SwePub
Sök i SwePub databas

  Utökad sökning

Träfflista för sökning "WFRF:(Nagel Björn) "

Sökning: WFRF:(Nagel Björn)

  • Resultat 1-50 av 104
Sortera/gruppera träfflistan
   
NumreringReferensOmslagsbildHitta
1.
  •  
2.
  •  
3.
  •  
4.
  •  
5.
  •  
6.
  •  
7.
  •  
8.
  •  
9.
  •  
10.
  •  
11.
  •  
12.
  •  
13.
  •  
14.
  • Borena, Wegene, et al. (författare)
  • A prospective study on metabolic risk factors and gallbladder cancer in the metabolic syndrome and cancer (Me-Can) collaborative study
  • 2014
  • Ingår i: PLOS ONE. - : Public Library of Science (PLoS). - 1932-6203. ; 9:2, s. e89368-
  • Tidskriftsartikel (refereegranskat)abstract
    • OBJECTIVE:To investigate the association between metabolic risk factors (individually and in combination) and risk of gallbladder cancer (GBC).METHODS:The metabolic syndrome and cancer project (Me-Can) includes cohorts from Norway, Austria, and Sweden with data on 578,700 men and women. We used Cox proportional hazard regression models to calculate relative risks of GBC by body mass index (BMI), blood pressure, and plasma levels of glucose, cholesterol, and triglycerides as continuous standardised variables and their standardised sum of metabolic syndrome (MetS) z-score. The risk estimates were corrected for random error in measurements.RESULTS:During an average follow-up of 12.0 years (SD = 7.8), 184 primary gallbladder cancers were diagnosed. Relative risk of gallbladder cancer per unit increment of z-score adjusted for age, smoking status and BMI (except for BMI itself) and stratified by birth year, sex and sub-cohorts, was for BMI 1.31 (95% confidence interval 1.11, 1.57) and blood glucose 1.76 (1.10, 2.85). Further analysis showed that the effect of BMI on GBC risk is larger among women in the premenopausal age group (1.84 (1.23, 2.78)) compared to those in the postmenopausal age group (1.29 (0.93, 1.79)). For the other metabolic factors no significant association was found (mid blood pressure 0.96 (0.71, 1.31), cholesterol 0.84 (0.66, 1.06) and serum triglycerides 1.16 (0.82, 1.64)). The relative risk per one unit increment of the MetS z-score was 1.37 (1.07, 1.73).CONCLUSION:This study showed that increasing BMI and impaired glucose metabolism pose a possible risk for gallbladder cancer. Beyond the individual factors, the results also showed that the metabolic syndrome as an entity presents a risk constellation for the occurrence of gallbladder cancer.
  •  
15.
  • Fritz, Josef, et al. (författare)
  • The triglyceride-glucose index as a measure of insulin resistance and risk of obesity-related cancers
  • 2020
  • Ingår i: International Journal of Epidemiology. - : Oxford University Press (OUP). - 0300-5771 .- 1464-3685. ; 49:1, s. 193-204
  • Tidskriftsartikel (refereegranskat)abstract
    • BACKGROUND: The role of insulin resistance as a mediator in the association of body mass index (BMI) with site-specific cancer risk has, to our knowledge, never been systematically quantified.METHODS: Altogether 510 471 individuals from six European cohorts, with a mean age of 43.1 years, were included. We used the triglyceride glucose product (TyG index) as a surrogate measure for insulin resistance. We fitted Cox models, adjusted for relevant confounders, to investigate associations of TyG index with 10 common obesity-related cancers, and quantified the proportion of the effect of BMI mediated through TyG index on the log-transformed hazard ratio (HR) scale.RESULTS: During a median follow-up of 17.2 years, 16 052 individuals developed obesity-related cancers. TyG index was associated with the risk of cancers of the kidney HR per one standard deviation increase 1.13, 95% confidence interval: 1.07 to 1.20], liver (1.13, 1.04 to 1.23), pancreas (1.12, 1.06 to 1.19), colon (1.07, 1.03 to 1.10) and rectum (1.09, 1.04 to 1.14). Substantial proportions of the effect of BMI were mediated by TyG index for cancers of the pancreas (42%), rectum (34%) and colon (20%); smaller proportions for kidney (15%) and liver (11%). Little or no mediation was observed for breast (postmenopausal), endometrial and ovarian cancer. Results were similar for males and females, except for pancreatic cancer where the proportions mediated were 20% and 91%, respectively.CONCLUSIONS: The TyG index was associated with increased risk of cancers of the digestive system and substantially mediated the effect of BMI, suggesting that insulin resistance plays a promoting role in the pathogenesis of gastrointestinal cancers.
