| 1. |
|
|
| 2. |
|
|
| 3. |
- Jensen, Kurt Villads, 1957-, et al.
(författare)
-
Introduction
- 2018
-
Ingår i: Fighting for the Faith. - Stockholm : Sällskapet Runica et mediævalia, Centre for Medieval Studies, Stockholm University. - 9789188568731 ; , s. 9-13
-
Bokkapitel (refereegranskat)
|
|
| 4. |
- Mahajan, Anubha, et al.
(författare)
-
Refining the accuracy of validated target identification through coding variant fine-mapping in type 2 diabetes
- 2018
-
Ingår i: Nature Genetics. - : Nature Publishing Group. - 1061-4036 .- 1546-1718. ; 50:4, s. 559-571
-
Tidskriftsartikel (refereegranskat)abstract
- We aggregated coding variant data for 81,412 type 2 diabetes cases and 370,832 controls of diverse ancestry, identifying 40 coding variant association signals (P < 2.2 × 10−7); of these, 16 map outside known risk-associated loci. We make two important observations. First, only five of these signals are driven by low-frequency variants: even for these, effect sizes are modest (odds ratio ≤1.29). Second, when we used large-scale genome-wide association data to fine-map the associated variants in their regional context, accounting for the global enrichment of complex trait associations in coding sequence, compelling evidence for coding variant causality was obtained for only 16 signals. At 13 others, the associated coding variants clearly represent ‘false leads’ with potential to generate erroneous mechanistic inference. Coding variant associations offer a direct route to biological insight for complex diseases and identification of validated therapeutic targets; however, appropriate mechanistic inference requires careful specification of their causal contribution to disease predisposition.
|
|
| 5. |
|
|
| 6. |
- Ainegren, Mats, 1963-, et al.
(författare)
-
Breathing resistance in automated metabolic systems is high in comparison with the Douglas Bag method and previous recommendations
- 2018
-
Ingår i: Proceedings of the Institution of Mechanical Engineers, Part P. - : SAGE Publications. - 1754-3371. ; 232:2, s. 122-130
-
Tidskriftsartikel (refereegranskat)abstract
- The purpose of this study was to investigate the resistance (RES) to breathing in metabolic systems used for the distribution and measurement of pulmonary gas exchange. A mechanical lung simulator was used to standardize selected air flow rates ( , L/s). The delta pressure (∆p, Pa) between ambient air and the air inside the equipment was measured in the breathing valve’s mouthpiece adapter for four metabolic systems and four types of breathing valves. RES for the inspiratory and expiratory sides was calculated as RES = ∆p / , Pa/L/s. The results for RES showed significant (p < 0.05) between-group variance among the tested metabolic systems, as well as the breathing valves and between most of the completed . The lowest RES among the metabolic systems was found for a Douglas Bag system, with approximately half of the RES compared to the automated metabolic systems. The automated systems were found to have higher RES already at low in comparison to previous recommendations. For the hardware components, the highest RES was found for the breathing valves while the lowest RES was found for the hoses. Conclusion: The results showed that RES in metabolic systems can be minimized through conscious choices of system design and hardware components.
|
|
| 7. |
- Bregnsbo, Michael, et al.
(författare)
-
Introduction
- 2016
-
Ingår i: Schleswig Holstein. - Odense : University Press of Southern Denmark. - 9788776748708 ; , s. 7-14
-
Bokkapitel (övrigt vetenskapligt/konstnärligt)
|
|
| 8. |
- Dehghan, Abbas, et al.
