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Muala, Ala
Publikasjoner (10 av 22) Visa alla publikasjoner
Uski, O., Rankin, G. D., Wingfors, H., Magnusson, R., Boman, C., Muala, A., . . . Sandström, T. (2024). In vitro toxicity evaluation in A549 cells of diesel particulate matter from two different particle sampling systems and several resuspension media. Journal of Applied Toxicology
Åpne denne publikasjonen i ny fane eller vindu >>In vitro toxicity evaluation in A549 cells of diesel particulate matter from two different particle sampling systems and several resuspension media
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2024 (engelsk)Inngår i: Journal of Applied Toxicology, ISSN 0260-437X, E-ISSN 1099-1263Artikkel i tidsskrift (Fagfellevurdert) Epub ahead of print
Abstract [en]

In urban areas, inhalation of fine particles from combustion sources such as diesel engines causes adverse health effects. For toxicity testing, a substantial amount of particulate matter (PM) is needed. Conventional sampling involves collection of PM onto substrates by filtration or inertial impaction. A major drawback to those methodologies is that the extraction process can modify the collected particles and alter their chemical composition. Moreover, prior to toxicity testing, PM samples need to be resuspended, which can alter the PM sample even further. Lastly, the choice of the resuspension medium may also impact the detected toxicological responses. In this study, we compared the toxicity profile of PM obtained from two alternative sampling systems, using in vitro toxicity assays. One system makes use of condensational growth before collection in water in an impinger – BioSampler (CG-BioSampler), and the other, a Dekati® Gravimetric Impactor (DGI), is based on inertial impaction. In addition, various methods for resuspension of DGI collected PM were compared. Tested endpoints included cytotoxicity, formation of cellular reactive oxygen species, and genotoxicity. The alternative collection and suspension methods affected different toxicological endpoints. The water/dimethyl sulfoxide mixture and cell culture medium resuspended particles, along with the CG-BioSampler sample, produced the strongest responses. The water resuspended sample from the DGI appeared least toxic. CG-BioSampler collected PM caused a clear increased response in apoptotic cell death. We conclude that the CG-BioSampler PM sampler is a promising alternative to inertial impaction sampling.

sted, utgiver, år, opplag, sider
John Wiley & Sons, 2024
Emneord
apoptosis, diesel exhaust, extraction, impinger, particulate matter, reactive oxygen species, sampling, soot, toxicity
HSV kategori
Identifikatorer
urn:nbn:se:umu:diva-224261 (URN)10.1002/jat.4616 (DOI)001214370400001 ()38705171 (PubMedID)2-s2.0-85192155238 (Scopus ID)
Tilgjengelig fra: 2024-05-14 Laget: 2024-05-14 Sist oppdatert: 2024-05-14
Rahman, M., Upadhyay, S., Ganguly, K., Introna, M., Ji, J., Boman, C., . . . Palmberg, L. (2023). Comparable response following exposure to biodiesel and diesel exhaust particles in advanced multicellular human lung models. Toxics, 11(6), Article ID 532.
Åpne denne publikasjonen i ny fane eller vindu >>Comparable response following exposure to biodiesel and diesel exhaust particles in advanced multicellular human lung models
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2023 (engelsk)Inngår i: Toxics, E-ISSN 2305-6304, Vol. 11, nr 6, artikkel-id 532Artikkel i tidsskrift (Fagfellevurdert) Published
Abstract [en]