  •  
16.
  • Häggström, Christel, et al. (författare)
  • Competing risk analysis of metabolic factors and prostate cancer
  • Annan publikation (övrigt vetenskapligt/konstnärligt)abstract
    • Background: Men at risk of prostate cancer are also at risk of competing events but this has been ignored in most studies of metabolic aberrations and prostate cancer. The aim of this study was to assess probabilities of prostate cancer and prostate cancer death by use of competing risk analysis.Methods: In the Metabolic syndrome and Cancer project (Me-Can), data on body mass index, blood pressure, glucose, total cholesterol, and triglycerides were collected from 285 040 men. Probabilities of prostate cancer, prostate cancer death and competing events, i.e. all-cause death or death from other causes, respectively, were calculated for men with normal (bottom 84%) and high (top 16%) levels of each metabolic factor and a composite score based on all metabolic factorsResults: During follow up, 5893 men were diagnosed with prostate cancer, 1013 men died of prostate cancer, and 26 328 men died of other causes. Men with high levels of metabolic factors had decreased probability of prostate cancer, similar probability of prostate cancer death, and increased probability of other causes of death compared to men with normal levels. After 1996, when prostate specific antigen was used for detection of prostate cancer, men up to 80 years with normal levels of metabolic factors had 13% probability of prostate cancer and 37% probability of death from all causes. For men with high levels of metabolic factors, corresponding probabilities were 12% and 47%.Conclusions: Men with metabolic aberrations had a decreased probability of prostate cancer but a substantially higher probability of death from all causes.
  •  
17.
  • Häggström, Christel, et al. (författare)
  • Prostate Cancer, Prostate Cancer Death, and Death from Other Causes, Among Men with Metabolic Aberrations
  • 2014
  • Ingår i: Epidemiology. - 1044-3983 .- 1531-5487. ; 25:6, s. 823-828
  • Tidskriftsartikel (refereegranskat)abstract
    • Background: Few previous studies of metabolic aberrations and prostate cancer risk have taken into account the fact that men with metabolic aberrations have an increased risk of death from causes other than prostate cancer. The aim of this study was to calculate, in a real-life scenario, the risk of prostate cancer diagnosis, prostate cancer death, and death from other causes.Methods: In the Metabolic Syndrome and Cancer Project, prospective data on body mass index, blood pressure, glucose, cholesterol, and triglycerides were collected from 285,040 men. Risks of prostate cancer diagnosis, prostate cancer death, and death from other causes were calculated by use of competing risk analysis for men with normal (bottom 84%) and high (top 16%) levels of each factor, and a composite score.Results: During a mean follow-up period of 12 years, 5,893 men were diagnosed with prostate cancer, 1,013 died of prostate cancer, and 26,328 died of other causes. After 1996, when prostate-specific antigen testing was introduced, men up to age 80 years with normal metabolic levels had 13% risk of prostate cancer, 2% risk of prostate cancer death, and 30% risk of death from other causes, whereas men with metabolic aberrations had corresponding risks of 11%, 2%, and 44%.Conclusions: In contrast to recent studies using conventional survival analysis, in a real-world scenario taking risk of competing events into account, men with metabolic aberrations had lower risk of prostate cancer diagnosis, similar risk of prostate cancer death, and substantially higher risk of death from other causes compared with men who had normal metabolic levels.
