| 1. |
- Cornelissen, Johannes H C, et al.
(author)
-
Global negative vegetation feedback to climate warming responses of leaf litter decomposition rates in cold biomes
- 2007
-
In: Ecology Letters. - : Wiley. - 1461-023X .- 1461-0248. ; 10:7, s. 619-627
-
Journal article (peer-reviewed)abstract
- Whether climate change will turn cold biomes from large long-term carbon sinks into sources is hotly debated because of the great potential for ecosystem-mediated feedbacks to global climate. Critical are the direction, magnitude and generality of climate responses of plant litter decomposition. Here, we present the first quantitative analysis of the major climate-change-related drivers of litter decomposition rates in cold northern biomes worldwide.Leaf litters collected from the predominant species in 33 global change manipulation experiments in circum-arctic-alpine ecosystems were incubated simultaneously in two contrasting arctic life zones. We demonstrate that longer-term, large-scale changes to leaf litter decomposition will be driven primarily by both direct warming effects and concomitant shifts in plant growth form composition, with a much smaller role for changes in litter quality within species. Specifically, the ongoing warming-induced expansion of shrubs with recalcitrant leaf litter across cold biomes would constitute a negative feedback to global warming. Depending on the strength of other (previously reported) positive feedbacks of shrub expansion on soil carbon turnover, this may partly counteract direct warming enhancement of litter decomposition.
|
|
| 2. |
- Bolshakova, A., et al.
(author)
-
Extra-cellular matrix proteins induce re-distribution of a-actinin-1 and a-actinin-4 in A431 cells
- 2007
-
In: Cell Biology International. - : Wiley. - 1065-6995 .- 1095-8355. ; 31:4 SPEC. ISS., s. 360-365
-
Journal article (peer-reviewed)abstract
- Alpha-actinins are actin-binding proteins of non-muscle cells, which can participate in the regulation of transcription factor activity. We describe the distribution of a-actinin-1 and -4 depending on different actin cytoskeleton formed as a result of cell adhesion to extracellular matrix proteins, such as fibronectin and laminin 2/4. Immunofluorescent studies show a difference in the distribution of a-actinin and -4. Both isoforms localise along stress-fibres, but a-actinin-1 localises in the perinuclear region more abundantly than a-actinin-4. Western blot analysis demonstrated existence of truncated forms of both isoforms. Truncated a-actinin-1 appears in cells spread on fibronectin or laminin. Cell spreading also correlated with more tight association of a-actinin-4 with chromatin. Basing on our previous finding of an interaction of a-actinin-4 with p65 subunit of the NF-?B, we checked the possible influence of immobilised ligands on its redistribution in nuclear complexes containing p65. a-Actinin-4 seems to be present in some but not all nuclear complexes containing p65. Immobilised ligands may affect the interaction of a-actinin-4/p65 complexes with chromatin. The data suggest that adhesion to extra-cellular matrix may interfere in cellular reactions mediated by a-actinin-1 and -4. © 2007 International Federation for Cell Biology.
|
|
| 3. |
|
|
| 4. |
|
|
| 5. |
- Magnusson, Kerstin, et al.
(author)
-
Effect of dentifrices with antimicrobial agents on mutans streptococci in saliva and approximal dental plaque in orthodontic patients.
- 2007
-
In: Oral health & preventive dentistry. - 1602-1622. ; 5:3, s. 223-7
-
Journal article (peer-reviewed)abstract
- PURPOSE: The aim of the present investigation was to study the effect of daily use of fluoride dentifrices containing various antimicrobial agents on mutans streptococci (MS) in saliva and approximal dental plaque. MATERIALS AND METHODS: Fifty-nine healthy adolescents, 12-14 years old, undergoing orthodontic treatment with fixed appliances and harbouring high levels of MS in saliva and preferably also in interdental plaque, were randomly distributed into four groups, using dentifrices with: 1) zinc lactate (n = 16), 2) amine fluoride-stannous fluoride (n = 13), 3) triclosan (n = 15), and 4) no antimicrobial agent (control; n = 15). Changes of MS scores versus baseline were determined after 1, 3 and 6 months, using the Dentocult SM Strip mutans test. RESULTS: At the 6-month sampling occasion, the subjects using dentifrice with either amine fluoride-stannous fluoride or triclosan showed a tendency to lower MS scores in interdental plaque (p < 0.05). In saliva and in the 1- and 3-month plaque samples, no changes of MS were detected in any of the four groups. CONCLUSION: This 6-month clinical study showed that dentifrices with various antimicrobial agents only result in small or no changes of the MS scores in saliva and approximal dental plaque in orthodontic patients.
|
|
| 6. |
- Magnusson, Maria K, 1972, et al.
(author)
-
Adenovirus 5 vector genetically re-targeted by an Affibody molecule with specificity for tumor antigen HER2/neu.
