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Journal articles on the topic 'Sudden Infant Death Syndrome; Cot death'

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Published: 4 June 2021

Last updated: 9 February 2022

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1

Rambaud, Caroline, Cécile Cieuta, Danielle Canioni, et al. "Cot death and myocarditis." Cardiology in the Young 2, no. 3 (1992): 266–71. http://dx.doi.org/10.1017/s1047951100001025.

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SummaryWe have investigated the hearts from 153 infants found dead in their cots at ages ranging from one month to one year. The deaths occurred over a period of five years (January 1986 to December 1990) and were studied in a center for the study of the sudden infant death syndrome located in Paris. The epidemiological characteristics of this group are:male predominance (sex ratio 1.43), age less than four months (82%), and a predominance of winter deaths. These are the characteristic features ofthe sudden infant death syndrome. Ofthe 143 children studied with the permission of their parents,

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2

Howatson, A. G., W. J. A. Patrick, G. S. Fell, et al. "Cot mattresses and sudden infant death syndrome." Lancet 345, no. 8956 (1995): 1044–46. http://dx.doi.org/10.1016/s0140-6736(95)90781-5.

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3

Jenkins, R. O., P. J. Craig, W. Goessler, and K. J. Irgolic. "Biovolatilization of antimony and sudden infant death syndrome (SIDS)." Human & Experimental Toxicology 17, no. 4 (1998): 231–38. http://dx.doi.org/10.1177/096032719801700406.

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1 The aerobic filamentous fungus S. brevicaulis IMI 17297 methylated antimony from Sb2O3 substrate, with the formation of gaseous trimethylantimony (TMA). No evidence was found for the generation of other gaseous antimony compounds by this organism. 2 Biovolatilization of inorganic antimony was greatest during cultivation of the fungus on solid media at 258C, and occurred more readily from antimony (III) substrates than from antimony (V) substrates. 3 Under simulated cot environment conditions (CO2 enriched atmosphere, 338C) the fungus exhibited an altered morphology and a reduced capability t

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4

Richardson, B. A. "Cot mattresses and the sudden infant death syndrome." BMJ 310, no. 6986 (1995): 1071. http://dx.doi.org/10.1136/bmj.310.6986.1071b.

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5

Mitchell, E. A., A. W. Stewart, and M. Clements. "Immunisation and the sudden infant death syndrome. New Zealand Cot Death Study Group." Archives of Disease in Childhood 73, no. 6 (1995): 498–501. http://dx.doi.org/10.1136/adc.73.6.498.

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6

Jenkins, R. O., P. J. Craig, W. Goessler, and K. J. Irgolic. "Antimony leaching from cot mattresses and sudden infant death syndrome (SIDS)." Human & Experimental Toxicology 17, no. 3 (1998): 138–39. http://dx.doi.org/10.1177/096032719801700302.

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1 Polyvinyl chloride (PVC) cot mattress covers from SIDS cases were investigated as potential sources of soluble (potentially ingestable) antimony in the cot environment. 2 Body fluids (urine, saliva) and proprietary domestic detergents/sterilizing fluids markedly enhanced leaching of antimony from PVC. Release of antimony was also enhanced at both low and high pH and by elevated temperature. The extent of antimony leaching did not correlate well with PVC content of this element. 3 These data do not support the assumption that postmortem analysis of antimony content proves exposure to gaseous

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7

Jenkins, R. O., P. J. Craig, W. Goessler, and K. J. Irgolic. "Antimony leaching from cot mattresses and sudden infant death syndrome (SIDS)." Human & Experimental Toxicology 17, no. 3 (1998): 138–39. http://dx.doi.org/10.1191/096032798678908413.

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8

Tyler, J. W. "Sudden infant death and chronic infant disorders: The N.E.S.T. model versus the lethal Cot-death Syndrome hoax." Medical Hypotheses 30, no. 4 (1989): 271–75. http://dx.doi.org/10.1016/0306-9877(89)90036-4.

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9

Pisaniak, Paulina, Dominika Piękoś, Katarzyna Bąk, Patryk Stokłosa, and Dorota Ozga. "The battle with uneven opponent – Sudden Infant Death Syndrome." Pielegniarstwo XXI wieku / Nursing in the 21st Century 18, no. 2 (2019): 132–35. http://dx.doi.org/10.2478/pielxxiw-2019-0013.