  •  
18.
  • Johansen, Dorthe, et al. (författare)
  • Metabolic factors and the risk of pancreatic cancer : a prospective analysis of almost 580,000 men and women in the Metabolic Syndrome and Cancer Project
  • 2010
  • Ingår i: Cancer Epidemiology, Biomarkers and Prevention. - : American Association for Cancer Research. - 1055-9965 .- 1538-7755. ; 19:9, s. 2307-2317
  • Tidskriftsartikel (refereegranskat)abstract
    • BACKGROUND: The aim of this study was to investigate the association between factors in metabolic syndrome (MetS; single and combined) and the risk of pancreatic cancer. METHODS: The Metabolic Syndrome and Cancer Project is a pooled cohort containing data on body mass index, blood pressure, and blood levels of glucose, cholesterol, and triglycerides. During follow-up, 862 individuals were diagnosed with pancreatic cancer. Cox proportional hazards analysis was used to calculate relative risks (RR) with 95% confidence intervals using the above-mentioned factors categorized into quintiles and transformed into z-scores. All z-scores were summarized and a second z-transformation creating a composite z-score for MetS was done. All risk estimates were calibrated to correct for a regression dilution bias. RESULTS: The trend over quintiles was positively associated with the risk of pancreatic cancer for mid-blood pressure (mid-BP) and glucose in men and for body mass index, mid-BP, and glucose in women. The z-score for the adjusted mid-BP (RR, 1.10; 1.01-1.20) and the calibrated z-score for glucose (RR, 1.37; 1.14-1.34) were positively associated with pancreatic cancer in men. In women, a positive association was found for calibrated z-scores for mid-BP (RR, 1.34; 1.08-1.66), for the calibrated z-score for glucose (RR, 1.98; 1.41-2.76), and for the composite z-score for MetS (RR, 1.58; 1.34-1.87). CONCLUSION: Our study adds further evidence to a possible link between abnormal glucose metabolism and risk of pancreatic cancer. IMPACT: To our knowledge, this is the first study on MetS and pancreatic cancer using prediagnostic measurements of the examined factors.
  •  
19.
  • Jouannet, Christopher, et al. (författare)
  • SUSTAINABLE AVIATION FOR SWEDEN - TECHNOLOGY & CAPABILITY ASSESSMENT TARGETING 2045
  • 2022
  • Ingår i: 33rd CONGRESS OF THE INTERNATIONAL COUNCIL OF THE AERONAUTICAL SCIENCES. - 2958-4647.
  • Konferensbidrag (refereegranskat)abstract
    • The goal of this project is to analyse the possibilities offered by different technological solutions to achieve zero emission aviation, firstly in the Swedish/Nordic network context and secondly extend this to the European context. This project will investigate the potential and feasibility of new or upgraded aircraft types based on the different technologies mapped from both, various published roadmaps and national expertise from Swedish aerospace universities and companies. This involves developing aircraft conceptual designs studies and trade analysis with regards to different fuel types, propulsion technologies, structure, operations, network and fleet management, and all relevant technologies. The project will, on a common technology basis, analyse a range of zero carbon fuels and associated technologies through operational studies and optimization to accelerate the introduction of fossil free aircraft technology and choosing optimal paths for making aviation sustainable.
  •  
20.
