| 1. |
- Hagiwara, K, et al.
(författare)
-
Review of particle physics
- 2002
-
Ingår i: Physical Review D (Particles and Fields). - 0556-2821. ; 66:1
-
Forskningsöversikt (refereegranskat)abstract
- This biennial Review summarizes much of Particle Physics Using data from previous editions, plus 2205 new measurements from 667 papers, we list, evaluate, and average measured properties of gauge bosons, leptons, quarks, mesons, and baryons We also summarize searches for hypothetical particles such as Higgs bosons, heavy neutrinos, and supersymmetric particles All the particle properties and search limits are listed in Summary Tables We also give numerous tables, figures, formulae, and reviews of topics such as the Standard Model, particle detectors, probability, and statistics This edition features expanded coverage of CP violation in B mesons and of neutrino oscillations For the first time we cover searches for evidence of extra dimensions (both in the particle listings and in a new review) Another new review is on Grand Unified Theories A booklet is available containing the Summary Tables and abbreviated versions of some of the other sections of this full Review All tables, listings, and reviews (and errata) are also available on the Particle Data Group website http //pdg 1b1 gov.
|
|
| 2. |
- Li, Jian-Liang, et al.
(författare)
-
A genome scan for modifiers of age at onset in Huntington disease : The HD MAPS study.
- 2003
-
Ingår i: American Journal of Human Genetics. - : Elsevier BV. - 0002-9297 .- 1537-6605. ; 73:3, s. 682-7
-
Tidskriftsartikel (refereegranskat)abstract
- Huntington disease (HD) is caused by the expansion of a CAG repeat within the coding region of a novel gene on 4p16.3. Although the variation in age at onset is partly explained by the size of the expanded repeat, the unexplained variation in age at onset is strongly heritable (h2=0.56), which suggests that other genes modify the age at onset of HD. To identify these modifier loci, we performed a 10-cM density genomewide scan in 629 affected sibling pairs (295 pedigrees and 695 individuals), using ages at onset adjusted for the expanded and normal CAG repeat sizes. Because all those studied were HD affected, estimates of allele sharing identical by descent at and around the HD locus were adjusted by a positionally weighted method to correct for the increased allele sharing at 4p. Suggestive evidence for linkage was found at 4p16 (LOD=1.93), 6p21-23 (LOD=2.29), and 6q24-26 (LOD=2.28), which may be useful for investigation of genes that modify age at onset of HD.
|
|
| 3. |
|
|
| 4. |
|
|
| 5. |
|
|
| 6. |
- Winick, Jeremy R., et al.
(författare)
-
Thermospheric infrared radiance response to the April 2002 geomagnetic storm from SABER infrared and GUVI ultraviolet limb data
- 2004
-
Ingår i: Proceedings of SPIE, the International Society for Optical Engineering. - : SPIE. - 0277-786X .- 1996-756X. ; 5235, s. 250-263
-
Tidskriftsartikel (refereegranskat)abstract
- The SABER instrument on TIMED continuously measures certain infrared limb radiance profiles with unprecedented sensitivity. Among these are emissions of CO 2 v 3 at 4.3 μm, routinely recorded to tangent heights of ∼140-150 km, and NO at 5.3 μm, seen to above 200 km. Both of these are greatly enhanced during periods of strong auroral activity, when they can be measured to ∼200 km and ∼300 km, respectively. We use these infrared channels of SABER and coincident far ultraviolet (FUV) measurements from GUVI on TIMED, to study the geomagnetic storm of April 2002. These all give a consistent measure of auroral energy input into the lower thermosphere at high latitudes. Emission in yet another SABER channel, near 2.0 μm, correlates well with enhanced electron energy deposition. We also have, in the 5.3-μm emissions from the long-lived population of aurorally produced NO, a tracer of how this energy is transported equatorward and released over an extended period of time, a few days. In this paper, we discuss the global patterns of energy deposition into the expanded auroral oval, its transport to lower latitudes, and its loss as revealed by the NO 5.3-μm emissions.
|
|
| 7. |
|
|
| 8. |
|
|
| 9. |
|
|
| 10. |
- Ljungman, P., et al.
(författare)
-
Respiratory virus infections after stem cell transplantation : a prospective study from the Infectious Diseases Working Party of the European Group for Blood and Marrow Transplantation
- 2001
-
Ingår i: Bone Marrow Transplantation. - : Springer Science and Business Media LLC. - 0268-3369 .- 1476-5365. ; 28:5, s. 479-484
-
Tidskriftsartikel (refereegranskat)abstract
- Community-acquired respiratory virus infections are a cause of mortality after stem cell transplantation (SCT). A prospective study was performed at 37 centers to determine their frequency and importance. Additional cases were also collected to allow the analysis of risk factors for severe infection. Forty episodes were collected in the prospective study and 53 additional episodes through subsequent case collection. The frequency of documented respiratory virus infections was 3.5% among 819 allogeneic and 0.4% among 1154 autologous SCT patients transplanted during the study period. The frequency of lower respiratory tract infections (LRTI) was 2.1% among allogeneic and 0.2% among autologous SCT patients. The mortality within 28 days from diagnosis of a respiratory viral infection was 1.1% among allogeneic SCT while no autologous SCT patient died. The deaths of five patients (0.6%) were directly attributed to a respiratory virus infection (three RSV; two influenza A). On multivariate analysis, lymphocytopenia increased the risk for LRTI (P = 0.008). Lymphocytopenia was also a significant risk factor for LRTI in patients with RSV infections. The overall mortality in RSV infection was 30.4% and the direct RSV-associated mortality was 17.4%. For influenza A virus infection, the corresponding percentages were 23.0% and 15.3%. This prospective study supports the fact that community-acquired respiratory virus infections cause transplant-related mortality after SCT.
|
|
