NSIDRC Journal Article Alert — February 20, 2009
Prepared by the National Sudden and Unexpected Infant/Child Death and Pregnancy Loss Resource Center at Georgetown University.
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Sudden Infant Death
1. Highet AR, Berry AM, Bettelheim KA, Goldwater PN
The frequency of molecular detection of virulence genes encoding cytolysin A, high-pathogenicity island and cytolethal distending toxin of Escherichia coli in cases of sudden infant death syndrome does not differ from that in other infant deaths and healthy infants
J Med Microbiol. 2009 Mar;58(Pt 3):285-9
Department of Microbiology and Infectious Diseases, SA Pathology, Women's and Children's Hospital, 72 King William Road, North Adelaide, South Australia, Australia.
Consistent pathological findings in sudden infant death syndrome (SIDS) are seen which display similarities to the pathogenesis of toxaemic shock and/or sepsis. A key candidate infectious agent that is possibly involved is Escherichia coli, given its universal early colonization of the intestinal tract of infants and an increased frequency of toxigenic and mouse-lethal isolates from SIDS compared with comparison infants. An explanation for these findings has yet to be identified. Using PCR, we screened E. coli isolates from 145 SIDS and 101 dead control and healthy infants for three new candidate pathogenicity-related genes: clyA (cytolysin A), irp2 [high-pathogenicity island (HPI)-specific gene] and cdt (cytolethal distending toxin). The results failed to show a positive correlation with SIDS, instead proving that clyA and irp2 genes were common to the infant intestinal E. coli. Interestingly we observed a high rate of carriage of these two potentially pathogenic genes in E. coli from healthy infants in the absence of diarrhoeal disease, and we report that in a number of cases, the detection of HPI-specific genes was predictable by serotype. Despite the lack of associations defined so far, there remains the likelihood that genetic determinants influence the interactions between E. coli and the host, so these factors may be part of the multi-factorial aspect of SIDS.
2. Myers MM
Sudden infant death syndrome: A developmental psychobiologist's perspective
Dev Psychobiol. 2009 Feb 10. [Epub ahead of print]
Division of Developmental Neuroscience, Department of Psychiatry, New York State Psychiatric Institute, Columbia University, Unit 40, 1051 Riverside Drive, New York, NY 10032.
3. Rickert CH, Groß O, Nolte KW, Vennemann M, Bajanowski
T, Brinkmann B
Leptomeningeal neurons are a common finding in infants and are increased in sudden infant death syndrome
Acta Neuropathol. 2009 Feb 11. [Epub ahead of print]
Institute of Neuropathology, University Hospital Münster, Munster, Germany, christian.rickert@mh.org.au
Developmental abnormalities of the brain, in particular, the brainstem potentially affecting centers for breathing, circulation and sleep regulation, are thought to be involved in the etiology of sudden infant death syndrome (SIDS). In order to investigate whether leptomeningeal neurons could serve as morphological indicators for a developmental failure or retardation in cerebral maturation, we evaluated the density of isolated leptomeningeal neurons (without associated glia) in 15 brain regions of 24 SIDS and 8 control cases, representing part of the German Study on sudden infant death. Leptomeningeal neurons were encountered in 79% of SIDS and 68% of control cases. More leptomeningeal neurons in SIDS versus control cases were found in lower pons (p = 0.002), upper pons (p = 0.016), cerebellar hemispheres (p = 0.012), lower medulla oblongata (p = 0.039), and temporal lobe (p = 0.041). Summarizing the data according to gross anatomical region of origin (i.e., brainstem, cerebellum or cerebrum), higher numbers of leptomeningeal neurons in SIDS cases were only found in the brainstem (p = 0.006 vs. 0.13 and 0.19, respectively). Our data show that single leptomeningeal neurons are present in most normal infantile brains. The age-dependent increase of leptomeningeal neurons among SIDS cases may either (a) represent a delayed maturation or retardation, i.e., a later or slower reduction of neurons or a delayed peak in occurrence (shift toward an older age), or (b) may be interpreted as a generally increased occurrence of leptomeningeal neurons among SIDS cases as a result of a diffuse developmental abnormality during central nervous system maturation.
4. Kinney HC
Neuropathology provides new insight in the pathogenesis of the sudden infant death syndrome
Acta Neuropathol. 2009 Feb 10. [Epub ahead of print]
Department of Pathology, Enders Building 1112, Children's Hospital Boston, Harvard Medical School, 300 Longwood Avenue, Boston, MA, 02115, USA, Hannah.kinney@childrens.harvard.edu.
Other Infant Death
1. Menifield CE, Dawson J
Infant mortality in southern states: a bureaucratic nightmare
J Health Hum Serv Adm. 2008 Winter;31(3):385-402
University of Memphis, Division of Public and Nonprofit Administration, USA.
