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Svensson, Lovisa
Publications (10 of 16) Show all publications
Bunse, C., Lundin, D., Karlsson, C. M. G., Akram, N., Vila-Costa, M., Palovaara, J., . . . Pinhassi, J. (2016). Response of marine bacterioplankton pH homeostasis gene expression to elevated CO2. Nature Climate Change, 6(5), 483-487
Open this publication in new window or tab >>Response of marine bacterioplankton pH homeostasis gene expression to elevated CO2
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2016 (English)In: Nature Climate Change, ISSN 1758-678X, E-ISSN 1758-6798, Vol. 6, no 5, p. 483-487Article in journal (Refereed) Published
Abstract [en]

Human-induced ocean acidification impacts marine life. Marine bacteria are major drivers of biogeochemical nutrient cycles and energy fluxes1; hence, understanding their performance under projected climate change scenarios is crucial for assessing ecosystem functioning. Whereas genetic and physiological responses of phytoplankton to ocean acidification are being disentangled2, 3, 4, corresponding functional responses of bacterioplankton to pH reduction from elevated CO2 are essentially unknown. Here we show, from metatranscriptome analyses of a phytoplankton bloom mesocosm experiment, that marine bacteria responded to lowered pH by enhancing the expression of genes encoding proton pumps, such as respiration complexes, proteorhodopsin and membrane transporters. Moreover, taxonomic transcript analysis showed that distinct bacterial groups expressed different pH homeostasis genes in response to elevated CO2. These responses were substantial for numerous pH homeostasis genes under low-chlorophyll conditions (chlorophyll a <2.5 μg l−1); however, the changes in gene expression under high-chlorophyll conditions (chlorophyll a >20 μg l−1) were low. Given that proton expulsion through pH homeostasis mechanisms is energetically costly, these findings suggest that bacterioplankton adaptation to ocean acidification could have long-term effects on the economy of ocean ecosystems.

National Category
Microbiology Ecology Climate Research
Research subject
Ecology, Microbiology
Identifiers
urn:nbn:se:lnu:diva-49969 (URN)10.1038/nclimate2914 (DOI)000375125200015 ()2-s2.0-84964949342 (Scopus ID)
Projects
EcoChange
Available from: 2016-02-29 Created: 2016-02-29 Last updated: 2018-10-24Bibliographically approved
Bonnedahl, J., Stedt, J., Waldenström, J., Svensson, L., Drobni, M. & Olsen, B. (2015). Comparison of Extended-Spectrum beta-Lactamase (ESBL) CTX-M Genotypes in Franklin Gulls from Canada and Chile. PLoS ONE, 10(10), Article ID e0141315.
Open this publication in new window or tab >>Comparison of Extended-Spectrum beta-Lactamase (ESBL) CTX-M Genotypes in Franklin Gulls from Canada and Chile
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2015 (English)In: PLoS ONE, ISSN 1932-6203, E-ISSN 1932-6203, Vol. 10, no 10, article id e0141315Article in journal (Refereed) Published
Abstract [en]

Migratory birds have been suggested to contribute to long-distance dispersal of antimicrobial resistant bacteria, but tests of this hypothesis are lacking. In this study we determined resistance profiles and genotypes of ESBL-producing bacteria in randomly selected Escherichia coli from Franklin's gulls (Leucophaeus pipixcan) at breeding sites in Canada and compared with similar data from the gulls' wintering grounds in Chile. Resistant E. coli phenotypes were common, most notably to ampicillin (30.1%) and cefadroxil (15.1%). Furthermore, 17.0% of the gulls in Canada carried ESBL producing bacteria, which is higher than reported from human datasets from the same country. However, compared to gulls sampled in Chile (30.1%) the prevalence of ESBL was much lower. The dominant ESBL variants in Canada were bla(CTX-M-14) and bla(CTX-M-15) and differed in proportions to the data from Chile. We hypothesize that the observed differences in ESBL variants are more likely linked to recent exposure to bacteria from anthropogenic sources, suggesting high local dissemination of resistant bacteria both at breeding and non-breeding times rather than a significant trans-hemispheric exchange through migrating birds.

