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Hoffmann, R. A wiki for the life sciences where authorship matters. Nature Genetics (2008)
MeSH Review

Sudden Infant Death

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Disease relevance of Sudden Infant Death

  • Because patients who have long QT syndrome with sodium channel gene (SCN5A) defects have an increased frequency of cardiac events during sleep, and a recent case is reported of a sporadic SCN5A mutation in an infant with near SIDS, SCN5A has emerged as the leading candidate ion channel gene for SIDS [1].
  • Administration of dopamine inhibits respiration by direct action on the carotid body, and it is suggested that the elevated levels of endogenous catecholamines found in victims of sudden infant death syndrome may compromise the normal function of the carotid body, particularly the ventilatory response to hypoxia [2].
  • These data suggest that medullary 5-HT dysfunction can lead to sleep-related, sudden death in affected SIDS infants, and confirm the same binding abnormalities reported by us in a larger dataset of non-American Indian SIDS and control infants [3].
  • We evaluated the white matter immunoreactivity for betaAPP from a variety of pediatric medicolegal autopsies: natural disease (non-Sudden Infant Death Syndrome [SIDS]), SIDS, motor vehicle accidents, drowning, near-drowning, overlay, carbon monoxide toxicity, miscellaneous trauma, and mechanical asphyxia [4].
  • Nicotine from cigarette smoke affects respiration and is a risk factor for sudden infant death syndrome (SIDS) and sleep-disordered breathing [5].

Psychiatry related information on Sudden Infant Death


High impact information on Sudden Infant Death

  • The NMR structure of the complex formed by the PAH2 domain of mammalian Sin3A with the transrepression domain (SID) of human Mad1 reveals that both domains undergo mutual folding transitions upon complex formation generating an unusual left-handed four-helix bundle structure and an amphipathic alpha helix, respectively [9].
  • SCD has also been linked to sudden infant death syndrome [10].
  • High thiamine levels in sudden infant-death syndrome [11].
  • The levels of biotin in the livers of infants who had died of sudden infant death syndrom (SIDS; cot death) were significantly lower than those in livers of infants of similar age, who had died of explicable causes [12].
  • Biotin and the sudden infant death syndrome [12].

Chemical compound and disease context of Sudden Infant Death


Biological context of Sudden Infant Death

  • RESULTS: Two of the 93 cases of SIDS possessed SCN5A mutations: a 6-week-old white male with an A997S missense mutation in exon 17 and a 1-month old white male with an R1826H mutation in exon 28 [1].
  • Reports from the Netherlands, Great Britain, Australia, and New Zealand indicate that avoiding the prone position for infants in the first 6 months of life could reduce the number of SIDS deaths by as much as 50% [18].
  • A fusion protein comprising the Mad1 SID linked to a Ga14 DNA binding domain mediates repression of minimal as well as complex promoters dependent on Ga14 DNA binding sites [19].
  • In addition, the SID represses the transcriptional activity of linked VP16 and c-Myc transactivation domains [19].
  • We have previously identified polymorphisms in the serotonin transporter gene promoter region and in intron 2 that were more common among sudden infant death syndrome (SIDS) cases compared with control subjects [20].

Anatomical context of Sudden Infant Death


Gene context of Sudden Infant Death

  • Furthermore, wild-type Mnt suppresses Myc+Ras cotransformation of primary cells, whereas Mnt containing a SID deletion cooperates with Ras in the absence of Myc to transform cells [25].
  • Postmortem molecular analysis of SCN5A defects in sudden infant death syndrome [1].
  • We also define a 72-amino-acid sequence in CBP necessary for SRC1 binding, designated the SRC1 interaction domain (SID) [26].
  • Furthermore, consanguineous parents of a child with sudden infant death syndrome should be examined for IGHMBP2 mutations [27].
  • Deletion mutants of E1A and Ets-2 lacking the conserved motif were unable to bind the CBP SID [28].