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AbstractSIDS is one of the biggest problems of modern medicine. In the diagnosis of SIDS, we take into account all possible diseases that may be the cause of death, as well as factors indicating an accident or murder. The etiology of SIDS is not yet known. There are several pathogenetic concepts, most of which refer to pathophysiological changes associated with nervous system hypoplasia. The most important risk factors include the effects of tobacco smoke, obstetric history, and incorrect sleep position. The role of risk factors in the pathogenesis of SIDS and their interdependence is still th

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10

Becroft, David M. O., John M. D. Thompson, and Edwin A. Mitchell. "Epidemiology of Intrathoracic Petechial Hemorrhages in Sudden Infant Death Syndrome." Pediatric and Developmental Pathology 1, no. 3 (1998): 200–209. http://dx.doi.org/10.1007/s100249900027.

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The possible effects of a wide range of sociodemographic and environmental factors on the incidence and distribution of petechiae were investigated in 485 sudden infant death syndrome (SIDS) cases from the New Zealand Cot Death Study. The number (nil, few, many) of macroscopic petechial hemorrhages in the visceral pleura, capsule of thymus, and epicardium was recorded in 458 of 474 autopsied SIDS cases. Other information was obtained from parental interview and obstetric records. Univariate analysis showed highly significant relationships ( P ≤ 0.005) between the frequency of petechiae at one

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11

Scragg, R., E. A. Mitchell, B. J. Taylor, et al. "Bed sharing, smoking, and alcohol in the sudden infant death syndrome. New Zealand Cot Death Study Group." BMJ 307, no. 6915 (1993): 1312–18. http://dx.doi.org/10.1136/bmj.307.6915.1312.

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12

STEWART, AJ, SM WILLIAMS, EA MITCHELL, BJ TAYLOR, RPK FORD, and EM ALLEN. "Antenatal and intrapartum factors associated with Sudden Infant Death Syndrome in the New Zealand Cot Death Study." Journal of Paediatrics and Child Health 31, no. 5 (1995): 473–78. http://dx.doi.org/10.1111/j.1440-1754.1995.tb00861.x.

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13

Becroft, David M. O., John M. D. Thompson, and Edwin A. Mitchell. "Pulmonary Interstitial Hemosiderin in Infancy: A Common Consequence of Normal Labor." Pediatric and Developmental Pathology 8, no. 4 (2005): 448–52. http://dx.doi.org/10.1007/s10024-005-0033-8.

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Deposits of hemosiderin are found frequently in the interstitium of the lungs of infants who die suddenly and have been a suggested marker for hypoxia during previous episodes of apnea. We studied the epidemiology of pulmonary interstitial hemosiderin (PIH) in 94 infants with a diagnosis of the sudden infant death syndrome that was established during the New Zealand Cot Death Study. Twenty-seven infants (29%) had widely distributed PIH. Associations were sought between PIH and variables on which information had been obtained from parental interviews or from medical records. Previous suggestion

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14

Williams, S. M., B. J. Taylor, E. A. Mitchell, R. Scragg, R. P. Ford, and A. W. Stewart. "Sudden infant death syndrome in New Zealand: are risk scores useful? New Zealand National Cot Death Study Group." Journal of Epidemiology & Community Health 49, no. 1 (1995): 94–101. http://dx.doi.org/10.1136/jech.49.1.94.

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15

Sherburn, R. E., and R. O. Jenkins. "Aerial release of bacteria from cot mattress materials and the sudden infant death syndrome." Journal of Applied Microbiology 98, no. 2 (2005): 293–98. http://dx.doi.org/10.1111/j.1365-2672.2004.02456.x.

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16

SHERBURN, R. "Cot mattresses as reservoirs of potentially harmful bacteria and the sudden infant death syndrome." FEMS Immunology and Medical Microbiology 42, no. 1 (2004): 76–84. http://dx.doi.org/10.1016/j.femsim.2004.06.011.

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17

Leditschke, J. Fred. "Surviving Childhood." Children Australia 14, no. 1-2 (1989): 25–27. http://dx.doi.org/10.1017/s0312897000002216.

