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NSIDRC Journal Article Alert — April 29, 2010

Prepared by the National Sudden and Unexpected Infant/Child Death and Pregnancy Loss Resource Center at Georgetown University.

These articles have been selected from PubMed, a service of the National Library of Medicine that includes over 19 million citations from MEDLINE and other life science journals for biomedical articles back to 1948. PubMed includes links to full text articles and other related resources.

Availability of full-text journal articles is often limited to subscribers or through inter-library loan. Please see your local library for copies of these articles, or view PubMed's How to Get the Journal Article or Partners in Information Access for the Public Health Workforce's How to Access Journal Articles for more details.


Sudden Infant Death

1. Darnall RA
The role of CO(2) and central chemoreception in the control of breathing in the fetus and the neonate
Respir Physiol Neurobiol. 2010 Apr 22. [Epub ahead of print]

Departments of Physiology and Neurobiology and Pediatrics, Dartmouth Medical School, Borwell Building, 1 Medical Center Drive, Lebanon, NH 03756, United States.

Central chemoreception is active early in development and likely drives fetal breathing movements, which are influenced by a combination of behavioral state and powerful inhibition. In the premature human infant and newborn rat ventilation increases in response to CO(2); in the rat the sensitivity of the response increases steadily after approximately P12. The premature human infant is more vulnerable to instability than the newborn rat and exhibits periodic breathing that is augmented by hypoxia and eliminated by breathing oxygen or CO(2) or the administration of respiratory stimulants. The sites of central chemoreception active in the fetus are not known, but may involve the parafacial respiratory group which may be a precursor to the adult RTN. The fetal and neonatal rat brainstem-spinal-cord preparations promise to provide important information about central chemoreception in the developing rodent and will increase our understanding of important clinical problems, including The Sudden Infant Death Syndrome, Congenital Central Hypoventilation Syndrome, and periodic breathing and apnea of prematurity. Copyright © 2010. Published by Elsevier B.V.


Other Infant Death

1. Donovan EF, Besl J, Paulson J, Rose B, Iams J; Ohio Perinatal Quality Collaborative
Infant death among Ohio resident infants born at 32 to 41 weeks of gestation
Am J Obstet Gynecol. 2010 Apr 22. [Epub ahead of print]

Child Policy Research Center, Cincinnati Children's Hospital Medical CenterThe Ohio State University, Cincinnati, OH; Ohio Perinatal Quality Collaborative, Columbus, OH.

OBJECTIVE: The aim of this study was to determine gestational age-specific, adjusted infant mortality rates for Ohio. STUDY DESIGN: Using a retrospective cohort design, all births and infant deaths from 2003-2005 were included in multivariable regression analyses. Variations in cause and timing of infant death were determined. RESULTS: Compared with births at 39 or 40 weeks, adjusted likelihood of infant death increased progressively between 38-32 weeks' gestational age. At later gestational ages, death was more likely caused by sudden infant death syndrome or intentional injury compared with congenital malformations and asphyxia or cerebral palsy at earlier gestational ages. Less mature infants tended to die earlier. CONCLUSION: The current study confirms for Ohio and extends the findings of others that infant mortality risk is increased for births at late preterm and near-term gestational ages. Decisions to deliver before 39 weeks should consider increased likelihood of infant death that may be unrelated to fetal malformations or maternal illness. Copyright © 2010 Mosby, Inc. All rights reserved.


Miscarriage/Stillbirth/Prenatal Issues

1. Olive DL, Pritts EA
Fibroids and reproduction
Semin Reprod Med. 2010 May;28(3):218-27. Epub 2010 Apr 22

Wisconsin Fertility Institute, Middleton, Wisconsin 53562, USA. lapskyboy@aol.com

Uterine fibroids are commonly seen in women with reproductive disorders such as infertility, spontaneous abortion (SAB), and obstetric complications. Although it is certain that these tumors can occasionally cause such pathophysiology, it is critical to understand the rate of such occurrences, the degree of causality of the fibroids, and our ability to ameliorate the problems via surgical treatment. Evaluation of the available data is hampered by poor quality studies, heterogeneity of the disease, and confounding factors affecting outcomes. Nevertheless, the best available evidence suggests the following: (1) Submucous myomas decrease fertility and increase SAB rates; myomectomy is likely to be of value; (2) intramural myomas may decrease fertility, but the issue is less clear; they do seem to increase rates of miscarriage; there is no solid evidence that myomectomy restores the patient to normal; (3) subserosal myomas do not impair fertility but may enhance the rate of SAB; and (4) fibroids increase the risk of several obstetric complications, including cesarean delivery, malpresentation, postpartum hemorrhage, retained placenta, intrauterine growth retardation, preterm labor, placenta previa, and abruption. Higher quality studies are desperately needed to add confidence to these tenuous conclusions. Thieme Medical Publishers.


Prepared by the
National Sudden and Unexpected Infant/Child Death and Pregnancy Loss Resource Center
Georgetown University
2115 Wisconsin Avenue, N.W., Suite 601
Washington, DC  20007
(866) 866-7437 toll free
(202) 687-7466 local
(202) 784-9777 fax
info@sidscenter.org
http://www.sidscenter.org


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