Sudden Infant Death Syndrome Research Today is a free monthly online journal that collates and summarizes the latest research about Sudden Infant Death Syndrome, including details on sids, causes, prevention, statistics. | |||||||
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Analysis of the spatial distribution of infant mortality by cause of death in Austria in 1984 to 2006.Waldhoer T, Wald M, Heinzl H Center of Public Health, Department of Epidemiology, Medical University of Vienna, Borschkegasse 8a, 1090 Vienna, Austria. thomas.waldhoer@meduniwien.ac.at BACKGROUND: In Austria, over the last 20 years infant mortality declined from 11.2 per 1,000 life births (1985) to 4.7 per 1,000 in1997 but remained rather constant since then. In addition to this time trend we already reported a non-random spatial distribution of infant mortality rates in a recent study covering the time period 1984 to 2002. This present study includes four additional years and now covers about 1.9 million individual birth certificates. It aimes to elucidate the observed non-random spatial distribution in more detail. We split up infant mortality into six groups according to the underlying cause of death. The underlying spatial distribution of standardized mortality ratios (SMR) is estimated by univariate models as well as by two models incorporating all six groups simultaneously. RESULTS: We observe strong correlations between the individual spatial patterns of SMR's except for "Sudden Infant Death Syndrome" and to some extent for "Peripartal Problems". The spatial distribution of SMR's is non-random with an area of decreased risk in the South-East of Austria. The group "Sudden Infant Death Syndrome" clearly and the group "Peripartal Problems" slightly show deviations from the common pattern. When comparing univariate and multivariate SMR estimates we observe that the resulting spatial distributions are very similar. CONCLUSION: We observe different non-random spatial distributions of infant mortality rates when grouped by cause of death. The models applied were based on individual data thereby avoiding ecological regression bias. The estimated spatial distributions do not substantially depend on the employed estimation method. The observed non-random spatial patterns of Austrian infant mortality remain to appear ambiguous. Published 20 June 2008 in Int J Health Geogr, 7: 21. Articles on Sudden Infant Death Syndrome published 20 June 2008: Prenatal Cigarette Smoke Exposure Attenuates Recovery from Hypoxemic Challenge in Preterm Infants. Am J Respir Crit Care Med. RATIONALE: The effects of prenatal cigarette smoke exposure and hypoxemia on cardio-respiratory control have been investigated in full term infants. However, little data are available in preterm infants, who form a particularly vulnerable population, with developmentally immature cardiorespiratory control. OBJECTIVES: To investigate the effects of prenatal cigarette smoke exposure on the duration and recovery of breathing pauses and oxygen saturation levels under baseline and hypoxemic ... [Abstract] [Full-text] Peptidergic Agonists of Activity-Dependent Neurotrophic Factor Protect Against Prenatal Alcohol-Induced Neural Tube Defects and Serotonin Neuron Loss. Alcohol Clin Exp Res. Introduction: Prenatal alcohol exposure via maternal liquid diet consumption by C57BL/6 (B6) mice causes conspicuous midline neural tube deficit (dysraphia) and disruption of genesis and development of serotonin (5-HT) neurons in the raphe nuclei, together with brain growth retardation. The current study tested the hypothesis that concurrent treatment with either an activity-dependent neurotrophic factor (ADNF) agonist peptide [SALLRSIPA, (SAL)] or an activity-dependent neurotrophic protein ... [Abstract] [Full-text] Articles on Sudden Infant Death Syndrome published 19 June 2008: Evidence for infection, inflammation and shock in sudden infant death: parallels between a neonatal rat model of sudden death and infants who died of sudden infant death syndrome. Innate Immun, 14(3): 145-52. This study compared pathological findings from a neonatal rat model of sudden death with those from 40 sudden infant death syndrome (SIDS) infants collected at autopsy. In the rat model, influenza A virus was administered intranasally on postnatal day 10, and on day 12 a sublethal, intraperitoneal dose of Escherichia coli endotoxin; mortality was 80%. Tissue samples from the animals and infants were fixed in formaldehyde, embedded in paraffin, and sections stained with hematoxylin and eosin. ... [Abstract] [Full-text] Articles on Sudden Infant Death Syndrome published 16 June 2008: Ocular Findings in Pediatric Deaths Under 2 Years of Age (1994-2004). J Forensic Sci. Our purpose is to highlight novel ocular findings of 102 forensic pediatric cases under 2 years of age who die suddenly. Forensic information, grossing, and microscopic eye protocol was followed. The most common diagnosis was Sudden Infant Death Syndrome (SIDS) (57/102). Novel cytoid bodies were present in the retina of 72/102 cases and they were located predominantly 90% (65/72) at the anterior part of the retina (p < 0.001). Of the SIDS cases, 85% (47/57) showed the presence of cytoid ... [Abstract] [Full-text] Articles on Sudden Infant Death Syndrome published 13 June 2008: Heterozygous nonsense SCN5A mutation W822X explains a simultaneous sudden infant death syndrome. Virchows Arch. The sudden, unexpected, and unexplained death of both members of a set of healthy twins (simultaneous sudden infant death syndrome (SSIDS)) is defined as a case in which both infants meet the definition of sudden infant death syndrome individually. A search of the world medical literature resulted in only 42 reported cases of SSIDS. We report the case of a pair of identical, male, monozygotic twins, 138 days old, who suddenly died, meeting the full criteria of SSIDS and where a genetic screen ... [Abstract] [Full-text] Articles on Sudden Infant Death Syndrome published 9 June 2008: Genes regulating the serotonin metabolic pathway in the brain stem and their role in the etiopathogenesis of the sudden infant death syndrome. Genomics, 91(6): 485-91. Genotypes and allelic frequencies of TPH2, 5-HTTLPR, the 5-HTT (SLC6A4) intron 2 variable-number tandem repeat (VNTR) region, and the MAOA VNTR region were determined in brain-stem samples of 20 "genuine" SIDS cases and compared with results obtained from 150 healthy controls. The SNP G1463A responsible for 80% functionality loss of TPH2 (tryptophan hydroxylase 2) was not detected, neither in SIDS infants nor in the controls. In contrast, a strict relation was found between the ... [Abstract] [Full-text] beta-Tryptase and quantitative mast-cell increase in a sudden infant death following hexavalent immunization. Forensic Sci Int. The association between sudden infant death syndrome and immunization is frequently discussed. Serious adverse events following vaccination have generally been defined as those adverse events that result in permanent disability, hospitalization or prolongation of hospitalization, life threatening illness, congenital anomaly or death. They are generally referred to the inherent properties of the vaccine (vaccine reaction) or some error in the immunization process (programme error).The event ... [Abstract] [Full-text] Articles on Sudden Infant Death Syndrome published 6 June 2008: Helicobacter pylori antigen in stool is associated with SIDS and sudden infant deaths due to infectious disease. Pediatr Res. Infection with Helicobacter pylori has been proposed to be a common cause of Sudden Infant Death Syndrome, SIDS. We investigated the frequency of H. pylori infection in 160 infant deaths and 156 live controls by means of the HpSA immunoassay. Histology was performed in 26 randomly selected cases. H. pylori antigen was detected in 8% (12/156) of the live controls compared to 25% (30/122) of SIDS cases (p<0.001), 53% (9/17) of deaths due to infection (p<0.001) and 9% (1/11) of ... [Abstract] [Full-text] © 2005-2008 Sudden Infant Death Syndrome Research Today. All Rights Reserved. |
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