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<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/?rss=yes"><title>Seminars in Fetal &amp; Neonatal Medicine</title><description>Seminars in Fetal &amp; Neonatal Medicine RSS feed: Current Issue.    
 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/?rss=yes</link><dc:publisher>Elsevier Inc.</dc:publisher><dc:language>en</dc:language><dc:rights> © 2011 Published by Elsevier Inc. All rights reserved. </dc:rights><prism:publicationName>Seminars in Fetal &amp; Neonatal Medicine</prism:publicationName><prism:issn>1744-165X</prism:issn><prism:volume>17</prism:volume><prism:number>1</prism:number><prism:publicationDate>February 2012</prism:publicationDate><prism:copyright> © 2011 Published by Elsevier Inc. All rights reserved. </prism:copyright><prism:rightsAgent>healthpermissions@elsevier.com</prism:rightsAgent><items><rdf:Seq><rdf:li rdf:resource="http://www.sfnmjournal.com/article/PIIS1744165X11001120/abstract?rss=yes"/><rdf:li rdf:resource="http://www.sfnmjournal.com/article/PIIS1744165X11001107/abstract?rss=yes"/><rdf:li rdf:resource="http://www.sfnmjournal.com/article/PIIS1744165X11001089/abstract?rss=yes"/><rdf:li rdf:resource="http://www.sfnmjournal.com/article/PIIS1744165X11000977/abstract?rss=yes"/><rdf:li rdf:resource="http://www.sfnmjournal.com/article/PIIS1744165X11000916/abstract?rss=yes"/><rdf:li rdf:resource="http://www.sfnmjournal.com/article/PIIS1744165X11000953/abstract?rss=yes"/><rdf:li rdf:resource="http://www.sfnmjournal.com/article/PIIS1744165X11000904/abstract?rss=yes"/><rdf:li rdf:resource="http://www.sfnmjournal.com/article/PIIS1744165X11001090/abstract?rss=yes"/><rdf:li rdf:resource="http://www.sfnmjournal.com/article/PIIS1744165X11000989/abstract?rss=yes"/><rdf:li rdf:resource="http://www.sfnmjournal.com/article/PIIS1744165X11000941/abstract?rss=yes"/><rdf:li rdf:resource="http://www.sfnmjournal.com/article/PIIS1744165X11000898/abstract?rss=yes"/><rdf:li rdf:resource="http://www.sfnmjournal.com/article/PIIS1744165X11000990/abstract?rss=yes"/></rdf:Seq></items></channel><item rdf:about="http://www.sfnmjournal.com/article/PIIS1744165X11001120/abstract?rss=yes"><title>Title Page/Aims and Scope/Editorial Board</title><link>http://www.sfnmjournal.com/article/PIIS1744165X11001120/abstract?rss=yes</link><description></description><dc:title>Title Page/Aims and Scope/Editorial Board</dc:title><dc:creator></dc:creator><dc:identifier>10.1016/S1744-165X(11)00112-0</dc:identifier><dc:source>Seminars in Fetal &amp; Neonatal Medicine 17, 1 (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><prism:volume>17</prism:volume><prism:number>1</prism:number><prism:issueIdentifier>S1744-165X(11)X0007-0</prism:issueIdentifier><prism:section></prism:section><prism:startingPage>IFC</prism:startingPage><prism:endingPage>IFC</prism:endingPage></item><item rdf:about="http://www.sfnmjournal.com/article/PIIS1744165X11001107/abstract?rss=yes"><title>Editorial</title><link>http://www.sfnmjournal.com/article/PIIS1744165X11001107/abstract?rss=yes</link><description>Research efforts over the past decade have yielded substantial insights into the mechanisms by which chorioamnionitis leads to preterm labor. Unfortunately, the majority of this scientific knowledge has not translated into novel clinical strategies for the prevention and treatment of this adverse pregnancy outcome. Timely diagnosis, effective obstetrical management and the reduction of neonatal morbidities remain formidable challenges for clinicians caring for these mothers and infants. Furthermore, we are just beginning to understand relationships between maternal conditions such as periodontitis, the microbiome responsible for chorioamnionitis and preterm birth and the mechanisms responsible for brain and lung injury. The following issue of Seminars in Maternal and Fetal Medicine will review what is known about the pathogenesis of chorioamnionitis and the subsequent inflammatory response, discuss current strategies for diagnosis and treatment, and describe selected neonatal morbidities observed in associated with intrauterine infection. We are indebted to all the authors for their scientific contributions to this field and superbly written manuscripts in this issue of the Seminars.