| 1. |
- Berg, Aase, et al.
(författare)
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Complement Activation Correlates With Disease Severity and Contributes to Cytokine Responses in Plasmodium falciparum Malaria
- 2015
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Ingår i: The Internet Journal of Infectious Diseases. - : Oxford University Press (OUP). - 1528-8366 .- 0022-1899 .- 1537-6613. ; 212:11, s. 1835-1840
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Tidskriftsartikel (refereegranskat)abstract
- The impact of complement activation and its possible relation to cytokine responses during malaria pathology was investigated in plasma samples from patients with confirmed Plasmodium falciparum malaria and in human whole-blood specimens stimulated with malaria-relevant agents ex vivo. Complement was significantly activated in the malaria cohort, compared with healthy controls, and was positively correlated with disease severity and with certain cytokines, in particular interleukin 8 (IL-8)/CXCL8. This was confirmed in ex vivo-stimulated blood specimens, in which complement inhibition significantly reduced IL-8/CXCL8 release. P. falciparum malaria is associated with systemic complement activation and complement-dependent release of inflammatory cytokines, of which IL-8/CXCL8 is particularly prominent.
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| 2. |
- Burström, Lage, 1954-, et al.
(författare)
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Acute effects of vibration on thermal perception thresholds
- 2006
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Ingår i: Diagnosis of injuries caused by hand-transmitted vibration - 2nd International workshop, Göteborg, 2006. - : Springer Science and Business Media LLC.
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Konferensbidrag (refereegranskat)abstract
- Objective This study focuses on the acute effects of vibration and how vibrations influence the measures of the thermal perception thresholds during different vibration magnitudes, frequencies, and durations.Methods The fingers of ten healthy subjects, five males and five females, were exposed to vibration under 16 conditions with a combination of different frequency, intensity and exposure time. The vibration frequency was 31.5 and 125 Hz and exposure lasted between 2 and 16 min. The energy-equivalent frequency weighted acceleration, according to ISO 5349-1, for the experimental time of 16 min was 2.5 or 5.0 m/s(2) (r.m.s.), corresponding to a 8-h equivalent acceleration, A(8) of 0.46 and 0.92 m/s(2), respectively. A measure of the thermal perception of cold and warmth was conducted before the different exposures to vibration. Immediately after the vibration exposure the acute effect was measured continuously on the exposed index finger for the first 75 s, followed by 30 s of measures at every minute for a maximum of 10 min. If the subject's thermal thresholds had not recovered, the measures continued for a maximum of 30 min with measurements taken every 5 min.Results For all experimental conditions and 30 s after exposure, the mean changes of the thresholds compared with the pre-test were found to be 0.05 and -0.67C for the warmth and cold thresholds, respectively. The effect of the vibration exposure was only significant on the cold threshold and only for the first minute after exposure when the threshold was decreased. The warmth threshold was not significantly affected at all. The frequency and the exposure time of the vibration stimuli had no significant influence on the perception thresholds for the sensation of cold or warmth. Increased equivalent frequency weighted acceleration resulted in a significant decrease of the subjects' cold threshold, not the warmth. The thresholds were unaffected when changes in the vibration magnitude were expressed as the frequency weighted acceleration or the unweighted acceleration.Conclusion When testing for the thermotactile thresholds, exposure to vibration on the day of a test might influence the results. Until further knowledge is obtained the previous praxis of 2 h avoidance of vibration exposure before assessment is recommended.
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| 3. |
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| 4. |
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| 5. |
- Barker, Abigail, et al.