Biodiesel is considered to be a sustainable alternative for fossil fuels such as petroleum-based diesel. However, we still lack knowledge about the impact of biodiesel emissions on humans, as airways and lungs are the primary target organs of inhaled toxicants. This study investigated the effect of exhaust particles from well-characterized rapeseed methyl ester (RME) biodiesel exhaust particles (BDEP) and petro-diesel exhaust particles (DEP) on primary bronchial epithelial cells (PBEC) and macrophages (MQ). The advanced multicellular physiologically relevant bronchial mucosa models were developed using human primary bronchial epithelial cells (PBEC) cultured at air–liquid interface (ALI) in the presence or absence of THP-1 cell-derived macrophages (MQ). The experimental set-up used for BDEP and DEP exposures (18 µg/cm2 and 36 µg/cm2) as well as the corresponding control exposures were PBEC-ALI, MQ-ALI, and PBEC co-cultured with MQ (PBEC-ALI/MQ). Following exposure to both BDEP and DEP, reactive oxygen species as well as the stress protein heat shock protein 60 were upregulated in PBEC-ALI and MQ-ALI. Expression of both pro-inflammatory (M1: CD86) and repair (M2: CD206) macrophage polarization markers was increased in MQ-ALI after both BDEP and DEP exposures. Phagocytosis activity of MQ and the phagocytosis receptors CD35 and CD64 were downregulated, whereas CD36 was upregulated in MQ-ALI. Increased transcript and secreted protein levels of CXCL8, as well as IL-6 and TNF-α, were detected following both BDEP and DEP exposure at both doses in PBEC-ALI. Furthermore, the cyclooxygenase-2 (COX-2) pathway, COX-2-mediated histone phosphorylation and DNA damage were all increased in PBEC-ALI following exposure to both doses of BDEP and DEP. Valdecoxib, a COX-2 inhibitor, reduced the level of prostaglandin E2, histone phosphorylation, and DNA damage in PBEC-ALI following exposure to both concentrations of BDEP and DEP. Using physiologically relevant multicellular human lung mucosa models with human primary bronchial epithelial cells and macrophages, we found BDEP and DEP to induce comparable levels of oxidative stress, inflammatory response, and impairment of phagocytosis. The use of a renewable carbon-neutral biodiesel fuel does not appear to be more favorable than conventional petroleum-based alternative, as regards of its potential for adverse health effects.

sted, utgiver, år, opplag, sider
MDPI, 2023
Emneord
biodiesel, COX-2, DNA damage, lung, MQ-ALI, oxidative stress, particles, PBEC-ALI, petro-diesel, PGE2, phagocytosis
HSV kategori
Identifikatorer
urn:nbn:se:umu:diva-212077 (URN)10.3390/toxics11060532 (DOI)001017713500001 ()37368632 (PubMedID)2-s2.0-85163637334 (Scopus ID)
Forskningsfinansiär
Swedish Research Council, 2018-03233Swedish Fund for Research Without Animal ExperimentsSwedish Heart Lung Foundation
Tilgjengelig fra: 2023-07-17 Laget: 2023-07-17 Sist oppdatert: 2023-07-17bibliografisk kontrollert
Friberg, M., Behndig, A. F., Bosson, J., Muala, A., Barath, S., Dove, R., . . . Pourazar, J. (2023). Human exposure to diesel exhaust induces CYP1A1 expression and AhR activation without a coordinated antioxidant response. Particle and Fibre Toxicology, 20(1), Article ID 47.
Åpne denne publikasjonen i ny fane eller vindu >>Human exposure to diesel exhaust induces CYP1A1 expression and AhR activation without a coordinated antioxidant response
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2023 (engelsk)Inngår i: Particle and Fibre Toxicology, E-ISSN 1743-8977, Vol. 20, nr 1, artikkel-id 47Artikkel i tidsskrift (Fagfellevurdert) Published
Abstract [en]

Background: Diesel exhaust (DE) induces neutrophilia and lymphocytosis in experimentally exposed humans. These responses occur in parallel to nuclear migration of NF-κB and c-Jun, activation of mitogen activated protein kinases and increased production of inflammatory mediators. There remains uncertainty regarding the impact of DE on endogenous antioxidant and xenobiotic defences, mediated by nuclear factor erythroid 2-related factor 2 (Nrf2) and the aryl hydrocarbon receptor (AhR) respectively, and the extent to which cellular antioxidant adaptations protect against the adverse effects of DE.

Methods: Using immunohistochemistry we investigated the nuclear localization of Nrf2 and AhR in the epithelium of endobronchial mucosal biopsies from healthy subjects six-hours post exposure to DE (PM10, 300 µg/m3) versus post-filtered air in a randomized double blind study, as a marker of activation. Cytoplasmic expression of cytochrome P450s, family 1, subfamily A, polypeptide 1 (CYP1A1) and subfamily B, Polypeptide 1 (CYP1B1) were examined to confirm AhR activation; with the expression of aldo–keto reductases (AKR1A1, AKR1C1 and AKR1C3), epoxide hydrolase and NAD(P)H dehydrogenase quinone 1 (NQO1) also quantified. Inflammatory and oxidative stress markers were examined to contextualize the responses observed.

