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  • 1995-1999  (3)
  • Critically ill  (2)
  • Alzheimer's disease
  • 1
    Electronic Resource
    Electronic Resource
    Springer
    Intensive care medicine 22 (1996), S. 575-581 
    ISSN: 1432-1238
    Keywords: Low T3 syndrome ; Selenium ; Deiodination ; Glutathione peroxidase ; Balance study ; Critically ill ; Trauma
    Source: Springer Online Journal Archives 1860-2000
    Topics: Medicine
    Notes: Abstract Objective Thyroxine (T4) is deiodinated to triiodothyronine (T3) by the hepatic type I iodothyronine deiodinase, a selenoprotein that is sensitive to selenium (Se) deficiency. After severe injury, T4 deiodination is decreased, leading to the low T3 syndrome. Injury increases free radical production, which inactivates the iodothyronine deiodinase. The aims were to study the Se status after major trauma and to investigate its relation to the low T3 syndrome. Design Preliminary prospective descriptive study. Setting Intensive care unit at a university teaching hospital. Patients and methods 11 patients aged 41±4 years (mean±SEM), with severe multiple injuries (Injury Severity Score 29±2 points). A balance study was performed from day 1 to day 7. Serum and urine samples were collected from the time of admission until day 7, then on days 10, 15, 20, 25 and 30. Nonparametric tests and Pearson's correlation coefficients were used for analysis. Results Cumulated Se losses were 0.88±0.1 μmol/24h. Serum Se was decreased from admission to day 7. T3, free T3, and the T3/T4 ratio were low until day 5, being lowest on day 2; T4 and thyroid stimulating hormone were normal. Serum Se was correlated with T3 (r=0.55,p=0.0001), and with free T3 (r=0.35). Conclusion Se status is altered after trauma, with decreased Se serum levels upon admission to the ICU but with no major Se losses. Se is probably redistributed to the tissues. The correlation between Se and T3, along with the parallel decrease in T4 deiodination, indicates that reduced deiodination might be related to the transient decrease in serum Se.
    Type of Medium: Electronic Resource
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  • 2
    Electronic Resource
    Electronic Resource
    Springer
    Intensive care medicine 22 (1996), S. 575-581 
    ISSN: 1432-1238
    Keywords: Key words Low T3 syndrome ; Selenium ; Deiodination ; Glutathione peroxidase ; Balance study ; Critically ill ; Trauma
    Source: Springer Online Journal Archives 1860-2000
    Topics: Medicine
    Notes: Abstract Objective: Thyroxine (T4) is deiodinated to triiodothyronine (T3) by the hepatic type I iodothyronine deiodinase, a selenoprotein that is sensitive to selenium (Se) deficiency. After severe injury, T4 deiodination is decreased, leading to the low T3 syndrome. Injury increases free radical production, which inactivates the iodothyronine deiodinase. The aims were to study the Se status after major trauma and to investigate its relation to the low T3 syndrome. Design: Preliminary prospective descriptive study. Setting: Intensive care unit at a university teaching hospital. Patients and methods: 11 patients aged 41±4 years (mean±SEM), with severe multiple injuries (Injury Severity Score 29±2 points). A balance study was performed from day 1 to day 7. Serum and urine samples were collected from the time of admission until day 7, then on days 10, 15, 20, 25 and 30. Non-parametric tests and Pearson‘s correlation coefficients were used for analysis. Results: Cumulated Se losses were 0.88±0.1 μmol/24 h. Serum Se was decreased from admission to day 7. T3, free T3, and the T3/T4 ratio were low until day 5, being lowest on day 2; T4 and thyroid stimulating hormone were normal. Serum Se was correlated with T3 (r=0.55, p=0.0001), and with free T3 (r=0.35). Conclusion: Se status is altered after trauma, with decreased Se serum levels upon admission to the ICU but with no major Se losses. Se is probably redistributed to the tissues. The correlation between Se and T3, along with the parallel decrease in T4 deiodination, indicates that reduced deiodination might be related to the transient decrease in serum Se.
    Type of Medium: Electronic Resource
    Library Location Call Number Volume/Issue/Year Availability
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  • 3
    Electronic Resource
    Electronic Resource
    Springer
    European archives of psychiatry and clinical neuroscience 246 (1996), S. 124-128 
    ISSN: 1433-8491
    Keywords: Senile plaques ; Primitive plaques ; Alzheimer's disease ; Interleukin-6
    Source: Springer Online Journal Archives 1860-2000
    Topics: Medicine
    Notes: Abstract In recent years many studies have indicated an involvement of inflammatory mechanisms in Alzheimer's disease (AD). Acute-phase proteins such as α1-antichymotrypsin and c-reactive protein, elements of the complement system, and activated microglial and astroglial cells are consistently found in brains of AD patients. Most importantly, also cytokines such as interleukin-6 (IL-6) have been detected in the cortices of AD patients, indicating a local activation of components of the unspecific inflammatory system. Up to now it has remained unclear whether inflammatory mechanisms represent a primary event or only an unspecific reaction to brain tissue damage. Therefore, we investigated whether IL-6 immunoreactivity could be found in plaques prior to the onset of neuritic changes, or whether the presence of this cytokine is restricted to later stages of plaque pathology. we confirmed our previous observation that IL-6 is detectable in a significant proportion of plaques in the brains of demented patients. In AD patients IL-6 was found in diffuse plaques in a significant higher ratio as would have been expected from a random distribution of IL-6 among all plaque types. This observation suggests that IL-6 may precede neuritic changes, and that immunological mechanism may be involved both in the transformation from diffuse to neuritic plaques in AD and in the development of dementia.
    Type of Medium: Electronic Resource
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