639 research outputs found
An Empirical Relation Between The Large-Scale Magnetic Field And The Dynamical Mass In Galaxies
The origin and evolution of cosmic magnetic fields as well as the influence
of the magnetic fields on the evolution of galaxies are unknown. Though not
without challenges, the dynamo theory can explain the large-scale coherent
magnetic fields which govern galaxies, but observational evidence for the
theory is so far very scarce. Putting together the available data of
non-interacting, non-cluster galaxies with known large-scale magnetic fields,
we find a tight correlation between the integrated polarized flux density,
S(PI), and the rotation speed, v(rot), of galaxies. This leads to an almost
linear correlation between the large-scale magnetic field B and v(rot),
assuming that the number of cosmic ray electrons is proportional to the star
formation rate, and a super-linear correlation assuming equipartition between
magnetic fields and cosmic rays. This correlation cannot be attributed to an
active linear alpha-Omega dynamo, as no correlation holds with global shear or
angular speed. It indicates instead a coupling between the large-scale magnetic
field and the dynamical mass of the galaxies, B ~ M^(0.25-0.4). Hence, faster
rotating and/or more massive galaxies have stronger large-scale magnetic
fields. The observed B-v(rot) correlation shows that the anisotropic turbulent
magnetic field dominates B in fast rotating galaxies as the turbulent magnetic
field, coupled with gas, is enhanced and ordered due to the strong gas
compression and/or local shear in these systems. This study supports an
stationary condition for the large-scale magnetic field as long as the
dynamical mass of galaxies is constant.Comment: 23 pages, 4 figures, accepted for publication in the Astrophysical
Journal Letter
Gain of chromosome arm 17q is associated with unfavourable prognosis in neuroblastoma, but does not involve mutations in the somatostatin receptor 2 (SSTR2) gene at 17q24
Deletion of chromosome arm 1p and amplification of the MYCN oncogene are well-recognized genetic alterations in neuroblastoma cells. Recently, another alteration has been reported; gain of the distal part of chromosome arm 17q. In this study 48 neuroblastoma tumours were successfully analysed for 17q status in relation to known genetic alterations. Chromosome 17 status was detected by fluorescence in situ hybridization (FISH). Thirty-one of the 48 neuroblastomas (65%) showed 17q gain, and this was significantly associated with poor prognosis. As previously reported, 17q gain was significantly associated with metastatic stage 4 neuroblastoma and more frequently detected than both deletion of chromosome arm 1p and MYCN amplification in tumours of all stages. 17q gain also showed a strong correlation to survival probability (P = 0.0009). However, the most significant correlation between 17q gain and survival probability was observed in children with low-stage tumours (stage 1, 2, 3 and 4S), with a survival probability of 100% at 5 years from diagnosis for children with tumours showing no 17q gain compared to 52.5% for those showing 17q gain (P = 0.0021). This suggests that 17q gain as a prognostic factor plays a more crucial role in low-stage tumours. Expression of the somatostatin receptor 2 (SSTR2), localized in chromosome region 17q24, has in previous studies been shown to be positively related to survival in neuroblastoma. A point mutation in the SSTR2 gene has earlier been reported in a human small-cell lung cancer. In this study, mutation screening of the SSTR2 gene in 43 neuroblastoma tumours was carried out with polymerase chain reaction-based single-stranded conformation polymorphism/heteroduplex (SSCP/HD) and DNA sequencing, and none of the tumours showed any aberrations in the SSTR2 gene. These data suggest that mutations in the SSTR2 gene are uncommon in neuroblastoma tumours and do not correlate with either the 17q gain often seen or the reason some tumours do not express SSTR2 receptors. Overall, this study indicates that gain of chromosome arm 17q is the most frequently occurring genetic alteration, and that it is associated with established prognostic factors. © 1999 Cancer Research Campaig
Gaseous mercury distribution in the upper troposphere and lower stratosphere observed onboard the CARIBIC passenger aircraft
Positional Concerns among the Poor: Does Reference Group Matter? Evidence from Survey Experiments
Analyses of apoptotic regulators CASP9 and DFFA at 1P36.2, reveal rare allele variants in human neuroblastoma tumours
The genes encoding Caspase-9 and DFF45 have both recently been mapped to chromosome region 1p36.2, that is a region alleged to involve one or several tumour suppressor genes in neuroblastoma tumours. This study presents an update contig of the ‘Smallest Region of Overlap of deletions’ in Scandinavian neuroblastoma tumours and suggests that DFF45 is localized in the region. The genomic organization of the human DFF45 gene, deduced by in-silico comparisons of DNA sequences, is described for the first time in this paper. In the present study 44 primary tumours were screened for mutation by analysis of the genomic sequences of the genes. In two out of the 44 tumours this detected in the DFFA gene one rare allele variant that caused a non-polar to a polar amino acid exchange in a preserved hydrophobic patch of DFF45. One case was hemizygous due to deletion of the more common allele of this polymorphism. Out of 194 normal control alleles only one was found to carry this variant allele, so in respect of it, no healthy control individual out of 97 was homozygous. Moreover, our RT–PCR expression studies showed that DFF45 is preferably expressed in low-stage neuroblastoma tumours and to a lesser degree in high-stage neuroblastomas. We conclude that although coding mutations of Caspase-9 and DFF45 are infrequent in neuroblastoma tumours, our discovery of a rare allele in two neuroblastoma cases should be taken to warrant further studies of the role of DFF45 in neuroblastoma genetics