  • Lindkvist, Björn, et al. (författare)
  • Metabolic risk factors for esophageal squamous cell carcinoma and adenocarcinoma: a prospective study of 580 000 subjects within the Me-Can project
  • 2014
  • Ingår i: BMC Cancer. - London : Springer Science and Business Media LLC. - 1471-2407. ; 14
  • Tidskriftsartikel (refereegranskat)abstract
    • Background: Obesity is associated with an increased risk of esophageal adenocarcinoma (EAC) and a decreased risk of esophageal squamous cell carcinoma (ESCC). However, little is known about the risk of EAC and ESCC related to other metabolic risk factors. We aimed to examine the risk of EAC and ESCC in relation to metabolic risk factors, separately and combined in a prospective cohort study. Methods: The Metabolic Syndrome and Cancer cohort includes prospective cohorts in Austria, Norway and Sweden, with blood pressure, lipids, glucose and BMI available from 578 700 individuals. Relative risk (RR) for EAC and ESCC was calculated using Cox's proportional hazards analysis for metabolic risk factors categorized into quintiles and transformed into z-scores. The standardized sum of all z-scores was used as a composite score for the metabolic syndrome (MetS). Results: In total, 324 histologically verified cases of esophageal cancer were identified (114 EAC, 184 ESCC and 26 with other histology). BMI was associated with an increased risk of EAC (RR 7.34 (95% confidence interval, 2.88-18.7) top versus bottom quintile) and negatively associated with the risk of ESCC (RR 0.38 (0.23-0.62)). The mean value of systolic and diastolic blood pressure (mid blood pressure) was associated with the risk of ESCC (RR 1.77 (1.37-2.29)). The composite MetS score was associated with the risk of EAC (RR 1.56 (1.19-2.05) per one unit increase of z-score) but not ESCC. Conclusions: In accordance with previous studies, high BMI was associated with an increased risk of EAC and a decreased risk of ESCC. An association between high blood pressure and risk of ESCC was observed but alcohol consumption is a potential confounding factor that we were not able to adjust for in the analysis. The MetS was associated with EAC but not ESCC. However this association was largely driven by the strong association between BMI and EAC. We hypothesize that this association is more likely to be explained by factors directly related to obesity than the metabolic state of the MetS, considering that no other metabolic factor than BMI was associated with EAC.
  •  
21.
  • Lindkvist, Björn, et al. (författare)
  • Prospective cohort study of metabolic risk factors and gastric adenocarcinoma risk in the Metabolic Syndrome and Cancer Project (Me-Can)
  • 2013
  • Ingår i: Cancer Causes and Control. - : Springer Science and Business Media LLC. - 1573-7225 .- 0957-5243. ; 24:1, s. 107-116
  • Tidskriftsartikel (refereegranskat)abstract
    • Little is known about the association between the metabolic syndrome (MetS) and the risk of gastric adenocarcinoma. The aim of this study was to investigate whether metabolic risk factors, together or combined, were associated with the risk of gastric adenocarcinoma. The Metabolic Syndrome and Cancer Project (Me-Can) is a pooling of prospective cohorts in Austria, Norway, and Sweden with information on blood pressure, lipids, glucose, and BMI available in 578,700 individuals. Cox proportional hazards analysis was used to calculate hazard ratio (HR) of gastric adenocarcinoma using metabolic risk factors categorized into quintiles and transformed into z-scores (with mean = 0 and SD = 1). The standardized sum of all z-scores created a composite MetS score. In total, 1,210 incident cases of gastric adenocarcinoma were identified. Glucose was significantly associated with the risk of gastric adenocarcinoma [calibrated HR 1.58 (1.14-2.20) per one unit increment in z-score] in women. There was a statistically significant association between triglycerides and risk of gastric adenocarcinoma per mmol increment in triglycerides [HR 1.20 (1.06-1.36) per mmol] but not for the adjusted z-score in women. There were no significant association between any metabolic factors and gastric cancer among men. The composite MetS score was associated with the risk of gastric adenocarcinoma in women [HR 1.18 (1.00-1.38) per one unit increment in z-score] but not in men. Glucose and high levels of the composite MetS score were associated with an increased risk of gastric adenocarcinoma in women but not in men.
  •  
22.
  •  
23.
