| 1. |
- Berlowski, M., et al.
(författare)
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Measurement of eta meson decays into lepton-antilepton pairs
- 2008
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Ingår i: Physical Review D. Particles and fields. - : American Physical Society. - 0556-2821 .- 1089-4918. ; 77:3, s. 032004-
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Tidskriftsartikel (refereegranskat)abstract
- A search for rare lepton decays of the eta meson was performed using the WASA detector at CELSIUS. Two candidates for double Dalitz decay eta -> e(+)e(-)e(+)e(-) events are reported with a background of 1.3 +/- 0.2 events. This allows to set an upper limit to the branching ratio of 9.7x10(-5) (90% CL). The branching ratio for the decay eta -> e(+)e(-)gamma is determined to (7.8 +/- 0.5(stat)+/- 0.8(syst))x10(-3) in agreement with world average value. An upper limit (90% CL) for the branching ratio for the eta -> e(+)e(-) decay is 2.7x10(-5) and a limit for the sum of the eta ->mu(+)mu(-)mu(+)mu(-) and eta ->pi(+)pi(-)mu(+)mu(-) decays is 3.6x10(-4).
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| 2. |
- Keleta, S, et al.
(författare)
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Exclusive measurement of two-pion production in the dd -> He-4 pi pi reaction
- 2009
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Ingår i: Nuclear Physics A. - : Elsevier BV. - 0375-9474 .- 1873-1554. ; 825:1-2, s. 71-90
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Tidskriftsartikel (refereegranskat)abstract
- The results from the first kinematically complete measurement of the dd -> He-4 pi pi reaction are reported. The aim was to investigate a long standing puzzle regarding the origin of the peculiar pi pi-invariant mass distributions appearing in double pion production in light ion collisions, the so-called ABC effect. The measurements were performed at the incident deuteron energies of 712 MeV and 1029 MeV. with the WASA detector assembly at CELSIUS in Uppsala, Sweden. We report the observation of a characteristic enhancement at low pi pi-invariant mass at 712 MeV, the lowest energy yet. At the higher energy, in addition to confirming previous experimental observations, Our results reveal a strong angular dependence of the pions in the overall centre of mass system. The results are qualitatively reproduced by a theoretical model, according to which the ABC effect is described as resulting from a kinematical enhancement in the production of the pion pairs from two parallel and independent NN -> d pi sub-processes. (C) 2009 Elsevier B.V. All rights reserved.
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| 3. |
- Bargholtz, Chr., et al.
(författare)
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Measurement of the eta -> pi(+)pi(-)e(+)e(-) decay branching ratio
- 2007
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Ingår i: Physics Letters B. - : Elsevier BV. - 0370-2693 .- 1873-2445. ; 644:5-6, s. 299-303
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Tidskriftsartikel (refereegranskat)abstract
- The reaction pd -> He-3 eta at threshold was used to provide a clean source of eta mesons for decay studies with the WASA detector at CELSIUS. The branching ratio of the decay eta -> pi(+)pi(-)e(+)e(-) is measured to be (4.3 +/- 1.3 +/- 0.4) x 10(-4).
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| 4. |
- Schönning, Karin, et al.
(författare)
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Production of eta and 3 pi mesons in the pd -> (HeX)-He-3 reaction at 1360 and 1450 MeV
- 2010
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Ingår i: European Physical Journal A. - : Springer Science and Business Media LLC. - 1434-6001 .- 1434-601X. ; 45:1, s. 11-21
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Tidskriftsartikel (refereegranskat)abstract
- The cross-sections of the pd -> He-3 eta, pd -> He-3 pi(0)pi(0)pi(0) and pd -> He-3 pi(+)pi(-)pi(0) reactions have been measured at the beam kinetic energies T-p = 1360 MeV and T-p = 1450 MeV using the CELSIUS/WASA detector setup. At both energies, the differential cross-section d sigma/d Omega of the eta meson in the pd -> He-3 eta reaction shows a strong forward-backward asymmetry in the CMS. The ratio between the pd -> He-3 pi(+)pi(-)pi(0) and pd -> He-3 pi(0)pi(0)pi(0) cross-sections has been analysed in terms of isospin amplitudes. The reconstructed invariant-mass distributions of the pi pi, He-3 pi and (3)He2 pi systems provide hints on the role of nucleon resonances in the 3 pi production process.
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| 5. |
- Ekström, Per A R, et al.
