(C) 2013 Elsevier Ireland Ltd. All rights reserved.”
“Background: The cardiovascular system is the part of the fetal anatomy that most frequently suffers from congenital pathology. This study shows our preliminary experience with fetal cardiovascular magnetic resonance (CMR) to evaluate congenital cardiovascular abnormalities.
Methods: Between January 2006 and June 2011, Prenatal routine obstetric ultrasound (US),
echocardiography and CMR data from 68 pregnant women carrying fetuses with congenital cardiovascular anomalies were compared BMS202 Immunology & Inflammation inhibitor with postnatal diagnoses (postnatal imagings, surgery and autopsy). All prenatal CMR was performed at 1.5 T. Imaging sequences included steady-state free-precession (SSFP) sequences, real-time SSFP and single-shot turbo spin echo (SSTSE) sequences. The images were analyzed with an anatomic segmental approach by two radiologists.
Results: Fetal CMR yielded the same diagnosis as postnatal findings in 79% (54/68) of patients. The diagnostic sensitivity of routine obstetric US for cardiac anomalies was 46% (31/68). The diagnostic sensitivity of VX-770 in vitro fetal echocardiographic examination by a fetal cardiac specialist was 82% (56/68). In 2 (3%) of 68 cases, diagnoses with
both echocardiography and CMR were incorrect when compared with postnatal diagnosis. In ten (15%) cases, diagnosis at echocardiography was incorrect and that at CMR was correct. In twelve (18%) cases, diagnosis at echocardiography was correct and that at CMR was incorrect. Ten cases missed or misdiagnosed by echocardiography but correctly diagnosed by fetal CMR included asplenia syndrome (n = 2), interrupted inferior vena cava of polysplenia syndrome (n = 1), tricuspid incompetence (n = 1), double outlet right ventricle (n = 2), double aortic arch (n = 1), right pulmonary artery hypoplasia (n = 1), right-sided aortic arch of tetralogy of Fallot (n = 1) and hypoplastic left heart syndrome of a twin fetus (n = 1).
Conclusion: Fetal CMR is a promising diagnostic tool for assessment
of congenital cardiovascular abnormalities, especially in situations that limit echocardiography.”
“Purpose of review
To describe our current understanding of the mechanisms involved BIIB057 in the regulation of linear growth in childhood obesity.
Recent findings
The developmental origins hypothesis has focused on low birth weight individuals with subsequent obesity, identifying a cascade of neuroendocrine regulatory factors involved in the progressive increase in body fat and metabolic risk. Yet, tall stature is the common clinical outcome of childhood obesity. Recent data have expanded our understanding of environmental influences on developing systems. Here, we review the elements of neuroendocrine systems contributing to the integration of metabolic controls involved in growth regulation in the obese child with particular emphasis on growth hormone, ghrelin, insulin-like growth factors and insulin.