  • Nagel, G., et al. (författare)
  • Metabolic factors and blood cancers among 578,000 adults in the metabolic syndrome and cancer project (Me-Can)
  • 2012
  • Ingår i: Annals of Hematology. - New York : Springer Science and Business Media LLC. - 0939-5555 .- 1432-0584. ; 91:10, s. 1519-1531
  • Tidskriftsartikel (refereegranskat)abstract
    • We investigated associations between metabolic factors and blood cancer subtypes. Data on body mass index (BMI), blood pressure, blood glucose, total cholesterol, and triglycerides from seven prospective cohorts were pooled (n = 578,700; mean age = 44 years). Relative risks of blood cancers were calculated from Cox regression models. During mean follow-up of 12 years, 2,751 incident and 1,070 fatal cases of blood cancers occurred. Overall, higher BMI was associated with an increased blood cancer risk. In gender-specific subgroup analyses, BMI was positively associated with blood cancer risk (p = 0.002), lymphoid neoplasms (p = 0.01), and Hodgkin's lymphoma (p = 0.02) in women. Further associations with BMI were found for high-grade B-cell lymphoma (p = 0.02) and chronic lymphatic leukemia in men (p = 0.05) and women (p = 0.01). Higher cholesterol levels were inversely associated with myeloid neoplasms in women (p = 0.01), particularly acute myeloid leukemia (p = 0.003), and glucose was positively associated with chronic myeloid leukemia in women (p = 0.03). In men, glucose was positively associated with risk of high-grade B-cell lymphoma and multiple myeloma, while cholesterol was inversely associated with low-grade B-cell lymphoma. The metabolic syndrome score was related to 48 % increased risk of Hodgkin's lymphoma among women. BMI showed up as the most consistent risk factor, particularly in women. A clear pattern was not found for other metabolic factors.
  •  
24.
  • Oprea, Alexandra, 1987- (författare)
  • On aircraft simulation in conceptual design
  • 2022
  • Licentiatavhandling (övrigt vetenskapligt/konstnärligt)abstract
    • The aerospace industry has a long tradition of using Model Based Systems Engineering in its development processes. Throughout the years an extensive library of system simulation models has been created, expanding with every new model being developed. Nevertheless, modelling and simulation engineers prefer developing their own models from scratch, as the reuse of legacy models seems cumbersome, leading to the simultaneous existence of multiple simulation models of the same system in a project. Not only does the development, verification and validation and maintenance of these multiple simulation models incur extra costs, but they also represent a potential threat to the aircraft development, as data consistency is more difficult to be ensured. The aim of this thesis is to investigate simulation model reuse during the aircraft development process, with the goal of creating an easy-to-reconfigure simulation framework, allowing for the inclusion of simulation models of various levels of fidelity. Through an industry-as-laboratory approach, the inclusion of industry-grade legacy system simulation models is investigated, with the help of simulation model integration standards such as Functional Mock-up Interface and System Structure and Parametrisation. The results of the work include the development of a proof-of-concept simulation framework that enables the aggregation, integration and reuse of simulation models from different technological domains and with different levels of fidelity. Moreover, the work proposes a workflow that streamlines the decision milestones when faced with the possibility of selecting between creating a new system simulation model or reusing a legacy one, and highlights the challenges associated with model reuse from both a technical and an organisational perspective. 
  •  
25.
  •  
26.