</description><dc:title>Editorial</dc:title><dc:creator>Richard A. Polin, Tara M. Randis</dc:creator><dc:identifier>10.1016/j.siny.2011.11.001</dc:identifier><dc:source>Seminars in Fetal &amp; Neonatal Medicine 17, 1 (2012)</dc:source><dc:date>2011-11-24</dc:date><prism:publicationName>Seminars in Fetal &amp; Neonatal Medicine</prism:publicationName><prism:publicationDate>2011-11-24</prism:publicationDate><prism:volume>17</prism:volume><prism:number>1</prism:number><prism:issueIdentifier>S1744-165X(11)X0007-0</prism:issueIdentifier><prism:section></prism:section><prism:startingPage>1</prism:startingPage><prism:endingPage>1</prism:endingPage></item><item rdf:about="http://www.sfnmjournal.com/article/PIIS1744165X11001089/abstract?rss=yes"><title>Diversity of microbes in amniotic fluid</title><link>http://www.sfnmjournal.com/article/PIIS1744165X11001089/abstract?rss=yes</link><description>Summary: Recent polymerase chain reaction (PCR)-based studies estimate the prevalence of microbial invasion of the amniotic cavity (MIAC) to be ≥30–50% higher than that detected by cultivation-based methods. Some species that have been long implicated in causing MIAC remain among the common invaders (e.g. Ureaplasma spp., Mycoplasma spp., Fusobacterium spp. Streptococcus spp., Bacteroides spp. and Prevotella spp.). Yet we now know from studies based on PCR of the 16S ribosomal DNA that cultivation-resistant anaerobes belonging to the family Fusobacteriaceae (particularly Sneathia sanguinegens, and Leptotrichia spp.) are also commonly found in amniotic fluid. Other diverse microbes detected by PCR of amniotic fluid include as-yet uncultivated and uncharacterized species. The presence of some microbial taxa is associated with specific host factors (e.g. Candida spp. and an indwelling intrauterine device). It appears that MIAC is polymicrobial in 24–67% of cases, but the potential role of pathogen synergy is poorly understood. A causal relationship between diverse microbes, as detected by PCR, and preterm birth is supported by types of association (e.g. space, time and dose) proposed as alternatives to Koch's postulates for inferring causality from molecular findings. The microbial census of the amniotic cavity remains unfinished. A more complete understanding may inform future research directions leading to improved strategies for preventing, diagnosing and treating MIAC.</description><dc:title>Diversity of microbes in amniotic fluid</dc:title><dc:creator>Daniel B. DiGiulio</dc:creator><dc:identifier>10.1016/j.siny.2011.10.001</dc:identifier><dc:source>Seminars in Fetal &amp; Neonatal Medicine 17, 1 (2012)</dc:source><dc:date>2011-12-05</dc:date><prism:publicationName>Seminars in Fetal &amp; Neonatal Medicine</prism:publicationName><prism:publicationDate>2011-12-05</prism:publicationDate><prism:volume>17</prism:volume><prism:number>1</prism:number><prism:issueIdentifier>S1744-165X(11)X0007-0</prism:issueIdentifier><prism:section></prism:section><prism:startingPage>2</prism:startingPage><prism:endingPage>11</prism:endingPage></item><item rdf:about="http://www.sfnmjournal.com/article/PIIS1744165X11000977/abstract?rss=yes"><title>Intrauterine infection and preterm labor</title><link>http://www.sfnmjournal.com/article/PIIS1744165X11000977/abstract?rss=yes</link><description>Summary: Preterm labor is defined as labor that begins before 37 completed weeks of pregnancy. More than 12% of infants born in the USA are preterm. At least 40% of preterm births are associated with intrauterine infection. Toll-like receptors (TLRs) are members of a family of cell-surface proteins responsible for recognition of a diverse spectrum of bacterial, viral and fungal pathogens. TLRs initiate the host innate (i.e. non-adaptive) immune response, inducing a proinflammatory cascade involving cytokines, chemokines, prostaglandins, and other effector molecules that result in the characteristic phenomena of labor, such as uterine contractions and rupture of fetal membranes. These cascades may also be activated by mechanisms that are not primarily infectious but are accompanied by inflammatory responses. Now that the molecular mechanisms linking infection and labor have been, to a large extent, elucidated, the challenge is to identify points of overlap with non-infectious causes of labor and to find intervention strategies that can minimize the negative impact of preterm delivery.