Vascular malformations cause discomfort and pain in children and are often as sociated with skeletal hypertrophy. Their molecular basis is poorly understood. Ephrin ligands and Eph receptor tyrosine kinases are involv...Vascular malformations cause discomfort and pain in children and are often as sociated with skeletal hypertrophy. Their molecular basis is poorly understood. Ephrin ligands and Eph receptor tyrosine kinases are involved in embryonic vascu lar development. In mice, some ephrin/Eph family members show a complementary ex pression pattern in blood vessels, with eph- rinB2 being expressed on arterial and EphB4 on venous endothelium. Targeted deletions of the genes reveal their es sential roles for conduit vessel development in mice, suggesting similar functio ns during human vascular development and deregulation in vascular malformations. Here, we have defined the expression patterns of human ephrinB2, EphB4, and Eph B2 in normal vessels of neonates (i.e. umbilici) and adults and compared them wi th those in congenital venous malformations. In adults, normal vessels of the sk in, muscle, and legs express ephrinB2 and EphB2 on arterial endothelial cells (E Cs), whereas EphB4 is found in arteries and veins. In the umbilicus, EphB2 is a specific marker of arterial ECs, whereas ephrinB2 is additionally expressed in v enous ECs, suggesting an arterial function of the veins. In venous malformations , the expression of EphB4 is not altered, but both ephrinB2 and EphB2 are ectopi cally expressed in venous ECs. This may reflect a nonphysiologic arterialization of malformed veins. Our study shows that the arterial markers ephrin B2 and Eph B2 are expressed in a subset of veins, and it remains to be studied whether this is cause or consequence of an altered vascular identity.展开更多
Background: Few and conflicting data are available in the literature on the association between Lp(a) levels and the severity of coronary artery disease(CAD) in diabetic patients. In addition, no studies took into acc...Background: Few and conflicting data are available in the literature on the association between Lp(a) levels and the severity of coronary artery disease(CAD) in diabetic patients. In addition, no studies took into account the role of apo(a) polymorphism. The purpose of the present study was to analyse the association of the degree of coronary atherosclerosis with Lp(a) levels and apo(a)polymorphism in a large group of type 2 diabetic patients. Methods: The study population consisted of 227 consecutive type 2 diabetic patients undergoing a routine coronary angiography to evaluate chest pain or suspected CAD. The patients were subdivided into four subgroups according to the number of coronary arteries diseased: normal arteries(n=26), mono-vessel disease(n=67), bi-vessel disease(n=54) and multi-vessel disease(n=80). Results: Lp(a) levels(normal arteries: 14.6± 19.6 mg/dl; mono-vessel disease: 19.0± 16.4 mg/dl; bi-vessel disease: 19.3± 15.1 mg/dl; multi-vessel disease: 26.5± 16.8 mg/dl; p< 0.001) and the percentages of patients with at least one isoform of low molecular weight(normal arteries: 23.1% ; mono-vessel disease: 38.8% ; bi-vessel disease: 75.9% ; multi-vessel disease: 81.2% ; p< 0.001) were significantly correlated with increasing number of coronary vessels diseased. Multiple logistic regression analysis showed that both Lp(a) levels(OR: 1.31; 95% CI: 1.02-4.11) and apo(a) polymorphism(OR: 3.43; 95% CI: 1.67-7.05) were independent predictors of CAD severity. Conclusions: Our data suggest that Lp(a) levels and apo(a) polymorphism may be reliable predictors of CAD severity in type 2 diabetic patients.展开更多
文摘Vascular malformations cause discomfort and pain in children and are often as sociated with skeletal hypertrophy. Their molecular basis is poorly understood. Ephrin ligands and Eph receptor tyrosine kinases are involved in embryonic vascu lar development. In mice, some ephrin/Eph family members show a complementary ex pression pattern in blood vessels, with eph- rinB2 being expressed on arterial and EphB4 on venous endothelium. Targeted deletions of the genes reveal their es sential roles for conduit vessel development in mice, suggesting similar functio ns during human vascular development and deregulation in vascular malformations. Here, we have defined the expression patterns of human ephrinB2, EphB4, and Eph B2 in normal vessels of neonates (i.e. umbilici) and adults and compared them wi th those in congenital venous malformations. In adults, normal vessels of the sk in, muscle, and legs express ephrinB2 and EphB2 on arterial endothelial cells (E Cs), whereas EphB4 is found in arteries and veins. In the umbilicus, EphB2 is a specific marker of arterial ECs, whereas ephrinB2 is additionally expressed in v enous ECs, suggesting an arterial function of the veins. In venous malformations , the expression of EphB4 is not altered, but both ephrinB2 and EphB2 are ectopi cally expressed in venous ECs. This may reflect a nonphysiologic arterialization of malformed veins. Our study shows that the arterial markers ephrin B2 and Eph B2 are expressed in a subset of veins, and it remains to be studied whether this is cause or consequence of an altered vascular identity.
文摘Background: Few and conflicting data are available in the literature on the association between Lp(a) levels and the severity of coronary artery disease(CAD) in diabetic patients. In addition, no studies took into account the role of apo(a) polymorphism. The purpose of the present study was to analyse the association of the degree of coronary atherosclerosis with Lp(a) levels and apo(a)polymorphism in a large group of type 2 diabetic patients. Methods: The study population consisted of 227 consecutive type 2 diabetic patients undergoing a routine coronary angiography to evaluate chest pain or suspected CAD. The patients were subdivided into four subgroups according to the number of coronary arteries diseased: normal arteries(n=26), mono-vessel disease(n=67), bi-vessel disease(n=54) and multi-vessel disease(n=80). Results: Lp(a) levels(normal arteries: 14.6± 19.6 mg/dl; mono-vessel disease: 19.0± 16.4 mg/dl; bi-vessel disease: 19.3± 15.1 mg/dl; multi-vessel disease: 26.5± 16.8 mg/dl; p< 0.001) and the percentages of patients with at least one isoform of low molecular weight(normal arteries: 23.1% ; mono-vessel disease: 38.8% ; bi-vessel disease: 75.9% ; multi-vessel disease: 81.2% ; p< 0.001) were significantly correlated with increasing number of coronary vessels diseased. Multiple logistic regression analysis showed that both Lp(a) levels(OR: 1.31; 95% CI: 1.02-4.11) and apo(a) polymorphism(OR: 3.43; 95% CI: 1.67-7.05) were independent predictors of CAD severity. Conclusions: Our data suggest that Lp(a) levels and apo(a) polymorphism may be reliable predictors of CAD severity in type 2 diabetic patients.