(författare)
-
Genome-Wide Association Study for Incident Myocardial Infarction and Coronary Heart Disease in Prospective Cohort Studies : The CHARGE Consortium
- 2016
-
Ingår i: PLOS ONE. - : Public Library of Science (PLoS). - 1932-6203. ; 11:3
-
Tidskriftsartikel (refereegranskat)abstract
- Background Data are limited on genome-wide association studies (GWAS) for incident coronary heart disease (CHD). Moreover, it is not known whether genetic variants identified to date also associate with risk of CHD in a prospective setting. Methods We performed a two-stage GWAS analysis of incident myocardial infarction (MI) and CHD in a total of 64,297 individuals (including 3898 MI cases, 5465 CHD cases). SNPs that passed an arbitrary threshold of 5x10(-6) in Stage I were taken to Stage II for further discovery. Furthermore, in an analysis of prognosis, we studied whether known SNPs from former GWAS were associated with total mortality in individuals who experienced MI during follow-up. Results In Stage I 15 loci passed the threshold of 5x10(-6); 8 loci for MI and 8 loci for CHD, for which one locus overlapped and none were reported in previous GWAS meta-analyses. We took 60 SNPs representing these 15 loci to Stage II of discovery. Four SNPs near QKI showed nominally significant association with MI (p-value<8.8x10(-3)) and three exceeded the genome-wide significance threshold when Stage I and Stage II results were combined (top SNP rs6941513: p = 6.2x10(-9)). Despite excellent power, the 9p21 locus SNP (rs1333049) was only modestly associated with MI (HR = 1.09, p-value = 0.02) and marginally with CHD (HR = 1.06, p-value = 0.08). Among an inception cohort of those who experienced MI during follow-up, the risk allele of rs1333049 was associated with a decreased risk of subsequent mortality (HR = 0.90, p-value = 3.2x10(-3)). Conclusions QKI represents a novel locus that may serve as a predictor of incident CHD in prospective studies. The association of the 9p21 locus both with increased risk of first myocardial infarction and longer survival after MI highlights the importance of study design in investigating genetic determinants of complex disorders.
|
|
| 9. |
- Forouzanfar, Mohammad H, et al.
(författare)
-
Global, regional, and national comparative risk assessment of 79 behavioural, environmental and occupational, and metabolic risks or clusters of risks in 188 countries, 1990-2013 : a systematic analysis for the Global Burden of Disease Study 2013.
- 2015
-
Ingår i: The Lancet. - 0140-6736 .- 1474-547X. ; 386:10010, s. 2287-2323
-
Tidskriftsartikel (refereegranskat)abstract
- BACKGROUND: The Global Burden of Disease, Injuries, and Risk Factor study 2013 (GBD 2013) is the first of a series of annual updates of the GBD. Risk factor quantification, particularly of modifiable risk factors, can help to identify emerging threats to population health and opportunities for prevention. The GBD 2013 provides a timely opportunity to update the comparative risk assessment with new data for exposure, relative risks, and evidence on the appropriate counterfactual risk distribution.METHODS: Attributable deaths, years of life lost, years lived with disability, and disability-adjusted life-years (DALYs) have been estimated for 79 risks or clusters of risks using the GBD 2010 methods. Risk-outcome pairs meeting explicit evidence criteria were assessed for 188 countries for the period 1990-2013 by age and sex using three inputs: risk exposure, relative risks, and the theoretical minimum risk exposure level (TMREL). Risks are organised into a hierarchy with blocks of behavioural, environmental and occupational, and metabolic risks at the first level of the hierarchy. The next level in the hierarchy includes nine clusters of related risks and two individual risks, with more detail provided at levels 3 and 4 of the hierarchy. Compared with GBD 2010, six new risk factors have been added: handwashing practices, occupational exposure to trichloroethylene, childhood wasting, childhood stunting, unsafe sex, and low glomerular filtration rate. For most risks, data for exposure were synthesised with a Bayesian meta-regression method, DisMod-MR 2.0, or spatial-temporal Gaussian process regression. Relative risks were based on meta-regressions of published cohort and intervention studies. Attributable burden for clusters of risks and all risks combined took into account evidence on the mediation of some risks such as high body-mass index (BMI) through other risks such as high systolic blood pressure and high cholesterol.FINDINGS: All risks combined account for 57·2% (95% uncertainty interval [UI] 55·8-58·5) of deaths and 41·6% (40·1-43·0) of DALYs. Risks quantified account for 87·9% (86·5-89·3) of cardiovascular disease DALYs, ranging to a low of 0% for neonatal disorders and neglected tropical diseases and malaria. In terms of global DALYs in 2013, six risks or clusters of risks each caused more than 5% of DALYs: dietary risks accounting for 11·3 million deaths and 241·4 million DALYs, high systolic blood pressure for 10·4 million deaths and 208·1 million DALYs, child and maternal malnutrition for 1·7 million deaths and 176·9 million DALYs, tobacco smoke for 6·1 million deaths and 143·5 million DALYs, air pollution for 5·5 million deaths and 141·5 million DALYs, and high BMI for 4·4 million deaths and 134·0 million DALYs. Risk factor patterns vary across regions and countries and with time. In sub-Saharan Africa, the leading risk factors are child and maternal malnutrition, unsafe sex, and unsafe water, sanitation, and handwashing. In women, in nearly all countries in the Americas, north Africa, and the Middle East, and in many other high-income countries, high BMI is the leading risk factor, with high systolic blood pressure as the leading risk in most of Central and Eastern Europe and south and east Asia. For men, high systolic blood pressure or tobacco use are the leading risks in nearly all high-income countries, in north Africa and the Middle East, Europe, and Asia. For men and women, unsafe sex is the leading risk in a corridor from Kenya to South Africa.INTERPRETATION: Behavioural, environmental and occupational, and metabolic risks can explain half of global mortality and more than one-third of global DALYs providing many opportunities for prevention. Of the larger risks, the attributable burden of high BMI has increased in the past 23 years. In view of the prominence of behavioural risk factors, behavioural and social science research on interventions for these risks should be strengthened. Many prevention and primary care policy options are available now to act on key risks.FUNDING: Bill & Melinda Gates Foundation.