Despite numerous advances in technology, medicine, and health care, infant mortality continues to reach very high levels in southern states. The purpose of this paper is to examine demographic, economic, and health care factors that are likely to affect infant mortality. In so doing, we first compare infant mortality and other critical factors in southern states to other regions of the country. Second, we use cross tabulation tables to determine if there is a correlation between infant mortality and several independent variables. Third, we use regression analysis to determine how each of these variables affects the change in infant mortality for the 1990-2003 periods. The results of the cross tabulation tables indicate relationships between infant mortality and each of the independent variables. When these variables were placed in a regression model, high school graduation rates, race, geographic region, unemployment rates, uninsured rates, teenage pregnancy rates, single parent families, and the number of doctors and hospitals were significant.
Miscarriage/Stillbirth/Prenatal Issues
1. Raffaelli F, Nanetti L, Vignini A, Mazzanti L, Giannubilo SR, Curzi CM, Turi A, Vitali P, Tranquilli AL
Nitric oxide platelet production in spontaneous miscarriage in the first trimester
Fertil Steril. 2009 Feb 11. [Epub ahead of print]
Department of Biochemistry, Biology and Genetics, Marche Polytechnic University, Ancona, Italy.
OBJECTIVE: To investigate the role played by platelet nitric oxide (NO) metabolism in patients with spontaneous miscarriage (SM) and recurrent spontaneous miscarriage (RSM) compared with healthy pregnant women. DESIGN: Retrospective case-control study. SETTING: Patients and controls in an academic research environment. INTERVENTION(S): None. PATIENT(S): Thirty singleton pregnant women who experienced SM, nine singleton pregnant women who presented with RSM, and 30 singleton healthy pregnant women matched for age, parity, and gestational age were enrolled. MAIN OUTCOME MEASURE(S): NO levels and peroxynitrite (ONOO(-)) production; moreover, inducible NO synthase (iNOS), endothelial NO synthase (eNOS), and nitrotyrosine expression (N-Tyr) were observed in the same samples. RESULT(S): A significant increase was shown in platelet NO and ONOO(-) levels and in iNOS and N-Tyr both in SM and in RSM pregnant women compared with controls. CONCLUSION(S): The data herein reported imply that a modified NO pathway might play a key role in the physiological changes of advancing gestation but may also contribute to the pathophysiology of spontaneous miscarriage. Thus, any factors balancing NO metabolism might be useful in the treatment of miscarriage, thus reducing the substantial morbidity and associated mortality.
2. Zhang YX, Zhang YP, Gu Y, Guan FJ, Li SL, Xie JS, Shen Y, Wu BL, Ju W, Jenkins EC, Brown WT, Zhong
Genetic analysis of first-trimester miscarriages with a combination of cytogenetic karyotyping, microsatellite genotyping and arrayCGH
N Clin Genet. 2009 Feb;75(2):133-40
Peking University Center of Medical Genetics, Beijing, China.
Miscarriage is the spontaneous loss of an embryo or fetus before the 20th week of pregnancy. Most miscarriages occur before the end of the first trimester (<13 weeks). Although many risk factors relate to this occurrence, genetic factors play the most important role. Chromosomal abnormalities, including both numerical and structural anomalies, underlie the majority of miscarriages. In this study, we employed a comprehensive approach using cytogenetic karyotyping, polymerase chain reaction (PCR)-based genotyping, and microarray-based comparative genomic hybridization (arrayCGH) in combination to analyze chromosomal profiles of 115 first-trimester miscarriages of Chinese women. Seventy cases (61%) were found to have chromosomal anomalies, of which 90% were numerical and 10% were structural. Cytogenetic karyotyping identified 78.6% (55/70), PCR assays 2.9% (2 triploids), and arrayCGH 18.6% (13/70) of the anomalies. In this study, a microdeletion of 108 kb and four microduplications sizing from 300 to 1460 kb were observed. An advantage of using this combination approach is that microsatellite genotyping and arrayCGH can be accomplished in spite of culture failure and maternal cell contamination. In addition, arrayCGH can detect submicroscopic chromosomal anomalies and gene dosage alterations.
3. Challis JR, Lockwood CJ, Myatt L, Norman JE, Strauss JF 3rd, Petraglia F
Inflammation and pregnancy
Reprod Sci. 2009 Feb;16(2):206-15
Michael Johnson Foundation for Health Research, Vancouver, Canada.
Inflammation is a process by which tissues respond to various insults. It is characterized by upregulation of chemokines, cytokines, and pattern recognition receptors that sense microbes and tissue breakdown products. During pregnancy, the balance of Th1 (cell-mediated immunity) and Th2 (humoral immunity) cytokines is characterized by an initial prevalence of Th2 cytokines, followed by a progressive shift toward Th1 predominance late in gestation, that when is abnormal, may initiate and intensify the cascade of inflammatory cytokine production involved in adverse pregnancy outcomes. Maternal and placental hormones may affect the inflammatory pathway. Hypoxia and the innate immune response are 2 adaptive mechanisms by which organisms respond to perturbation in organ function, playing a major role in spontaneous abortion, intrauterine growth restriction, preeclampsia, and preterm delivery. The interaction between tissue remodeling factors, like matrix metalloproteinases, and vasoactive/hemostatic factors, like prostaglandin and coagulation factors, mediates this adaptive response.
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