<?xml version="1.0" encoding="UTF-8"?>
<rdf:RDF xmlns:rdf="http://www.w3.org/1999/02/22-rdf-syntax-ns#" xmlns:dcterms="http://purl.org/dc/terms/" xmlns:prism="http://prismstandard.org/namespaces/1.2/basic/" xmlns:dc="http://purl.org/dc/elements/1.1/" xmlns="http://purl.org/rss/1.0/"><channel rdf:about="http://www.sfnmjournal.com//inpress?rss=yes"><title>Seminars in Fetal &amp; Neonatal Medicine - Articles in Press</title><description>Seminars in Fetal &amp; Neonatal Medicine RSS feed: Articles in Press.    
 Seminars in Fetal &amp; Neonatal Medicine  (formerly  Seminars in Neonatology ) is a bi-monthly journal which publishes 
topic-based issues, including current 'Hot Topics' on the latest advances in fetal and neonatal medicine. The change in title relates 
to the growing interest amongst obstetricians, midwives and fetal medicine specialists.  
 
The Journal commissions review-based content 
covering current clinical opinion on the care and treatment of the neonate and draws on the necessary specialist knowledge, including 
that of the respiratory physician, the infectious disease physician, the surgeon, as well as the paediatrician and obstetrician.  
 

Each topic-based issue is edited by an authority in their field and contains 8-10 articles.  
 
Recent Issues have included: 
 


• 
Newer Concepts in Neonatal Respiratory Care  •  Perinatal Infection: Detection and Prevention  •  Multiple Births  

•  Neonatal Jaundice  • Inborn Errors of Metabolism  
 
 Seminars in Fetal &amp; Neonatal Medicine  provides: 

 
 • coverage of major developments in neonatal care;  • value to practising neonatologists, consultant and trainee paediatricians, 
obstetricians, midwives and fetal medicine specialists wishing to extend their knowledge in this field; • up-to-date information 
in an attractive and relevant format.  
 
