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- Andersson, JLR, et al.
(författare)
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Regional cerebral blood flow and oxygen metabolism during migraine with and without aura
- 1997
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Ingår i: CEPHALALGIA. - : SCANDINAVIAN UNIVERSITY PRESS. - 0333-1024. ; 17:5, s. 570-579
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Tidskriftsartikel (övrigt vetenskapligt/konstnärligt)abstract
- Eleven cases of migraine with and without aura were investigated with positron emission tomography (PET). Regional cerebral blood flow (rCBF), oxygen metabolism (rCMRO(2)) and oxygen extraction (rOER) were measured during baseline (n = 11), aura (n = 6),
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| 4. |
- Bulhak, AA, et al.
(författare)
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PPAR-alpha activation protects the type 2 diabetic myocardium against ischemia-reperfusion injury: involvement of the PI3-Kinase/Akt and NO pathway
- 2009
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Ingår i: American journal of physiology. Heart and circulatory physiology. - : American Physiological Society. - 0363-6135 .- 1522-1539. ; 296:3, s. H719-H727
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Tidskriftsartikel (refereegranskat)abstract
- Several clinical studies have shown the beneficial cardiovascular effects of fibrates in patients with diabetes and insulin resistance. The ligands of peroxisome proliferator-activated receptor-α (PPAR-α) reduce ischemia-reperfusion injury in nondiabetic animals. We hypothesized that the activation of PPAR-α would exert cardioprotection in type 2 diabetic Goto-Kakizaki (GK) rats, involving mechanisms related to nitric oxide (NO) production via the phosphatidylinositol 3-kinase (PI3K)/Akt pathway. GK rats and age-matched Wistar rats (n ≥ 7) were given either 1) the PPAR-α agonist WY-14643 (WY), 2) dimethyl sulfoxide (DMSO), 3) WY and the NO synthase inhibitor NG-nitro-l-arginine (l-NNA), 4) l-NNA, 5) WY and the PI3K inhibitor wortmannin, or 6) wortmannin alone intravenously before a 35-min period of coronary artery occlusion followed by 2 h of reperfusion. Infarct size (IS), expression of endothelial NO synthase (eNOS), inducible NO synthase, and Akt as well as nitrite/nitrate were determined. The IS was 75 ± 3% and 72 ± 4% of the area at risk in the Wistar and GK DMSO groups, respectively. WY reduced IS to 56 ± 3% in Wistar ( P < 0.05) and to 46 ± 5% in GK rats ( P < 0.001). The addition of either l-NNA or wortmannin reversed the cardioprotective effect of WY in both Wistar (IS, 70 ± 5% and 65 ± 5%, respectively) and GK (IS, 66 ± 4% and 64 ± 4%, P < 0.05, respectively) rats. The expression of eNOS and eNOS Ser1177 in the ischemic myocardium from both strains was increased after WY. The expression of Akt, Akt Ser473, and Akt Thr308 was also increased in the ischemic myocardium from GK rats following WY. Myocardial nitrite/nitrate levels were reduced in GK rats ( P < 0.05). The results suggest that PPAR-α activation protects the type 2 diabetic rat myocardium against ischemia-reperfusion injury via the activation of the PI3K/Akt and NO pathway.
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| 5. |
- Engler, Henry, et al.
(författare)
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Imaging astrocytosis with PET in Creutzfeldt-Jakob disease : case report with histopathological findings
- 2012
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Ingår i: International Journal of Clinical and Experimental Medicine. - 1940-5901. ; 5:2, s. 201-207
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Tidskriftsartikel (refereegranskat)abstract
- In a previous study, patients with suspect Creutzfeldt-Jakob's disease (CJD) have been examined with Positron Emission Tomography (PET) combining N-[11C-methyl]-L-deuterodeprenyl (DED) and [(18)F] 2- fluorodeoxyglucose (FDG) in an attempt to detect astrocytosis and neuronal dysfunction, two of the hallmarks in CJD. Increased DED uptake with pronounced hypometabolism matching the areas with high DED retention was found in the fronto-parieto-occipital areas and cerebellum of patients with confirmed CJD. However, the temporal lobes did not present such a pattern. In 6 of the 15 examined patients the autopsy was performed, but a strict comparison between the PET results and the histopathology could not be done. Recently, one patient with suspect CJD was examined with PET using DED and FDG. The results of the examinations in this patient showed a pattern similar to that found in the brain of the CJD patients from the first study. The patient died shortly after the examination and an autopsy could be performed. The autopsy showed neuronal death, astrocytosis and spongiform changes in the brain. The diagnosis of definite sporadic CJD was established by the Western blot analysis, confirming the presence of the prion resistant protein (PrPres). The PET data demonstrated high DED uptake and extreme low glucose uptake in the left brain hemisphere whereas the right side was less affected. The autopsy was performed allowing the comparison between high DED uptake and the histopathological findings of reactive astrocytosis revealed by immunostaining with antibodies against glial fibrillary acid protein (GFAP). The results confirmed the presence of a pattern with high ratio DED/FDG, similar to that found in the previous study and revealing for the first time, a good correlation between high DED uptake and high density of reactive astrocytes as demonstrated by immunostaining.