|
|
| 10. |
- Gejl, Kasper D., et al.
(författare)
-
Changes in metabolism but not myocellular signaling by training with CHO-restriction in endurance athletes
- 2018
-
Ingår i: Physiological Reports. - : Wiley. - 2051-817X. ; 6:17
-
Tidskriftsartikel (refereegranskat)abstract
- Carbohydrate (CHO) restricted training has been shown to increase the acute training response, whereas less is known about the acute effects after repeated CHO restricted training. On two occasions, the acute responses to CHO restriction were examined in endurance athletes. Study 1 examined cellular signaling and metabolic responses after seven training-days including CHO manipulation (n = 16). The protocol consisted of 1 h high-intensity cycling, followed by 7 h recovery, and 2 h of moderate-intensity exercise (120SS). Athletes were randomly assigned to low (LCHO: 80 g) or high (HCHO: 415 g) CHO during recovery and the 120SS. Study 2 examined unaccustomed exposure to the same training protocol (n = 12). In Study 1, muscle biopsies were obtained at rest and 1 h after 120SS, and blood samples drawn during the 120SS. In Study 2, substrate oxidation and plasma glucagon were determined. In Study 1, plasma insulin and proinsulin C-peptide were higher during the 120SS in HCHO compared to LCHO (insulin: 0 min: +37%; 60 min: +135%; 120 min: +357%, P = 0.05; proinsulin C-peptide: 0 min: +32%; 60 min: +52%; 120 min: +79%, P = 0.02), whereas plasma cholesterol was higher in LCHO (+15-17%, P = 0.03). Myocellular signaling did not differ between groups. p-AMPK and p-ACC were increased after 120SS (+35%, P = 0.03; +59%, P = 0.0004, respectively), with no alterations in p-p38, p-53, or p-CREB. In Study 2, glucagon and fat oxidation were higher in LCHO compared to HCHO during the 120SS (+26-40%, P = 0.03; +44-76%, P = 0.01 respectively). In conclusion, the clear respiratory and hematological effects of CHO restricted training were not translated into superior myocellular signaling after accustomization to CHO restriction.
|
|
| 11. |
- Gejl, Kasper Degn, et al.