(författare)
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Impaired nerve regeneration in streptozotocin-diabetic rats. Effects of treatment with an aldose reductase inhibitor
- 1989
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Ingår i: Journal of the Neurological Sciences. - 0022-510X. ; 93:2-3, s. 231-237
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Forskningsöversikt (refereegranskat)abstract
- Rats with streptozotocin-induced diabetes have a decreased rate of sciatic nerve regeneration. We studied the effects on this defect of treatment with the aldose reductase inhibitor, ponalrestat (25 mg/kg per day via an endogastric tube). The nerves of diabetic rats were crush-injured at 5 weeks of diabetes and regeneration evaluated 7 days later with the pinch-reflex test. Ponalrestat treatment was started at day 3 after streptozotocin injection and was continued for the whole experimental period, i.e. until 6 weeks of diabetes. The treatment prevented effectively the accumulation of sorbitol and fructose in the nerves of diabetic rats, but was without effect on the sciatic nerve regeneration (controls 21.8 ± 1.2 mm/7 days (mean ± SEM, n = 6), untreated diabetics 15.8 ± 1.8 (n = 7), ponalrestat-treated diabetics 16.2 ± 1.0 (n = 10)). The results indicate that there is no connection between increased sorbitol pathway flux and impaired regeneration in streptozotocin diabetic rats.
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| 6. |
- Ahuja, Sat pal, et al.
(författare)
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Physiopathology of retinal degeneration in rd1 mouse model of retinitis pigmentosa : TGF-Β1, proteinases and oxidative stress mechanisms
- 2009
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Ingår i: Retinal Degeneration: Causes, Diagnosis and Treatment. - 9781607410072 ; , s. 1-41
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Bokkapitel (refereegranskat)abstract
- The rd1 (retinal degeneration) mouse retina shows degeneration homologous to a form of retinitis pigmentosa with a rapid loss of rod photoreceptors and deficiency of retinal blood vessels. Due to Pde6brd1 gene mutation, β subunit of phosphodiesterase (PDE) of rd1 retina has an inactive PDE which elevates cGMP and Ca2+ ions level. In vitro retinal explants provide a system close to the in vivo situation, so both approaches were used to compare the status of oxidative stress, transforming growth factor-β1 (TGF-β1), sialylation, galactosylation of proteoglycans, and different proteinases-endogenous inhibitors systems participating in extracellular matrix (ECM) remodeling/degeneration and programmed cell death (PCD)/apoptosis in wt and rd1 mouse retinas. Proteins and desialylated sulfated glucosaminoglycan parts of proteoglycans in ECM of rd1 retina were, respectively, decreased and increased due to enhanced activities of proteinases. Desialylation increases the susceptibility of cells to phoagocytosis/apoptosis, decreased neurogenesis and faulty guidance cues for synaptogenesis. In vivo activities of total proteinases, matrix metalloproteinase-9 (MMP-9) and cathepsin B were increased in rd1 retina on postnatal day 14 (PN14), -21 and -28, due to relatively lower levels of tissue inhibitor of MMPs (TIMP-1) and cystatin C, respectively. This corresponded with increased in vitro secretion of these proteinases by rd1 retina. Cells including end-feet of Mueller cells in degenerating rd1 retina showed intense immunolabeling for MMP-9, MMP-2/TIMP-1, TIMP-2 and cathepsin B/cystatin C, and proteinases pool was increased by Mueller cells. Intense immunolabeling of ganglion cell (RGC) layer for cathepsin B and of inner-plexiform layer of both PN2/PN7 rd1 and wt retinas indicated importance of cathepsin B in synaptogenesis and PCD of RGC. Increased levels of TGF-β1 in vitro transiently increased the secretion of MMPs and cathepsins activities by wt explants which activate TGF-β1 and remodel the ECM for angiogenesis and ontogenetic PCD. Whereas, lower level of TGF-β1 and persistently higher activities of MMPs and cathepsins in rd1 retinas and conditioned medium, suggested that proteinases degraded TGF-β1 and ECM and caused retinal degeneration. Lower activities of glutathione-S-transferase and glutathione-peroxidase in rd1 retina contribute to oxidative stress which damages membranes and increased the expression, release/secretion of proteinases relative to their endogenous inhibitors. Participation of oxidative stress in rd1 retinal degeneration was further confirmed from the partial protection of rd1 photoreceptors by in vitro and/or in vivo supplementation with glutathione-S-transferase or a combination of antioxidants namely lutein, zeaxanthin, α-lipoic acid and reduced-L-glutathione. Treatment with combination(s) of broad spectrum proteinase inhibitor(s) and antioxidants needs investigation.
