Recovering Joys Law as a Function of Solar Cycle, Hemisphere, and Longitude

Bipolar active regions in both hemispheres tend to be tilted with respect to the East West equator of the Sun in accordance with Joys law that describes the average tilt angle as a function of latitude. Mt. Wilson observatory data from 1917 to 1985 are used to analyze the active-region tilt angle as a function of solar cycle, hemisphere, and longitude, in addition to the more common dependence on latitude. Our main results are as follows: i) We recommend a revision of Joys law toward a weaker dependence on latitude (slope of 0.13 to 0.26) and without forcing the tilt to zero at the Equator. ii) We determine that the hemispheric mean tilt value of active regions varies with each solar cycle, although the noise from a stochastic process dominates and does not allow for a determination of the slope of Joys law on an 11-year time scale. iii) The hemispheric difference in mean tilt angles, 1.1 degrees + 0.27, over Cycles 16 to 21 was significant to a three-sigma level, with average tilt angles in the northern and southern hemispheres of 4.7 degrees + 0.26 and 3.6 degrees + 0.27 respectively. iv) Area-weighted mean tilt angles normalized by latitude for Cycles 15 to 21 anticorrelate with cycle strength for the southern hemisphere and whole-Sun data, confirming previous results by Dasi-Espuig, Solanki, Krivova, et al. (2010, Astron. Astrophys. 518, A7). The northern hemispheric mean tilt angles do not show a dependence on cycle strength. vi) Mean tilt angles do not show a dependence on longitude for any hemisphere or cycle. In addition, the standard deviation of the mean tilt is 29 to 31 degrees for all cycles and hemispheres indicating that the scatter is due to the same consistent process even if the mean tilt angles vary.Comment: 13 pages, 4 figures, 3 table

Fitting the integrated Spectral Energy Distributions of Galaxies

Fitting the spectral energy distributions (SEDs) of galaxies is an almost universally used technique that has matured significantly in the last decade. Model predictions and fitting procedures have improved significantly over this time, attempting to keep up with the vastly increased volume and quality of available data. We review here the field of SED fitting, describing the modelling of ultraviolet to infrared galaxy SEDs, the creation of multiwavelength data sets, and the methods used to fit model SEDs to observed galaxy data sets. We touch upon the achievements and challenges in the major ingredients of SED fitting, with a special emphasis on describing the interplay between the quality of the available data, the quality of the available models, and the best fitting technique to use in order to obtain a realistic measurement as well as realistic uncertainties. We conclude that SED fitting can be used effectively to derive a range of physical properties of galaxies, such as redshift, stellar masses, star formation rates, dust masses, and metallicities, with care taken not to over-interpret the available data. Yet there still exist many issues such as estimating the age of the oldest stars in a galaxy, finer details ofdust properties and dust-star geometry, and the influences of poorly understood, luminous stellar types and phases. The challenge for the coming years will be to improve both the models and the observational data sets to resolve these uncertainties. The present review will be made available on an interactive, moderated web page (sedfitting.org), where the community can access and change the text. The intention is to expand the text and keep it up to date over the coming years.Comment: 54 pages, 26 figures, Accepted for publication in Astrophysics & Space Scienc

Plasma lipid profiles discriminate bacterial from viral infection in febrile children

Fever is the most common reason that children present to Emergency Departments. Clinical signs and symptoms suggestive of bacterial infection ar

Novel Loci for Adiponectin Levels and Their Influence on Type 2 Diabetes and Metabolic Traits : A Multi-Ethnic Meta-Analysis of 45,891 Individuals

J. Kaprio, S. Ripatti ja M.-L. Lokki työryhmien jäseniä.Peer reviewe

The Deoxygenation and Isomerization of Artemisinin and Artemether and Their Relevance to Antimalarial Action

The treatment of artemisinin (1) and ß-artemether (6) with Zn dissolving in AcOH for a few hours results in mono-deoxygenation giving deoxyartemisinin (5) and deoxy-ß-artemether (7), respectively, as the sole product. In contrast, submission of 1 to FeCl2 · 4 H2O in MeCN at room temperature for 15 min causes only isomerization, (3aS,4R,6aS,7R,10S,10aR)-octahydro-4,7-dimethyl-8-oxo-2H-10H-furo[3,2-i] benzopyran-10-yl acetate (8) and (3R)-3-hydroxydeoxyartemisinin (9) being produced in 78 and 17% yield, respectively. The action of FeCl2 · 4 H2O in MeCN on 6 is similar. Under the same conditions, 6 gives products analogous to 8 and 9 accompanied by an epimeric mixture of 2-[4-methyl-2-oxo-3-(3-oxobutyl)cyclohexyl]propanaldehyde in yields of 32, 23, and 16%, respectively. No epoxide is formed on repeating the last two experiments in the presence of cyclohexene. The deoxygenation of 1 and 6 by Zn is rationalized in terms of its oxophilic nature. The catalyzed isomerization of 1 and 6 by Fe2+ is attributed to the redox properties of the Fe2+/Fe3+ system

Leydig cell hypoplasia: cases with new mutations, new polymorphisms and cases without mutations in the luteinizing hormone receptor gene.

BACKGROUND: Defective male sex differentiation in patients with hypoplasia of Leydig cells (LCH) is caused by deficient LH receptor signal transduction. To further investigate the variety of LH receptor gene mutations present in LCH patients and their influence on the phenotype, we examined 10 nonrelated patients with the clinical presentation of LCH. PATIENTS AND METHODS: Ten patients with a clinical phenotype of LCH were analysed for mutations in the complete coding region of the LH receptor gene. Exons 1-10 and two overlapping fragments of exon 11 of the LH receptor gene including all intron-exon boundaries were amplified by polymerase chain reaction and sequenced. To screen for frequencies of DNA changes, mutation analysis was performed on 45-59 healthy persons using denaturation high-performance liquid chromatography. RESULTS: Six new DNA alterations were identified. Three of them appear to be new polymorphisms. A G to C change at the 28th nucleotide of intron 1 on one allele and a heterozygous CGA to CAA transition at codon 124 (R124Q) were found. Both findings in these two patients are polymorphisms that occur with a frequency of 17% and 1.7%, respectively. A silent heterozygous CTA to TTA change at codon 204 was identified. In a patient with micropenis, the analysis revealed a homozygous missense mutation at codon 625 (I625K). As reported previously, this alteration significantly impaired signal transduction and explains the partial phenotype. Finally, in one compound heterozygous patient, two different mutations were discovered. At the polymorphic site in exon 1, a 27-bp insertion (CTG)2 AAG (CTG)5 CAG and a premature stop codon in the transmembrane segment 4 (W491*) were found. Both mutations disrupt signal transduction and explain the complete phenotype of this patient. In five patients, no DNA alterations could be identified. CONCLUSIONS: Three mutations (33 bp insertion in exon 1; W491* and I625K) were identified that explain the phenotype in two patients. In addition, most of the patients with the clinical phenotype of LCH did not have causative mutations, suggesting that changes in other regions of the LH receptor gene, such as the large introns or the promoter region, may be responsible for the majority of cases. Alternatively, the displayed phenotype may be the result of other genetic defects. Our work further underscores the importance of thorough clinical analysis of patients before molecular analysis of a particular gene is performed