   </description><link>http://www.sfnmjournal.com//inpress?rss=yes</link><dc:publisher>Elsevier Inc.</dc:publisher><dc:language>en</dc:language><dc:rights> © 2012 Elsevier Ltd. All rights reserved. </dc:rights><prism:publicationName>Seminars in Fetal &amp; Neonatal Medicine</prism:publicationName><prism:issn>1744-165X</prism:issn><prism:publicationDate>2012-02-02</prism:publicationDate><prism:copyright> © 2012 Elsevier Ltd. All rights reserved. </prism:copyright><prism:rightsAgent>healthpermissions@elsevier.com</prism:rightsAgent><items><rdf:Seq><rdf:li rdf:resource="http://www.sfnmjournal.com/article/PIIS1744165X12000108/abstract?rss=yes"/><rdf:li rdf:resource="http://www.sfnmjournal.com/article/PIIS1744165X12000091/abstract?rss=yes"/><rdf:li rdf:resource="http://www.sfnmjournal.com/article/PIIS1744165X12000029/abstract?rss=yes"/><rdf:li rdf:resource="http://www.sfnmjournal.com/article/PIIS1744165X12000042/abstract?rss=yes"/><rdf:li rdf:resource="http://www.sfnmjournal.com/article/PIIS1744165X12000054/abstract?rss=yes"/><rdf:li rdf:resource="http://www.sfnmjournal.com/article/PIIS1744165X12000066/abstract?rss=yes"/><rdf:li rdf:resource="http://www.sfnmjournal.com/article/PIIS1744165X12000030/abstract?rss=yes"/><rdf:li rdf:resource="http://www.sfnmjournal.com/article/PIIS1744165X12000078/abstract?rss=yes"/><rdf:li rdf:resource="http://www.sfnmjournal.com/article/PIIS1744165X1200008X/abstract?rss=yes"/></rdf:Seq></items></channel><item rdf:about="http://www.sfnmjournal.com/article/PIIS1744165X12000108/abstract?rss=yes"><title>Long term respiratory outcomes of very premature birth (&lt;32 weeks) - Corrected Proof</title><link>http://www.sfnmjournal.com/article/PIIS1744165X12000108/abstract?rss=yes</link><description>Summary: Many very prematurely born infants develop bronchopulmonary dysplasia (BPD), remaining oxygen dependent for many months and requiring frequent rehospitalisations. Troublesome, recurrent respiratory symptoms requiring treatment and lung function abnormalities at follow-up are common. The most severely affected may remain symptomatic with evidence of airways obstruction even as adults. Data from adolescents and adults on the respiratory outcome of extreme prematurity, however, are usually from patients who have had ‘classical’ BPD with severe respiratory failure in the neonatal period. Nowadays, infants have ‘new’ BPD developing chronic oxygen dependence despite initially minimal or even no respiratory distress. Affected patients do suffer chronic respiratory morbidity and their lung function may deteriorate during the first year after birth. Infants who suffer respiratory syncytial virus lower respiratory tract infections are most likely to require rehospitalisation and suffer chronic respiratory morbidity, but this may reflect greater abnormal premorbid lung function.</description><dc:title>Long term respiratory outcomes of very premature birth (&lt;32 weeks) - Corrected Proof</dc:title><dc:creator>Anne Greenough</dc:creator><dc:identifier>10.1016/j.siny.2012.01.009</dc:identifier><dc:source>Seminars in Fetal &amp; Neonatal Medicine (2012)</dc:source><dc:date>2012-02-02</dc:date><prism:publicationName>Seminars in Fetal &amp; Neonatal Medicine</prism:publicationName><prism:publicationDate>2012-02-02</prism:publicationDate></item><item rdf:about="http://www.sfnmjournal.com/article/PIIS1744165X12000091/abstract?rss=yes"><title>Long term respiratory outcomes of congenital diaphragmatic hernia, esophageal atresia, and cardiovascular anomalies - Corrected Proof</title><link>http://www.sfnmjournal.com/article/PIIS1744165X12000091/abstract?rss=yes</link><description>Summary: Intrathoracic congenital malformations may be associated with long-term pulmonary morbidity. This certainly is the case for congenital diaphragmatic hernia, esophageal atresia and cardiac and aortic arch abnormalities. These conditions have variable degrees of impaired development of both the airways and lung vasculature, with a postnatal impact on lung function and bronchial reactivity. Pulmonary complications are themselves frequently associated to non-pulmonary morbidities, including gastrointestinal and orthopaedic complications. These are best recognized in a structured multidisciplinary follow-up clinic so that they can be actively managed.</description><dc:title>Long term respiratory outcomes of congenital diaphragmatic hernia, esophageal atresia, and cardiovascular anomalies - Corrected Proof</dc:title><dc:creator>Christophe Delacourt, Alice Hadchouel, Jaan Toelen, Maissa Rayyan, Jacques de Blic, Jan Deprest</dc:creator><dc:identifier>10.1016/j.siny.2012.01.008</dc:identifier><dc:source>Seminars in Fetal &amp; Neonatal Medicine (2012)</dc:source><dc:date>2012-02-01</dc:date><prism:publicationName>Seminars in Fetal &amp; Neonatal Medicine</prism:publicationName><prism:publicationDate>2012-02-01</prism:publicationDate></item><item rdf:about="http://www.sfnmjournal.com/article/PIIS1744165X12000029/abstract?rss=yes"><title>Long term respiratory outcomes of perinatal lung disease - Corrected Proof</title><link>http://www.sfnmjournal.com/article/PIIS1744165X12000029/abstract?rss=yes</link><description>Perinatal and infant mortality rates have decreased rapidly over the last few decades especially in industrialised countries. This has been partly attributed to the improved survival of infants born preterm, particularly those born extremely preterm. Contributions have undoubtedly been made by improvements in obstetric care, neonatal practice and surgical advances. However, with such progress important questions are raised regarding the longer term outcomes, especially the neurodevelopmental, respiratory and growth outlook for the survivors. This issue of Seminars focuses on long term respiratory outcomes of perinatal lung disease as these infants reach childhood and adulthood.