The Experts below are selected from a list of 504 Experts worldwide ranked by ideXlab platform
Anne Cathrine Staff - One of the best experts on this subject based on the ideXlab platform.
-
failure of physiological transformation and spiral artery atherosis their roles in preeclampsia
American Journal of Obstetrics and Gynecology, 2020Co-Authors: Anne Cathrine Staff, Heidi Elisabeth Fjeldstad, Ingrid Knutsdotter Fosheim, Kjartan Moe, Gitta Turowski, Guro Mork Johnsen, Patji Alnaeskatjavivi, Meryam SugulleAbstract:Physiological transformation with remodeling of the uteroplacental spiral arteries is key to a successful placentation and normal placental function. It is an intricate process that involves, but is not restricted to, complex interactions between maternal decidual immune cells and invasive trophoblasts in the uterine wall. In normal pregnancy, the smooth muscle cells of the arterial tunica media of uteroplacental spiral arteries are replaced by invading trophoblasts and fibrinoid, and the arterial diameter increases 5- to 10-fold. Poor remodeling of the uteroplacental spiral arteries is linked to early-onset preeclampsia and several other major obstetrical syndromes, including fetal growth restriction, placental abruption, and spontaneous preterm premature rupture of membranes. Extravillous endoglandular and endovenous trophoblast invasions have recently been put forth as potential contributors to these syndromes as well. The well-acknowledged disturbed extravillous invasion of maternal spiral arteries in preeclampsia is summarized, as are briefly novel concepts of disturbed extravillous endoglandular and endovenous trophoblast invasions. Acute atherosis is a foam cell lesion of the uteroplacental spiral arteries associated with poor remodeling. It shares some morphologic features with early stages of atherosclerosis, but several molecular differences between these lesions have also recently been revealed. Acute atherosis is most prevalent at the maternal-fetal interface, at the tip of the spiral arteries. The localization of acute atherosis downstream of poorly remodeled arteries suggests that alterations in blood flow may trigger inflammation and foam cell development. Acute atherosis within the decidua basalis is not, however, confined to unremodeled areas of spiral arteries or to hypertensive disorders of pregnancy and may even be present in some clinically uneventful pregnancies. Given that foam cells of atherosclerotic lesions are known to arise from smooth muscle cells or macrophages activated by multiple types of inflammatory stimulation, we have proposed that multiple forms of decidual vascular inflammation may cause acute atherosis, with or without poor remodeling and/or preeclampsia. Furthermore, we propose that acute atherosis may develop at different gestational ages, depending on the type and degree of the inflammatory insult. This review summarizes the current knowledge of spiral artery remodeling defects and acute atherosis in preeclampsia. Some controversies will be presented, including endovascular and interstitial trophoblast invasion depths, the concept of 2-stage trophoblast invasion, and whether the replacement of maternal spiral artery endothelium by fetal endovascular trophoblasts is permanent. We will discuss the role of acute atherosis in the pathophysiology of preeclampsia and short- and long-term health correlates. Finally, we suggest future opportunities for research on this intriguing uteroplacental interface between the mother and fetus.
-
learning from the placenta acute atherosis and vascular remodeling in preeclampsia novel aspects for atherosclerosis and future cardiovascular health
Hypertension, 2010Co-Authors: Anne Cathrine Staff, Ralf Dechend, Robert PijnenborgAbstract:Preeclampsia is a common and potentially lethal pregnancy complication for women and offspring. Women who develop preeclampsia also run a long-term augmented risk of cardiovascular disease and premature death, and two theories are discussed. Women developing preeclampsia and persons developing cardiovascular disease may have common risk factors, which are unmasked by the "stress" of pregnancy. Alternatively, a new risk factor might occur de novo during the preeclamptic pregnancy. In preeclampsia, lipid deposition in walls of the maternal uterine arteries leading to the placenta, named spiral arteries, regularly occurs. These vascular lesions resemble early stages of atherosclerosis and are named "acute atherosis" and is thought to regress after delivery. The mechanisms that contribute to acute atherosis in preeclampsia are largely unknown, but are related to the impaired vascular remodeling of the spiral arteries in the first half of pregnancy. One striking feature is that the development of these "atherosclerosis-like" lesions requires a few months in pregnancy and may be partly linked to invasion of trophoblasts (specialized fetally derived placenta cells). We summarize normal and pathological vessel remodeling in pregnancy and discuss similarities and differences between preeclampsia and arteriosclerosis. The transient appearance of acute atherosis of uterine wall spiral arteries seen in pregnancy complications and the molecular interaction between trophoblast, smooth muscle and vascular cells could add important elements to explain arteriosclerosis and stenosis in cardiovascular disease. Further understanding of the process underlying spiral artery atherosis in the months of pregnancy may cast light on development of cardiovascular disease later in life.