A novel 1p36.2 located gene, APITD1, with tumour-suppressive properties and a putative p53-binding domain, shows low expression in neuroblastoma tumours
Neuroblastoma is characterised by a lack of TP53 mutations and no other tumour suppressor gene consistently inactivated has yet been identified in this childhood cancer form. Characterisation of a new gene, denoted APITD1, in the neuroblastoma tumour suppressor candidate region in chromosome 1p36.22 reveals that APITD1 contains a predicted TFIID-31 domain, representing the TATA box-binding protein-associated factor, TAFII31, which is required for p53-mediated transcription activation. Two different transcripts of this gene were shown to be ubiquitously expressed, one of them with an elevated expression in foetal tissues. Primary neuroblastoma tumours of all different stages showed either very weak or no measurable APITD1 expression, contrary to the level of expression observed in neuroblastoma cell lines. A reduced pattern of expression was also observed in a set of various tumour types. APITD1 was functionally tested by adding APITD1 mRNA to neuroblastoma cells, leading to the cell growth to be reduced up to 90% compared to control cells, suggesting APITD1 to have a role in a cell death pathway. Furthermore, we determined the genomic organisation of APITD1. Automated genomic DNA sequencing of the coding region of the gene as well as the promoter sequence in 44 neuroblastoma tumours did not reveal any loss-of-function mutations, indicating that mutations in APITD1 is not a common abnormality of neuroblastoma tumours. We suggest that low expression of this gene might interfere with the ability for apoptosis through the p53 pathway
Mercury distribution in the upper troposphere and lowermost stratosphere according to measurements by the IAGOS-CARIBIC observatory: 2014-2016
Mercury was measured onboard the IAGOSCARIBIC passenger aircraft from May 2005 until February 2016 during near monthly sequences of mostly four intercontinental flights from Germany to destinations in North and South America, Africa and South and East Asia. Most of these mercury data were obtained using an internal default signal integration procedure of the Tekran instrument but since April 2014 more precise and accurate data were obtained using post-flight manual integration of the instrument raw signal. In this paper we use the latter data. Increased upper tropospheric total mercury (TM) concentrations due to large scale biomass burning were observed in the upper troposphere (UT) at the equator and southern latitudes during the flights to Latin America and South Africa in boreal autumn (SON) and boreal winter (DJF). TM concentrations in the lowermost stratosphere (LMS) decrease with altitude above the thermal tropopause but the gradient is less steep than reported before. Seasonal variation of the vertical TM distribution in the UT and LMS is similar to that of other trace gases with surface sources and stratospheric sinks. Speciation experiments suggest comparable TM and gaseous elementary mercury (GEM) concentrations at and below the tropopause leaving little space for Hg2+ (TM-GEM) being the dominating component of TM here. In the stratosphere significant GEM concentrations were found to exist up to 4 km altitude above the thermal tropopause. Correlations with N2O as a reference tracer suggest stratospheric lifetimes of 72 ± 37 and 74 ± 27 years for TM and GEM, respectively, comparable to the stratospheric lifetime of COS. This coincidence, combined with pieces of evidence from us and other researchers, corroborates the hypothesis that Hg2+ formed by oxidation in the stratosphere attaches to sulfate particles formed mainly by oxidation of COS and is removed with them from the stratosphere by air mass exchange, gravitational sedimentation and cloud scavenging processes
Two-Dimensional Electronic Spectroscopy of Chlorophyll a: Solvent Dependent Spectral Evolution
The interaction of the monomeric chlorophyll Q-band electronic transition with solvents of differing physical-chemical properties is investigated through two-dimensional electronic spectroscopy (2DES). Chlorophyll constitutes the key chromophore molecule in light harvesting complexes. It is well-known that the surrounding protein in the light harvesting complex fine-tunes chlorophyll electronic transitions to optimize energy transfer. Therefore, an understanding of the influence of the environment on the monomeric chlorophyll electronic transitions is important. The Q-band 2DES is inhomogeneous at early times, particularly in hydrogen bonding polar solvents, but also in nonpolar solvents like cyclohexane. Interestingly this inhomogeneity persists for long times, even up to the nanosecond time scale in some solvents. The reshaping of the 2DES occurs over multiple time scales and was assigned mainly to spectral diffusion. At early times the reshaping is Gaussian-like, hinting at a strong solvent reorganization effect. The temporal evolution of the 2DES response was analyzed in terms of a Brownian oscillator model. The spectral densities underpinning the Brownian oscillator fitting were recovered for the different solvents. The absorption spectra and Stokes shift were also properly described by this model. The extent and nature of inhomogeneous broadening was a strong function of solvent, being larger in H-bonding and viscous media and smaller in nonpolar solvents. The fastest spectral reshaping components were assigned to solvent dynamics, modified by interactions with the solute
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