(författare)
-
No Superior Adaptations to Carbohydrate Periodization in Elite Endurance Athletes
- 2017
-
Ingår i: Medicine & Science in Sports & Exercise. - 0195-9131 .- 1530-0315. ; 49:12, s. 2486-2497
-
Tidskriftsartikel (refereegranskat)abstract
- Purpose The present study investigated the effects of periodic carbohydrate (CHO) restriction on endurance performance and metabolic markers in elite endurance athletes. Methods Twenty-six male elite endurance athletes (maximal oxygen consumption (VO2max), 65.0 mL O(2)kg(-1)min(-1)) completed 4 wk of regular endurance training while being matched and randomized into two groups training with (low) or without (high) CHO manipulation 3 dwk(-1). The CHO manipulation days consisted of a 1-h high-intensity bike session in the morning, recovery for 7 h while consuming isocaloric diets containing either high CHO (414 2.4 g) or low CHO (79.5 1.0 g), and a 2-h moderate bike session in the afternoon with or without CHO. VO2max, maximal fat oxidation, and power output during a 30-min time trial (TT) were determined before and after the training period. The TT was undertaken after 90 min of intermittent exercise with CHO provision before the training period and both CHO and placebo after the training period. Muscle biopsies were analyzed for glycogen, citrate synthase (CS) and -hydroxyacyl-coenzyme A dehydrogenase (HAD) activity, carnitine palmitoyltransferase (CPT1b), and phosphorylated acetyl-CoA carboxylase (pACC). Results The training effects were similar in both groups for all parameters. On average, VO2max and power output during the 30-min TT increased by 5% +/- 1% (P < 0.05) and TT performance was similar after CHO and placebo during the preload phase. Training promoted overall increases in glycogen content (18% +/- 5%), CS activity (11% +/- 5%), and pACC (38% +/- 19%; P < 0.05) with no differences between groups. HAD activity and CPT1b protein content remained unchanged. Conclusions Superimposing periodic CHO restriction to 4 wk of regular endurance training had no superior effects on performance and muscle adaptations in elite endurance athletes.
|
|
| 12. |
- Harrison, Dick, et al.
(författare)
-
Förord
- 2017
-
Ingår i: Korstågen : européer i heligt krig under 500 år - européer i heligt krig under 500 år. - 9789175043135 ; , s. 6-13
-
Bokkapitel (refereegranskat)
|
|
| 13. |
- Jackson, Victoria E, et al.
(författare)
-
Meta-analysis of exome array data identifies six novel genetic loci for lung function.
- 2018
-
Ingår i: Wellcome open research. - : F1000 Research Ltd. - 2398-502X. ; 3
-
Tidskriftsartikel (refereegranskat)abstract
- Background: Over 90 regions of the genome have been associated with lung function to date, many of which have also been implicated in chronic obstructive pulmonary disease. Methods: We carried out meta-analyses of exome array data and three lung function measures: forced expiratory volume in one second (FEV 1), forced vital capacity (FVC) and the ratio of FEV 1 to FVC (FEV 1/FVC). These analyses by the SpiroMeta and CHARGE consortia included 60,749 individuals of European ancestry from 23 studies, and 7,721 individuals of African Ancestry from 5 studies in the discovery stage, with follow-up in up to 111,556 independent individuals. Results: We identified significant (P<2·8x10 -7) associations with six SNPs: a nonsynonymous variant in RPAP1, which is predicted to be damaging, three intronic SNPs ( SEC24C, CASC17 and UQCC1) and two intergenic SNPs near to LY86 and FGF10. Expression quantitative trait loci analyses found evidence for regulation of gene expression at three signals and implicated several genes, including TYRO3 and PLAU. Conclusions: Further interrogation of these loci could provide greater understanding of the determinants of lung function and pulmonary disease.
|
|
| 14. |
|
|
| 15. |
- Jensen, Kurt Villads, 1957-
(författare)
-
Bishops on crusade
- 2018
-
Ingår i: Dominus Episcopus. - Stockholm : Kungl. Vitterhets Historie och Antikvitets Akademien. - 9789174024630 ; , s. 83-99
-
Bokkapitel (refereegranskat)
|
|
| 16. |
|
|
| 17. |
|
|
| 18. |
|
|
| 19. |
- Jensen, Kurt Villads, 1957-
(författare)
-
Conclusion : Is it Good to be Peripheral?
- 2017
-
Ingår i: Livland – eine Region am Ende der Welt?. - Köln : Böhlau. - 9783412508050 ; , s. 483-493
-
Bokkapitel (refereegranskat)
|
|
| 20. |
|
|
| 21. |
- Jensen, Kurt Villads, 1957-
(författare)
-
Crusading at the Edges of Europe : Denmark and Portugal c. 1000 - c. 1250
- 2017
-
Bok (refereegranskat)abstract
- Communication in the Middle Ages was better developed than often assumed and institutions, ideas, and military technology was exchanged rapidly, meaning it was possible to coordinate great military expeditions across the geographical periphery of Western Europe. Both Denmark and Portugal were closely connected to the sea and developed strong fleets, at the entrance to the Baltic and in the Mediterranean Seas respectively. They also both had religious borders, to the pagan Wends and to the Muslims, that were pushed forward in almost continuous crusades throughout the centuries. Crusading at the Edges of Europe follows the major campaigns of the kings and crusaders in Denmark and Portugal and compares war-technology and crusading ideology, highlighting how the countries learned from each other and became organised for war.
