et al

in Journal of Vascular Surgery (2003), 37(2), 340-5

OBJECTIVE: This study investigated a large number of families in which at least two individuals were diagnosed with abdominal aortic aneurysms to identify the relationship of the affected relatives to the ... [more ▼]

OBJECTIVE: This study investigated a large number of families in which at least two individuals were diagnosed with abdominal aortic aneurysms to identify the relationship of the affected relatives to the proband. Subjects and Methods: Families for the study were recruited through various vascular surgery centers in the United States, Finland, Belgium, Canada, the Netherlands, Sweden, and the United Kingdom and through our patient recruitment website (www.genetics.wayne.edu/ags). RESULTS: We identified 233 families with at least two individuals diagnosed with abdominal aortic aneurysms. The families originated from nine different nationalities, but all were white. There were 653 aneurysm patients in these families, with an average of 2.8 cases per family. Most of the families were small, with only two affected individuals. There were, however, six families with six, three with seven, and one with eight affected individuals. Most of the probands (82%) and the affected relatives (77%) were male, and the most common relationship to the proband was brother. Most of the families (72%) appeared to show autosomal recessive inheritance pattern, whereas in 58 families (25%), abdominal aortic aneurysms were inherited in autosomal dominant manner, and in eight families, the familial aggregation could be explained by autosomal dominant inheritance with incomplete penetrance. In the 66 families where abdominal aortic aneurysms were inherited in a dominant manner, 141 transmissions of the disease from one generation to another were identified, and the male-to-male, male-to-female, female-to-male, and female-to-female transmissions occurred in 46%, 11%, 32%, and 11%, respectively. CONCLUSION: Our study supports previous studies about familial aggregation of abdominal aortic aneurysms and suggests that first-degree family members, male relatives, in particular, are at increased risk. No single inheritance mode could explain the occurrence of abdominal aortic aneurysms in the 233 families studied here, suggesting that abdominal aortic aneursyms are a multifactorial disorder with multiple genetic and environmental risk factors. [less ▲]

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See detailFamilial Acromegaly : Case report and review of the litterature
Beckers, Albert ULg; Stevenaert, Achille ULg; Teh, B. T. et al

in The 6th International Pituitary Congress - Abstract book (1999)

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See detailFamilial Acromegaly : Family screening and assetment in the familial isolated pituitary adenoma (FIPA)
Fajardo, C.; Camara, R.; Daly, Adrian ULg et al

in 10th European Congress of Endocrinology - Abstract book (2008)

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See detailFamilial Acromegaly: Case Report and Review of the Literature
Verloes, Alain ULg; Stevenaert, Achille ULg; Teh, B. T. et al

in Pituitary (1999), 1(3-4), 273-277

Familial acromegaly is an exceptional clinical entity when not associated with features of multiple endocrine neoplasia type 1 (MEN1). We report here 3 pedigrees in each of which 2 patients have been ... [more ▼]

Familial acromegaly is an exceptional clinical entity when not associated with features of multiple endocrine neoplasia type 1 (MEN1). We report here 3 pedigrees in each of which 2 patients have been shown to develop acromegaly. In 4 patients, clinical follow-up, and biological screening allowed to confidently exclude MEN1. Absence of mutation in the MEN1 gene after direct DNA analysis in 2 pedigrees reinforces the conviction that the families do not have MEN1. In families 1 and 2, diagnosis was made at a very early age and voluminous adenomas with suprasellar expansion were already present at the time of diagnosis. We review the 20 previous reports of familial acromegaly, some of them questionable. Our 3 families, combined with some other published pedigrees, allow the delineation of a familial form of acromegaly, distinct from MEN1. Dominant inheritance with reduced, age-dependant penetrance is the most parsimonious model to explain the recurrences. Gs protein pathway could be the site of action of the gene responsible of familial acromegaly, but no data have been published to sustain or reject this hypothesis. [less ▲]

