| 1. |
- Aoyama, T., et al.
(författare)
-
The anomalous magnetic moment of the muon in the Standard Model
- 2020
-
Ingår i: Physics reports. - : Elsevier BV. - 0370-1573 .- 1873-6270. ; 887, s. 1-166
-
Forskningsöversikt (refereegranskat)abstract
- We review the present status of the Standard Model calculation of the anomalous magnetic moment of the muon. This is performed in a perturbative expansion in the fine-structure constant α and is broken down into pure QED, electroweak, and hadronic contributions. The pure QED contribution is by far the largest and has been evaluated up to and including O(α5) with negligible numerical uncertainty. The electroweak contribution is suppressed by (mμ/MW)2 and only shows up at the level of the seventh significant digit. It has been evaluated up to two loops and is known to better than one percent. Hadronic contributions are the most difficult to calculate and are responsible for almost all of the theoretical uncertainty. The leading hadronic contribution appears at O(α2) and is due to hadronic vacuum polarization, whereas at O(α3) the hadronic light-by-light scattering contribution appears. Given the low characteristic scale of this observable, these contributions have to be calculated with nonperturbative methods, in particular, dispersion relations and the lattice approach to QCD. The largest part of this review is dedicated to a detailed account of recent efforts to improve the calculation of these two contributions with either a data-driven, dispersive approach, or a first-principle, lattice-QCD approach. The final result reads aμSM = 116 591 810(43) x 10-11 and is smaller than the Brookhaven measurement by 3.7 σ. The experimental uncertainty will soon be reduced by up to a factor four by the new experiment currently running at Fermilab, and also by the future J-PARC experiment. This and the prospects to further reduce the theoretical uncertainty in the near future - which are also discussed here - make this quantity one of the most promising places to look for evidence of new physics.
|
|
| 2. |
|
|
| 3. |
- Agostoni, Angelo, et al.
(författare)
-
Hereditary and acquired angioedema: problems and progress: proceedings of the third C1 esterase inhibitor deficiency workshop and beyond
- 2004
-
Ingår i: Journal of Allergy and Clinical Immunology. - : Elsevier BV. - 1097-6825 .- 0091-6749. ; 114:3 Suppl, s. 51-131
-
Tidskriftsartikel (refereegranskat)abstract
- Hereditary angioedema (HAE), a rare but life-threatening condition, manifests as acute attacks of facial, laryngeal, genital, or peripheral swelling or abdominal pain secondary to intra-abdominal edema. Resulting from mutations affecting C1 esterase inhibitor (C1-INH), inhibitor of the first complement system component, attacks are not histamine-mediated and do not respond to antihistamines or corticosteroids. Low awareness and resemblance to other disorders often delay diagnosis; despite availability of C1-INH replacement in some countries, no approved, safe acute attack therapy exists in the United States. The biennial C1 Esterase Inhibitor Deficiency Workshops resulted from a European initiative for better knowledge and treatment of HAE and related diseases. This supplement contains work presented at the third workshop and expanded content toward a definitive picture of angioedema in the absence of allergy. Most notably, it includes cumulative genetic investigations; multinational laboratory diagnosis recommendations; current pathogenesis hypotheses; suggested prophylaxis and acute attack treatment, including home treatment; future treatment options; and analysis of patient subpopulations, including pediatric patients and patients whose angioedema worsened during pregnancy or hormone administration. Causes and management of acquired angioedema and a new type of angioedema with normal C1-INH are also discussed. Collaborative patient and physician efforts, crucial in rare diseases, are emphasized. This supplement seeks to raise awareness and aid diagnosis of HAE, optimize treatment for all patients, and provide a platform for further research in this rare, partially understood disorder.
|
|
| 4. |
- Boyle, Peter, et al.
(författare)
-
Isospin-breaking corrections to light leptonic decays in lattice QCD+QED at the physical point
- 2023
-
Ingår i: The 39th International Symposium on Lattice Field Theory (LATTICE2022). - Trieste, Italy : Sissa Medialab. - 1824-8039. ; 430
-
Konferensbidrag (refereegranskat)abstract
- We report on the physical-point RBC/UKQCD calculation of the leading isospin-breaking corrections to light-meson leptonic decays. This is highly relevant for future precision tests in the flavour physics sector, in particular the first-row unitarity of the Cabibbo-Kobayashi-Maskawa matrix containing the elements Vus and Vud. The simulations were performed using Domain-Wall fermions for 2 + 1 flavours, and with isospin-breaking effects included perturbatively in the path integral through order α and (mu - md)/ΛQCD. We use QEDL for the inclusion of electromagnetism, and discuss here the non-locality of this prescription which has significant impact on the infinite-volume extrapolation.
|
|
| 5. |
- Gulez, N., et al.