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In the first month of life, prematurity and congenital anomalies account for the majority of deaths to children. Between one month and one year of age, the still unexplained Sudden Infant Death Syndrome (SIDS) or cot death remains very much an unsolved problem causing untold distress and grief to parents.If, however, we consider the childhood commencing at one month of age and carrying through until the completion of at least primary school and possibly secondary schooling, then accidents cause over a quarter of the deaths and, in considering those deaths in the first five years of life, drown

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18

Kelley, Joan, Dennis Allsopp, and David L. Hawksworth. "Sudden Infant Death Syndrome (SIDS) and the Toxic Gas Hypothesis: Microbiological Studies of Cot Mattresses." Human & Experimental Toxicology 11, no. 5 (1992): 347–55. http://dx.doi.org/10.1177/096032719201100508.

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1 Fifty infants' mattresses were studied to investigate the occurrence of viable fungal and bacterial propagules, with particular reference to Scopulariopsis brevicaulis which had been suggested to be implicated in SIDS cases. A total of 19 SIDS cases mattresses, 1 non-SIDS death, 20 used controls, and 10 new unused controls were examined. 2 Differences were found between SIDS and used controls in the variety of fungal species isolated and the numbers isolated from fillings; bacterial numbers were similar. 3 S. brevicaulis was isolated from only four mattresses, three of which were SIDS cases.

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19

Jenkins, R. O., and R. E. Sherburn. "Growth and survival of bacteria implicated in sudden infant death syndrome on cot mattress materials." Journal of Applied Microbiology 99, no. 3 (2005): 573–79. http://dx.doi.org/10.1111/j.1365-2672.2005.02620.x.

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20

WILSON, C. A., B. J. TAYLOR, R. M. LAING, S. M. WILLIAMS, and E. A. MITCHELL. "Clothing and bedding and its relevance to sudden infant death syndrome: Further results from the New Zealand Cot Death Study." Journal of Paediatrics and Child Health 30, no. 6 (1994): 506–12. http://dx.doi.org/10.1111/j.1440-1754.1994.tb00722.x.

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21

Saadi, A. T., C. C. Blackwell, M. W. Raza, et al. "Factors enhancing adherence of toxigenic Staphylococcus aureus to epithelial cells and their possible role in sudden infant death syndrome." Epidemiology and Infection 110, no. 3 (1993): 507–17. http://dx.doi.org/10.1017/s0950268800050937.

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SUMMARYToxigenic strains of Staphylococcus aureus have been suggested to play a role in sudden infant death syndrome (SIDS). In this study we examined two factors that might enhance binding of toxigenic staphylococci to epithelial cells of infants in the age range in which cot deaths are prevalent: expression of the Lewisa antigen and infection with respiratory syncytial virus (RSV). By flow cytometry we demonstrated that binding of three toxigenic strains of S. aureus to cells from non-secretors was significantly greater than to cells of secretors. Pre-treatment of epithelial cells with monoc

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22

HOLGATE, S. T., C. WALTERS, A. F. WALLS, et al. "The anaphylaxis hypothesis of sudden infant death syndrome (SIDS): mast cell degranulation in cot death revealed by elevated concentrations of tryptase in serum." Clinical & Experimental Allergy 24, no. 12 (1994): 1115–22. http://dx.doi.org/10.1111/j.1365-2222.1994.tb03316.x.

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23

Patel, Aloka L., Kathy Harris, and Bradley T. Thach. "Inspired CO2 and O2 in sleeping infants rebreathing from bedding: relevance for sudden infant death syndrome." Journal of Applied Physiology 91, no. 6 (2001): 2537–45. http://dx.doi.org/10.1152/jappl.2001.91.6.2537.

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Some infants sleep facedown for long periods with no ill effects, whereas others become hypoxemic. Rebreathing of expired air has been determined by CO2 measurement; however, O2 levels under such conditions have not been determined. To evaluate this and other factors influencing inspired gas concentrations, we studied 21 healthy infants during natural sleep while facedown on soft bedding. We measured gas exchange with the environment and bedding, ventilatory response to rebreathing, and concentrations of inspired CO2 and O2. Two important factors influencing inspired gas concentrations were 1)

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24

Curran, Aidan K., Robert A. Darnall, James J. Filiano, Aihua Li, and Eugene E. Nattie. "Muscimol dialysis in the rostral ventral medulla reduced the CO2 response in awake and sleeping piglets." Journal of Applied Physiology 90, no. 3 (2001): 971–80. http://dx.doi.org/10.1152/jappl.2001.90.3.971.