</description><dc:title>Intrauterine infection and preterm labor</dc:title><dc:creator>Varkha Agrawal, Emmet Hirsch</dc:creator><dc:identifier>10.1016/j.siny.2011.09.001</dc:identifier><dc:source>Seminars in Fetal &amp; Neonatal Medicine 17, 1 (2012)</dc:source><dc:date>2011-09-26</dc:date><prism:publicationName>Seminars in Fetal &amp; Neonatal Medicine</prism:publicationName><prism:publicationDate>2011-09-26</prism:publicationDate><prism:volume>17</prism:volume><prism:number>1</prism:number><prism:issueIdentifier>S1744-165X(11)X0007-0</prism:issueIdentifier><prism:section></prism:section><prism:startingPage>12</prism:startingPage><prism:endingPage>19</prism:endingPage></item><item rdf:about="http://www.sfnmjournal.com/article/PIIS1744165X11000916/abstract?rss=yes"><title>Inflammatory response in acute chorioamnionitis</title><link>http://www.sfnmjournal.com/article/PIIS1744165X11000916/abstract?rss=yes</link><description>Summary: Acute chorioamnionitis is the principal antecedent of premature birth and an important contributor to specific neonatal and other complications that may extend throughout subsequent life. A large number of studies have addressed surrogate markers of in-utero inflammation including cytokines, chemokines, pathogen-associated molecular patterns, and elicited host proteins. However, chorioamnionitis means inflammation occurring within the chorioamnion and the only practical direct measure available to assess this finding in most placentas is histopathology. The maternal and fetal inflammatory response to the presence of organisms within the placental membranes, so-called histologic chorioamnionitis, is the focus of this review. The issues addressed are the nature and origin of the eliciting antigen, mode of spread to the placenta, general characteristics of placental immunity, and a specific characterization of the spectrum of pathologic lesions observed in placentas with membrane infection.</description><dc:title>Inflammatory response in acute chorioamnionitis</dc:title><dc:creator>Raymond W. Redline</dc:creator><dc:identifier>10.1016/j.siny.2011.08.003</dc:identifier><dc:source>Seminars in Fetal &amp; Neonatal Medicine 17, 1 (2012)</dc:source><dc:date>2011-08-25</dc:date><prism:publicationName>Seminars in Fetal &amp; Neonatal Medicine</prism:publicationName><prism:publicationDate>2011-08-25</prism:publicationDate><prism:volume>17</prism:volume><prism:number>1</prism:number><prism:issueIdentifier>S1744-165X(11)X0007-0</prism:issueIdentifier><prism:section></prism:section><prism:startingPage>20</prism:startingPage><prism:endingPage>25</prism:endingPage></item><item rdf:about="http://www.sfnmjournal.com/article/PIIS1744165X11000953/abstract?rss=yes"><title>Perinatal infection, inflammation, and retinopathy of prematurity</title><link>http://www.sfnmjournal.com/article/PIIS1744165X11000953/abstract?rss=yes</link><description>Summary: The major known risk factors for retinopathy of prematurity (ROP) are extremely low gestational age, exposure to high levels of oxygen early after birth (phase I) and relatively lower oxygen levels later (phase II). In this review, we summarize recent data suggesting that exposure to perinatal infection/inflammation is associated with an increased risk for ROP. Part of this effect might be due to direct exposure of the developing retina to circulating products of infection and/or inflammation. Another potential mechanism that deserves exploration is that inflammation and/or oxidative stress can modify the known increased risk of oxygen-associated ROP. Taken together, accumulating evidence suggests that prenatal, perinatal, and postnatal systemic inflammation contribute to a ‘pre-phase’, sensitizing the pre-ROP retina for subsequent insults, setting the stage for what are now called phase I and phase II of ROP pathogenesis. Strategies targeting inflammatory responses might help reduce the risk for ROP in extremely low gestational age newborns.