References of "SAKALIHASAN, Natzi"
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See detailAneurysm : epidemiology, aetiology and pathology.
SAKALIHASAN, Natzi ULg; KUIVANIEMI, HELENA; Nusgens, Betty ULg et al

Book published by SPRINGER (2011)

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See detailNovel aspects of the pathogenesis of aneurysms of the abdominal aorta in humans.
Michel, Jérôme ULg; Martin-Ventura, J. L.; Egido, J. et al

in Cardiovascular Research (2011)

Aneurysm of the abdominal aorta (AAA) is a particular, specifically localized form of atherothrombosis, providing a unique human model of this disease. The pathogenesis of AAA is characterized by a ... [more ▼]

Aneurysm of the abdominal aorta (AAA) is a particular, specifically localized form of atherothrombosis, providing a unique human model of this disease. The pathogenesis of AAA is characterized by a breakdown of the extracellular matrix due to an excessive proteolytic activity, leading to potential arterial wall rupture. The roles of matrix metalloproteinases and plasmin generation in progression of AAA have been demonstrated both in animal models and in clinical studies. In the present review, we highlight recent studies addressing the role of the haemoglobin-rich, intraluminal thrombus and the adventitial response in the development of human AAA. The intraluminal thrombus exerts its pathogenic effect through platelet activation, fibrin formation, binding of plasminogen and its activators, and trapping of erythrocytes and neutrophils, leading to oxidative and proteolytic injury of the arterial wall. These events occur mainly at the intraluminal thrombus-circulating blood interface, and pathological mediators are conveyed outwards, where they promote matrix degradation of the arterial wall. In response, neo-angiogenesis, phagocytosis by mononuclear cells, and a shift from innate to adaptive immunity in the adventitia are observed. Abdominal aortic aneurysm thus represents an accessible spatiotemporal model of human atherothrombotic progression towards clinical events, the study of which should allow further understanding of its pathogenesis and the translation of pathogenic biological activities into diagnostic and therapeutic applications. [less ▲]

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See detailResponse to Comment on “High Levels of 18F-FG Uptake in Aortic Aneurysm Wall are Associated with High Wall Stress”
Sakalihasan, Natzi ULg; Defraigne, Jean-Olivier ULg; Xu, Yun

in European Journal of Vascular and Endovascular Surgery (2010), 39

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See detailMR Imaging of Iron Phagocytosis in Intraluminal Thrombi of Abdominal Aortic Aneurysms in Humans.
NCHIMI LONGANG, Alain ULg; Defawe, Olivier; Brisbois, Denis ULg et al

in Radiology (2010), 254(3), 973-81

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See detailHigh Levels of 18F-FDG Uptake in Aortic Aneurysm Wall are Associated with High Wall Stress
Xu, Yun; Borghi, Alexandre; NCHIMI LONGANG, Alain ULg et al

in European Journal of Vascular and Endovascular Surgery (2010), 39

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See detailGenome-wide association study identifies sequence variants within the DAB2IP gene conferring susceptibility to abdominal aortic aneurysm.
Gretarsdottir, Solveig; Baas, Annette F.; Thorleifsson, G. et al

in Nature Genetics (2010)

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See detailFunctional imaging of abdominal aortic aneurysms : can it predict probability of rupture.
Sakalihasan, Natzi ULg; Hustinx, Roland ULg; Gomez, Pierre et al

in VASCULAR ANEURYSMS (2009)

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See detailFunctional imaging of atherosclerosis to advance vascular biology. Invited overview.
Sakalihasan, Natzi ULg; Michel, Jean-Baptiste

in European Journal of Vascular and Endovascular Surgery (2009), 37

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See detailEvaluation of inflammatory cells in abdominal aortic aneurysmal wall by tomography emission positron
Sakalihasan, Natzi ULg; Hustinx, Roland ULg; Gomez, Pierre et al

in Médecine Nucléaire : Imagerie Fonctionnelle et Métabolique (2009), 33/5

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See detailFunctional imaging of abdominal aortic aneurysms
Sakalihasan, Natzi ULg; Hustinx, Roland ULg; Gomez, Pierre et al

in Aortic Aneurysms, new insights of an old problem (2008)