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See detailFamilial adenomatous polyposis: clinical presentation, detection and surveillance.
Laurent, S.; Franchimont, D.; Vander Auwera, Jacqueline ULg et al

in Acta Gastro-Enterologica Belgica (2011), 74(3), 415-20

Colorectal cancer (CRC) is a leading cause of cancer related death in the western countries. It remains an important health problem, often under-diagnosed. The symptoms can appear very late and about 25 ... [more ▼]

Colorectal cancer (CRC) is a leading cause of cancer related death in the western countries. It remains an important health problem, often under-diagnosed. The symptoms can appear very late and about 25% of the patients are diagnosed at metastatic stage. Familial adenomatous polyposis (FAP) is an inherited colorectal cancer syndrome, characterized by the early onset of hundred to thousands of adenomatous polyps in the colon and rectum. Left untreated, there is a nearly 100% cumulative risk of progression to CRC by the age of 35-40 years, as well as an increased risk of various other malignancies. CRC can be prevented by the identification of the high risk population and by the timely implementation of rigid screening programs which will lead to special medico-surgical interventions. [less ▲]

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See detailFamilial aggregation and antimicrobial response dose-dependently affect the risk for Crohn's disease.
Joossens, Marie; Van Steen, Kristel ULg; Branche, Julien et al

in Inflammatory Bowel Diseases (2010), 16(1), 58-67

BACKGROUND:: An increased risk of Crohn's disease (CD) has been reported consistently in first-degree relatives of patients. Our aim was to test whether a combination of CD-associated genes involved in ... [more ▼]

BACKGROUND:: An increased risk of Crohn's disease (CD) has been reported consistently in first-degree relatives of patients. Our aim was to test whether a combination of CD-associated genes involved in innate immunity and/or antibody responses to microbial antigens may be valuable in identifying healthy relatives at risk. METHODS:: We investigated 86 families from Belgium and northern France, 45 with at least 3 first-degree relatives with CD, 24 with a single case, and 17 control families without inflammatory bowel disease (IBD). The cohort consisted of 186 CD patients, 290 healthy relatives, and 142 controls (total 618). Genetic (NOD2, NOD1, TLR4, CARD8) and serologic markers (ASCA, ACMA, ALCA, ACCA, ASigmaMA, OmpC, CBir1, I2) were determined in all subjects. All Belgian families were prospectively followed up for 54 months. RESULTS:: In multiple-affected families, an increment of affected first-degree relatives and of positive antibodies were additive risks factors for CD (P < 0.0001), independent of NOD2 mutations. When comparing subjects from multiple-affected families, having 3 additional first-degree relatives with CD and 1 additional positive antibody increased the odds for CD to 9.19 (95% confidence interval [CI]: 4.07-20.80). After a follow-up of 54 months among all Belgian families, a total of 4 new diagnoses of IBD were confirmed in the multiple-affected families only, resulting in a 57-fold increase in incidence within multiple-affected families compared to the known incidence of IBD in our region. CONCLUSIONS:: We found an additive risk increment for CD in subjects from multicase families per additional affected relative and per additional positive antibody, independent of NOD2. Furthermore, a very high disease incidence was observed in these multiple-affected families. Inflamm Bowel Dis 2010. [less ▲]

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See detailFamilial amyloidosis caused by lysozyme mutations
Dumoulin, Mireille ULg

in Ramirez-Alvarado, M.; Kelly, J. W.; Dobson, C. (Eds.) Protein Misfolding Diseases: Basis of Protein Misfolding, Pathophysiology, Current, and Emerging Therapies (2010)

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See detailFamilial and Other Conversations: Special Issue on Caryl Phillips
Ledent, Bénédicte ULg

in Moving Worlds : A Journal of Transcultural Writings (2007), 7(1), 123

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See detailFamilial aspects in acromegaly
Verloes, Alain ULg; Beckers, Albert ULg; Pétrossians, E. et al

in 26th Annual meeting of European society of Human Genetics. Abstract book (1994)