| 1. |
- De Vries, Henk, et al.
(author)
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Standardization : Towards an agenda for research
- 2018
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In: International Journal of Standardization Research. - 2470-8542. ; 16:1, s. 52-59
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Journal article (peer-reviewed)abstract
- Standardization research is a fairly new and is a still-evolving field of research, with possibly major practical ramifications. This article presents a summary of the authors' subjective views of the most pressing research topics in the field. These include, among others, standards (e.g. incorporation of ethical issues), the potential impact of standards, the corporate management of standardization and legal issues like Intellectual Property Rights (IPR). In addition, gaps have been identified with a respect to a basic understanding of standardization, suggesting a need for better education in the field.
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| 2. |
- Karlsson, Britt M., et al.
(author)
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Nimodipine affects the microcirculation and modulates the vascular effects of acetylcholinesterase inhibition
- 2003
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In: Upsala Journal of Medical Sciences. - : Taylor & Francis. - 0300-9734 .- 2000-1967. ; 108:2, s. 141-149
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Journal article (peer-reviewed)abstract
- The present investigation was undertaken in order to study whether microvascular effects of the calcium antagonist nimodipine induces changes that can explain an increased detoxification of the highly toxic cholinesterase inhibitor soman. Anaesthetised, tracheotomised and artificially ventilated rats were treated intra-peritoneally (ip) with nimodipine, 10 mg kg(-1) or vehicle followed one hour later by the exposure to 45 microg kg(-1) soman (iv). Nimodipine per se induced a vasodilation in the intestine, myocardium and other muscles. In the abdominal skin soman elicited a significant vasoconstriction that was turned into an increased blood flow after nimodipine pre-treatment. A slight vasoconstriction in diaphragm of soman intoxicated rats was turned into a significant vasodilation by nimodipine pre-treatment. In the intestinal parts no effect of soman was detected. However, in nimodipine pretreated animals soman induced a significant vasoconstriction. The capacity of soman detoxifying processes, i.e. enzymatic hydrolysis and covalent binding to different esterases, is unequally distributed throughout the body. Together with the knowledge of the detoxifying processes of cholinesterase inhibition the results support our theory, that nimodipine alters the peripheral blood flow in a beneficial way resulting in improved detoxification ability.
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| 3. |
- Koskinen, Lars-Owe D., et al.
(author)
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Cerebral microvascular effects of nimodipine in combination with soman
- 2012
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In: Environmental Toxicology and Pharmacology. - : Elsevier BV. - 1382-6689 .- 1872-7077. ; 34:3, s. 905-910
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Journal article (peer-reviewed)abstract
- Nimodipine, a calcium antagonist, has been shown to increase the detoxification of soman. In this study the cerebral microcirculatory effects of nimodipine and the acetylcholinesterase inhibitor soman was studied. Anaesthetised rats were administered nimodipine, 10 mg kg(-1) or vehicle intra-peritoneally, and 1 h later exposed to 45 mu g kg(-1) soman intravenously. The regional blood flows were measured using the microsphere method. Nimodipine and soman markedly increased the cerebral blood flow (CBF) and reduced the vascular resistance. Total CBF increased by 146% after nimodipine and by 105% after soman administration. Combined administration of nimodipine and soman caused additional but not fully additive effects on CBF and vascular resistance, indicating possible different mechanisms of the two agents. A part of the nimodipine induced increased detoxification after AChE-inhibition may be associated with this cerebral vasodilation. (C) 2012 Elsevier B.V. All rights reserved.
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| 4. |
- Koskinen, Lars-Owe D., Professor, 1955-, et al.
(author)
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Cerebrovascular effects of the TRH analogues pGlu-3-methyl-His-Pro amide and pGlu-Glu-Pro amide : a comparison with TRH.
- 2000
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In: Upsala Journal of Medical Sciences. - : Upsala Medical Society. - 0300-9734 .- 2000-1967. ; 105:1, s. 73-83
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Journal article (peer-reviewed)abstract
- The goal of the study was to assess whether TRH analogues possess cerebrovascular effects similar to the native peptide. The neuropeptide thyrotropin releasing hormone (TRH) elicits cerebrovasodilation in several species under various conditions. The laser-Doppler method was employed to study the effects of TRH and the analogues pGlu-3-methyl-His-Pro amid (M-TRH) and pGlu-Glu-Pro amide. Intravenous (i.v.) injection of 300 microg kg(-1) of TRH elicited cerebrovasodilation and a 62% increase in blood flow within 1 minute. M-TRH, in a dose of 300 microg kg(-1) i.v., elicited a 80% increase in cerebral blood flow. Even a minute dose of M-TRH (625 ng kg(-1)) caused an increase in cerebral blood flow. No clear difference in effects on the cerebral blood flow was observed between spontaneously and mechanically ventilated animals, pGlu-Glu-Pro amide had no cerebrovascular effect.
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| 5. |
- Koskinen, Lars-Owe D., Professor, 1955-, et al.
(author)
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Nitric oxide inhibition by L-NAME but not 7-NI induces a transient increase in cortical cerebral blood flow and affects the cerebrovasodilation induced by TRH
- 2003
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In: Peptides. - : Elsevier. - 0196-9781 .- 1873-5169. ; 24:4, s. 579-583
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Journal article (peer-reviewed)abstract
- The tripeptide thyrotropin releasing hormone (TRH) has multiple interesting and complex physiological effects. One of these is the cerebrovasodilating effect, which has been described under several different conditions. The final mechanism for this effect is unknown. In the present study, we found an initial atropine-resistant cerebral vasodilation (24%) elicited by the NOS inhibitor L-NAME in the rat. D-NAME and 7-NI did not produce this effect. TRH (300 microg kg(-1), i.v.) induced an increase in cerebral blood flow by 62%. L-NAME reduced this effect significantly. The cerebrovasodilating mechanism of TRH, at least in part, is endothelial NO dependent as the neuronal 7-NI NOS inhibitor does not affect the TRH response.
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| 6. |
- Koskinen, Lars-Owe D., Professor, 1955-, et al.
(author)
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The neuropeptide TRH has a minor effect on the enzymatic activity of acetylcholinesterase in vitro.
- 1998
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In: Peptides. - : Elsevier BV. - 0196-9781 .- 1873-5169. ; 19:10, s. 1675-1677
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Journal article (peer-reviewed)abstract
- The neuropeptide thyrotropin-releasing hormone (TRH) elicits a variety of physiological effects of which some are due to cholinergic mechanisms. TRH modulates in vivo the effects of compounds affecting acetylcholinesterase (AChE). In the present study the in vitro effects of TRH on the activity of AChE were explored. TRH has no effect at physiologically relevant concentrations. At unphysiologically high concentrations (>5 mM) a slight inhibition was found. This was noticed also when the enzyme was exposed to the amide-free tripeptide analog p-Glu-His-Pro. We conclude that any cholinergic effect of TRH observed in vivo is unlikely to be due to a direct interaction of the peptide with AChE.
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