(författare)
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Unravelling the Crustal Architecture of Cape Verde from the Seamount Xenolith Record
- 2019
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Ingår i: Minerals. - : MDPI. - 2075-163X. ; 9:2
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Tidskriftsartikel (refereegranskat)abstract
- The Cape Verde oceanic plateau hosts 10 islands and 11 seamounts and provides an extensive suite of alkaline lavas and pyroclastic rocks. The volcanic rocks host a range of crustal and mantle xenoliths. These xenoliths provide a spectrum of lithologies available to interact with magma during transport through the lithospheric mantle and crust. We explore the origin and depth of formation of crustal xenoliths to develop a framework of magma-crust interaction and a model for the crustal architecture beneath the Cape Verde oceanic plateau. The host lavas are phononephelinites to phonolites and the crustal xenoliths are mostly mafic plutonic assemblages with one sedimentary xenolith. REE profiles of clinopyroxene in the host lavas are light rare-earth element (LREE) enriched whereas clinopyoxene from the plutonic xenoliths are LREE depleted. Modelling of REE melt compositions indicates the plutonic xenoliths are derived from mid-ocean ridge basalt (MORB)-type ocean crust. Thermobarometry indicates that clinopyroxene in the host lavas formed at depths of 17 to 46 km, whereas those in the xenoliths formed at 5 to 20 km. This places the depth of origin of the plutonic xenoliths in the oceanic crust. Therefore, the xenoliths trace magma-crust interaction to the MORB oceanic crust and overlying sediments located beneath the Cape Verde oceanic plateau.
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| 6. |
- Berg, Ina, 1982-, et al.
(författare)
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Curcumin alleviates Aβ indcuced neurotoxicity and vice versa without removing amyloid deposits in transgenic Drosophila
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Annan publikation (övrigt vetenskapligt/konstnärligt)abstract
- Curcumin has been proposed to facilitate clearance of toxic amyloid formed by the Aβ peptide. To further address this notion, different concentrations of curcumin were tried for its effects in various Drosophila Alzheimer’s disease (AD) models. This study entailed five different Drosophila AD models (four Aβ expressing lines, and one tau expressing line), expressing the AD associated proteins using the Gal4/UAS system. These were assayed for several aspects of neurological impairment, including survival, climbing behavior, as well as locomotor activity. In addition, amyloid deposition was assessed by histological analysis. Curcumin treatment substantially prolonged the lifespan and improved climbing and locomotor activity for flies with severe disease geneotypes (Aβ1-42 E22G and double expressing Aβ1-42). In comparison, curcumin feeding of control flies resulted in a concentration-dependent shortened lifespan, whereas no such toxic side effects were found for AD genotypes with a mild phenotype (single expressors of Aβ1-40 and Aβ1-42). All flies expressing Aβ and tau displayed a higher total locomotor activity, and a continuation of the activity over a larger number of hours upon curcumin treatment. Unexpectedly, no change in tissue amyloid deposition upon curcumin treatment was observed. In vitro fibrillation of Aβ1-42, followed by Western blot and transmission electron microscopy in the presence and absence of curcumin, displayed enhanced fibrillation into large aggregates and decreased population of oligomers in curcumin samples. The decrease in oligomer formation by curcumin may explain why it increases the lifespan and activity without removing of the amyloid deposits seen in tissues. We also suggest that Aβ, at least in the context of Drosophila, functions as a chemical detoxifier sequestering curcumin and thereby mitigating its toxicity.
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| 7. |
- Berg, Ina, 1982-, et al.
(författare)
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Efficient imaging of amyloid deposits in Drosophila models of human amyloidoses
- 2010
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Ingår i: Nature Protocols. - : Macmillan Publishers Ltd.. - 1754-2189 .- 1750-2799. ; 5:5, s. 935-944
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Tidskriftsartikel (refereegranskat)abstract
- Drosophila melanogaster is emerging as an important model system for neurodegenerative disease research. In this protocol, we describe an efficient method for imaging amyloid deposits in the Drosophila brain, by the use of a luminescent-conjugated oligothiophene (lco), p-Ftaa polymer probe. We also demonstrate the feasibility of co-staining with antibodies and compare the lco staining with standard amyloid-specific probes. the lco protocol enables high-resolution imaging of several different protein aggregates, such as aβ1-42, aβ1-42e22G, transthyretin V30M and human tau, in the Drosophila brain. aβ and tau aggregates could also be distinguished from each other because of distinct lco emission spectra. Furthermore, this protocol enables threedimensional brain mapping of amyloid distribution in whole-mount Drosophila brains. the use of p-Ftaa combined with other probes, antibodies and/or dyes will aid the rapid characterization of various amyloid deposits in the rapidly growing number of Drosophila models of neurodegenerative diseases.