National Category
Microbiology
Research subject
Ecology, Zoonotic Ecology
Identifiers
urn:nbn:se:lnu:diva-47229 (URN)10.1371/journal.pone.0141315 (DOI)000363309200092 ()26496629 (PubMedID)2-s2.0-84949488537 (Scopus ID)
Available from: 2015-11-16 Created: 2015-11-13 Last updated: 2019-05-20Bibliographically approved
Demirel, I., Vumma, R., Mohlin, C., Svensson, L., Säve, S. & Persson, K. (2012). Nitric Oxide Activates IL-6 Production and Expression in Human Renal Epithelial Cells. American Journal of Nephrology, 36(6), 524-530
Open this publication in new window or tab >>Nitric Oxide Activates IL-6 Production and Expression in Human Renal Epithelial Cells
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2012 (English)In: American Journal of Nephrology, ISSN 0250-8095, E-ISSN 1421-9670, Vol. 36, no 6, p. 524-530Article in journal (Refereed) Published
Abstract [en]

Background/Aims: Increased nitric oxide (NO) production or inducible form of NO synthase activity have been documented in patients suffering from urinary tract infection (UTI), but the role of NO in this infection is unclear. We investigated whether NO can affect the host response in human renal epithelial cells by modulating IL-6 production and mRNA expression. Methods: The human renal epithelial cell line A498 was infected with a uropathogenic Escherichia coli (UPEC) strain and/or the NO donor DETA/NO. The IL-6 production and mRNA expression were evaluated by ELISA and real-time RT-PCR. IL-6 mRNA stability was evaluated by analyzing mRNA degradation by real-time RT-PCR. Results: DETA/NO caused a significant (p < 0.05) increase in IL-6 production. Inhibitors of p38 MAPK and ERK1/2 signaling, but not JNK, were shown to significantly suppress DETA/NO-induced IL-6 production. UPEC-induced IL-6 production was further increased (by 73 +/- 23%, p < 0.05) in the presence of DETA/NO. The IL-6 mRNA expression increased 2.1 +/- 0.17-fold in response to DETA/NO, while the UPEC-evoked increase was pronounced (20 +/- 4.5-fold). A synergistic effect of DETA/NO on UPEC-induced IL-6 expression was found (33 +/- 7.2-fold increase). The IL-6 mRNA stability studies showed that DETA/NO partially attenuated UPEC-induced degradation of IL-6 mRNA. Conclusions: NO was found to stimulate IL-6 in renal epithelial cells through p38 MAPK and ERK1/2 signaling pathways and also to increase IL-6 mRNA stability in UPEC-infected cells. This study proposes a new role for NO in the host response during UTI by modulating the transcription and production of the cytokine IL-6. Copyright (C) 2012 S. Karger AG, Basel

Keywords
Nitric oxide, Urinary tract infections, IL-6, MAPK signaling, Renal epithelial cells
National Category
Urology and Nephrology Immunology in the medical area
Research subject
Natural Science, Biomedical Sciences
Identifiers
urn:nbn:se:lnu:diva-24513 (URN)10.1159/000345351 (DOI)000312916200004 ()2-s2.0-84869889861 (Scopus ID)
Available from: 2013-02-22 Created: 2013-02-22 Last updated: 2018-01-11Bibliographically approved
Axelsson Olsson, D., Olofsson, J., Svensson, L., Griekspoor, P., Waldenström, J., Ellström, P. & Olsen, B. (2010). Amoebae and algae can prolong the survival of Campylobacter species in co-culture. Experimental parasitology, 126, 59-64
Open this publication in new window or tab >>Amoebae and algae can prolong the survival of Campylobacter species in co-culture
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2010 (English)In: Experimental parasitology, ISSN 0014-4894, E-ISSN 1090-2449, Vol. 126, p. 59-64Article in journal (Refereed) Published
Abstract [en]