|
|
| 22. |
|
|
| 23. |
- Jensen, Kurt Villads, 1957-
(författare)
-
Crying Crusaders
- 2017
-
Ingår i: Tears, sighs and laughter. - Stockholm : Kungl. Vitterhets Historie och Antikvitets Akademien. - 9789174024470 ; , s. 98-108
-
Bokkapitel (refereegranskat)
|
|
| 24. |
- Jensen, Kurt Villads, 1957-, et al.
(författare)
-
Det danske imperium
- 2017
-
Ingår i: Imperier. - København : Forlaget Columbus. - 9788779703551 ; , s. 117-146
-
Bokkapitel (refereegranskat)
|
|
| 25. |
|
|
| 26. |
- Jensen, Kurt Villads, 1957-
(författare)
-
Doktor Dampe og Koranens etik
- 2016
-
Ingår i: Krig, korstog og kulturmøder i 1700-tallet. - Nyborg : Østfyns Museer. - 9788792620330 ; , s. 143-171
-
Bokkapitel (övrigt vetenskapligt/konstnärligt)
|
|
| 27. |
|
|
| 28. |
|
|
| 29. |
|
|
| 30. |
- Jensen, Kurt Villads, 1957-
(författare)
-
Fra konge til korstog
- 2017
-
Konferensbidrag (övrigt vetenskapligt/konstnärligt)
|
|
| 31. |
|
|
| 32. |
|
|
| 33. |
|
|
| 34. |
- Jensen, Kurt Villads, 1957-
(författare)
-
Jerusalem på jorden : Rundkyrkor och korståg
- 2018
-
Ingår i: Bromma Kyrka 850 år. - Bromma : Bromma församling. - 9789163981166 ; , s. 17-23
-
Bokkapitel (övrigt vetenskapligt/konstnärligt)
|
|
| 35. |
|
|
| 36. |
|
|
| 37. |
- Jensen, Kurt Villads, 1957-
(författare)
-
Langekapellet og Birgittakapellet
- 2018
-
Ingår i: Ribe Domkirke kirkeblad. ; :4, s. 4-9
-
Tidskriftsartikel (populärvet., debatt m.m.)
|
|
| 38. |
- Jensen, Kurt Villads, 1957-
(författare)
-
Prisoners of war in the Baltic in the XII-XIII centuries
- 2017
-
Ingår i: E-strategica. - 2530-9951. ; :1, s. 285-295
-
Tidskriftsartikel (refereegranskat)abstract
- Warfare was cruel along the religious borders in the Baltic in the twelfth and thirteenth century and oscillated between mass killing and mass enslavement. Prisoners of war were often problematic to control and guard, but they were also of huge economic importance. Some were used in production, some were ransomed, some held as hostages, all depending upon status of the prisoners and needs of the slave owners.
|
|
| 39. |
|
|
| 40. |
- Jensen, Kurt Villads, 1957-
(författare)
-
Ristiretket
- 2019
-
Bok (refereegranskat)
|
|
| 41. |
|
|
| 42. |
- Jensen, Kurt Villads, 1957-, et al.
(författare)
-
Rude : Zisterzienser
- 2019
-
Ingår i: Klosterbuch Schleswig-Holstein und Hamburg. - Regensburg : Verlag Schnell + Steiner GmbH. - 9783795428969 ; , s. 509-532
-
Bokkapitel (refereegranskat)
|
|
| 43. |
|
|
| 44. |
- Jensen, Kurt Villads, 1957-
(författare)
-
Saints at War in the Baltic Region
- 2018
-
Ingår i: Saints and Sainthood around the Baltic Sea. - Michigan : Medieval Institute Publications. - 9781580443234 - 9781580443241 ; , s. 251-271
-
Bokkapitel (refereegranskat)
|
|
| 45. |
|
|
| 46. |
|
|
| 47. |
|
|
| 48. |
|
|
| 49. |
|
|
| 50. |
|
|