  • Stocks, Tanja, et al. (författare)
  • Blood pressure and risk of cancer incidence and mortality in the metabolic syndrome and cancer project
  • 2012
  • Ingår i: Hypertension. - Philadelphia : Lippincott Williams & Wilkins. - 0194-911X .- 1524-4563. ; 59:4, s. 802-810
  • Tidskriftsartikel (refereegranskat)abstract
    • Observational studies have shown inconsistent results for the association between blood pressure and cancer risk. We investigated the association in 7 cohorts from Norway, Austria, and Sweden. In total, 577799 adults with a mean age of 44 years were followed for, on average, 12 years. Incident cancers were 22184 in men and 14744 in women, and cancer deaths were 8724 and 4525, respectively. Cox regression was used to calculate hazard ratios of cancer per 10-mmHg increments of midblood pressure, which corresponded with 0.7 SDs and, for example, an increment of systolic/diastolic blood pressure of 130/80 to 142/88 mmHg. All of the models used age as the time scale and were adjusted for possible confounders, including body mass index and smoking status. In men, midblood pressure was positively related to total incident cancer (hazard ratio per 10 mmHg increment: 1.07 [95% CI: 1.04-1.09]) and to cancer of the oropharynx, colon, rectum, lung, bladder, kidney, malignant melanoma, and nonmelanoma skin cancer. In women, midblood pressure was not related to total incident cancer but was positively related to cancer of the liver, pancreas, cervix, uterine corpus, and malignant melanoma. A positive association was also found for cancer mortality, with HRs per 10-mmHg increment of 1.12 (95% CI: 1.08-1.15) for men and 1.06 (95% CI: 1.02-1.11) for women. These results suggest a small increased cancer risk overall in men with elevated blood pressure level and a higher risk for cancer death in men and women. © 2012 American Heart Association, Inc.
  •  
27.
  • Aad, G., et al. (författare)
  • 2013
  • Tidskriftsartikel (refereegranskat)
  •  
28.
  • Aad, G., et al. (författare)
  • 2013
  • Ingår i: New Journal of Physics. - : IOP Publishing. - 1367-2630. ; 15
  • Tidskriftsartikel (refereegranskat)
  •  
29.
  • Aad, G., et al. (författare)
  • 2013
  • Tidskriftsartikel (refereegranskat)
  •  
30.
  • Aad, G., et al. (författare)
  • 2013
  • Ingår i: The European Physical Journal C. - : Springer Science and Business Media LLC. - 1434-6052. ; 73:1
  • Tidskriftsartikel (refereegranskat)
  •  
31.
  • Aad, G., et al. (författare)
  • 2013
  • Tidskriftsartikel (refereegranskat)
  •  
32.
  • Aad, G., et al. (författare)
  • 2013
  • Tidskriftsartikel (refereegranskat)
  •  
33.
  • Aad, G., et al. (författare)
  • 2012
  • Tidskriftsartikel (refereegranskat)
  •  
34.
  • Aad, G., et al. (författare)
  • 2013
  • Tidskriftsartikel (refereegranskat)
  •  
35.
  • Aad, G., et al. (författare)
  • 2012
  • Tidskriftsartikel (refereegranskat)
  •  
36.
  • Aad, G., et al. (författare)
  • 2012
  • Tidskriftsartikel (refereegranskat)
  •  
37.
  • Aad, G., et al. (författare)
  • 2012
  • Tidskriftsartikel (refereegranskat)
  •  
38.
  • Aad, G., et al. (författare)
  • 2013
  • Tidskriftsartikel (refereegranskat)
  •  
39.
  • Aad, G., et al. (författare)
  • 2013
  • Ingår i: The European Physical Journal C. - : Springer Science and Business Media LLC. - 1434-6052. ; 73:3
  • Tidskriftsartikel (refereegranskat)
  •  
40.
  • Aad, G., et al. (författare)
  • 2013
  • Ingår i: New Journal of Physics. - : IOP Publishing. - 1367-2630. ; 15
  • Tidskriftsartikel (refereegranskat)
  •  
41.
  • Aad, G., et al. (författare)
  • 2013
  • Ingår i: New Journal of Physics. - : IOP Publishing. - 1367-2630. ; 15
  • Tidskriftsartikel (refereegranskat)
  •  
42.
  • Aad, G., et al. (författare)
  • 2013
  • Tidskriftsartikel (refereegranskat)
  •  
43.
  • Aad, G., et al. (författare)
  • 2012
  • Tidskriftsartikel (refereegranskat)
  •  
44.
