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  • 1
    Electronic Resource
    Electronic Resource
    IMPROVED REVERSE OSMOSIS PERMEATION BY HEATING (1973)
    Oxford, UK : Blackwell Publishing Ltd
    Journal of food science 38 (1973), S. 0 
    Details
    ISSN: 1750-3841
    Source: Blackwell Publishing Journal Backfiles 1879-2005
    Topics: Agriculture, Forestry, Horticulture, Fishery, Domestic Science, Nutrition , Process Engineering, Biotechnology, Nutrition Technology
    Notes: At higher temperatures reverse osmosis membrane coefficients increase and cause permeation rates to increase. Diffusion coefficients also increase and viscosity coefficients decrease causing concentration polarization to decrease and improve permeation. Experiments were performed with 15% (w/w) sucrose solutions in tubular cellulose acetate reverse osmosis membranes at 500 psig for low flow rates (Reynolds numbers between 10 and 1000). Depending upon the flow rate and mode of heating, raising the temperature from 25 to 35°C increased permeation rates up to 20%, and from 25 to 45°C up to 55%. Two methods of heating were tested: preheating the entire feed to the system, and heating the boundary layer at the membrane surface. Comparisons with theory are discussed
    Type of Medium: Electronic Resource
    URL: http://dx.doi.org/10.1111/j.1365-2621.1973.tb02830.x
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  • 2
    Electronic Resource
    Electronic Resource
    Stimulation of pyruvate kinase phosphatase activity by insulin in isolated rat hepatocytes
    Amsterdam : Elsevier
    Biochemical and Biophysical Research Communications 134 (1986), S. 292-298 
    Details
    ISSN: 0006-291X
    Source: Elsevier Journal Backfiles on ScienceDirect 1907 - 2002
    Topics: Biology , Chemistry and Pharmacology , Physics
    Type of Medium: Electronic Resource
    URL: http://dx.doi.org/10.1016/0006-291X(86)90561-9
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  • 3
    Electronic Resource
    Electronic Resource
    Pudendal neuropathy in diabetic patients with faecal incontinence (1994)
    Springer
    International journal of colorectal disease 9 (1994), S. 105-109 
    Details
    ISSN: 1432-1262
    Source: Springer Online Journal Archives 1860-2000
    Topics: Medicine
    Description / Table of Contents: Résumé Afin d'étudier la pathophysiologie de l'incontinence fécale en cas de diabète, deux groupes de patients diabétiques ont été analysés: 14 sujets incontinents (7 femmes et 7 hommes dont l'âge moyen est de 57±9 ans) (groupe A) et 15 sujets sans incontinence mais porteurs d'une neuropathie périphérique (6 femmes et 9 hommes dont l'âge moyen est de 54,7±8 ans). Un troisième groupe (groupe C) constitué de 10 volontaires sains a servi de groupe contrôle. Tous les sujets ont subi des investigations électroneurographiques de leur neuropathie périphérique, une mesure du temps de latence du nerf honteux interne, une manométrie anorectale et des tests de sensibilité rectale. Tous les patients du groupe A présentent une neuropathie somatique périphérique. La pression maximale de rétention est plus basse dans le groupe A que dans le groupe C (P〈0,025) et peut être maintenue moins longtemps dans le groupe A que dans le groupe B (P〈0,0005) ou que dans le groupe C (P〈0,0005). Les seuils de sensibilité rectale sont plus élevés dans le groupe A que dans les groupes B et C. Le temps de latence du nerf honteux interne est allongé chez 92,9% des patients étudiés dans le groupe A et 73,3% des patients du groupe B (A vs B,P〈0,005); la différence est encore plus significative en comparaison avec le groupe C (A vs CP〈0,0005, B vs CP〈0,005). Nos constations suggèrent que la neuropathie somatique joue un rôle important dans la genèse de l'incontinence chez les patients diabétiques, en combinaison avec des altérations du seuil de sensibilité rectale en tant que symptôme d'une atteinte autonome.