Results: DE exposure caused an influx of neutrophils to the bronchial airway surface (p = 0.013), as well as increased bronchial submucosal neutrophil (p < 0.001), lymphocyte (p = 0.007) and mast cell (p = 0.002) numbers. In addition, DE exposure enhanced the nuclear translocation of the AhR and increased the CYP1A1 expression in the bronchial epithelium (p = 0.001 and p = 0.028, respectively). Nuclear translocation of AhR was also increased in the submucosal leukocytes (p < 0.001). Epithelial nuclear AhR expression was negatively associated with bronchial submucosal CD3 numbers post DE (r = −0.706, p = 0.002). In contrast, DE did not increase nuclear translocation of Nrf2 and was associated with decreased NQO1 in bronchial epithelial cells (p = 0.02), without affecting CYP1B1, aldo–keto reductases, or epoxide hydrolase protein expression.

Conclusion: These in vivo human data confirm earlier cell and animal-based observations of the induction of the AhR and CYP1A1 by diesel exhaust. The induction of phase I xenobiotic response occurred in the absence of the induction of antioxidant or phase II xenobiotic defences at the investigated time point 6 h post-exposures. This suggests DE-associated compounds, such as polycyclic aromatic hydrocarbons (PAHs), may induce acute inflammation and alter detoxification enzymes without concomitant protective cellular adaptations in human airways.

sted, utgiver, år, opplag, sider
BioMed Central (BMC), 2023
Emneord
Aryl hydrocarbon receptor, Diesel exhaust, Immunohistochemistry, Oxidative stress, Xenobiotic metabolism
HSV kategori
Identifikatorer
urn:nbn:se:umu:diva-218128 (URN)10.1186/s12989-023-00559-1 (DOI)38062420 (PubMedID)2-s2.0-85178874563 (Scopus ID)
Forskningsfinansiär
Västerbotten County CouncilSwedish Heart Lung FoundationUmeå University
Tilgjengelig fra: 2023-12-15 Laget: 2023-12-15 Sist oppdatert: 2023-12-15bibliografisk kontrollert
Hansson, A., Rankin, G., Uski, O., Sehlstedt, M., Pourazar, J., Lindgren, R., . . . Muala, A. (2023). Reduced bronchoalveolar macrophage phagocytosis and cytotoxic effects after controlled short-term exposure to wood smoke in healthy humans. Particle and Fibre Toxicology, 20(1), Article ID 30.
Åpne denne publikasjonen i ny fane eller vindu >>Reduced bronchoalveolar macrophage phagocytosis and cytotoxic effects after controlled short-term exposure to wood smoke in healthy humans
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2023 (engelsk)Inngår i: Particle and Fibre Toxicology, E-ISSN 1743-8977, Vol. 20, nr 1, artikkel-id 30Artikkel i tidsskrift (Fagfellevurdert) Published
Abstract [en]

Background: Exposure to wood smoke has been shown to contribute to adverse respiratory health effects including airway infections, but the underlying mechanisms are unclear. A preceding study failed to confirm any acute inflammation or cell influx in bronchial wash (BW) or bronchoalveolar lavage (BAL) 24 h after wood smoke exposure but showed unexpected reductions in leukocyte numbers. The present study was performed to investigate responses at an earlier phase, regarding potential development of acute inflammation, as well as indications of cytotoxicity.

Methods: In a double-blind, randomised crossover study, 14 healthy participants were exposed for 2 h to filtered air and diluted wood smoke from incomplete wood log combustion in a common wood stove with a mean particulate matter concentration of 409 µg/m3. Bronchoscopy with BW and BAL was performed 6 h after exposure. Differential cell counts, assessment of DNA-damage and ex vivo analysis of phagocytic function of phagocytosing BAL cells were performed. Wood smoke particles were also collected for in vitro toxicological analyses using bronchial epithelial cells (BEAS-2B) and alveolar type II-like cells (A549).

Results: Exposure to wood smoke increased BAL lactate dehydrogenase (LDH) (p = 0.04) and reduced the ex vivo alveolar macrophage phagocytic capacity (p = 0.03) and viability (p = 0.02) vs. filtered air. BAL eosinophil numbers were increased after wood smoke (p = 0.02), while other cell types were unaffected in BW and BAL. In vitro exposure to wood smoke particles confirmed increased DNA-damage, decreased metabolic activity and cell cycle disturbances.