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See detailModern look at a pathology of the millenium : abdominal aortic aneurysms.
Limet, Raymond ULg; Sakalihasan, Natzi ULg

in Bulletins et Mémoires de l’Académie Royale de Médecine de Belgique (2008), 163(5), 205-11

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See detailThree arginine to cysteine substitutions in the pro-alpha (I)-collagen chain cause Ehlers-Danlos syndrome with a propensity to arterial rupture in early adulthood.
Malfait, Fransiska; Symoens, Sofie; De Backer, Julie et al

in Human Mutation (2007), 28(4), 387-95

Mutations in the COL1A1 and COL1A2 genes, encoding the proalpha1 and 2 chains of type I collagen, cause osteogenesis imperfecta (OI) or Ehlers-Danlos syndrome (EDS) arthrochalasis type. Although the ... [more ▼]

Mutations in the COL1A1 and COL1A2 genes, encoding the proalpha1 and 2 chains of type I collagen, cause osteogenesis imperfecta (OI) or Ehlers-Danlos syndrome (EDS) arthrochalasis type. Although the majority of missense mutations in the collagen type I triple helix affect glycine residues in the Gly-Xaa-Yaa repeat, few nonglycine substitutions have been reported. Two arginine-to-cysteine substitutions in the alpha1(I)-collagen chain are associated with classic EDS [R134C (p.R312C)] or autosomal dominant Caffey disease with mild EDS features [R836C (p.R1014C)]. Here we show alpha1(I) R-to-C substitutions in three unrelated patients who developed iliac or femoral dissection in early adulthood. In addition, manifestations of classic EDS in Patient 1 [c.1053C>T; R134C (p.R312C); X-position] or osteopenia in Patients 2 [c.1839C>T; R396C (p.R574C); Y-position] and 3 [c.3396C>T; R915C (p.R1093C); Y-position] are seen. Dermal fibroblasts from the patients produced disulfide-bonded alpha1(I)-dimers in approximately 20% of type I collagen, which were efficiently secreted into the medium in case of the R396C and R915C substitution. Theoretical stability calculations of the collagen type I heterotrimer and thermal denaturation curves of monomeric mutant alpha1(I)-collagen chains showed minor destabilization of the collagen helix. However, dimers were shown to be highly unstable. The R134C and R396C caused delayed procollagen processing by N-proteinase. Ultrastructural findings showed collagen fibrils with variable diameter and irregular interfibrillar spaces, suggesting disturbed collagen fibrillogenesis. Our findings demonstrate that R-to-C substitutions in the alpha1(I) chain may result in a phenotype with propensity to arterial rupture in early adulthood. This broadens the phenotypic range of nonglycine substitutions in collagen type I and has important implications for genetic counseling and follow-up of patients carrying this type of mutation. [less ▲]

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See detailL’image du mois - Fistule coronaro-pulmonaire.
Verscheure, Sara ULg; Sakalihasan, Natzi ULg; Limet, Raymond ULg

in Revue Médicale de Liège (2007), 62

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See detailEvidence for association between the HLA-DQA locus and abdominal aortic aneurysms in the Belgian population: a case control study.
Ogata, Toru; Gregoire, Lucie; Goddard, Katrina A B et al

in BMC Medical Genetics (2006), 7

BACKGROUND: Chronic inflammation and autoimmunity likely contribute to the pathogenesis of abdominal aortic aneurysms (AAAs). The aim of this study was to investigate the role of autoimmunity in the ... [more ▼]

