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- Anderson, Leif G, 1951, et al.
(författare)
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Source and formation of the upper halocline of the Arctic Ocean
- 2013
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Ingår i: Journal of Geophysical Research - Oceans. - 0148-0227 .- 2156-2202. ; 118:1, s. 410-421
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Tidskriftsartikel (refereegranskat)abstract
- The upper halocline of the Arctic Ocean has a distinct chemical signature with high nutrient concentrations as well as low oxygen and pH values. This signature is formed in the Chukchi and East Siberian Seas, by a combination of mineralization of organic matter and release of decay products to the sea ice brine enriched bottom water. Salinity and total alkalinity data show that the fraction of sea ice brine in the nutrient enriched upper halocline water in the central Arctic Ocean is up to 4%. In the East Siberian Sea the bottom waters with exceptional high nutrient concentration and low pH have typically between 5 and 10% of sea ice brine as computed from salinity and oxygen-18 values. On the continental slope, over bottom depths of 15-200 m, the brine contribution was 6% at the nutrient maximum depth (50-100 m). At the same location as well as over the deeper basin the silicate maximum was found over a wider salinity range than traditionally found in the Canada Basin, in agreement with earlier observations east of the Chukchi Plateau. A detailed evaluation of the chemical and the temperature-salinity properties suggests at least two different areas for the formation of the nutrient rich halocline within the East Siberian Sea. This has not been observed before 2004 and it could be a sign of a changing marine climate in the East Siberian Sea, caused by more open water in the summer season followed by more sea ice formation and brine production in the fall/winter.
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- Andersson, Irene, 1978
(författare)
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Cardiovascular effects of growth hormone. Studies in genetically engineered mice
- 2004
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Doktorsavhandling (övrigt vetenskapligt/konstnärligt)abstract
- The general aim of this thesis was to enhance the understanding on the relationships between growth hormone (GH) and cardiovascular disease using genetically engineered mice. More specifically the effects of GH on blood pressure (BP), vascular and cardiac function, atherosclerosis and autonomic control of heart rate were studied. Two genetically engineered mice models were used, bovine GH transgenic (bGH) and GH receptor/binding protein knock-out mice (GHR KO). In addition a third mouse model was generated through crossbreeding of bGH and an atherosclerosis prone mouse strain, apoE-/-, yielding apoE-/-/bGH mice. bGH mice had increased mean arterial BP compared to control mice as measured by telemetry. The hypertension was not salt sensitive but associated with increased resistance of the hindquarter vasculature. Mesenteric arteries from bGH mice displayed intact endothelial function and decreased sensitivity to noradrenaline, as assessed by myograph technique, while carotid artery and aorta displayed impaired endothelial function. Treatment of the vessels with a super oxide dismutase (SOD) mimetic appeared to abolish differences in endothelium dependent vasodilation between bGH and control mice. However, aorta from young bGH mice had intact endothelial function accompanied by increased mRNA levels of SOD and endothelial nitric oxide synthase, semi quantified by real-time PCR. Heart rate responses measured by telemetry, to pharmacological challenging of the sympathetic and parasympathetic nervous system, showed that bGH mice had reduced ability for sympathetic activation but intact reflex activation of parasympathetic nervous system. bGH mice also had decreased heart rate variability and reduced noradrenaline concentrations in plasma and tissue, measured by high performance liquid chromatography. Systolic BP, measured by tail-cuff technique, was increased in female apoE-/-/bGH mice compared to apoE-/- control mice. Atherosclerotic plaque area in the thoracic aorta, quantified en face after lipid staining, was significantly increased in male apoE-/-/bGH compared to control, and tended to be increased in female apoE-/-/bGH. Interestingly, female apoE-/-/bGH had a more atherogenic serum lipid profile than male. Finally, GHR KO mice had decreased systolic BP measured by tail-cuff technique and reduced cardiac and vascular structure but intact endothelial function. Furthermore, GHR KO mice had impaired cardiac function as assessed by echocardiography. In summary, this thesis has generated new knowledge on the effects of GH on cardiovascular function and development of atherosclerosis. It has presented a novel mouse model that facilitates direct studies on the mechanism involved in GH induced atherogenesis. A further important finding is that GH appears to have profound effects on sympathetic nervous system function and tissue noradrenaline levels. This may be an interesting future target for treatment of diseases associated with autonomic dysfunction.
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- Andersson, Iréne, et al.
(författare)
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Complement split products and pro-inflammatory cytokines in salvaged blood after hip and knee arthroplasty.
- 2001
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Ingår i: Canadian journal of anaesthesia = Journal canadien d'anesthésie. - 0832-610X. ; 48:3, s. 251-5
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Tidskriftsartikel (refereegranskat)abstract
- PURPOSE: To determine whether salvaged autologous blood collected postoperatively contains complement split products (SC5b-9), and pro-inflammatory cytokines (IL-6 and IL-8) and whether there are any differences between blood collected during hip or knee surgery. METHODS: Fifty-eight consecutive patients undergoing hip or knee replacement surgery were studied. Thirty-eight had postoperative bleeding large enough to require infusion of salvaged blood. The salvaged blood was filtered during collection through a 200 microm filter and before infusion a 40 microm filter was used. Samples for complement and cytokine determinations were drawn from the circulation and from the collected blood. RESULTS: High concentrations of SC5b-9, IL-6, and IL-8 were found in salvaged blood. The concentrations were higher than in the circulation (P < 0.05). The circulating concentrations of IL-6 and IL-8 were increased 60 min and 12-18 hr after transfusion. There were no differences regarding SC5b-9, IL-6, and IL-8 in the blood collected after hip or knee surgery. CONCLUSION: Blood collected from a surgical wound contains large concentrations of inflammatory mediators. There were no differences between blood collected during hip or knee surgery.