</description><dc:title>Perinatal infection, inflammation, and retinopathy of prematurity</dc:title><dc:creator>Jennifer Lee, Olaf Dammann</dc:creator><dc:identifier>10.1016/j.siny.2011.08.007</dc:identifier><dc:source>Seminars in Fetal &amp; Neonatal Medicine 17, 1 (2012)</dc:source><dc:date>2011-09-07</dc:date><prism:publicationName>Seminars in Fetal &amp; Neonatal Medicine</prism:publicationName><prism:publicationDate>2011-09-07</prism:publicationDate><prism:volume>17</prism:volume><prism:number>1</prism:number><prism:issueIdentifier>S1744-165X(11)X0007-0</prism:issueIdentifier><prism:section></prism:section><prism:startingPage>26</prism:startingPage><prism:endingPage>29</prism:endingPage></item><item rdf:about="http://www.sfnmjournal.com/article/PIIS1744165X11000904/abstract?rss=yes"><title>Perinatal inflammation and lung injury</title><link>http://www.sfnmjournal.com/article/PIIS1744165X11000904/abstract?rss=yes</link><description>Summary: Bronchopulmonary dysplasia (BPD) remains the major morbidity of extreme preterm birth. The incidence of BPD has remained stable despite recent efforts to reduce postnatal exposures to volutrauma and hyperoxia. This review will focus on recent clinical and experimental insights that provide support for the concept that the ‘new BPD’ is the result of inflammation-mediated injury and altered lung development during a window of vulnerability in genetically susceptible infants that is modified by maternal and postnatal exposures.</description><dc:title>Perinatal inflammation and lung injury</dc:title><dc:creator>Rose Marie Viscardi</dc:creator><dc:identifier>10.1016/j.siny.2011.08.002</dc:identifier><dc:source>Seminars in Fetal &amp; Neonatal Medicine 17, 1 (2012)</dc:source><dc:date>2011-08-22</dc:date><prism:publicationName>Seminars in Fetal &amp; Neonatal Medicine</prism:publicationName><prism:publicationDate>2011-08-22</prism:publicationDate><prism:volume>17</prism:volume><prism:number>1</prism:number><prism:issueIdentifier>S1744-165X(11)X0007-0</prism:issueIdentifier><prism:section></prism:section><prism:startingPage>30</prism:startingPage><prism:endingPage>35</prism:endingPage></item><item rdf:about="http://www.sfnmjournal.com/article/PIIS1744165X11001090/abstract?rss=yes"><title>Proteomics/diagnosis of chorioamnionitis and of relationships with the fetal exposome</title><link>http://www.sfnmjournal.com/article/PIIS1744165X11001090/abstract?rss=yes</link><description>Summary: Proteomics, a relatively young science, originally emerged as a complement to genomics research. By definition, the goal of proteomics is to provide a snapshot of all the proteins within an organism, tissue or biological sample at a given moment. Proteomics has the ability to single out one or more proteins (biomarkers) that change consistently in affected subjects as compared to those disease-free. From a proteomics perspective, chorioamnionitis poses both challenges and opportunities. Challenges relate to the dynamic course of the inflammatory process, and compartmentalization of the gestational sac in relation to the maternal compartment. An inability to evaluate the amniotic fluid non-invasively and repeatedly for meaningful changes in its proteome, and lack of a true gold standard for diagnosis of inflammation and/or infection, represent additional challenges. On the other hand, the unbiased and holistic nature of proteomics offers a real opportunity to improve the current diagnostic and prognostic algorithms for chorioamnionitis. Even at this current stage there are reasons to believe that proteomic biomarkers will improve the understanding of how chorioamnionitis programs or affects the fetus in utero, thus defining its exposome (sum of interactions between genetic make-up of the fetus and the intrauterine environment) of pregnancies affected by infection and/or inflammation. This review summarizes the results of proteomics studies that have aimed or reached these goals.