Analytical, diagnostic and therapeutic context of Sudden Infant Death


  1. Postmortem molecular analysis of SCN5A defects in sudden infant death syndrome. Ackerman, M.J., Siu, B.L., Sturner, W.Q., Tester, D.J., Valdivia, C.R., Makielski, J.C., Towbin, J.A. JAMA (2001) [Pubmed]
  2. Sudden infant death syndrome: increased carotid-body dopamine and noradrenaline content. Perrin, D.G., Cutz, E., Becker, L.E., Bryan, A.C., Madapallimatum, A., Sole, M.J. Lancet (1984) [Pubmed]
  3. Serotonergic brainstem abnormalities in Northern Plains Indians with the sudden infant death syndrome. Kinney, H.C., Randall, L.L., Sleeper, L.A., Willinger, M., Belliveau, R.A., Zec, N., Rava, L.A., Dominici, L., Iyasu, S., Randall, B., Habbe, D., Wilson, H., Mandell, F., McClain, M., Welty, T.K. J. Neuropathol. Exp. Neurol. (2003) [Pubmed]
  4. Beta-amyloid precursor protein staining in nonhomicidal pediatric medicolegal autopsies. Reichard, R.R., White, C.L., Hladik, C.L., Dolinak, D. J. Neuropathol. Exp. Neurol. (2003) [Pubmed]
  5. Mechanisms underlying regulation of respiratory pattern by nicotine in preBötzinger complex. Shao, X.M., Feldman, J.L. J. Neurophysiol. (2001) [Pubmed]
  6. Olfactory deficits, cognition and negative symptoms in early onset psychosis. Corcoran, C., Whitaker, A., Coleman, E., Fried, J., Feldman, J., Goudsmit, N., Malaspina, D. Schizophr. Res. (2005) [Pubmed]
  7. Plasma progesterone levels, infant temperament, arousals from sleep, and the sudden infant death syndrome. Weissbluth, M. Med. Hypotheses (1982) [Pubmed]
  8. A preliminary understanding of mania: roles for melatonin, vasotocin and rapid-eye-movement sleep. Maurizi, C.P. Med. Hypotheses (2000) [Pubmed]
  9. Solution structure of the interacting domains of the Mad-Sin3 complex: implications for recruitment of a chromatin-modifying complex. Brubaker, K., Cowley, S.M., Huang, K., Loo, L., Yochum, G.S., Ayer, D.E., Eisenman, R.N., Radhakrishnan, I. Cell (2000) [Pubmed]
  10. Primary systemic carnitine deficiency is caused by mutations in a gene encoding sodium ion-dependent carnitine transporter. Nezu, J., Tamai, I., Oku, A., Ohashi, R., Yabuuchi, H., Hashimoto, N., Nikaido, H., Sai, Y., Koizumi, A., Shoji, Y., Takada, G., Matsuishi, T., Yoshino, M., Kato, H., Ohura, T., Tsujimoto, G., Hayakawa, J., Shimane, M., Tsuji, A. Nat. Genet. (1999) [Pubmed]
  11. High thiamine levels in sudden infant-death syndrome. Davis, R.E., Icke, G.C., Hilton, J.M. N. Engl. J. Med. (1980) [Pubmed]
  12. Biotin and the sudden infant death syndrome. Johnson, A.R., Hood, R.L., Emery, J.L. Nature (1980) [Pubmed]
  13. Decreased muscarinic receptor binding in the arcuate nucleus in sudden infant death syndrome. Kinney, H.C., Filiano, J.J., Sleeper, L.A., Mandell, F., Valdes-Dapena, M., White, W.F. Science (1995) [Pubmed]
  14. Normal thyroxine levels in sudden infant death. Bader, M. JAMA (1982) [Pubmed]
  15. Carbon monoxide and near-miss cot death. Kahn, A., Haesaerts, D., Blum, D. Lancet (1985) [Pubmed]
  16. Letter: Vitamin-E deficiency in cot deaths. Tapp, E., Anfield, C. Lancet (1975) [Pubmed]
  17. Toxic gas generation from plastic mattresses and sudden infant death syndrome. Warnock, D.W., Delves, H.T., Campell, C.K., Croudace, I.W., Davey, K.G., Johnson, E.M., Sieniawska, C. Lancet (1995) [Pubmed]
  18. Sleeping prone and the risk of sudden infant death syndrome. Guntheroth, W.G., Spiers, P.S. JAMA (1992) [Pubmed]