</description><dc:title>Long term respiratory outcomes of perinatal lung disease - Corrected Proof</dc:title><dc:creator>Sailesh Kotecha, Sarah J. Kotecha</dc:creator><dc:identifier>10.1016/j.siny.2012.01.001</dc:identifier><dc:source>Seminars in Fetal &amp; Neonatal Medicine (2012)</dc:source><dc:date>2012-01-25</dc:date><prism:publicationName>Seminars in Fetal &amp; Neonatal Medicine</prism:publicationName><prism:publicationDate>2012-01-25</prism:publicationDate><prism:section>EDITORIAL</prism:section></item><item rdf:about="http://www.sfnmjournal.com/article/PIIS1744165X12000042/abstract?rss=yes"><title>Long term respiratory consequences of intrauterine growth restriction - Corrected Proof</title><link>http://www.sfnmjournal.com/article/PIIS1744165X12000042/abstract?rss=yes</link><description>Summary: Epidemiological studies demonstrate that in-utero growth restriction and low birth weight are associated with impaired lung function and increased respiratory morbidity from infancy, throughout childhood and into adulthood. Chronic restriction of nutrients and/or oxygen during late pregnancy causes abnormalities in the airways and lungs of offspring, including smaller numbers of enlarged alveoli with thicker septal walls and basement membranes. The structural abnormalities and impaired lung function seen soon after birth persist or even progress with age. These changes are likely to cause lung symptomology through life and hasten lung aging.</description><dc:title>Long term respiratory consequences of intrauterine growth restriction - Corrected Proof</dc:title><dc:creator>Katharine Pike, J. Jane Pillow, Jane S. Lucas</dc:creator><dc:identifier>10.1016/j.siny.2012.01.003</dc:identifier><dc:source>Seminars in Fetal &amp; Neonatal Medicine (2012)</dc:source><dc:date>2012-01-25</dc:date><prism:publicationName>Seminars in Fetal &amp; Neonatal Medicine</prism:publicationName><prism:publicationDate>2012-01-25</prism:publicationDate></item><item rdf:about="http://www.sfnmjournal.com/article/PIIS1744165X12000054/abstract?rss=yes"><title>Long term respiratory outcomes of late preterm-born infants - Corrected Proof</title><link>http://www.sfnmjournal.com/article/PIIS1744165X12000054/abstract?rss=yes</link><description>Summary: In recent years, the rate of preterm births has risen in many industrialised countries with late preterm births forming a substantial proportion of the preterm births. Late preterm infants are delivered at the immature saccular stage of lung development when surfactant and antioxidant systems are still developing. It is now increasingly recognised that late preterm infants have increased respiratory morbidity in the neonatal period. In addition, late preterm infants are at an increased risk of lower respiratory tract infections in infancy from respiratory viruses such as respiratory syncytial virus. There is a paucity of data reporting lung function in infancy and childhood in late preterm born children. The available data suggest that children born late preterm may be at risk of decreased lung function in later life. However, further studies are required to assess the medium and long term respiratory consequences of late preterm birth.</description><dc:title>Long term respiratory outcomes of late preterm-born infants - Corrected Proof</dc:title><dc:creator>Sarah J. Kotecha, Frank D. Dunstan, Sailesh Kotecha</dc:creator><dc:identifier>10.1016/j.siny.2012.01.004</dc:identifier><dc:source>Seminars in Fetal &amp; Neonatal Medicine (2012)</dc:source><dc:date>2012-01-25</dc:date><prism:publicationName>Seminars in Fetal &amp; Neonatal Medicine</prism:publicationName><prism:publicationDate>2012-01-25</prism:publicationDate></item><item rdf:about="http://www.sfnmjournal.com/article/PIIS1744165X12000066/abstract?rss=yes"><title>Maternal and fetal origins of lung disease in adulthood - Corrected Proof</title><link>http://www.sfnmjournal.com/article/PIIS1744165X12000066/abstract?rss=yes</link><description>Summary: This review focuses on genetic and environmental influences that result in long term alterations in lung structure and function. Environmental factors operating during fetal and early postnatal life can have persistent effects on lung development and so influence lung function and respiratory health throughout life. Common factors affecting the quality of the intrauterine environment that can alter lung development include fetal nutrient and oxygen availability leading to intrauterine growth restriction, fetal intrathoracic space, intrauterine infection or inflammation, maternal tobacco smoking and other drug exposures. Similarly, factors that operate during early postnatal life, such as mechanical ventilation and high FiO2 in the case of preterm birth, undernutrition, exposure to tobacco smoke and respiratory infections, can all lead to persistent alterations in lung structure and function. Greater awareness of the many prenatal and early postnatal factors that can alter lung development will help to improve lung development and hence respiratory health throughout life.