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Some victims of sudden infant death syndrome have arcuate nucleus abnormalities. The arcuate nucleus may be homologous with ventral medullary structures in the cat known to be involved in the control of breathing and the response to systemic hypercapnia. We refer to putative arcuate homologues in the piglet collectively as the rostral ventral medulla (RVM). We inhibited the RVM in awake and sleeping, chronically instrumented piglets by microdialysis of the GABAA receptor agonist muscimol. Muscimol dialysis (10 and 40 mM) had no effect on eupnea but caused a significant reduction in the respons

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25

Blair, P. S., P. J. Fleming, I. J. Smith, et al. "Babies sleeping with parents: case-control study of factors influencing the risk of the sudden infant death syndrome Commentary: Cot death---the story so far." BMJ 319, no. 7223 (1999): 1457–62. http://dx.doi.org/10.1136/bmj.319.7223.1457.

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26

Jenkins, R. O., T.-A. Morris, P. J. Craig, W. Goessler, N. Ostah, and K. M. Wills. "Evaluation of cot mattress inner foam as a potential site for microbial generation of toxic gases." Human & Experimental Toxicology 19, no. 12 (2000): 693–702. http://dx.doi.org/10.1191/096032700670028460.

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Recent reports of biovolatilisation of phosphorus and antimony by anaerobic bacteria and of leaching of phosphorus and antimony fire-retardant additives from PVC cot mattress covers, indicate that the polyurethane inner-foam of cot mattresses could be a site for generation of toxic gases of group 15 elements. A toxic gas hypothesis for sudden infant death syndrome (SIDS) involving polyurethane foam of cot mattresses was proposed and tested experimentally. Levels of antimony, phosphorus, arsenic and bismuth were determined at four sites for 44 SIDS and 50 control (no death) cot mattress foams.

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27

Miller, Marvin E., John G. Brooks, Nicholas Forbes, and Richard Insel. "Frequency of Medium-Chain Acyl-CoA Dehydrogenase Deficiency G-985 Mutation in Sudden Infant Death Syndrome." Pediatric Research 31, no. 4 (1992): 305–7. http://dx.doi.org/10.1203/00006450-199204000-00001.

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28

Carolan, Patrick L., James S. Kemp, James Ross, and William B. Wheeler. "Effect on CO2 Dispersal Rate of Commercial Products Marketed to Reduce Sudden Infant Death Syndrome Risk." Pediatric Research 45, no. 4, Part 2 of 2 (1999): 350A. http://dx.doi.org/10.1203/00006450-199904020-02083.

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29

Kaku, Noriyuki, Kenji Ihara, Yuichiro Hirata, et al. "Diagnostic potential of stored dried blood spots for inborn errors of metabolism: a metabolic autopsy of medium-chain acyl-CoA dehydrogenase deficiency." Journal of Clinical Pathology 71, no. 10 (2018): 885–89. http://dx.doi.org/10.1136/jclinpath-2017-204962.

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AimIt is estimated that 1–5% of sudden infant death syndrome (SIDS) cases might be caused by undiagnosed inborn errors of metabolism (IEMs); however, the postmortem identification of IEMs remains difficult. This study aimed to evaluate the usefulness of dried blood spots (DBSs) stored after newborn screening tests as a metabolic autopsy to determine the causes of death in infants and children who died suddenly and unexpectedly.MethodsInfants or toddlers who had suddenly died without a definite diagnosis between July 2008 and December 2012 at Kyushu University Hospital in Japan were enrolled in

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30

Young, Jacob O., Aron Geurts, Matthew R. Hodges, and Kevin J. Cummings. "Active sleep unmasks apnea and delayed arousal in infant rat pups lacking central serotonin." Journal of Applied Physiology 123, no. 4 (2017): 825–34. http://dx.doi.org/10.1152/japplphysiol.00439.2017.

