| 1. |
- Choularton, T. W., et al.
(författare)
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The Great Dun Fell Cloud Experiment 1993 : An overview
- 1997
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Ingår i: Atmospheric Environment. - 1352-2310. ; 31:16, s. 2393-2405
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Tidskriftsartikel (refereegranskat)abstract
- The 1993 Ground-based Cloud Experiment on Great Dun Fell used a wide range of measurements of trace gases, aerosol particles and cloud droplets at five sites to study their sources and sinks especially those in cloud. These measurements have been interpreted using a variety of models. The conclusions add to our knowledge of air pollution, acidification of the atmosphere and the ground, eutrophication and climate change. The experiment is designed to use the hill cap cloud as a flow-through reactor, and was conducted in varying levels of pollution typical of much of the rural temperate continental northern hemisphere in spring-time.
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| 2. |
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| 3. |
- Fredlund, K.M, et al.
(författare)
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NADH-ferricyanide reductases in plant membranes
- 1996
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Ingår i: Plant Membrane Biology- Proceedings of the Phytochemical Society of Europe -38. ; , s. 143-151
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Konferensbidrag (övrigt vetenskapligt/konstnärligt)
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| 4. |
- Agius, Stephanie C, et al.
(författare)
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The internal rotenone-insensitive NADPH dehydrogenase contributes to malate oxidation by potato tuber and pea leaf mitochondria
- 1998
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Ingår i: Physiologia Plantarum. - : Wiley. - 0031-9317. ; 104:3, s. 329-336
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Tidskriftsartikel (refereegranskat)abstract
- Inside-out submitochondrial particles from both potato (Solanum tuberosum L. cv. Bintje) tubers and pea (Pisum sativum L. cv. Oregon) leaves possess three distinct dehydrogenase activities: Complex I catalyzes the rotenone-sensitive oxidation of deamino-NADH, NDin(NADPH) catalyzes the rotenone-insensitive and Ca2+-dependent oxidation of NADPH and NDin(NADH) catalyzes the rotenone-insensitive and Ca2+-independent oxidation of NADH. Diphenylene iodonium (DPI) inhibits complex I, NDin(NADPH) and NDin (NADH) activity with a Ki of 3.7, 0.17 and 63 µM, respectively, and the 400-fold difference in Ki between the two NDin made possible the use of DPI inhibition to estimate NDin (NADPH) contribution to malate oxidation by intact mitochondria. The oxidation of malate in the presence of rotenone by intact mitochondria from both species was inhibited by 5 µM DPI. The maximum decrease in rate was 10–20 nmol O2 mg-1 min-1. The reduction level of NAD(P) was manipulated by measuring malate oxidation in state 3 at pH 7.2 and 6.8 and in the presence and absence of an oxaloacetate-removing system. The inhibition by DPI was largest under conditions of high NAD(P) reduction. Control experiments showed that 125 µM DPI had no effect on the activities of malate dehydrogenase (with NADH or NADPH) or malic enzyme (with NAD+ or NADP+) in a matrix extract from either species. Malate dehydrogenase was unable to use NADP+ in the forward reaction. DPI at 125 µM did not have any effect on succinate oxidation by intact mitochondria of either species. We conclude that the inhibition caused by DPI in the presence of rotenone in plant mitochondria oxidizing malate is due to inhibition of NDin(NADPH) oxidizing NADPH. Thus, NADP turnover contributes to malate oxidation by plant mitochondria.
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| 5. |
- Möller, J, et al.
(författare)
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Do episodes of anger trigger myocardial infarction? A case-crossover analysis in the Stockholm Heart Epidemiology Program (SHEEP).
- 1999
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Ingår i: Psychosomatic Medicine. - : Ovid Technologies (Wolters Kluwer Health). - 0033-3174 .- 1534-7796. ; 61:6, s. 842-9
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Tidskriftsartikel (refereegranskat)abstract
- OBJECTIVE: Our objectives were to study anger as a trigger of acute myocardial infarction (MI) and to explore potential effect modification by usual behavioral patterns related to hostility. METHODS: This study was a case-crossover study within the Stockholm Heart Epidemiology Program. Exposure in the period immediately preceding MI was compared with exposure during a control period for each case. From April 1993 to December 1994, 699 patients admitted to coronary care units in Stockholm County were interviewed. RESULTS: During a period of 1 hour after an episode of anger, with an intensity of at least "very angry," the relative risk of MI was 9.0 (95% CI, 4.4-18.2). In patients with premonitory symptoms, the time of disease initiation may be misclassified. When restricting the analyses to those without such symptoms, the trigger risk was 15.7 (95% CI, 7.6-32.4). The possibility of examining effect modification was limited by a lack of statistical power (eight exposed cases). Results of the analyses suggested, however, an increased trigger effect among subjects reporting nonhostile usual behavior patterns, nonovert strategies of coping with aggressive situations (not protesting when being treated unfairly), and nonuse of beta-blockers. CONCLUSIONS: The hypothesis that anger may trigger MI is further supported, with an increased risk lasting for approximately 1 hour after an outburst of anger. It is suggested that the trigger risk may be modified by personal behavior patterns.
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