Several species of free-living amoebae can cause disease in humans. However, in addition to the direct pathogenicity of e.g. Acanthamoebae and Naegleria species, they are recognized as environmental hosts, indirectly involved in the epidemiology of many pathogenic bacteria. Although several studies have demonstrated intracellular survival of many different bacteria in these species, the extent of such interactions as well as the implications for the epidemiology of the bacterial species involved, are largely unknown and probably underestimated. In this study, we evaluated eight different unicellular eukaryotic organisms, for their potential to serve as environmental hosts for Campylobacter species. These organisms include four amoebozoas (Acanthamoeba polyphaga, Acanthamoeba castellanii, Acanthamoeba rhysodes and Hartmanella vermiformis), one alveolate (Tetrahymena pyriformis), one stramenopile (Dinobryon sertularia), one eugoenozoa (Euglena gracilis) and one heterolobosea (Naegleria americana). Campylobacter spp. including Campylobacter jejuni, Campylobacter coli and Campylobacter lari are the most common cause of gastroenteritis in the western world. Survival and replication of these three species as well as Campylobacter hyointestinalis were assessed in co-cultures with the eukaryotic organisms. Campylobacter spp. generally survived longer in co-cultures, compared to when incubated in the corresponding growth media. The eukaryotic species that best promoted bacterial survival was the golden algae D. sertularia. Three species of amoebozoas, of the genus Acanthamoeba promoted both prolonged survival and replication of Campylobacter spp. The high abundance in lakes, ponds and water distribution networks of these organisms indicate that they might have a role in the epidemiology of campylobacteriosis, possibly contributing to survival and dissemination of these intestinal pathogens to humans and other animals. The results suggest that not only C. jejuni, but a variety of Campylobacter spp. can interact with different eukaryotic unicellular organisms.

National Category
Infectious Medicine
Research subject
Natural Science, Biomedical Sciences
Identifiers
urn:nbn:se:lnu:diva-7086 (URN)10.1016/j.exppara.2009.12.016 (DOI)000278917000012 ()
Available from: 2010-08-10 Created: 2010-08-10 Last updated: 2017-12-12Bibliographically approved
Waldenström, J., Axelsson Olsson, D., Olsen, B., Hasselquist, D., Griekspoor, P., Jansson, L., . . . Ellström, P. (2010). Campylobacter jejuni colonization in wild birds: Results from an infection experiment. PLoS ONE, 5(2), Article ID e9082.
Open this publication in new window or tab >>Campylobacter jejuni colonization in wild birds: Results from an infection experiment
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2010 (English)In: PLoS ONE, ISSN 1932-6203, E-ISSN 1932-6203, Vol. 5, no 2, article id e9082Article in journal (Refereed) Published
Abstract [en]

Campylobacter jejuni is a common cause of bacterial gastroenteritis in most parts of the world. The bacterium has a broad host range and has been isolated from many animals and environments. To investigate shedding patterns and putative effects on an avian host, we developed a colonization model in which a wild bird species, the European Robin Erithacus rubecula, was inoculated orally with C. jejuni from either a human patient or from another wild bird species, the Song Thrush Turdus philomelos. These two isolates were genetically distinct from each other and provoked very different host responses. The Song Thrush isolate colonized all challenged birds and colonization lasted 6.8 days on average. Birds infected with this isolate also showed a transient but significant decrease in body mass. The human isolate did not colonize the birds and could be detected only in the feces of the birds shortly after inoculation. European Robins infected with the wild bird isolate generated a specific antibody response to C. jejuni membrane proteins from the avian isolate, which also was cross-reactive to membrane proteins of the human isolate. In contrast, European Robins infected with the human isolate did not mount a significant response to bacterial membrane proteins from either of the two isolates. The difference in colonization ability could indicate host adaptations.

National Category
Microbiology
Research subject
Ecology, Zoonotic Ecology
Identifiers
urn:nbn:se:lnu:diva-7083 (URN)10.1371/journal.pone.0009082 (DOI)2-s2.0-77949373747 (Scopus ID)
Available from: 2010-08-10 Created: 2010-08-10 Last updated: 2017-12-12Bibliographically approved
Axelsson Olsson, D., Svensson, L., Olofsson, J., Salomon, P., Waldenström, J., Ellström, P. & Olsen, B. (2010). Increase in Acid Tolerance of Campylobacter jejuni through Coincubation with Amoebae. Applied and Environmental Microbiology, 76(13), 4194-4200
Open this publication in new window or tab >>Increase in Acid Tolerance of Campylobacter jejuni through Coincubation with Amoebae
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2010 (English)In: Applied and Environmental Microbiology, ISSN 0099-2240, E-ISSN 1098-5336, Vol. 76, no 13, p. 4194-4200Article in journal (Refereed) Published
Abstract [en]