    Notes: Abstract To investigate the pathophysiology of faecal incontinence in diabetes mellitus, two groups of diabetic patients were studied: 14 subjects (7 females and 7 males, mean age 57±9 years) with faecal incontinence (Group A) and 15 subjects (6 females and 9 males, mean age 54.7±8 years) without faecal incontinence but affected by somatic peripheral neuropathy. A third group (C) of 10 healthy volunteers was used as controls. All subjects underwent electroneurographic evaluation of peripheral neuropathy, pudendal nerve terminal motor latency, anorectal manometry and rectal sensitivity tests. All the patients of group A had somatic peripheral neuropathy. Maximum squeeze pressure was lower in A compared to C (P〈0.025) and sustained for a shorter period in A compared with B (P〈0.0005) and C (P〈0.0005). All rectal sensitivity thresholds were higher in A compared with B and C. Pudendal Nerve Terminal Motor Latency was prolonged in 93% of patients studied in group A and in 73% of patients in group B (A vs BP〈0.005), with a significant difference in comparison with C: A vs CP〈0.0005, B vs CP〈0.005. Our findings suggest that somatic neuropathy plays an important role in faecal incontinence in diabetic patients, combined with sesation threshold impairment as a feature of an autonomic involvement.
    Type of Medium: Electronic Resource
    URL: http://dx.doi.org/10.1007/BF00699423
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  • 4
    Electronic Resource
    Electronic Resource
    Effect of neuropeptide Y on the sympathetic contraction of the rabbit central ear artery during cooling (2000)
    Springer
    Pflügers Archiv 440 (2000), S. 548-555 
    Details
    ISSN: 1432-2013
    Keywords: Alpha-adrenoceptor vasoconstriction Cutaneous arteries Nitric oxide Purinoceptor vasoconstriction Y1 receptors
    Source: Springer Online Journal Archives 1860-2000
    Topics: Medicine
    Notes: Abstract. In order to analyse the effect of neuropeptide Y (NPY) on the cutaneous vascular response to sympathetic nerve stimulation during cooling, the isometric response of isolated 2-mm segments of the rabbit central ear (cutaneous) artery was recorded at 37°C and during cooling (30°C). Electrical field stimulation (4–16 Hz) at 37°C produced a frequency-dependent contraction, which was reduced during cooling (45% for 16 Hz) and potentiated by NPY (10–8, 3×10–8 and 10–7 M), this potentiation being greater at 30°C than at 37°C. The NPY-induced potentiation of the contraction elicited by electrical field stimulation (8 Hz) was abolished by an antagonist of Y1 subtype NPY receptors, BIBP3226 (10–6 M), at 37°C and 30°C, reduced by phentolamine (10–6 M) at 30°C but not at 37°C, was not modified by the purinoceptor antagonist PPADS (3×10–5 M) and was reduced by application of both phentolamine and PPADS at both temperatures. Both NiCl2 (10–3 M) and verapamil (10–5 M) abolished the potentiating effect of NPY at 37°C and reduced it at 30°C. Neither application of an inhibitor of nitric oxide synthesis, l-N ω-nitro-arginine (l-NOARG, 10–4 M), nor endothelium removal modified the potentiating effect of NPY at 37°C or 30°C. NPY (10–8, 3×10–8 and 10–7 M) potentiated in a concentration-dependent way the arterial contraction in response to exogenous noradrenaline (10–8–10–4 M) at 30°C but not at 37°C, and it increased the response to ATP (10–4–10–2 M) at both temperatures. Therefore, in cutaneous (ear) arteries: (1) NPY potentiates the sympathetic response at 37°C and at 30°C, (2) this potentiating effect of NPY was more marked at 30°C than at 37°C, probably because of greater potentiation of the α-adrenoceptor response during cooling, and (3) the potentiating effect of NPY at both temperatures is mediated by NPY receptors of the Y1 subtype, is dependent of Ca2+ channels and is independent of the release of endothelial nitric oxide.
    Type of Medium: Electronic Resource
    URL: http://dx.doi.org/10.1007/s004240000323
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