Conclusions: Exposure to wood smoke from incomplete combustion did not induce any acute airway inflammatory cell influx at 6 h, apart from eosinophils. However, there were indications of a cytotoxic reaction with increased LDH, reduced cell viability and impaired alveolar macrophage phagocytic capacity. These findings are in accordance with earlier bronchoscopy findings at 24 h and may provide evidence for the increased susceptibility to infections by biomass smoke exposure, reported in population-based studies.

sted, utgiver, år, opplag, sider
BioMed Central (BMC), 2023
Emneord
Air pollution, Biomass combustion, Bronchoscopy, Controlled human exposure, Cytotoxicity, In vitro, Macrophages, Phagocytosis, Wood smoke
HSV kategori
Identifikatorer
urn:nbn:se:umu:diva-212714 (URN)10.1186/s12989-023-00541-x (DOI)37517998 (PubMedID)2-s2.0-85165871931 (Scopus ID)
Forskningsfinansiär
Swedish Heart Lung FoundationVästerbotten County CouncilSwedish Energy AgencyUmeå University
Tilgjengelig fra: 2023-08-15 Laget: 2023-08-15 Sist oppdatert: 2023-08-15bibliografisk kontrollert
Martikainen, M.-V., Aakko-Saksa, P., Broek, L. v., Cassee, F. R., Carare, R. O., Chew, S., . . . Jalava, P. I. (2022). TUBE project: Transport-derived ultrafines and the brain effects. International Journal of Environmental Research and Public Health, 19(1), Article ID 311.
Åpne denne publikasjonen i ny fane eller vindu >>TUBE project: Transport-derived ultrafines and the brain effects
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2022 (engelsk)Inngår i: International Journal of Environmental Research and Public Health, ISSN 1661-7827, E-ISSN 1660-4601, Vol. 19, nr 1, artikkel-id 311Artikkel i tidsskrift (Fagfellevurdert) Published
Abstract [en]

The adverse effects of air pollutants on the respiratory and cardiovascular systems are unquestionable. However, in recent years, indications of effects beyond these organ systems have become more evident. Traffic-related air pollution has been linked with neurological diseases, exacerbated cognitive dysfunction, and Alzheimer’s disease. However, the exact air pollutant compositions and exposure scenarios leading to these adverse health effects are not known. Although several components of air pollution may be at play, recent experimental studies point to a key role of ultrafine particles (UFPs). While the importance of UFPs has been recognized, almost nothing is known about the smallest fraction of UFPs, and only >23 nm emissions are regulated in the EU. Moreover, the role of the semivolatile fraction of the emissions has been neglected. The Transport-Derived Ultrafines and the Brain Effects (TUBE) project will increase knowledge on harmful ultrafine air pollutants, as well as semivolatile compounds related to adverse health effects. By including all the major current combustion and emission control technologies, the TUBE project aims to provide new information on the adverse health effects of current traffic, as well as information for decision makers to develop more effective emission legislation. Most importantly, the TUBE project will include adverse health effects beyond the respiratory system; TUBE will assess how air pollution affects the brain and how air pollution particles might be removed from the brain. The purpose of this report is to describe the TUBE project, its background, and its goals.

sted, utgiver, år, opplag, sider
MDPI, 2022
Emneord
Air pollution, Brain, CNS, Particulate matter, Toxicology, Traffic, UFP
HSV kategori
Identifikatorer
urn:nbn:se:umu:diva-190968 (URN)10.3390/ijerph19010311 (DOI)000742434400001 ()2-s2.0-85121690427 (Scopus ID)
Forskningsfinansiär
EU, Horizon 2020, 814978
Tilgjengelig fra: 2022-01-04 Laget: 2022-01-04 Sist oppdatert: 2023-09-05bibliografisk kontrollert
Pourazar, J., Sehlstedt, M., Rankin, G., Uski, O., Boman, C., Lopez, N., . . . Muala, A. (2019). Exposure to wood smoke induced activation of lymphocyte subtypes in peripheral blood. Paper presented at European-Respiratory-Society (ERS) International Congress, Madrid, SPAIN, SEP 28-OCT 02, 2019.. European Respiratory Journal, 54
Åpne denne publikasjonen i ny fane eller vindu >>Exposure to wood smoke induced activation of lymphocyte subtypes in peripheral blood
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2019 (engelsk)Inngår i: European Respiratory Journal, ISSN 0903-1936, E-ISSN 1399-3003, Vol. 54Artikkel i tidsskrift, Meeting abstract (Annet vitenskapelig) Published
sted, utgiver, år, opplag, sider
Sheffield: European Respiratory Society Journals, 2019
Emneord
Air pollution, Systemic effect, Inflammation
HSV kategori
Identifikatorer
urn:nbn:se:umu:diva-168164 (URN)10.1183/13993003.congress-2019.PA1983 (DOI)000507372402143 ()
Konferanse
European-Respiratory-Society (ERS) International Congress, Madrid, SPAIN, SEP 28-OCT 02, 2019.
Prosjekter
Bio4Energy
Forskningsfinansiär
Bio4Energy
Merknad