BACKGROUND: Chronic inflammation and autoimmunity likely contribute to the pathogenesis of abdominal aortic aneurysms (AAAs). The aim of this study was to investigate the role of autoimmunity in the etiology of AAAs using a genetic association study approach with HLA polymorphisms. METHODS: HLA-DQA1, -DQB1, -DRB1 and -DRB3-5 alleles were determined in 387 AAA cases (180 Belgian and 207 Canadian) and 426 controls (269 Belgian and 157 Canadian) by a PCR and single-strand oligonucleotide probe hybridization assay. RESULTS: We observed a potential association with the HLA-DQA1 locus among Belgian males (empirical p = 0.027, asymptotic p = 0.071). Specifically, there was a significant difference in the HLA-DQA1*0102 allele frequencies between AAA cases (67/322 alleles, 20.8%) and controls (44/356 alleles, 12.4%) in Belgian males (empirical p = 0.019, asymptotic p = 0.003). In haplotype analyses, marginally significant association was found between AAA and haplotype HLA-DQA1-DRB1 (p = 0.049 with global score statistics and p = 0.002 with haplotype-specific score statistics). CONCLUSION: This study showed potential evidence that the HLA-DQA1 locus harbors a genetic risk factor for AAAs suggesting that autoimmunity plays a role in the pathogenesis of AAAs. [less ▲]

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See detailPrimary sarcoma of an abdominal aortic aneurysm
Defawe, O.D.; Thiry, Albert ULg; Lapiere, C.M. et al

in Abdominal Imaging (2006), 31(1, Jan-Feb), 117-119

Primary tumors of the aorta are extremely rare and the diagnosis is made most often after surgery or autopsy. Because clinical symptoms of abdominal sarcoma are similar to those of occlusive or aneurysmal ... [more ▼]

Primary tumors of the aorta are extremely rare and the diagnosis is made most often after surgery or autopsy. Because clinical symptoms of abdominal sarcoma are similar to those of occlusive or aneurysmal disease, aortic sarcomas are frequently mistaken for these lesions. The imaging findings are frequently nonspecific and therefore do not allow a definitive preoperative diagnosis. We report a case of an epithelioid angiosarcoma in the vessel wall of an abdominal aortic aneurysm. [less ▲]

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See detailHLA-DQA is associated with abdominal aortic aneurysms in the Belgian population
Tromp, Gerard; Ogata, Toru; Grégoire, Lucie et al

in Annals of the New York Academy of Sciences (2006), 1085

Chronic inflammation and autoimmunity likely contribute to the pathogenesis of abdominal aortic aneurysms (AAAs). The aim of this study was to investigate the role of autoimmunity in the etiology of AAAs ... [more ▼]

Chronic inflammation and autoimmunity likely contribute to the pathogenesis of abdominal aortic aneurysms (AAAs). The aim of this study was to investigate the role of autoimmunity in the etiology of AAAs using a genetic association study approach with human leukocyte antigen (HLA) polymorphisms (HLA-DQA1, -DQB1, -DRB1 and -DRB3-5 alleles) in 387 AAA cases and 426 controls. We observed an association with the HLA-DQA1 locus among Belgian males, and found a significant difference in the HLA-DQA1 *0102 allele frequencies between AAA cases and controls. In conclusion, this study showed potential evidence that the HLA-DQA1 locus harbors a genetic risk factor for AAAs suggesting that autoimmunity plays a role in the pathogenesis of AAAs. [less ▲]

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See detailGenetic analysis of polymorphisms in biologically relevant candidate genes in patients with abdominal aortic aneurysms
Ogata, Toru; Shibamura, Hidenori; Tromp, Gerard et al

in Journal of Vascular Surgery (2005), 41(6), 1036-1042

Background: Abdominal aortic aneurysms (AAAs) are characterized by histologic signs of chronic inflammation, destructive remodeling of extracellular matrix, and depletion of vascular smooth muscle cells ... [more ▼]