Campylobacter jejuni is a recognized and common gastrointestinal pathogen in most parts of the world. Human infections are often food borne, and the bacterium is frequent among poultry and other food animals. However, much less is known about the epidemiology of C. jejuni in the environment and what mechanisms the bacterium depends on to tolerate low pH. The sensitive nature of C. jejuni stands in contrast to the fact that it is difficult to eradicate from poultry production, and even more contradictory is the fact that the bacterium is able to survive the acidic passage through the human stomach. Here we expand the knowledge on C. jejuni acid tolerance by looking at protozoa as a potential epidemiological pathway of infection. Our results showed that when C. jejuni cells were coincubated with Acanthamoeba polyphaga in acidified phosphate-buffered saline (PBS) or tap water, the bacteria could tolerate pHs far below those in their normal range, even surviving at pH 4 for 20 h and at pH 2 for 5 h. Interestingly, moderately acidic conditions (pH 4 and 5) were shown to trigger C. jejuni motility as well as to increase adhesion/internalization of bacteria into A. polyphaga. Taken together, the results suggest that protozoa may act as protective hosts against harsh conditions and might be a potential risk factor for C. jejuni infections. These findings may be important for our understanding of C. jejuni passage through the gastrointestinal tract and for hygiene practices used in poultry settings.

National Category
Microbiology
Research subject
Ecology, Microbiology
Identifiers
urn:nbn:se:lnu:diva-7087 (URN)10.1128/AEM.01219-09 (DOI)2-s2.0-77954258414 (Scopus ID)
Available from: 2010-08-10 Created: 2010-08-10 Last updated: 2017-12-12Bibliographically approved
Jourdain, E., Gunnarsson, G., Wahlgren, J., Latorre-Margalef, N., Bröjer, C., Sahlin, S., . . . Olsen, B. (2010). Influenza Virus in a Natural Host, the Mallard: Experimental Infection Data. PLoS ONE, 5(1), Article ID e8935.
Open this publication in new window or tab >>Influenza Virus in a Natural Host, the Mallard: Experimental Infection Data
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2010 (English)In: PLoS ONE, ISSN 1932-6203, E-ISSN 1932-6203, Vol. 5, no 1, article id e8935Article in journal (Refereed) Published
Abstract [en]

Wild waterfowl, particularly dabbling ducks such as mallards (Anas platyrhynchos), are considered the main reservoir of low-pathogenic avian influenza viruses (LPAIVs). They carry viruses that may evolve and become highly pathogenic for poultry or zoonotic. Understanding the ecology of LPAIVs in these natural hosts is therefore essential. We assessed the clinical response, viral shedding and antibody production of juvenile mallards after intra-esophageal inoculation of two LPAIV subtypes previously isolated from wild congeners. Six ducks, equipped with data loggers that continually monitored body temperature, heart rate and activity, were successively inoculated with an H7N7 LPAI isolate (day 0), the same H7N7 isolate again (day 21) and an H5N2 LPAI isolate (day 35). After the first H7N7 inoculation, the ducks remained alert with no modification of heart rate or activity. However, body temperature transiently increased in four individuals, suggesting that LPAIV strains may have minor clinical effects on their natural hosts. The excretion patterns observed after both reinoculations differed strongly from those observed after the primary H7N7 inoculation, suggesting that not only homosubtypic but also heterosubtypic immunity exist. Our study suggests that LPAI infection has minor clinically measurable effects on mallards and that mallard ducks are able to mount immunological responses protective against heterologous infections. Because the transmission dynamics of LPAIVs in wild populations is greatly influenced by individual susceptibility and herd immunity, these findings are of high importance. Our study also shows the relevance of using telemetry to monitor disease in animals.

