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  • Key words: Beta-endorphin – Cerebrospinal fluid – Nucleus tractus solitarius – Sudden infant death  (1)
  • SID  (1)
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  • 1
    Electronic Resource
    Electronic Resource
    Inverse relationship between beta-endorphin immunoreactivity in cerebrospinal fluid and nucleus tractus solitarius in sudden infant death (1994)
    Springer
    European journal of pediatrics 153 (1994), S. 381-386 
    Details
    ISSN: 1432-1076
    Keywords: Key words: Beta-endorphin – Cerebrospinal fluid – Nucleus tractus solitarius – Sudden infant death
    Source: Springer Online Journal Archives 1860-2000
    Topics: Medicine
    Notes: Abstract. In nucleus tractus solitarius (NTS) beta-endorphin (BEND) induces bradycardia and respiratory depression which have been reported to precede death in sudden infant death (SID). Of SID victims, 50% have elevated levels of beta-endorphin immunoreactivity (BENDI) in the cerebrospinal fluid (CSF), and 50% had undetectable levels. We therefore investigated the relationship of BENDI in the CSF to BENDI levels in the NTS area. This study included SID victims (CSF from n=47, brain stem from n=16), borderline SID victims (CSF and brain stem from n=2), sudden death in childhood (CSF and brain stem from n=1), and controls (CSF from n=32, brain stem from n=11). BEND in CSF and NTS area, after extraction, was measured by radioimmunoassay. High performance liquid chromatography was used for closer identification of BENDI. We found that the SID victims divided into two subpopulations, one having a relatively high BENDI level in CSF and one having no detectable level (P〈0.01). Furthermore, an inverse relationship was found between BENDI level in CSF and BENDI level in NTS area in the SID victims (P〈0.05). We conclude that increased BENDI level in CSF is associated with low BENDI level in the NTS area in 50% of SID victims. The low BENDI level in the NTS area may be due to increased release of BEND.
    Type of Medium: Electronic Resource
    URL: http://dx.doi.org/10.1007/BF01956426
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    Paper (German National Licenses)
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  • 2
    Electronic Resource
    Electronic Resource
    Elevated beta-endorphin immunoreactivity in the cerebrospinal fluid in victims of sudden infant death correlates with hypoxanthine in vitreous humour (1993)
    Springer
    European journal of pediatrics 152 (1993), S. 935-938 
    Details
    ISSN: 1432-1076
    Keywords: Beta-endorphin ; Hypoxanthine ; Hypoxia ; SID
    Source: Springer Online Journal Archives 1860-2000
    Topics: Medicine
    Notes: Abstract Beta-endorphin (BEND) may induce respiratory depression. Elevated levels of beta-endorphin immunoreactivity (BENDI) in the CSF are found in children with apnoea and in about 50% of sudden infant death (SID) victims. Premortal hypoxia in SID victims has been indicated by elevated hypoxanthine (HX) levels in the vitreous humour (VH). In this study we correlated BENDI in CSF with HX in VH in SID victims (n=19) and controls (n=18). BEND in CSF was measured by RIA, and HPLC was used for identification of BENDI. HX in VH was measured by HPLC. All the SID victims had elevated levels of HX in VH. The BENDI in CSF divided the SID victims into two subpopulations (P〈0.01); one with undetectable levels (〈4.3 fmol/ml) (n=10) and one with high levels (160–400 fmol/ml) (n=9).In the SID subpopulation with high levels of BENDI in CSF,we found a correlation between BENDI in CSF and HX in VH (r=0.92). Control infants who died a stressful death, such as during heart operations (n=2), had high levels of BENDI in CSF and low levels of HX in VH. Controls who died of infections (n=11) had low levels of BENDI in CSF and elevated levels of HX in VH. Because hypoxia in itself does not increase BENDI in CSF, increased BENDI in CSF is probably not secondary to hypoxia but may be of aetiological significance. We therefore suggest that SID victims with high levels of BENDI in CSF, which correlate with the elevated levels of HX in VH, may die from premortal hypoxia possibly induced by BEND.
    Type of Medium: Electronic Resource
    URL: http://dx.doi.org/10.1007/BF01957536
    Library Location Call Number Volume/Issue/Year Availability
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    Paper (German National Licenses)
    Fulltext
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