Background: Abdominal aortic aneurysms (AAAs) are characterized by histologic signs of chronic inflammation, destructive remodeling of extracellular matrix, and depletion of vascular smooth muscle cells. We investigated the process of extracellular matrix remodeling by performing a genetic association study with polymorphisms in the genes for matrix metalloproteinases (MMPs), tissue inhibitors of metalloproteinases (TIMPs), and structural extracellular matrix molecules in AAA. Our hypothesis was that genetic variations in one or more of these genes contribute to greater or lesser activity of these gene products, and thereby contribute to susceptibility for developing AAAs. Methods: DNA samples from 812 unrelated white subject (AAA, n = 387; controls, n = 425) were genotyped for 14 polymorphisms in 13 different candidate genes: MMP1(nt-1607), MMP2(nt-955), MMP3(nt-1612), MMP9(nt-1562), MMP10(nt+180), MMP12(nt-82), MMP13(nt-77), TIMP1(nt+434), TIMP1(rs;2070584), TIMP2(rs2009196), TIMP3(nt-1296), TGFBI(nt-509), ELN(nt+422), and COL3A1(nt+581). Odds ratios and P values adjusted for gender and country of origin using logistic regression and stratified by family history of AAA were calculated to test for association between genotype and disease status. Haplotype analysis was carried out for the two TIMP1 polymorphisms; in male subjects. Results: Analyses with one polymorphism per test without interactions showed an association with the two TIMP1 gene polymorphisms (nt+434, P =.0047; rs2070584, P =.015) in male subjects without a family history of AAA. The association remained significant when analyzing TIMP1 haplotypes (x(2) p =.014 and empirical P =.009). In addition, we found a significant interaction between the polymorphism and gender for MMP10 (P=.037) in cases without a family history of AAA, as well as between the polymorphism and country of origin for ELN (P =.0169) and TIMP3 (P =.0023) in cases with a family history of AAA. Conclusions: These findings suggest that genetic variations in TIMP1, TIMP3, MMP10, and ELN genes may contribute to the pathogenesis of AAAs. Further work is needed to confirm the findings in an independent set of samples and to study the functional role of these variants in AAA. It is noteworthy that contrary to a previous study, we did not find an association between the MMP9 (nt-1562) polymorphism and AAA, suggesting genetic heterogeneity of the disease. Clinical Relevance: Abdominal aortic aneurysms (AAAs) are an important cardiovascular disease, but the genetic and environmental risk factors, which contribute to individual's risk to develop an aneurysm, are poorly understood. Histologically, AAAs are characterized by signs of chronic inflammation, destructive remodeling of the extracellular matrix, and depletion of vascular smooth muscle cells. We hypothesized that genes involved in these events could harbor changes that make individuals more susceptible to developing aneurysms. This study identified significant genetic associations between DNA sequence changes in tissue inhibitor of metalloproteinase I (TIMP1), TIMP3, matrix metalloproteinase 10 (MMP10) and elastin (ELN) genes, and AAA. The results will require confirmation using an independent set of samples. After replication it is possible that these sequence changes in combination with other risk factors could be used in the future to identify individuals who are at increased risk for developing an AAA. [less ▲]

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See detailDistribution of F-18 fluorodeoxyglucose (F-18 FDG) in abdominal aortic aneurysm: High accumulation in macrophages seen on PET Imaging and immunohistology
Defawe, O. D.; Hustinx, Roland ULg; Defraigne, Jean-Olivier ULg et al

in Clinical Nuclear Medicine (2005), 30(5), 340-341

A 68-year-old man was hospitalized for unstable angina and underwent emergency coronary artery bypass surgery. During the operation, a pulsatile large abdominal aortic aneurysm (AAA) was discovered. To ... [more ▼]

A 68-year-old man was hospitalized for unstable angina and underwent emergency coronary artery bypass surgery. During the operation, a pulsatile large abdominal aortic aneurysm (AAA) was discovered. To define the optimal treatment of the abdominal aneurysm, after bypass surgery, CT scans and positron emission tomography (PET) were performed, as we routinely do. PET imaging combined with immunohistologic examination showed a region of increased F-18 FDG uptake corresponding to an inflammatory infiltrate in the aortic wall in contrast to the thrombus in the aneurysm (devoid of inflammatory cells). The luminal area showed midlevel F-18 FDG uptake corresponding to circulating mediators. [less ▲]

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