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| 7. |
- Edbladh, Magnus, et al.
(författare)
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Early regeneration in vitro of adult mouse sciatic axons is dependent on local protein synthesis but may not involve neurotrophins
- 1994
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Ingår i: Neuroscience Letters. - : Elsevier BV. - 0304-3940. ; 168:1-2, s. 37-40
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Tidskriftsartikel (refereegranskat)abstract
- The sensory axons of the adult mouse sciatic nerve were shown to regenerate after a local test crush lesion in vitro in a serum-free medium. The average outgrowth distance of the leading axons after culturing for 3 days was 2.8 ± 0.1 mm, which was shorter than in vivo (3.8 ± 0.2 mm). With the use of a compartmentalised culture system we could show that regeneration was partially dependent on local protein synthesis in the injury region. The initial stages of regeneration did not seem to involve neurotrophins since both K252a and K252b, selective and nontoxic inhibitors of the neurotrophin actions, failed to inhibit axonal growth. The present in vitro model system offers favourable conditions to investigate the early events of the regeneration process in an adult mammalian peripheral nerve.
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| 8. |
- Ekström, Per A R
(författare)
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Insulin stimulates ganglionic protein synthesis and reduces thymidine incorporation in support cells of the in vitro regenerating adult frog sciatic sensory neurons
- 1991
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Ingår i: Neuroscience Letters. - : Elsevier BV. - 0304-3940. ; 132:2, s. 183-186
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Tidskriftsartikel (refereegranskat)abstract
- Insulin was tested for effects on crush injured, in vitro regenerating, adult frog sciatic sensory axons. A wide range of insulin concentrations (0.01-10 μg × ml-1) was found to stimulate incorporation of radioactive leucine into ganglionic protein by 50-80%. without affecting the regeneration distance. Simultaneously insulin inhibited the proliferation of the support cells at the crush region by 30%, as measured by thymidine incorporation. Experiments using compartmentalized culture dishes indicated that the proliferation inhibitory effect could be indirect and mediated by the neuronal cells. The results suggest that insulin influences the metabolism of adult peripheral neuronal cell bodies. The stimulated nerve cells could in turn affect the proliferation of support cells in the nerve trunk.
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| 9. |
- Ekström, Per A R, et al.
(författare)
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Leukemia inhibitory factor null mice : Unhampered in vitro outgrowth of sensory axons but reduced stimulatory potential by nerve segments
- 2000
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Ingår i: Neuroscience Letters. - 0304-3940. ; 281:2-3, s. 107-110
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Tidskriftsartikel (refereegranskat)abstract
- Leukemia inhibitory factor (LIF) is locally up-regulated after peripheral nerve injury and may be involved in the subsequent regeneration. Here, adult mice with or without LIF gene deletions were used to study the role of LIF in regeneration. The results show that axonal regeneration in vitro from dorsal root ganglia (DRGs) was unaffected by LIF deletion. However, segments from wild type mice promoted DRG axonal outgrowth better than segments from LIF deleted animals when in vivo-injured sciatic nerve segments were co-cultured with DRGs from normal adult mice. Addition of LIF could not restore the deficit. This suggests that LIF is engaged in the local regulation of regeneration but not in the regenerative events occuring at the cell body level. (C) 2000 Elsevier Science Ireland Ltd.
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| 10. |
- Ekström, Per A R, et al.
(författare)
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Nerve regeneration and serum levels of insulin-like growth factor-I in rats with streptozotocin-induced insulin deficiency
- 1989
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Ingår i: Brain Research. - : Elsevier BV. - 0006-8993. ; 496:1-2, s. 141-147
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Tidskriftsartikel (refereegranskat)abstract
- Peripheral nerve regeneration was studied in female Sprague-Dawley rats with streptozotocin-induced insulin deficiency. Nerve regeneration was provoked by a crush lesion on the sciatic nerve 21 days after the streptozotocin injection. The regeneration was assessed by a pinch test at different time-points after injury. The rate ofregeneration in insulin-deficient animals, 2.5 mm/day, was significantly lower than in control animals, 2.9 mm/day(P < 0.05). There was no difference in the initial delay, i.e. the period before regeneration attains a constant velocity. One group of insulin-deficient rats was treated with insulin during the regeneration period by means of implanted osmotic mini-pumps. This treatment prevented the decrease in regenerationsw. After 6 days the sciatic nerves of insulin-deficient rats had regenerated 12.3 ±0.3 mm (mean ±S.E.M.), while the corresponding value for insulin-treated rats was 15.7 ±0.6 mm (P > 0.01). The streptozotocin-treated rats were found to have a 39% reduction in the serum level of insulin-like 1 growth factor-I (IGF-I)_compared to control rats (0.33 ± 0.22 μg/ml and 0.54 ± ml respectively, (P < 0.001). Insulin treatment 1830 1732 during the regeneration period completely restored the IGF-I level back to normal.