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Sudden infant death syndrome (SIDS), occurring during sleep periods, is highly associated with abnormalities within serotonin (5-HT) neurons, including reduced 5-HT. There is evidence that future SIDS cases experience more apnea and have abnormal arousal from sleep. In rodents, a loss of 5-HT neurons is associated with apnea in early life and, in adulthood, delayed arousal. As the activity of 5-HT neurons changes with vigilance state, we hypothesized that the degree of apnea and delayed arousal displayed by rat pups specifically lacking central 5-HT varies with state. Two-week-old tryptophan h

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31

Itzhak, Nadav, and David Greenblatt. "Aerodynamic factors affecting rebreathing in infants." Journal of Applied Physiology 126, no. 4 (2019): 952–64. http://dx.doi.org/10.1152/japplphysiol.00784.2018.

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The rebreathing of expire air, with high carbon dioxide and low oxygen concentrations, has long been implicated in unexplained Sudden Infant Death Syndrome (SIDS) when infants are placed to sleep in a prone (facedown) position. This study elucidates the effect of the aerodynamic parameters Reynolds number, Strouhal number, and Froude number on the percentage of expired air that is reinspired (rebreathed). A nasal module was designed that served as a simplified geometric representation of infant nostrils and placed above a hard, flat surface. Quantitative and flow visualization experiments were

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32

Cushing, J. M. "Book Reviews : Cot Deaths, Coping with Sudden Infant Death Syndrome by Jacquelynn Luben. Published by Thorsons Publishing, 1986. Price: £5.99. Paperback. Pp 191. ISBN: 0 7225 1255 4." Journal of the Royal Society of Health 107, no. 4 (1987): 159. http://dx.doi.org/10.1177/146642408710700418.

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33

Penatti, E. M., A. V. Berniker, B. Kereshi, et al. "Ventilatory response to hypercapnia and hypoxia after extensive lesion of medullary serotonergic neurons in newborn conscious piglets." Journal of Applied Physiology 101, no. 4 (2006): 1177–88. http://dx.doi.org/10.1152/japplphysiol.00376.2006.

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Acute inhibition of serotonergic (5-HT) neurons in the medullary raphé (MR) using a 5-HT1A receptor agonist had an age-dependent impact on the “CO2 response” of piglets ( 33 ). Our present study explored the effect of chronic 5-HT neuron lesions in the MR and extra-raphé on the ventilatory response to hypercapnia and hypoxia in piglets, with possible implications on the role of 5-HT in the sudden infant death syndrome. We established four experimental groups. Group 1 ( n = 11) did not undergo any treatment. Groups 2, 3, and 4 were injected with either vehicle or the neurotoxin 5,7-dihydroxytry

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34

Highet, Amanda R., Anne M. Berry, Karl A. Bettelheim, and Paul N. Goldwater. "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." Journal of Medical Microbiology 58, no. 3 (2009): 285–89. http://dx.doi.org/10.1099/jmm.0.005322-0.

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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 candid

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35

Messier, Michelle L., Aihua Li, and Eugene E. Nattie. "Inhibition of medullary raphé serotonergic neurons has age-dependent effects on the CO2 response in newborn piglets." Journal of Applied Physiology 96, no. 5 (2004): 1909–19. http://dx.doi.org/10.1152/japplphysiol.00805.2003.

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Medullary raphé serotonergic neurons are chemosensitive in culture and are situated adjacent to blood vessels in the brain stem. Selective lesioning of serotonergic raphé neurons decreases the ventilatory response to systemic CO2 in awake and sleeping adult rats. Abnormalities in the medullary serotonergic system, including the raphé, have been implicated in the sudden infant death syndrome ( 48 ). In this study, we ask whether serotonergic neurons in the medullary raphé and extra-raphé regions are involved in the CO2 response in unanesthetized newborn piglets, 3-16 days old. Whole body plethy

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36

Sudhan, Lavanya, Leonardi, Neri, and Sekar. "Monitoring of Chemical Risk Factors for Sudden Infant Death Syndrome (SIDS) by Hydroxyapatite-Graphene-MWCNT Composite-Based Sensors." Sensors 19, no. 15 (2019): 3437. http://dx.doi.org/10.3390/s19153437.