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| 14. |
- Lundberg, PO
(författare)
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CJD cases in Sweden 1985-1996
- 1998
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Ingår i: Neuropathol Applied Neurobiol. ; 24, s. 410-
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Tidskriftsartikel (refereegranskat)
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| 18. |
- Lundberg, PO
(författare)
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Hovedpine og seksualitet
- 1997
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Ingår i: Kapitel 15, Hjerne & seksualitet, aspekter af teori & klinik. - : Munksgaard, København. ; , s. 227-
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Bokkapitel (övrigt vetenskapligt/konstnärligt)
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| 19. |
- Lundberg, PO
(författare)
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Läkemedel och sexualitetKap 35
- 2002
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Ingår i: SexologiPO Lundberg (red). - : Liber utbildning, Stockholm. ; , s. 361-
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Bokkapitel (övrigt vetenskapligt/konstnärligt)
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| 25. |
- Lundberg, Peter, et al.
(författare)
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Primary metabolism in N-2-fixing Alnus incana-Frankia symbiotic root nodules studied with N-15 and P-31 nuclear magnetic resonance spectroscopy
- 2004
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Ingår i: Planta. - : Springer Science and Business Media LLC. - 0032-0935 .- 1432-2048. ; 219:4, s. 661-672
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Tidskriftsartikel (refereegranskat)abstract
- The primary nitrogen metabolism of the N-2-fixing root nodule symbiosis Alnus incana (L.)-Frankia was investigated by P-31 and N-15 nuclear magnetic resonance (NMR) spectroscopy. Perfusion of root nodules in a pulse-chase approach with N-15- or N-14-labeled NH4+ revealed the presence of the amino acids alanine (Ala), gamma-amino butyric acid, glutamine (Gln), glutamic acid (Glu), citrulline (Cit) and arginine (Arg). Labeling kinetics of the Gln amide-N and alpha-amino acids suggested that the glutamine synthetase (GS, EC 6.3.1.2)-glutamate synthase (GOGAT, EC 1.4.1.13) pathway was active. Inhibition of the GS-catalyzed reaction by methionine sulphoximine abolished incorporation of N-15. Cit was labeled in all three N positions but most rapidly in the omega position, consistent with carbamoyl phosphate as the precursor to which Gln could be the amino donor catalyzed by carbamoyl phosphate synthase (CPS, EC 6.3.5.5). Ala biosynthesis occurred consistent with a flux of N in the sequence Gln-Glu-Ala. P-31 NMR spectroscopy in vivo and of extracts revealed several metabolites and was used in connection with the N-15 pulse-chase experiment to assess general metabolic status. Stable concentrations of ATP and UDP-glucose during extended perfusions showed that the overall root nodule metabolism appeared undisturbed throughout the experiments. The metabolic pathways suggested by the NMR results were confirmed by high activities of the enzymes GS, NADH-GOGAT and ornithine carbamoyltransferase (OCT, EC 2.1.3.3). We conclude that the primary pathway of NH4+ assimilation in A. incana root nodules occurs through the GS-GOGAT pathway. Biosynthesis of Cit through GS-CPS-OCT is important and is a link between the first amino acid Gln and this final transport and storage form of nitrogen.
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| 32. |
- Lundberg, PO
(författare)
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Vad är sexologi?kap 1
- 2002
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Ingår i: SexologiPO Lundberg (red). - : Liber utbildning Stockholm. ; , s. 13-
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Bokkapitel (övrigt vetenskapligt/konstnärligt)
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| 33. |
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| 35. |
- Skarpengland, T, et al.
(författare)
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Neil3-dependent base excision repair regulates lipid metabolism and prevents atherosclerosis in Apoe-deficient mice
- 2016
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Ingår i: Scientific reports. - : Springer Science and Business Media LLC. - 2045-2322. ; 6, s. 28337-
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Tidskriftsartikel (refereegranskat)abstract
- Increasing evidence suggests that oxidative DNA damage accumulates in atherosclerosis. Recently, we showed that a genetic variant in the human DNA repair enzyme NEIL3 was associated with increased risk of myocardial infarction. Here, we explored the role of Neil3/NEIL3 in atherogenesis by both clinical and experimental approaches. Human carotid plaques revealed increased NEIL3 mRNA expression which significantly correlated with mRNA levels of the macrophage marker CD68. Apoe−/−Neil3−/− mice on high-fat diet showed accelerated plaque formation as compared to Apoe−/− mice, reflecting an atherogenic lipid profile, increased hepatic triglyceride levels and attenuated macrophage cholesterol efflux capacity. Apoe−/−Neil3−/− mice showed marked alterations in several pathways affecting hepatic lipid metabolism, but no genotypic alterations in genome integrity or genome-wide accumulation of oxidative DNA damage. These results suggest a novel role for the DNA glycosylase Neil3 in atherogenesis in balancing lipid metabolism and macrophage function, potentially independently of genome-wide canonical base excision repair of oxidative DNA damage.
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| 36. |
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