</description><dc:title>Proteomics/diagnosis of chorioamnionitis and of relationships with the fetal exposome</dc:title><dc:creator>Irina A. Buhimschi, Catalin S. Buhimschi</dc:creator><dc:identifier>10.1016/j.siny.2011.10.002</dc:identifier><dc:source>Seminars in Fetal &amp; Neonatal Medicine 17, 1 (2012)</dc:source><dc:date>2011-11-21</dc:date><prism:publicationName>Seminars in Fetal &amp; Neonatal Medicine</prism:publicationName><prism:publicationDate>2011-11-21</prism:publicationDate><prism:volume>17</prism:volume><prism:number>1</prism:number><prism:issueIdentifier>S1744-165X(11)X0007-0</prism:issueIdentifier><prism:section></prism:section><prism:startingPage>36</prism:startingPage><prism:endingPage>45</prism:endingPage></item><item rdf:about="http://www.sfnmjournal.com/article/PIIS1744165X11000989/abstract?rss=yes"><title>Evidence for the clinical management of chorioamnionitis</title><link>http://www.sfnmjournal.com/article/PIIS1744165X11000989/abstract?rss=yes</link><description>Summary: Acute chorioamnionitis or intra-amniotic infection is defined by maternal fever in association with at least one additional clinical criterion including maternal or fetal tachycardia, maternal leukocytosis, uterine tenderness, or foul amniotic fluid odor. In clinically uncertain cases, the diagnosis can be augmented by routine laboratory studies (e.g. white blood cell count and differential count and acute phase reactants) and assays done on amniotic fluid. In general, the clinical management of chorioamnionitis is based on observational or cohort studies; only a few randomized controlled trials have been done. Prompt administration of antibiotics and delivery decrease maternal and neonatal morbidity. The most commonly used antibiotic regimen is ampicillin and gentamicin. Recent evidence supports daily rather than three-times-daily dosing of gentamicin for greater efficacy and decreased fetal toxicity. There is no evidence demonstrating harm with the administration of corticosteroids (to promote fetal lung maturity) in women with acute chorioamnionitis. Cesarean delivery should be reserved for standard obstetric indications</description><dc:title>Evidence for the clinical management of chorioamnionitis</dc:title><dc:creator>Shira G. Fishman, Shari E. Gelber</dc:creator><dc:identifier>10.1016/j.siny.2011.09.002</dc:identifier><dc:source>Seminars in Fetal &amp; Neonatal Medicine 17, 1 (2012)</dc:source><dc:date>2011-10-03</dc:date><prism:publicationName>Seminars in Fetal &amp; Neonatal Medicine</prism:publicationName><prism:publicationDate>2011-10-03</prism:publicationDate><prism:volume>17</prism:volume><prism:number>1</prism:number><prism:issueIdentifier>S1744-165X(11)X0007-0</prism:issueIdentifier><prism:section></prism:section><prism:startingPage>46</prism:startingPage><prism:endingPage>50</prism:endingPage></item><item rdf:about="http://www.sfnmjournal.com/article/PIIS1744165X11000941/abstract?rss=yes"><title>Microbiota of the upper and lower genital tract</title><link>http://www.sfnmjournal.com/article/PIIS1744165X11000941/abstract?rss=yes</link><description>Summary: Our understanding of the bacterial species inhabiting the female genital tract has been limited primarily by our ability to detect them. Early investigations using microscopy and culture-based techniques identified lactobacilli as the predominant members of the vaginal microbiota and suggested that these organisms might serve a protective function at the mucosal surface. Improvements in cultivation techniques and the development of molecular-based detection strategies validated these early findings and enabled us to recognize that the microbiota of the female genital tract is much more complex than previously suspected. Disruption of the vaginal microbial community due to invasion of exogenous organisms or by overgrowth of one or more endogenous species has important health implications for both the mother and newborn.