Keywords
A VIRUS, ANAS-PLATYRHYNCHOS, FEBRILE RESPONSE, IMMUNE-RESPONSE, NORTHERN EUROPE, WILD BIRDS, HEART-RATE, DUCKS, H5N1, REPLICATION
National Category
Microbiology in the medical area Microbiology in the medical area
Research subject
Ecology, Zoonotic Ecology; Ecology, Microbiology; Biomedical Sciences, Virology
Identifiers
urn:nbn:se:lnu:diva-2151 (URN)10.1371/journal.pone.0008935 (DOI)2-s2.0-77952481249 (Scopus ID)
Available from: 2010-04-06 Created: 2010-04-06 Last updated: 2018-01-12Bibliographically approved
Svensson, L., Poljakovic, M., Säve, S., Gilberthorpe, N., Schön, T., Strid, S., . . . Persson, K. (2010). Role of flavohemoglobin in combating nitrosative stress in uropathogenic Escherichia coli – implications for urinary tract infection. Microbial Pathogenesis, 49(3), 59-66
Open this publication in new window or tab >>Role of flavohemoglobin in combating nitrosative stress in uropathogenic Escherichia coli – implications for urinary tract infection
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2010 (English)In: Microbial Pathogenesis, ISSN 0882-4010, E-ISSN 1096-1208, Vol. 49, no 3, p. 59-66Article in journal (Refereed) Published
Abstract [en]

During the course of urinary tract infection (UTI) nitric oxide (NO) is generated as part of the host response. This study investigates the significance of the NO-detoxifying enzyme flavohemoglobin (Hmp) in protection of uropathogenic Escherichia coli (UPEC) against nitrosative stress. An hmp (J96Δhmp) knockout mutant of UPEC strain J96 was constructed using single-gene deletion. The viability of J96Δhmp was significantly reduced (P < 0.001) compared to the wild-type strain after exposure to the NO-donor DETA/NO. The NO consumption in J96Δhmp was significantly (P < 0.001) impaired compared to J96wt. Screening UPEC isolates from patients with UTI revealed increased hmp expression in all patients. In a competition-based mouse model of UTI, the hmp mutant strain was significantly (P < 0.05) out-competed by the wild-type strain. This study demonstrates, for the first time, that Hmp contributes to the protection of UPEC against NO-mediated toxicity in vitro. In addition, hmp gene expression occurs in UPEC isolates from the infected human urinary tract and UPEC that were hmp-deficient had a reduced ability to colonize the mouse urinary tract. Taken together the results suggest that NO detoxification by Hmp may be a fitness advantage factor in UPEC, and a potentially interesting target for development of novel treatment concepts for UTI.

National Category
Microbiology in the medical area
Research subject
Natural Science, Biomedical Sciences
Identifiers
urn:nbn:se:lnu:diva-29102 (URN)10.1016/j.micpath.2010.04.001 (DOI)2-s2.0-77954660611 (Scopus ID)
Note

Ingår i avhandlingen "Nitric oxide and bacteria-host interactions in Escherichia coli urinary tract infection" under titeln "Flavohemoglobin protects uropathogenic Escherichia coli against nitrosative stress; implication for urovirulence"

Available from: 2013-09-30 Created: 2013-09-30 Last updated: 2018-10-24Bibliographically approved
Svensson, L., Säve, S. & Persson, K. (2010). The effect of nitric oxide on adherence of P-fimbriated uropathogenic Escherichia coli to human renal epithelial cells. British Journal of Urology, 105(12), 1726-1731
Open this publication in new window or tab >>The effect of nitric oxide on adherence of P-fimbriated uropathogenic Escherichia coli to human renal epithelial cells
2010 (English)In: British Journal of Urology, ISSN 0007-1331, E-ISSN 1365-2176, Vol. 105, no 12, p. 1726-1731Article in journal (Refereed) Published
Abstract [en]

OBJECTIVES

To examine the effect of nitric oxide (NO), an endogenous component of the host defence in urinary tract infection, on the adherence of P-fimbriated uropathogenic Escherichia coli (UPEC) to human renal epithelial cells.