Joseph Jankovic - One of the best experts on this subject based on the ideXlab platform.
-
chorea Athetosis and ballism
Movement Disorders in Childhood (Second Edition), 2016Co-Authors: Harvey S. Singer, Donald L. Gilbert, Jonathan W. Mink, Joseph JankovicAbstract:This chapter discusses the large variety of diagnoses in childhood where chorea may be a prominent feature. Chorea is uncommon in children. It nearly always causes some interference with life activities and is perceived as involuntary by the individual. The terms “Athetosis” and “ballism” designate similar movements, and are reviewed in this chapter. The most common cause of chorea in childhood is Sydenham’s chorea. This chapter provides a systematic approach to diagnosis and treatment of chorea in childhood, based on childhood development, epidemiology, primary features, associated symptoms, and understanding of neuroanatomy and pathophysiology.
-
movement disorders in cerebrovascular disease
Lancet Neurology, 2013Co-Authors: Raja Mehanna, Joseph JankovicAbstract:Summary Movement disorders can occur as primary (idiopathic) or genetic disease, as a manifestation of an underlying neurodegenerative disorder, or secondary to a wide range of neurological or systemic diseases. Cerebrovascular diseases represent up to 22% of secondary movement disorders, and involuntary movements develop after 1–4% of strokes. Post-stroke movement disorders can manifest in parkinsonism or a wide range of hyperkinetic movement disorders including chorea, ballism, Athetosis, dystonia, tremor, myoclonus, stereotypies, and akathisia. Some of these disorders occur immediately after acute stroke, whereas others can develop later, and yet others represent delayed-onset progressive movement disorders. These movement disorders have been encountered in patients with ischaemic and haemorrhagic strokes, subarachnoid haemorrhage, cerebrovascular malformations, and dural arteriovenous fistula affecting the basal ganglia, their connections, or both.
Meryam Sugulle - One of the best experts on this subject based on the ideXlab platform.
-
failure of physiological transformation and spiral artery atherosis their roles in preeclampsia
American Journal of Obstetrics and Gynecology, 2020Co-Authors: Anne Cathrine Staff, Heidi Elisabeth Fjeldstad, Ingrid Knutsdotter Fosheim, Kjartan Moe, Gitta Turowski, Guro Mork Johnsen, Patji Alnaeskatjavivi, Meryam SugulleAbstract:Physiological transformation with remodeling of the uteroplacental spiral arteries is key to a successful placentation and normal placental function. It is an intricate process that involves, but is not restricted to, complex interactions between maternal decidual immune cells and invasive trophoblasts in the uterine wall. In normal pregnancy, the smooth muscle cells of the arterial tunica media of uteroplacental spiral arteries are replaced by invading trophoblasts and fibrinoid, and the arterial diameter increases 5- to 10-fold. Poor remodeling of the uteroplacental spiral arteries is linked to early-onset preeclampsia and several other major obstetrical syndromes, including fetal growth restriction, placental abruption, and spontaneous preterm premature rupture of membranes. Extravillous endoglandular and endovenous trophoblast invasions have recently been put forth as potential contributors to these syndromes as well. The well-acknowledged disturbed extravillous invasion of maternal spiral arteries in preeclampsia is summarized, as are briefly novel concepts of disturbed extravillous endoglandular and endovenous trophoblast invasions. Acute atherosis is a foam cell lesion of the uteroplacental spiral arteries associated with poor remodeling. It shares some morphologic features with early stages of atherosclerosis, but several molecular differences between these lesions have also recently been revealed. Acute atherosis is most prevalent at the maternal-fetal interface, at the tip of the spiral arteries. The localization of acute atherosis downstream of poorly remodeled arteries suggests that alterations in blood flow may trigger inflammation and foam cell development. Acute atherosis within the decidua basalis is not, however, confined to unremodeled areas of spiral arteries or to hypertensive disorders of pregnancy and may even be present in some clinically uneventful pregnancies. Given that foam cells of atherosclerotic lesions are known to arise from smooth muscle cells or macrophages activated by multiple types of inflammatory stimulation, we have proposed that multiple forms of decidual vascular inflammation may cause acute atherosis, with or without poor remodeling and/or preeclampsia. Furthermore, we propose that acute atherosis may develop at different gestational ages, depending on the type and degree of the inflammatory insult. This review summarizes the current knowledge of spiral artery remodeling defects and acute atherosis in preeclampsia. Some controversies will be presented, including endovascular and interstitial trophoblast invasion depths, the concept of 2-stage trophoblast invasion, and whether the replacement of maternal spiral artery endothelium by fetal endovascular trophoblasts is permanent. We will discuss the role of acute atherosis in the pathophysiology of preeclampsia and short- and long-term health correlates. Finally, we suggest future opportunities for research on this intriguing uteroplacental interface between the mother and fetus.