  • Aad, G., et al. (författare)
  • 2012
  • Tidskriftsartikel (refereegranskat)
  •  
45.
  • Aad, G., et al. (författare)
  • 2012
  • Tidskriftsartikel (refereegranskat)
  •  
46.
  • Aad, G., et al. (författare)
  • 2012
  • Tidskriftsartikel (refereegranskat)
  •  
47.
  • Aad, G., et al. (författare)
  • 2013
  • Tidskriftsartikel (refereegranskat)
  •  
48.
  • Aad, G., et al. (författare)
  • 2012
  • Ingår i: Nuclear Physics, Section B. - : Elsevier BV. - 0550-3213 .- 1873-1562. ; 864:3, s. 341-381
  • Tidskriftsartikel (refereegranskat)
  •  
49.
  • Aad, G., et al. (författare)
  • 2012
  • Tidskriftsartikel (refereegranskat)
  •  
50.
  • Aad, G., et al. (författare)
  • 2013
  • Tidskriftsartikel (refereegranskat)
  •  
Skapa referenser, mejla, bekava och länka
  • Resultat 1-50 av 104
Typ av publikation
tidskriftsartikel (101)
annan publikation (1)
konferensbidrag (1)
licentiatavhandling (1)
Typ av innehåll
refereegranskat (102)
övrigt vetenskapligt/konstnärligt (2)
Författare/redaktör
Aad, G (91)
Abbott, B. (91)
Abdinov, O (91)
Zwalinski, L. (91)
Abi, B. (91)
Abramowicz, H. (91)
visa fler...
Adams, D. L. (91)
Adelman, J. (91)
Adomeit, S. (91)
Adye, T. (91)
Aielli, G. (91)
Akimov, A. V. (91)
Albrand, S. (91)
Aleksa, M. (91)
Aleksandrov, I. N. (91)
Alexander, G. (91)
Alexandre, G. (91)
Alexopoulos, T. (91)
Alhroob, M. (91)
Alimonti, G. (91)
Alison, J. (91)
Allport, P. P. (91)
Almond, J. (91)
Amako, K. (91)
Amelung, C. (91)
Amram, N. (91)
Anastopoulos, C. (91)
Ancu, L. S. (91)
Andari, N. (91)
Anderson, K. J. (91)
Anghinolfi, F. (91)
Annovi, A. (91)
Antonaki, A. (91)
Antonelli, M. (91)
Antonov, A. (91)
Apolle, R. (91)
Arabidze, G. (91)
Arai, Y. (91)
Arguin, J-F. (91)
Arnaez, O. (91)
Arnal, V. (91)
Asai, S. (91)
Asquith, L. (91)
Assamagan, K. (91)
Avolio, G. (91)
Azuma, Y. (91)
Bachacou, H. (91)
Bachas, K. (91)
Backes, M. (91)
Backhaus, M. (91)
visa färre...
Lärosäte
Lunds universitet (99)
Uppsala universitet (95)
Stockholms universitet (91)
Kungliga Tekniska Högskolan (90)
Umeå universitet (9)
Göteborgs universitet (4)
visa fler...
Linköpings universitet (1)
Chalmers tekniska högskola (1)
Karolinska Institutet (1)
Naturhistoriska riksmuseet (1)
visa färre...
Språk
Engelska (104)
Forskningsämne (UKÄ/SCB)
Naturvetenskap (91)
Medicin och hälsovetenskap (9)
Teknik (2)
Samhällsvetenskap (1)
Humaniora (1)

År

Kungliga biblioteket hanterar dina personuppgifter i enlighet med EU:s dataskyddsförordning (2018), GDPR. Läs mer om hur det funkar här.
Så här hanterar KB dina uppgifter vid användning av denna tjänst.

 
pil uppåt Stäng

Kopiera och spara länken för att återkomma till aktuell vy