  19. Mad proteins contain a dominant transcription repression domain. Ayer, D.E., Laherty, C.D., Lawrence, Q.A., Armstrong, A.P., Eisenman, R.N. Mol. Cell. Biol. (1996) [Pubmed]
  20. Sudden infant death syndrome: case-control frequency differences at genes pertinent to early autonomic nervous system embryologic development. Weese-Mayer, D.E., Berry-Kravis, E.M., Zhou, L., Maher, B.S., Curran, M.E., Silvestri, J.M., Marazita, M.L. Pediatr. Res. (2004) [Pubmed]
  21. Involvement of mast cells in sudden infant death syndrome. Platt, M.S., Yunginger, J.W., Sekula-Perlman, A., Irani, A.M., Smialek, J., Mirchandani, H.G., Schwartz, L.B. J. Allergy Clin. Immunol. (1994) [Pubmed]
  22. Erythrocyte transketolase activity and sudden infant death. Peterson, D.R., Labbe, R.F., van Belle, G., Chinn, N.M. Am. J. Clin. Nutr. (1981) [Pubmed]
  23. Medullary serotonergic network deficiency in the sudden infant death syndrome: review of a 15-year study of a single dataset. Kinney, H.C., Filiano, J.J., White, W.F. J. Neuropathol. Exp. Neurol. (2001) [Pubmed]
  24. Similarities and differences in lectin cytochemistry of laryngeal and tracheal epithelium and subepithelial seromucous glands in cases of sudden infant death and controls. Paulsen, F.P., Tschernig, T., Debertin, A.S., Kleemann, W.J., Pabst, R., Tillmann, B.N. Thorax (2001) [Pubmed]
  25. Mnt, a novel Max-interacting protein is coexpressed with Myc in proliferating cells and mediates repression at Myc binding sites. Hurlin, P.J., Quéva, C., Eisenman, R.N. Genes Dev. (1997) [Pubmed]
  26. Analysis of the steroid receptor coactivator 1 (SRC1)-CREB binding protein interaction interface and its importance for the function of SRC1. Sheppard, H.M., Harries, J.C., Hussain, S., Bevan, C., Heery, D.M. Mol. Cell. Biol. (2001) [Pubmed]
  27. Infantile spinal muscular atrophy with respiratory distress type 1 (SMARD1). Grohmann, K., Varon, R., Stolz, P., Schuelke, M., Janetzki, C., Bertini, E., Bushby, K., Muntoni, F., Ouvrier, R., Van Maldergem, L., Goemans, N.M., Lochmüller, H., Eichholz, S., Adams, C., Bosch, F., Grattan-Smith, P., Navarro, C., Neitzel, H., Polster, T., Topaloğlu, H., Steglich, C., Guenther, U.P., Zerres, K., Rudnik-Schöneborn, S., Hübner, C. Ann. Neurol. (2003) [Pubmed]
  28. A Conserved alpha-helical motif mediates the binding of diverse nuclear proteins to the SRC1 interaction domain of CBP. Matsuda, S., Harries, J.C., Viskaduraki, M., Troke, P.J., Kindle, K.B., Ryan, C., Heery, D.M. J. Biol. Chem. (2004) [Pubmed]
  29. Submicrosecond surface-induced dissociation of peptide ions in a MALDI TOF MS. Gamage, C.M., Fernández, F.M., Kuppannan, K., Wysocki, V.H. Anal. Chem. (2004) [Pubmed]
  30. Crystalloid strong ion difference determines metabolic acid-base change during in vitro hemodilution. Morgan, T.J., Venkatesh, B., Hall, J. Crit. Care Med. (2002) [Pubmed]
  31. Increased mast cell tryptase in sudden infant death - anaphylaxis, hypoxia or artefact? Edston, E., Gidlund, E., Wickman, M., Ribbing, H., Van Hage-Hamsten, M. Clin. Exp. Allergy (1999) [Pubmed]
  32. Sensitive determination of phenothiazines in body fluids by gas chromatography with surface ionization detection. Hattori, H., Yamamoto, S., Iwata, M., Takashima, E., Yamada, T., Suzuki, O. J. Chromatogr. (1992) [Pubmed]
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