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Sensing properties of chemical sensors based on ternary hydroxyapatite-graphene-multiwalled carbon nanotube (HA-GN-MWCNT) nanocomposite in the detection of chemical substances representing risk factors for sudden infant death syndrome (SIDS), have been evaluated. Characterization data of the synthesized composite have shown that the graphene-MWCNT network serves as a matrix to uniformly disperse the hydroxyapatite nanoparticles and provide suitable electrical properties required for developing novel electrochemical and conductometric sensors. A HA-GN-MWCNT composite-modified glassy carbon elec

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37

Lecoq, I., E. Mallet, JB Bonte, and G. Travert. "The A985 to G mutation of the medium-chain acyl-CoA dehydrogenase gene and sudden infant death syndrome in Normandy." Acta Paediatrica 85, no. 2 (1996): 145–47. http://dx.doi.org/10.1111/j.1651-2227.1996.tb13980.x.

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38

Park, M. R., S. K. Cho, J. Y. Park, et al. "65RARE AND OFTEN UNRECOGNIZED CEREBROMENINGITIS AND HEPATOPNEUMONIC CONGESTION ARE MAJOR CAUSES OF SUDDEN DEATH IN CLONED MALE PIGLETS." Reproduction, Fertility and Development 16, no. 2 (2004): 154. http://dx.doi.org/10.1071/rdv16n1ab65.

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In this study, we investigated the relationship between the sex of cloned pigs and sudden infant death syndrome (SIDS). Three cell lines (2 male and 1 female) were obtained from F1 fetuses derived from 3 different dams (Yorkshire) inseminated by the same sire (Landrace); one female fibroblast cell line was obtained from a Duroc-strain fetus acquired from a slaughterhouse, the age of the fetus unknown. The fetal fibroblast cells were cultured in DMEM supplemented with 10% fetal bovine serum under 5% CO2 in air at 37°C. For NT, we used the 4 cell lines described above. All 37 cloned piglets deri

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39

Wang, S. S., P. M. Fernhoff, and M. J. Khoury. "Is the G985A Allelic Variant of Medium-Chain Acyl-CoA Dehydrogenase a Risk Factor for Sudden Infant Death Syndrome? A Pooled Analysis." PEDIATRICS 105, no. 5 (2000): 1175–76. http://dx.doi.org/10.1542/peds.105.5.1175.

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40

Duran, M., L. Bruinvis, D. Ketting, J. B. de Klerk, and S. K. Wadman. "Cis-4-decenoic acid in plasma: a characteristic metabolite in medium-chain acyl-CoA dehydrogenase deficiency." Clinical Chemistry 34, no. 3 (1988): 548–51. http://dx.doi.org/10.1093/clinchem/34.3.548.

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Abstract The profile of organic acids in plasma of patients with a deficiency of medium-chain acyl-CoA dehydrogenase (EC 1.3.99.3) was determined by gas-liquid chromatography of trimethylsilylated derivatives of the acids isolated by ethyl acetate extraction. All 13 patients had increased concentrations of free octanoate, cis-4-decenoate, and decanoate in their plasma. Cis-4-decenoate, an intermediary metabolite of linoleic acid, is pathognomonic of medium-chain acyl-CoA dehydrogenase deficiency. This metabolite does not accumulate in plasma after oral loading with medium-chain triglycerides,

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41

Buchanan, Gordon F., Haleigh R. Smith, Amanda MacAskill, and George B. Richerson. "5-HT2A receptor activation is necessary for CO2-induced arousal." Journal of Neurophysiology 114, no. 1 (2015): 233–43. http://dx.doi.org/10.1152/jn.00213.2015.

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Hypercapnia-induced arousal from sleep is an important protective mechanism pertinent to a number of diseases. Most notably among these are the sudden infant death syndrome, obstructive sleep apnea and sudden unexpected death in epilepsy. Serotonin (5-HT) plays a significant role in hypercapnia-induced arousal. The mechanism of 5-HT's role in this protective response is unknown. Here we sought to identify the specific 5-HT receptor subtype(s) involved in this response. Wild-type mice were pretreated with antagonists against 5-HT receptor subtypes, as well as antagonists against adrenergic, cho

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42

Lundemose, Jytte B., Niels Gregersen, Steen Karlvraa, et al. "The frequency of a disease-causing point mutation in the gene coding for medium-chain acyl-CoA dehydrogenase in sudden infant death syndrome." Acta Paediatrica 82, no. 6-7 (1993): 544–46. http://dx.doi.org/10.1111/j.1651-2227.1993.tb12749.x.