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| 11. |
- Remgård, Pär, et al.
(författare)
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A Fast Axonally Transported Protein of the Frog Sciatic Sensory Axons Undergoes Similar Qualitative Changes During Regeneration In Vitro and In Vivo
- 1991
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Ingår i: Journal of Neurochemistry. - : Wiley. - 0022-3042 .- 1471-4159. ; 57:6, s. 1907-1912
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Tidskriftsartikel (refereegranskat)abstract
- The adult frog sciatic sensory neurons have been shown to regenerate in vitro. If a crush injury is made at the beginning of culture, regeneration starts after 3.4 days and proceeds at a rate of ∼0.8 mm/day for several days. Two‐dimensional gel electrophoresis was used to study the patterns of radiolabeled, fast axonally transported proteins during the first 7 days of regeneration. Interest was focused on one protein, referred to as rrp31 (regeneration‐related protein 31), which changed in apparent pl from 4.9 to 5.3 when the outgrowth of new fibers started. The change was noticeable 3 days after injury and became prominent during day 5 of culturing. By day 7 the pl changed again, this time toward the original value. The in vitro results were supported by experiments in vivo. In this case the change occurred earlier, with a peak only 3 days after injury, after which the pl decreased. If adenosine at 1 mM was included in the culturing medium, the outgrowth of sensory axons was inhibited in a nontoxic way, and the pl changes of rrp31 were prevented. The temporal nature of the pl changes suggests a role for rrp31 in the initiation of the regeneration process.
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| 12. |
- Remgård, Pär, et al.
(författare)
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Growth cones of regenerating adult sciatic sensory axons release axonally transported proteins
- 1992
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Ingår i: Brain Research. - 0006-8993. ; 572:1-2, s. 139-145
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Tidskriftsartikel (refereegranskat)abstract
- Labelled, rapidly transported axonal proteins were shown to be released frog adult frog sciatic sensory neurons, regenerating in vitro after a crush injury. The spatial distribution of the transported, released proteins could accurately be resolved by culturing the nerve on nitrocellulose paper, which trapped the released proteins. The release was located to the crush and to the entire outgrowth region. When regeneration was inhibited by adenosine, the release was limited to the crush site, implying that the release was linked to the growing axons. Other experiments suggested that the release emanated from growth cones. Furthermore, two-dimensional electrophoretical analysis of both fast axonally transported and of released proteins showed that the represented a selection of the transported protein species.
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| 13. |
- Wiklund, Peter, et al.
(författare)
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Protein kinase C and mouse sciatic nerve regeneration
- 1996
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Ingår i: Brain Research. - : Elsevier BV. - 0006-8993. ; 715:1-2, s. 145-154
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Tidskriftsartikel (refereegranskat)abstract
- We have studied the role of protein kinase C (PKC) in peripheral nerve regeneration by using the cultured adult mouse sciatic nerve, which displays regrowth of sensory axons under serum-free conditions. By the use of immunohistochemistry we show that one of the isoforms of PKC, PKCβ, is present in the nerve cell bodies of normal nerves and is upregulated after injury. In spite of this, the specific PKC inhibitor chelerythrine at 5 μM, a concentration well above its IC50 value for PKC, failed to reduce the outgrowth distance of new axons. This was not due to impermeability of the drug, since the same concentration caused a clear reduction of the injury-induced proliferation of Schwann cells in the crush region. Likewise, HA-1004, an inhibitor of cyclic nucleotide-dependent protein kinases, also lacked effect on outgrowth when used on its own, even at very high concentrations (100 μM). In contrast, outgrowth was significantly reduced when 5 μM chelerythrine and 5 μM HA-1004 were used in combination. In conclusion, the present results suggest that PKC-activity is important but not indispensable for the regeneration process. Successful completion of the latter could be achieved by several, perhaps redundant, phosphorylation systems.
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