</description><dc:title>Maternal and fetal origins of lung disease in adulthood - Corrected Proof</dc:title><dc:creator>Richard Harding, Gert Maritz</dc:creator><dc:identifier>10.1016/j.siny.2012.01.005</dc:identifier><dc:source>Seminars in Fetal &amp; Neonatal Medicine (2012)</dc:source><dc:date>2012-01-25</dc:date><prism:publicationName>Seminars in Fetal &amp; Neonatal Medicine</prism:publicationName><prism:publicationDate>2012-01-25</prism:publicationDate></item><item rdf:about="http://www.sfnmjournal.com/article/PIIS1744165X12000030/abstract?rss=yes"><title>Early origins of chronic obstructive pulmonary disease - Corrected Proof</title><link>http://www.sfnmjournal.com/article/PIIS1744165X12000030/abstract?rss=yes</link><description>Summary: Chronic obstructive pulmonary disease (COPD) is a major cause of morbidity and mortality worldwide and a significant challenge for adult physicians. However, there is a misconception that COPD is a disease of only adult smokers. There is a growing body of evidence to support the hypothesis that chronic respiratory diseases such as COPD have their origins in early life. In particular, adverse maternal factors will interact with the environment in a susceptible host promoting altered lung growth and development antenatally and in early childhood. Subsequent lung injury and further gene–environment interactions may result in permanent lung injury manifest by airway obstruction predisposing to COPD. This review will discuss the currently available data regarding risk factors in early life and their role in determining the COPD phenotype.</description><dc:title>Early origins of chronic obstructive pulmonary disease - Corrected Proof</dc:title><dc:creator>Indra Narang, Andrew Bush</dc:creator><dc:identifier>10.1016/j.siny.2012.01.002</dc:identifier><dc:source>Seminars in Fetal &amp; Neonatal Medicine (2012)</dc:source><dc:date>2012-01-24</dc:date><prism:publicationName>Seminars in Fetal &amp; Neonatal Medicine</prism:publicationName><prism:publicationDate>2012-01-24</prism:publicationDate></item><item rdf:about="http://www.sfnmjournal.com/article/PIIS1744165X12000078/abstract?rss=yes"><title>Fetal origins of asthma - Corrected Proof</title><link>http://www.sfnmjournal.com/article/PIIS1744165X12000078/abstract?rss=yes</link><description>Summary: There is convincing evidence that asthma has its origins in early life. We review the epidemiological and biological evidence for fetal exposures that may have a causal role in asthma development. However, those factors that provoke asthma exacerbations are not necessarily the same as those associated with disease induction. Epidemiological studies have identified many potential exposures linked to asthma but these do not confirm causality and have not been replicated by experiment. Asthma is a heterogeneous disease and there are developmental influences on at least two pathways, airway structure and airway inflammation. The fetus is not immunologically naive and intrauterine exposures can act directly to invoke immunological sensitisation leading postnatally to airway inflammation. Other potential mechanisms include indirect effects on airway and lung growth through fetal nutrition and epigenetic modifications of DNA expression by environmental exposures. Identifying the causal factors will provide the targets for interventions to prevent disease.</description><dc:title>Fetal origins of asthma - Corrected Proof</dc:title><dc:creator>A. John Henderson, John O. Warner</dc:creator><dc:identifier>10.1016/j.siny.2012.01.006</dc:identifier><dc:source>Seminars in Fetal &amp; Neonatal Medicine (2012)</dc:source><dc:date>2012-01-24</dc:date><prism:publicationName>Seminars in Fetal &amp; Neonatal Medicine</prism:publicationName><prism:publicationDate>2012-01-24</prism:publicationDate></item><item rdf:about="http://www.sfnmjournal.com/article/PIIS1744165X1200008X/abstract?rss=yes"><title>Epidemiology of late and moderate preterm birth - Corrected Proof</title><link>http://www.sfnmjournal.com/article/PIIS1744165X1200008X/abstract?rss=yes</link><description>Summary: Preterm birth affects 12.5% of all births in the USA. Infants of Black mothers are disproportionately affected, with 1.5 times the risk of preterm birth and 3.4 times the risk of preterm-related mortality. The preterm birth rate has increased by 33% in the last 25 years, almost entirely due to the rise in late preterm births (34–36 weeks’ gestation). Recently attention has been given to uncovering the often subtle morbidity and mortality risks associated with moderate (32–33 weeks’ gestation) and late preterm delivery, including respiratory, infectious, and neurocognitive complications and infant mortality. This section summarizes the epidemiology of moderate and late preterm birth, case definitions, risk factors, recent trends, and the emerging body of knowledge of morbidity and mortality associated with moderate and late preterm birth.</description><dc:title>Epidemiology of late and moderate preterm birth - Corrected Proof</dc:title><dc:creator>Carrie K. Shapiro-Mendoza, Eve M. Lackritz</dc:creator><dc:identifier>10.1016/j.siny.2012.01.007</dc:identifier><dc:source>Seminars in Fetal &amp; Neonatal Medicine (2012)</dc:source><dc:date>2012-01-24</dc:date><prism:publicationName>Seminars in Fetal &amp; Neonatal Medicine</prism:publicationName><prism:publicationDate>2012-01-24</prism:publicationDate></item></rdf:RDF>