(författare)
-
Homozygosity For a Novel Mutation in the C1q C Chain Gene in a Turkish Family With Hereditary C1q Deficiency
- 2010
-
Ingår i: Journal of Investigational Allergology & Clinical Immunology. - 1698-0808. ; 20:3, s. 255-258
-
Tidskriftsartikel (refereegranskat)abstract
- Hereditary complete deficiency of complement component C1q is associated with a high prevalence of systemic lupus erythematosus and increased susceptibility to severe recurrent infections. An 11-year-old girl was screened for immunodeficiency due to a history of recurrent meningitis and pneumonia. Immunologic studies revealed absence of classic pathway hemolytic activity and undetectable levels of C1q. Exon-specific amplification of genomic DNA by polymerase chain reaction followed by direct sequence analysis revealed a novel homozygous missense mutation at codon 48 in the C1q C gene causing a glycine-to-arginine substitution affecting the collagen-like region of C1q. No changes were seen in the exons of the A and B chains. The mutation affected both the formation and the secretion of C1q variant molecules. We describe a novel mutation in the C1q C chain gene that leads to an interchange in amino acids resulting in absence of C1q in serum.
|
|
| 6. |
- Johanneson, B, et al.
(författare)
-
A comparison of genome-scans performed in multicase families with systemic lupus erythematosus from different population groups
- 1999
-
Ingår i: Journal of Autoimmunity. - : Elsevier BV. - 0896-8411. ; 13, s. 137-
-
Tidskriftsartikel (refereegranskat)abstract
- Systemic lupus erythematosus is a disease of unknown etiology. Multiple genetic factors are believed to be involved in its pathogenesis. In addition, and due to genetic heterogeneity, these factors and/or their combinations may be different in different ethnic groups, while some might be shared between populations. We have performed genome scans in multicase families from three different population groups, two from Northern Europe, with a high degree of homogeneity, and the third from a recently admixed population of Mexican Mestizos. Although our family material is relatively small, the results presented here show that using family sets from well defined populations are sufficient to detect susceptibility loci for SLE. Our results also reveal the chromosomal regions most likely to contain susceptibility genes for SLE.
|
|
| 7. |
- Jönsen, Andreas, et al.
(författare)
-
Genetically determined mannan-binding lectin deficiency is of minor importance in determining susceptibility to severe infections and vascular organ damage in systemic lupus erythematosus.
- 2007
-
Ingår i: Lupus. - : SAGE Publications. - 0961-2033 .- 1477-0962. ; 16:4, s. 245-253
-
Tidskriftsartikel (refereegranskat)abstract
- Deficiency of mannan-binding lectin (MBL) has been reported to impact susceptibility to severe nfections and atherosclerosis in systemic lupus erythematosus (SLE). In this study, MBL gene polymorphisms were analysed in 143 SLE patients and the frequency of severe infections and organ damage according to SLICC/ACR Damage Index regarding cerebrovascular accidents, angina pectoris, coronary by-pass surgery, myocardial infarction and peripheral arterial disease leading to significant tissue loss, were recorded during a mean follow-up time of 15 years from diagnosis. In a multiple logistic regression model, smoking (P = 0.001), hypertension (P = 0.030), alcohol intake (P = 0.027) and higher triglyceride concentration (P = 0.026) were associated with cerebrovascular, cardiovascular and peripheral arterial organ damage (CPAD), while the association with MBL deficiency did not reach significance (P = 0.098). Alcohol intake (> 15 g/month) was inversely correlated with CPAD (OR = 0.29, 95%Cl 0.096-0.87). MBL deficiency was not significantly more common in SLE patients with severe infections in a multivariate analysis (P > 0.3). In conclusion, classical risk factors such as smoking, hypertension, low alcohol intake and elevated triglyceride concentration were relatively more important for development of CPAD than MBL deficiency in SLE. Furthermore, MBL deficiency did not contribute to development of major infections in SLE.
|
|
| 8. |
- Linder, Astrid, et al.
(författare)
-
Dynamic performances of different seat designs for low to medium velocity rear impact.
- 2001
-
Ingår i: 45th Annual Proceedings. - : Association for the Advancement of Automotive Medicine. ; , s. 187-201
-
Konferensbidrag (refereegranskat)abstract
- There is good evidence that seat design and impact severities in terms of delta-V and acceleration plays a role in AIS 1 neck injury outcomes in the event of a rear impact. This study evaluates a number of current production seats to assess the AIS 1 neck injury protection potential at different impact severities. Five different seat designs were exposed to four different impact severities in a sled simulating a rear impact. The same delta-V produced with different peak accelerations generated very different dummy responses. Head restraint position influenced the angular and horizontal displacement of the head relative to torso and the time of head to head restraint contact. The lowest motion of the head relative to the torso was found in the two anti-whiplash seats tested. The results of the study can be used for the design of future vehicle seats and anti-whiplash systems.
|
|
| 9. |
|
|
| 10. |
- Orbai, A-M, et al.
(författare)
-
Anti-C1q antibodies in systemic lupus erythematosus.
- 2015
-
Ingår i: Lupus. - : SAGE Publications. - 0961-2033 .- 1477-0962. ; 24:1, s. 42-49
-
Tidskriftsartikel (refereegranskat)abstract
- Anti-C1q has been associated with systemic lupus erythematosus (SLE) and lupus nephritis in previous studies. We studied anti-C1q specificity for SLE (vs rheumatic disease controls) and the association with SLE manifestations in an international multicenter study.
|
|