</description><dc:title>Microbiota of the upper and lower genital tract</dc:title><dc:creator>Ryan Rampersaud, Tara M. Randis, Adam J. Ratner</dc:creator><dc:identifier>10.1016/j.siny.2011.08.006</dc:identifier><dc:source>Seminars in Fetal &amp; Neonatal Medicine 17, 1 (2012)</dc:source><dc:date>2011-09-15</dc:date><prism:publicationName>Seminars in Fetal &amp; Neonatal Medicine</prism:publicationName><prism:publicationDate>2011-09-15</prism:publicationDate><prism:volume>17</prism:volume><prism:number>1</prism:number><prism:issueIdentifier>S1744-165X(11)X0007-0</prism:issueIdentifier><prism:section></prism:section><prism:startingPage>51</prism:startingPage><prism:endingPage>57</prism:endingPage></item><item rdf:about="http://www.sfnmjournal.com/article/PIIS1744165X11000898/abstract?rss=yes"><title>Prevention of preterm birth</title><link>http://www.sfnmjournal.com/article/PIIS1744165X11000898/abstract?rss=yes</link><description>Summary: Preterm birth (delivery before 37 completed weeks of gestation) is common and rates are increasing. In the past, medical efforts focused on ameliorating the consequences of prematurity rather than preventing its occurrence. This approach resulted in improved neonatal outcomes, but it remains costly in terms of both the suffering of infants and their families and the economic burden on society. Increased understanding of the pathophysiology of preterm labor has altered the approach to this problem, with increased focus on preventive strategies. Primary prevention is a limited strategy which involves public education, smoking cessation, improved nutritional status and avoidance of late preterm births. Secondary prevention focuses on recurrent preterm birth which is the most recognisable risk factor. Widely accepted strategies include cervical cerclage, progesterone and dedicated clinics. However, more research is needed to explore the role of antibiotics and anti-inflammatory treatments in the prevention of this complex problem.</description><dc:title>Prevention of preterm birth</dc:title><dc:creator>Karen Flood, Fergal D. Malone</dc:creator><dc:identifier>10.1016/j.siny.2011.08.001</dc:identifier><dc:source>Seminars in Fetal &amp; Neonatal Medicine 17, 1 (2012)</dc:source><dc:date>2011-09-07</dc:date><prism:publicationName>Seminars in Fetal &amp; Neonatal Medicine</prism:publicationName><prism:publicationDate>2011-09-07</prism:publicationDate><prism:volume>17</prism:volume><prism:number>1</prism:number><prism:issueIdentifier>S1744-165X(11)X0007-0</prism:issueIdentifier><prism:section></prism:section><prism:startingPage>58</prism:startingPage><prism:endingPage>63</prism:endingPage></item><item rdf:about="http://www.sfnmjournal.com/article/PIIS1744165X11000990/abstract?rss=yes"><title>Alcohol, Drugs and Medication in Pregnancy</title><link>http://www.sfnmjournal.com/article/PIIS1744165X11000990/abstract?rss=yes</link><description>This textbook summarizes the long term consequences in children who have been exposed in utero to various drugs and substances of misuse. The authors have explored findings of recent research in this area and provided a scientific basis for the clinical decision-making process. The book is divided into four sections containing 16 chapters written by a group of authors from the UK, USA, Canada and France, thus truly providing a global perspective.</description><dc:title>Alcohol, Drugs and Medication in Pregnancy</dc:title><dc:creator>Ramesh Kumar</dc:creator><dc:identifier>10.1016/j.siny.2011.09.003</dc:identifier><dc:source>Seminars in Fetal &amp; Neonatal Medicine 17, 1 (2012)</dc:source><dc:date>2011-11-09</dc:date><prism:publicationName>Seminars in Fetal &amp; Neonatal Medicine</prism:publicationName><prism:publicationDate>2011-11-09</prism:publicationDate><prism:volume>17</prism:volume><prism:number>1</prism:number><prism:issueIdentifier>S1744-165X(11)X0007-0</prism:issueIdentifier><prism:section>Book review</prism:section><prism:startingPage>64</prism:startingPage><prism:endingPage>64</prism:endingPage></item></rdf:RDF>