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43

Wang, S. S., and M. J. Khoury. "An epidemiologic assessment of the relationship between the G985A medium chain acyl-coA dehydrogenase deficiency (MCADD) allelic variant and sudden infant death syndrome (SIDS)." Genetics in Medicine 1, no. 2 (1999): 43. http://dx.doi.org/10.1097/00125817-199901000-00017.

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44

Gozal, David, Evelyne Gozal, Stephen R. Reeves, and Andrew J. Lipton. "Gasping and autoresuscitation in the developing rat: effect of antecedent intermittent hypoxia." Journal of Applied Physiology 92, no. 3 (2002): 1141–44. http://dx.doi.org/10.1152/japplphysiol.00972.2001.

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Gasping is a critically important mechanism for autoresuscitation and survival during extreme tissue hypoxia. Evidence of antecedent hypoxia in sudden infant death syndrome suggests that intermittently occurring hypoxic episodes may modify gasping and autoresuscitation. To examine this issue, an intermittent hypoxia (IH) profile consisting of alternating room air and 10% O2-balance N2 every 90 s was applied to pregnant Sprague-Dawley rats (IHRA; n = 50) and to pups after a normal pregnancy (RAIH; n = 50) as well as to control pups (RARA; n = 50). At postnatal day 5, pups were exposed to 95% N2

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Cummings, Kevin J., Kathryn G. Commons, Julie C. Hewitt, et al. "Failed heart rate recovery at a critical age in 5-HT-deficient mice exposed to episodic anoxia: implications for SIDS." Journal of Applied Physiology 111, no. 3 (2011): 825–33. http://dx.doi.org/10.1152/japplphysiol.00336.2011.

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Mice deficient in the transcription factor Pet-1−/− have a ∼70% deficiency of brainstem serotonin [5-hydroxytryptamine (5-HT)] neurons and exhibit spontaneous bradycardias in room air at postnatal day (P)5 and P12 and delayed gasping in response to a single episode of anoxia at P4.5 and P9.5 (Cummings KJ, Li A, Deneris ES, Nattie EE. Am J Physiol Regul Integr Comp Physiol 298: R1333–R1342, 2010; and Erickson JT, Sposato BC. J Appl Physiol 106: 1785–1792, 2009). We hypothesized that at a critical age Pet-1−/− mice will fail to autoresuscitate during episodic anoxia, ultimately dying from a fail

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Curran, A. K., L. Xia, J. C. Leiter, and D. Bartlett. "Elevated body temperature enhances the laryngeal chemoreflex in decerebrate piglets." Journal of Applied Physiology 98, no. 3 (2005): 780–86. http://dx.doi.org/10.1152/japplphysiol.00906.2004.

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Hyperthermia and reflex apnea may both contribute to sudden infant death syndrome (SIDS). Therefore, we investigated the effect of increased body temperature on the inhibition of breathing produced by water injected into the larynx, which elicits the laryngeal chemoreflex (LCR). We studied decerebrated, vagotomized, neonatal piglets aged 3–15 days. Blood pressure, end-tidal CO2, body temperature, and phrenic nerve activity were recorded. To elicit the LCR, we infused 0.1 ml of distilled water through a polyethylene tube passed through the nose and positioned just rostral to the larynx. Three t

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Davis, Joseph H. "Sudden Infant Death Syndrome." Pediatric Pathology & Laboratory Medicine 15, no. 2 (1995): 359–61. http://dx.doi.org/10.3109/15513819509026971.

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Carroll, J. L., and G. M. Loughlin. "Sudden Infant Death Syndrome." Pediatrics in Review 14, no. 3 (1993): 83–93. http://dx.doi.org/10.1542/pir.14-3-83.

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Kim, Chang-Hwi. "Sudden Infant Death Syndrome." Journal of the Korean Medical Association 44, no. 9 (2001): 976. http://dx.doi.org/10.5124/jkma.2001.44.9.976.

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Fleming, Peter, and Peter S. Blair. "Sudden Infant Death Syndrome." Sleep Medicine Clinics 2, no. 3 (2007): 463–76. http://dx.doi.org/10.1016/j.jsmc.2007.05.003.

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