Supplement: 63. Meeting Abstract: PA1983.

Tilgjengelig fra: 2020-03-17 Laget: 2020-03-17 Sist oppdatert: 2023-05-09bibliografisk kontrollert
Lepzien, R., Rankin, G., Pourazar, J., Muala, A., Eklund, A., Grunewald, J., . . . Smed-Sorensen, A. (2019). Mapping mononuclear phagocytes in blood, lungs, and lymph nodes of sarcoidosis patients. Journal of Leukocyte Biology, 105(4), 797-807
Åpne denne publikasjonen i ny fane eller vindu >>Mapping mononuclear phagocytes in blood, lungs, and lymph nodes of sarcoidosis patients
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2019 (engelsk)Inngår i: Journal of Leukocyte Biology, ISSN 0741-5400, E-ISSN 1938-3673, Vol. 105, nr 4, s. 797-807Artikkel i tidsskrift (Fagfellevurdert) Published
Abstract [en]

Sarcoidosis is a T-cell driven inflammatory disease characterized by granuloma formation. Mononuclear phagocytes (MNPs)-macrophages, monocytes, and dendritic cells (DCs)-are likely critical in sarcoidosis as they initiate and maintain T cell activation and contribute to granuloma formation by cytokine production. Granulomas manifest primarily in lungs and lung-draining lymph nodes (LLNs) but these compartments are less studied compared to blood and bronchoalveolar lavage (BAL). Sarcoidosis can present with an acute onset (usually Lofgren's syndrome (LS)) or a gradual onset (non-LS). LS patients typically recover within 2 years while 60% of non-LS patients maintain granulomas for up to 5 years. Here, four LS and seven non-LS patients underwent bronchoscopy with endobronchial ultrasound-guided transbronchial needle aspiration (EBUS-TBNA). From each patient, blood, BAL, endobronchial biopsies (EBBs), and LLN samples obtained by EBUS-TBNA were collected and MNPs characterized using multicolor flow cytometry. Six MNP subsets were identified at varying frequencies in the anatomical compartments investigated. Importantly, monocytes and DCs were most mature with migratory potential in BAL and EBBs but not in the LLNs suggesting heterogeneity in MNPs in the compartments typically affected in sarcoidosis. Additionally, in LS patients, frequencies of DC subsets were lower or lacking in LLNs and EBBs, respectively, compared to non-LS patients that may be related to the disease outcome. Our work provides a foundation for future investigations of MNPs in sarcoidosis to identify immune profiles of patients at risk of developing severe disease with the aim to provide early treatment to slow down disease progression.