- 2007
-
In: Cancer gene therapy. - : Springer Science and Business Media LLC. - 0929-1903 .- 1476-5500. ; 14:5, s. 468-79
-
Journal article (peer-reviewed)abstract
- In order to use adenovirus (Ad) type 5 (Ad5) for cancer gene therapy, Ad needs to be de-targeted from its native receptors and re-targeted to a tumor antigen. A limiting factor for this has been to find a ligand that (i) binds a relevant target, (ii) is able to fold correctly in the reducing environment of the cytoplasm and (iii) when incorporated at an optimal position on the virion results in a virus with a low physical particle to plaque-forming units ratio to diminish the viral load to be administered to a future patient. Here, we present a solution to these problems by producing a genetically re-targeted Ad with a tandem repeat of the HER2/neu reactive Affibody molecule (ZH) in the HI-loop of a Coxsackie B virus and Ad receptor (CAR) binding ablated fiber genetically modified to contain sequences for flexible linkers between the ZH and the knob sequences. ZH is an Affibody molecule specific for the extracellular domain of human epidermal growth factor receptor 2 (HER2/neu) that is overexpressed in inter alia breast and ovarian carcinomas. The virus presented here exhibits near wild-type growth characteristics, infects cells via HER2/neu instead of CAR and represents an important step toward the development of genetically re-targeted adenoviruses with clinical relevance.
|
|
| 7. |
- Magnusson, Åsa, et al.
(author)
-
Carbon-14 levels in the vicinity of the Lithuanian nuclear power plant Ignalina
- 2007
-
In: Nuclear Instruments & Methods in Physics Research. Section B: Beam Interactions with Materials and Atoms. - : Elsevier BV. - 0168-583X. ; 259:1, s. 530-535
-
Journal article (peer-reviewed)abstract
- Carbon-14 levels in the vicinity of the Lithuanian nuclear power plant Ignalina have been investigated. During 2001-2004, approximately 70 samples were collected and analysed using accelerator mass spectrometry. The study included samples of leaves, grass, moss, soil and aquatic plants, covering a distance up to 32 km from the power plant. The highest C-14 specific activities were found in soil samples from moss-covered sites close to the power plant, probably indicating the release of particulate material. The results are compared with those from studies around other types of reactors also investigated within the project. (c) 2007 Elsevier B.V. All rights reserved.
|
|
| 8. |
|
|
| 9. |
- Pivoriunas, A., et al.
(author)
-
PI 3-K signaling pathway suppresses PMA-induced expression of p21WAF1/ Cip1 in human leukemia cells
- 2007
-
In: Molecular and Cellular Biochemistry. - : Springer Science and Business Media LLC. - 0300-8177 .- 1573-4919. ; 302:1-2
-
Journal article (peer-reviewed)abstract
- Despite the understanding of the importance of phosphoinositide 3-kinase (PI 3-K) signaling pathway in the regulation of cellular proliferation, little is known about its role during phorbol 12-myristate 13-acetate (PMA)-induced differentiation in human leukemia cells. Here, we report a novel finding that PI 3-K inhibition by LY294002 significantly increases p21WAF1/Cip1 expression in PMA-stimulated human leukemia cells NB4 and THP1. LY294002 potentiated expression of p21WAF1/Cip1 via a p53-independent mechanism and did not affect mitogen activated protein kinase (MAPK) activation. Electrophoretic mobility shift (EMSA) experiments revealed that blocking of PI 3-K was associated with increased binding of transcription factor Sp1 to the PMA-responsive sites on the p21WAF1/Cip1 promoter. Pretreatment with rapamycin, an inhibitor of mTOR kinase, decreased the expression of p21WAF1/Cip1 protein in PMA-stimulated NB4 cells. The level of PMA-induced p21WAF1/ Cip1 protein expression was lower in NB4 cells overexpressing wild type protein kinase C ? (PKC ?) compared to those transfected with empty vector or with kinase inactive PKC ?. Sp1 binding to the p21WAF1/Cip1 promoter was completely lost in a wild type PKC ? overexpressing and PMA-stimulated NB4 cells. We demonstrate that PI 3-K signaling pathway suppresses PMA-induced expression of p21WAF1/Cip1 in human leukemia cells, and that this effect is partly mediated by PKC ?. © Springer Science+Business Media, LLC 2007.
|
|
| 10. |
- Sahlin, Charlotte, et al.
(author)
-
The Arctic Alzheimer mutation favors intracellular amyloid-beta production by making amyloid precursor protein less available to alpha-secretase
- 2007
-
In: Journal of Neurochemistry. - : Wiley. - 0022-3042 .- 1471-4159. ; 101:3, s. 854-862
-
Journal article (peer-reviewed)abstract
- Mutations within the amyloid-β (Aβ) domain of the amyloid precursor protein (APP) typically generate hemorrhagic strokes and vascular amyloid angiopathy. In contrast, the Arctic mutation (APP E693G) results in Alzheimer's disease. Little is known about the pathologic mechanisms that result from the Arctic mutation, although increased formation of Aβ protofibrils in vitro and intraneuronal Aβ aggregates in vivo suggest that early steps in the amyloidogenic pathway are facilitated. Here we show that the Arctic mutation favors proamyloidogenic APP processing by increased β-secretase cleavage, as demonstrated by altered levels of N- and C-terminal APP fragments. Although the Arctic mutation is located close to the α-secretase site, APP harboring the Arctic mutation is not an inferior substrate to a disintegrin and metalloprotease-10, a major α-secretase. Instead, the localization of Arctic APP is altered, with reduced levels at the cell surface making Arctic APP less available for α-secretase cleavage. As a result, the extent and subcellular location of Aβ formation is changed, as revealed by increased Aβ levels, especially at intracellular locations. Our findings suggest that the unique clinical symptomatology and neuropathology associated with the Arctic mutation, but not with other intra-Aβ mutations, could relate to altered APP processing with increased steady-state levels of Arctic Aβ, particularly at intracellular locations.
|
|