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- Andersson, Irene, 1978, et al.
(författare)
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Endothelial dysfunction in growth hormone transgenic mice
- 2006
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Ingår i: Clinical Science. - 0143-5221 .- 1470-8736. ; 110:2, s. 217-25
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Tidskriftsartikel (refereegranskat)abstract
- Acromegaly [overproduction of GH (growth hormone)] is associated with cardiovascular disease. Transgenic mice overexpressing bGH (bovine GH) develop hypertension and hypercholesterolaemia and could be a model for cardiovascular disease in acromegaly. The aims of the present study were to investigate the effects of excess GH on vascular function and to test whether oxidative stress affects endothelial function in bGH transgenic mice. We studied the ACh (acetylcholine)-induced relaxation response in aortic and carotid rings of young (9-11 weeks) and aged (22-24 weeks) female bGH transgenic mice and littermate control mice, without and with the addition of a free radical scavenger {MnTBAP [Mn(III)tetrakis(4-benzoic acid)porphyrin chloride]}. We also measured mRNA levels of eNOS (endothelial nitric oxide synthase) and EC-SOD (extracellular superoxide dismutase). Intracellular superoxide anion production in the vascular wall was estimated using a dihydroethidium probe. Carotid arteries from bGH transgenic mice had an impaired ACh-induced relaxation response (young, 46 +/- 7% compared with 69 +/- 8%; aged, 52 +/- 5% compared with 80 +/- 3%; P < 0.05), whereas endothelial function in aorta was intact in young but impaired in aged bGH transgenic mice. Endothelial dysfunction was corrected by addition of MnTBAP in carotid arteries from young mice and in aortas from aged mice; however, MnTBAP did not correct endothelial dysfunction in carotid arteries from aged bGH transgenic mice. There was no difference in intracellular superoxide anion production between bGH transgenic mice and control mice, whereas mRNA expression of EC-SOD and eNOS was increased in aortas from young bGH transgenic mice compared with control mice (P < 0.05). We interpret these data to suggest that bGH overexpression is associated with a time- and vessel-specific deterioration in endothelial function, initially caused by increased oxidative stress and later by other alterations in vascular function.
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- Andersson, Irene, 1978, et al.
(författare)
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Increased atherosclerotic lesion area in apoE deficient mice overexpressing bovine growth hormone
- 2006
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Ingår i: Atherosclerosis. - : Elsevier BV. - 0021-9150. ; 188:2, s. 331-40
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Tidskriftsartikel (refereegranskat)abstract
- Human growth hormone (GH) excess is linked to increased cardiovascular morbidity and mortality. However, little is known about the effect of GH excess on atherosclerosis. We developed a new mouse model to assess the hypothesis that GH overexpression accelerates atherosclerotic lesion formation. apoE(-/-) mice were crossed with bovine GH (bGH) transgenic mice to yield apoE(-/-) mice overexpressing bGH (apoE(-/-)/bGH). The mice were fed either standard or Western diet. At 22 weeks, atherosclerotic lesion area of thoracic aorta was larger in apoE(-/-)/bGH mice compared with littermate apoE(-/-) mice fed either diet (standard: +161+/-50%, Western: +430+/-134%). Aortic sinus lesions were more severe in apoE(-/-)/bGH mice fed standard diet compared with littermate apoE(-/-) mice. apoE(-/-)/bGH mice had lower (VLDL+LDL)/HDL ratios compared with littermate apoE(-/-) mice, while systolic blood pressure was higher in apoE(-/-)/bGH mice, irrespective of diet. The levels of serum amyloid A and hepatic CRP mRNA were higher in apoE(-/-)/bGH mice than in littermate apoE(-/-) mice. In conclusion, this study shows that excess GH augments the development of atherosclerosis in apoE(-/-) mice. The mechanisms could be direct effects of GH on cellular processes in the vessel wall or the result of concomitant processes such as hypertension or a general inflammatory state.
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- Andersson, Irene, 1978, et al.
(författare)
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Reduced sympathetic responsiveness as well as plasma and tissue noradrenaline concentration in growth hormone transgenic mice
- 2004
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Ingår i: Acta Physiol Scand. - 0001-6772. ; 182:4, s. 369-78
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Tidskriftsartikel (refereegranskat)abstract
- AIMS: Acromegaly [overproduction of growth hormone (GH)] and GH deficiency have both been associated with alterations in autonomic nervous system function. The aim of this study was to investigate autonomic nervous system influence on heart rate (HR) in transgenic mice overexpressing bovine GH (bGH). METHODS: HR and HR variability (HRV) were measured in conscious young (8-13 weeks) and old (5-6 months) female bGH and control mice using telemetry. HR control was studied using antagonists and an agonist of adrenergic and muscarinic receptors. Noradrenaline was measured in plasma, heart and kidney using high performance liquid chromatography. RESULTS: Average 24 h resting HR did not differ between bGH and control mice. After saline injection and after muscarinic blockade with methylscopolamine HR increase was blunted (in old) or absent (in young) bGH mice compared with control mice (P < 0.05). Phenylephrine caused a baroreflex mediated decrease in HR from around 550 to 300-350 beats min(-1), not different between bGH and control mice. Time- and frequency-domain measures of HRV were reduced in old bGH compared with control mice (P < 0.05). Noradrenaline concentrations were reduced by 25-49% in plasma and tissue of bGH compared with control mice (P < 0.05). CONCLUSION: The current study suggests reduced autonomic modulation of HR in bGH transgenic mice. Thus, GH appears to have marked effects on autonomic tone, reducing sympathetic nervous system function possibly via reduced noradrenaline stores.
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