sted, utgiver, år, opplag, sider
Society for Leukocyte Biology, 2019
Emneord
dendritic cell, monocyte, sarcoidosis, lymph node, Lofgren's syndrome
HSV kategori
Identifikatorer
urn:nbn:se:umu:diva-158084 (URN)10.1002/JLB.5A0718-280RR (DOI)000462155000015 ()30742337 (PubMedID)2-s2.0-85061445996 (Scopus ID)
Forskningsfinansiär
Swedish Heart Lung FoundationSwedish Research Council
Tilgjengelig fra: 2019-04-15 Laget: 2019-04-15 Sist oppdatert: 2023-05-09bibliografisk kontrollert
Muala, A., Österdahl, R., Sehlstedt, M., Rankin, G., Pourazar, J., Bosson, J. A., . . . Öhberg, F. (2019). Small airways effects of exposure to wood smoke. Paper presented at European-Respiratory-Society (ERS) International Congress, Madrid, SPAIN, SEP 28-OCT 02, 2019.. European Respiratory Journal, 54
Åpne denne publikasjonen i ny fane eller vindu >>Small airways effects of exposure to wood smoke
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2019 (engelsk)Inngår i: European Respiratory Journal, ISSN 0903-1936, E-ISSN 1399-3003, Vol. 54Artikkel i tidsskrift, Meeting abstract (Annet vitenskapelig) Published
sted, utgiver, år, opplag, sider
Sheffield: European Respiratory Society Journals, 2019
Emneord
Asthma, Air pollution
HSV kategori
Identifikatorer
urn:nbn:se:umu:diva-168166 (URN)10.1183/13993003.congress-2019.PA2829 (DOI)000507372403325 ()
Konferanse
European-Respiratory-Society (ERS) International Congress, Madrid, SPAIN, SEP 28-OCT 02, 2019.
Prosjekter
Bio4Energy
Forskningsfinansiär
Bio4Energy
Tilgjengelig fra: 2020-03-17 Laget: 2020-03-17 Sist oppdatert: 2023-05-09bibliografisk kontrollert
Hansson, A., Rankin, G., Uski, O., Sehlstedt, M., Bosson, J. A., Pourazar, J., . . . Muala, A. (2019). Wood smoke effects on epithelial cell lines and human airway cells. Paper presented at European-Respiratory-Society (ERS) International Congress, Madrid, SPAIN, SEP 28-OCT 02, 2019.. European Respiratory Journal, 54
Åpne denne publikasjonen i ny fane eller vindu >>Wood smoke effects on epithelial cell lines and human airway cells
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2019 (engelsk)Inngår i: European Respiratory Journal, ISSN 0903-1936, E-ISSN 1399-3003, Vol. 54Artikkel i tidsskrift, Meeting abstract (Annet vitenskapelig) Published
sted, utgiver, år, opplag, sider
European Respiratory Society Journals, 2019
Emneord
Bronchoscopy, Immunology, Air pollution
HSV kategori
Identifikatorer
urn:nbn:se:umu:diva-168169 (URN)10.1183/13993003.congress-2019.PA5448 (DOI)000507372407158 ()
Konferanse
European-Respiratory-Society (ERS) International Congress, Madrid, SPAIN, SEP 28-OCT 02, 2019.
Prosjekter
Bio4Energy
Forskningsfinansiär
Bio4Energy
Merknad

Supplement: 63. Meeting Abstract: PA5448.

Tilgjengelig fra: 2020-03-17 Laget: 2020-03-17 Sist oppdatert: 2023-05-09bibliografisk kontrollert
Sehlstedt, M., Muala, A., Pourazar, J., Rankin, G., Uski, O., Behndig, A. F., . . . Blomberg, A. (2019). Wood smoke exposure induces the activation of bronchoalveolar lavage lymphocytes. Paper presented at European-Respiratory-Society (ERS) International Congress, Madrid, SPAIN, SEP 28-OCT 02, 2019.. European Respiratory Journal, 54
Åpne denne publikasjonen i ny fane eller vindu >>Wood smoke exposure induces the activation of bronchoalveolar lavage lymphocytes
Vise andre…
2019 (engelsk)Inngår i: European Respiratory Journal, ISSN 0903-1936, E-ISSN 1399-3003, Vol. 54Artikkel i tidsskrift, Meeting abstract (Annet vitenskapelig) Published
sted, utgiver, år, opplag, sider
European Respiratory Society Journals, 2019
Emneord
Air pollution, Bronchoalveolar lavage, Inflammation
HSV kategori
Identifikatorer
urn:nbn:se:umu:diva-168165 (URN)10.1183/13993003.congress-2019.PA2828 (DOI)000507372403324 ()
Konferanse
European-Respiratory-Society (ERS) International Congress, Madrid, SPAIN, SEP 28-OCT 02, 2019.
Prosjekter
Bio4Energy
Forskningsfinansiär
Bio4Energy
Merknad

Supplement: 63. Meeting Abstract: PA2828.

Tilgjengelig fra: 2020-03-17 Laget: 2020-03-17 Sist oppdatert: 2023-05-09bibliografisk kontrollert
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