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  • Opioid receptor blockade  (2)
  • Alzheimer  (1)
  • 1
    ISSN: 1432-1440
    Keywords: Human corticotropin-releasing factor (hCRF) ; C-peptide ; Naloxone ; Opioid receptor blockade ; Type 2 diabetes
    Source: Springer Online Journal Archives 1860-2000
    Topics: Medicine
    Notes: Summary Administration of synthetic human corticotropin-releasing factor (hCRF, 2 µg/kg body weight) during simultaneous application of the opioid antagonist naloxone (1.6 mg i.v. bolus, followed by an infusion at a rate of 1.2 mg/h) produced a significant increase in plasma C-peptide levels of six male Type 2 diabetic patients which even exceeded the postprandial values. This stimulatory effect of hCRF/naloxone on plasma C-peptide was less pronounced in six healthy men. hCRF alone did not provoke any reaction of plasma C-peptide in either group. The possibility of a paracrine, CRF-dependent mechanism in pancreatic islets which somehow involves inhibitory opioid receptors is preferentially discussed. Such a mechanism may underlie the stimulatory action of hCRF/naloxone on B cells and would explain the absent reaction of peripheral venous plasma C-peptide to hCRF alone as well as the amplifying effect of simultaneous opioid receptor blockade.
    Type of Medium: Electronic Resource
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  • 2
    Electronic Resource
    Electronic Resource
    Springer
    Journal of molecular medicine 65 (1987), S. 453-457 
    ISSN: 1432-1440
    Keywords: Human corticotropin-releasing factor (hCRF) ; ACTH ; Cortisol ; Naloxone ; Opioid receptor blockade
    Source: Springer Online Journal Archives 1860-2000
    Topics: Medicine
    Notes: Summary Administration of synthetic human corticotropin-releasing factor (hCRF; 2 µg/kg body weight) to six normal male subjects produced a significant rise in plasma ACTH, followed by an increase in circulating cortisol. Simultaneous treatment with the opioid antagonist naloxone (1.6 mg i.v. bolus, followed by an infusion at a rate of 1.2 mg/h) significantly potentiated the hCRF-induced rise in ACTH and enhanced the cortisol response to hCRF. It is suggested that naloxone acts by antagonizing an inhibitory ultra-short-loop feedback effect of coreleased β-endorphin on pituitary corticotrophs, thereby amplifying the net effect of hCRF, i.e., the release of ACTH.
    Type of Medium: Electronic Resource
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  • 3
    ISSN: 1573-6903
    Keywords: Prothrombin ; ELISA ; cerebrospinal fluid ; blood-CSF barrier ; Alzheimer ; neurological disorders
    Source: Springer Online Journal Archives 1860-2000
    Topics: Medicine
    Notes: Abstract Prothrombin, known to be expressed in brain and to possess growth modulating properties, has been suggested to be involved in the pathogenesis of Alzheimer's disease (AD). We studied prothrombin concentration in lumbar CSF (L-CSF) in patients with AD (n = 25), neurologic disease controls (NDC; n = 33) covering a wide range of neurologic disorders, and subjects with Guillain-Barré syndrome (GBS; n = 4) as well as in samples of non-pathological ventricular CSF (V-CSF; n = 4). The results were evaluated with respect to CSF flow rate, as indicated by the albumin quotient (QAlb). The concentrations of prothrombin in L-CSF in NDC (mean: 0.46 mg/l, range: 0.21–0.96), and AD (mean: 0.6 mg/l, range: 0.19–1.2) were in the normal range reported previously. Expectedly, prothrombin concentration in L-CSF of GBS was increased (mean: 6.3 mg/l, range: 2.3–9.7) corresponding to the increased QAlb in this group (mean 54.6 × 10−3, range: 17–88.1). The concentrations of both prothrombin and albumin were 5.5-fold higher in L-CSF than in V-CSF (mean QAlb : 1.1 × 10−3, mean concentration of prothrombin: 0.088 mg/l). In conclusion, CSF prothrombin in all conditions evaluated here is exclusively derived from blood.
    Type of Medium: Electronic Resource
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