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| 8. |
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| 9. |
- Bivik, Caroline, et al.
(författare)
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Novel Genes Involved in Controlling Specification of Drosophila FMRFamide Neuropeptide Cells
- 2015
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Ingår i: Genetics. - : Genetics Society of America. - 0016-6731 .- 1943-2631. ; 200:4, s. 1229-1244
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Tidskriftsartikel (refereegranskat)abstract
- The expression of neuropeptides is often extremely restricted in the nervous system, making them powerful markers for addressing cell specification . In the developing Drosophila ventral nerve cord, only six cells, the Ap4 neurons, of some 10,000 neurons, express the neuropeptide FMRFamide (FMRFa). Each Ap4/FMRFa neuron is the last-born cell generated by an identifiable and well-studied progenitor cell, neuroblast 5-6 (NB5-6T). The restricted expression of FMRFa and the wealth of information regarding its gene regulation and Ap4 neuron specification makes FMRFa a valuable readout for addressing many aspects of neural development, i.e., spatial and temporal patterning cues, cell cycle control, cell specification, axon transport, and retrograde signaling. To this end, we have conducted a forward genetic screen utilizing an Ap4-specific FMRFa-eGFP transgenic reporter as our readout. A total of 9781 EMS-mutated chromosomes were screened for perturbations in FMRFa-eGFP expression, and 611 mutants were identified. Seventy-nine of the strongest mutants were mapped down to the affected gene by deficiency mapping or whole-genome sequencing. We isolated novel alleles for previously known FMRFa regulators, confirming the validity of the screen. In addition, we identified novel essential genes, including several with previously undefined functions in neural development. Our identification of genes affecting most major steps required for successful terminal differentiation of Ap4 neurons provides a comprehensive view of the genetic flow controlling the generation of highly unique neuronal cell types in the developing nervous system.
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| 10. |
- Ceasar (Berg), Ina, et al.
(författare)
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Curcumin Promotes A-beta Fibrillation and Reduces Neurotoxicity in Transgenic Drosophila
- 2012
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Ingår i: PLOS ONE. - : Public Library of Science. - 1932-6203. ; 7:2
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Tidskriftsartikel (refereegranskat)abstract
- The pathology of Alzheimers disease (AD) is characterized by the presence of extracellular deposits of misfolded and aggregated amyloid-beta (A beta) peptide and intraneuronal accumulation of tangles comprised of hyperphosphorylated Tau protein. For several years, the natural compound curcumin has been proposed to be a candidate for enhanced clearance of toxic A beta amyloid. In this study we have studied the potency of feeding curcumin as a drug candidate to alleviate A beta toxicity in transgenic Drosophila. The longevity as well as the locomotor activity of five different AD model genotypes, measured relative to a control line, showed up to 75% improved lifespan and activity for curcumin fed flies. In contrast to the majority of studies of curcumin effects on amyloid we did not observe any decrease in the amount of A beta deposition following curcumin treatment. Conformation-dependent spectra from p-FTAA, a luminescent conjugated oligothiophene bound to A beta deposits in different Drosophila genotypes over time, indicated accelerated pre-fibrillar to fibril conversion of A beta(1-42) in curcumin treated flies. This finding was supported by in vitro fibrillation assays of recombinant A beta(1-42). Our study shows that curcumin promotes amyloid fibril conversion by reducing the pre-fibrillar/oligomeric species of A beta, resulting in a reduced neurotoxicity in Drosophila.
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