Tanja Kersnik Levart - One of the best experts on this subject based on the ideXlab platform.
-
Rare variant of Lesch-Nyhan syndrome without self-mutilation or nephrolithiasis.
Pediatric Nephrology, 2007Co-Authors: Tanja Kersnik LevartAbstract:Lesch–Nyhan syndrome is a very rare X-linked recessive disorder characterized by mental retardation, spasticity resembling cerebral palsy, choreo-Athetosis, self-mutilation and hyperuricemia. Self-mutilative behavior is a hallmark of the disease. Hyperuricemia leads to hyperuricuria and uric acid nephrolithiasis. The underlying defect is a deficiency of hypoxanthine-guanine-phosphoribosyl transferase. We report on a 7-year-old boy with Lesch–Nyhan syndrome, lacking self-mutilative behavior, who was erroneously diagnosed as having athetotic cerebral palsy. He also had no renal stones; hyperechoic renal medullary pyramids were the only renal abnormality detected and were sonographically indistinguishable from medullary nephrocalcinosis.
Bas B Van Rijn - One of the best experts on this subject based on the ideXlab platform.
-
spiral artery remodeling and maternal cardiovascular risk the spiral artery remodeling spar study
Journal of Hypertension, 2016Co-Authors: Jan H W Veerbeek, Laura Brouwers, Maria P H Koster, Steven V Koenen, Elvira O G Van Vliet, Peter G J Nikkels, Arie Franx, Bas B Van RijnAbstract:BACKGROUND:: Women with a history of placental bed disorders, including preeclampsia and intrauterine growth restriction have an increased long-term risk of cardiovascular disease (CVD). Further, similarities exist between atherosclerosis and abnormalities observed in placental bed spiral arteries in pregnancies affected by preeclampsia and intrauterine growth restriction, such as acute atherosis and defective remodeling. This suggests a common pathophysiological pathway underlying both disorders. OBJECTIVES:: The aim of this study was to investigate vascular and inflammatory lesions in the placental bed of women with preeclampsia and normal pregnancy using a systematic approach to characterize lesions of the placental bed, and relate spiral artery pathology to postpartum CVD risk assessment. METHODS:: Placental bed punch biopsies were performed following caesarean section and systematically studied to assess vascular pathology, arterial remodeling, and the presence of CD3, CD56, and CD68 cells. In addition, levels of modifiable CVD risk factors were assessed immediately postpartum. RESULTS:: We found fewer spiral arteries with complete remodeling in women with preeclampsia than in the control group (21 vs. 68%; P?=?0.008). Further, women with preeclampsia showed less presence of CD3 cells in both the decidua and the myometrium. Preliminary findings of CVD risk factor assessment postpartum suggest a correlation between acute atherosis and higher triglyceride and low-density lipoprotein cholesterol levels. CONCLUSION:: Systematic study of vascular pathology in uterine spiral artery biopsy samples in relation to CVD risk factors provides valuable insight into the link between cardiovascular health and placental bed disorders.