MATERIALS AND METHODS

Two wild-type UPEC strains (AD110 and IA2) and the P-fimbriated recombinant strain HB101pPIL-75 were used. Bacteria were allowed to adhere to the human renal epithelial cell line A498 and attachment was evaluated in the absence or presence of the NO donor DETA/NONOate (1 mm). Total RNA was extracted from NO-exposed bacteria in static urine cultures, followed by semi-quantitative reverse transcription-polymerase chain reaction (RT-PCR) analysis of the papG gene that encodes the P-fimbriae adhesin PapG.

RESULTS

Bacterial adherence to A498 cells was fimbriae-dependent and the ability to agglutinate human P1 positive erythrocytes confirmed that the used strains were P-fimbriated. UPEC strains AD110 and IA2 attached by a mean of 8 bacteria/cell and 20 bacteria/cell, respectively. In the presence of DETA/NONOate, the attachment of AD110 and IA2 to A498 cells was significantly reduced by a mean (sem) of 34 (3.9)% and 45 (14)%, respectively. The expression of papG was decreased after DETA/NONOate exposure as shown by semiquantitative RT-PCR.

CONCLUSION

NO disrupted functional adhesion of P-fimbriated UPEC to kidney epithelial cells, suggesting that NO-production from epithelial cells in the urinary tract may limit bacterial colonization at the mucosal surface. The reduced adherence may involve transcriptional effects of NO on papG expression, but further studies are needed to establish the underlying mechanisms.

National Category
Microbiology in the medical area
Research subject
Natural Science, Biomedical Sciences
Identifiers
urn:nbn:se:lnu:diva-29101 (URN)10.1111/j.1464-410X.2009.08986.x (DOI)
Available from: 2013-09-30 Created: 2013-09-30 Last updated: 2018-10-24Bibliographically approved
Axelsson Olsson, D., Olofsson, J., Svensson, L., Ellström, P., Waldenström, J. & Olsen, B. (2009). Campylobacter jejuni acid tolerance increases when co-incubated with amoebae. In: : . Paper presented at CHRO 2009, 15th International Workshop on Campylobacter, Helicobacter and Related Organisms, Niigata, Japan, September 2-5th 2009.
Open this publication in new window or tab >>Campylobacter jejuni acid tolerance increases when co-incubated with amoebae
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2009 (English)Conference paper, Oral presentation with published abstract (Refereed)
Abstract [en]

Background: Although Campylobacter jejuni is a frequent cause of bacterial gastroenteritis, one of the enigmas is how thisfragile organism can survive the transit through the acid milieu of the stomach. C. jejuni is very sensitive to low pH, but cansurvive in moderately acid environment for short periods of time. We have previously shown that C. jejuni can colonize andeven replicate in different species of amoebas, thereby gaining protection from adverse environments.

Objectives: We evaluated the effects of hydrochloric acid (HCl) on C. jejuni at various pH and time intervals, to study whetherco-cultivation with amoeba influenced C.jejuni acid tolerance. The setup was chosen to mimic the acidified milieu of the humangastrointestinal tract.

Methods: Cultures of C. jejuni (CCUG 11284) were co-cultured with Acanthamoeba polyphaga in either PBS or tap wateracidified with HCl to pH 1, 2, 3 and 4. We also evaluated different treatments effect on campylobacter survival, by exposingsome bacterial samples to an acid shock and some to a slower acidification process.

Results and conclusions: We show that C. jejuni can withstand pH below the normal range of survival, when co-cultured withA. polyphaga. C. jejuni co-cultured with amoebae survived acidified conditions at pH 3 for 20 hours and pH 2 for approximately5 hours. We also found a pH increase during the experiment, which correlated with campylobacter survival. These results pointto an unknown mechanism for C.jejuni to survive at low pH levels. This could be in the form of excretion of pH-increasingsubstances and simultaneous chemotaxic orientation towards a protective host. Our results could give one possible explanationto C. jejuni survival through the low pH of the gastrointestinal tract.

National Category
Microbiology
Research subject
Ecology, Microbiology
Identifiers
urn:nbn:se:lnu:diva-55450 (URN)
Conference
CHRO 2009, 15th International Workshop on Campylobacter, Helicobacter and Related Organisms, Niigata, Japan, September 2-5th 2009
Available from: 2016-08-15 Created: 2016-08-15 Last updated: 2018-05-22Bibliographically approved
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