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  • 1
    Electronic Resource
    Electronic Resource
    s.l. : American Chemical Society
    Analytical chemistry 44 (1972), S. 2081-2081 
    ISSN: 1520-6882
    Source: ACS Legacy Archives
    Topics: Chemistry and Pharmacology
    Type of Medium: Electronic Resource
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  • 2
    Electronic Resource
    Electronic Resource
    Oxford, UK : Blackwell Publishing Ltd
    Clinical and experimental pharmacology and physiology 15 (1988), S. 0 
    ISSN: 1440-1681
    Source: Blackwell Publishing Journal Backfiles 1879-2005
    Topics: Medicine
    Notes: 1. Clonidine, an α2-adrenergic agonist, is thought to inhibit noradrenergic neuronal activity (NNA) in the central nervous system (CNS) by a presynaptic α2-receptor mechanism. Central NNA is thought to be the primary monoaminergic stimulus to pituitary ACTH release. Fenfluramine, a serotonin releasing agent and uptake inhibitor, causes ACTH release in normal man.2. The present study investigated the effect of clonidine on fenfluramine-induced ACTH release in six normal volunteers. Four protocols were used: 1.5 mg/kg body weight oral fenfluramine; 4.3 μg/kg body weight oral clonidine; oral clonidine + oral fenfluramine 1 h later; placebo clonidine. Plasma ACTH and cortisol were measured at intervals for 5 h after clonidine and for 4 h after fenfluramine.3. The mean plasma ACTH and cortisol levels and the mean maximal changes in these levels were significantly lower during the clonidine + fenfluramine test than during fenfluramine alone. Plasma ACTH and cortisol levels were not lowered significantly more by clonidine than by placebo.4. In conclusion, clonidine blocked the ACTH-releasing activity of fenfluramine in normal humans. This inhibition of active ACTH release may result from clonidine blockade of fenfluramine-induced activation of central NNA. Clonidine alone was no more effective than placebo in lowering plasma ACTH and cortisol.
    Type of Medium: Electronic Resource
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  • 3
    Electronic Resource
    Electronic Resource
    Oxford, UK : Blackwell Publishing Ltd
    Clinical and experimental pharmacology and physiology 14 (1987), S. 0 
    ISSN: 1440-1681
    Source: Blackwell Publishing Journal Backfiles 1879-2005
    Topics: Medicine
    Notes: 1. Adrenaline causes ACTH release from cultured rat pituitary corticotrophs (Vale et al. 1983) and there is evidence that it causes ACTH release in rats in vivo (Plotsky et al. 1985).2. The present study examined the effects of intravenous adrenaline infusion with and without simultaneous administration of the known ACTH secretagog, arginine vasopressin, in normotensive and mild essential hypertensive men on their plasma ACTH and cortisol levels.3. Low dose adrenaline infusion (0.013 μg/kg per min) does not cause ACTH or cortisol release, but appears to blunt the ACTH and cortisol rise caused by arginine vasopressin (0.14 pressor units/kg, i.m.).
    Type of Medium: Electronic Resource
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  • 4
    Electronic Resource
    Electronic Resource
    Oxford, UK : Blackwell Publishing Ltd.
    Child 29 (2003), S. 0 
    ISSN: 1365-2214
    Source: Blackwell Publishing Journal Backfiles 1879-2005
    Topics: Medicine , Psychology
    Notes: Background  The concept of visual impairment (VI) in childhood has changed over the last 30 years. There has been a decrease in the number of children with an isolated visual problem and an increase in the numbers with VI and coexisting neurological disability. This study aimed to produce a profile of VI in childhood with a view to informing future services and to raise awareness of the need for comprehensive assessment including developmental remediation and educational advice.Methods  Children with a VI were identified from multiple sources including hospital- and community-based paediatricians and statutory blind registers.Results  Seventy-six children with a VI were identified giving a childhood prevalence of 1.61 per 1000. Thirty-two per cent had a normal pattern of development. Global delays/severe learning difficulty were found in 43%. Only 21% of the children had an isolated VI. Additional medical problems were present in 79% of which cerebral palsy, occurring in 33%, was the most common. Nine per cent of the children were classified as totally blind. Cortical visual impairment was diagnosed in 45%. Twenty-two per cent of the children were registered blind or partially sighted.Conclusions  Most cases of VI in children did not appear on the statutory blind or partially sighted registers, thus these have limited value for service development. The implications for practice highlight the need for early assessment and advice from a co-ordinated team to optimize visual potential in childhood.
    Type of Medium: Electronic Resource
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  • 5
    Electronic Resource
    Electronic Resource
    Springer
    International ophthalmology 9 (1986), S. 161-172 
    ISSN: 1573-2630
    Keywords: corneal endothelium ; intraocular lens ; specular microscopy ; trauma
    Source: Springer Online Journal Archives 1860-2000
    Topics: Medicine
    Notes: Abstract In 1965 the patient, aged 6, sustained a perforating eye injury which was repaired and a traumatic cataract was aspirated within five weeks. Five years later a Ridley Mk 2 A/C intraocular lens was inserted. Several episodes of blunt trauma occurred over a three year period following this procedure. This paper reports the clinical, corneal pachometric and specular microscopic findings of both traumatized and normal fellow eyes 18 years after the initial incident. The corneal endothelial mosaic of the traumatized right eye was very irregular in the vicinity of the initial site of perforation. These marked variations in cell size and shape were less apparent at peripheral corneal areas. The estimated cell loss to the traumatized eye was in the region of 74% although in spite of this corneal function was maintained. The effects of trauma on the corneal endothelium are discussed and a brief review of the literature presented.
    Type of Medium: Electronic Resource
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