211 research outputs found

    Genetics of tension-type headache

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    The objective of this study was to investigate the importance of genetics in tension-type headache. A MEDLINE search from 1966 to December 2006 was performed for “tension-type headache and prevalence” and “tension-type headache and genetics” The prevalence of tensiontype headache varies from 11 to 93%, with a slight female preponderance. Co-occurrence of migraine increases the frequency of tension-type headache. A family study of chronic tension-type headache suggests that genetic factors are important. A twin study analysing tension-type headache in migraineurs found that genetic factors play a minor role in episodic tension-type headache. Another twin study analysing twin pairs without co-occurrence of migraine showed a significantly higher concordance rate among monozygotic than same-gender dizygotic twin pairs with no or frequent episodic tension-type headache, while the difference was minor in twin pairs with infrequent episodic tensiontype headache. Frequent episodic and chronic tension-type headache is caused by a combination of genetic and environmental factors, while infrequent episodic tensiontype headache is caused primarily by environmental factors

    No V-Fe-Zn isotopic variation in basalts from the 2021 Fagradalsfjall eruption

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    The Earth’s mantle is chemically heterogeneous in space and time, which is often reflected by variable isotopic compositions of mantle derived basalts. Basalts from the first 40 days of the 2021 Fagradalsfjall eruption, Reykjanes Peninsula, Iceland, display systematic temporal variations in the ratios of incompatible elements alongside resolvable variations in Sr, Nd and Pb radiogenic isotopes. These variations reflect progressive influx of magma derived from melting of a deeper, more enriched and potentially lithologically distinct source. We use this eruptive time series to conduct the first combined V-Fe-Zn isotope study, exploring the sensitivity of the combined isotopic approach, with particular focus on fingerprinting source lithological heterogeneity. We find no analytically resolvable change in V (ÎŽ51VAA between −0.95 ± 0.09 ‰ 2 s.d. and −0.86 ± 0.07 ‰ 2 s.d.), Fe (ÎŽ56FeIRMM-524 between +0.047 ± 0.042 ‰ 2 s.d. and +0.094 ± 0.049 ‰ 2 s.d.) and Zn (ÎŽ66ZnAA-ETH between −0.042 ± 0.003 ‰ 2 s.d. and +0.013 ± 0.027 ‰ 2 s.d.) isotopic compositions. The lack of variability in V-Fe-Zn isotopes, despite the evolving trace element and radiogenic isotope ratios, suggests there is no significant contribution of melts from a lithologically distinct (pyroxenite) mantle component under the Reykjanes Peninsula

    Francisella tularensis Schu S4 lipopolysaccharide core sugar and o-antigen mutants are attenuated in a mouse model of tularemia

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    The virulence factors mediating Francisella pathogenesis are being investigated, with an emphasis on understanding how the organism evades innate immunity mechanisms. Francisella tularensis produces a lipopolysaccharide (LPS) that is essentially inert and a polysaccharide capsule that helps the organism to evade detection by components of innate immunity. Using an F. tularensis Schu S4 mutant library, we identified strains that are disrupted for capsule and O-antigen production. These serum-sensitive strains lack both capsule production and O-antigen laddering. Analysis of the predicted protein sequences for the disrupted genes (FTT1236 and FTT1238c) revealed similarity to those for waa (rfa) biosynthetic genes in other bacteria. Mass spectrometry further revealed that these proteins are involved in LPS core sugar biosynthesis and the ligation of O antigen to the LPS core sugars. The 50% lethal dose (LD(50)) values of these strains are increased 100- to 1,000-fold for mice. Histopathology revealed that the immune response to the F. tularensis mutant strains was significantly different from that observed with wild-type-infected mice. The lung tissue from mutant-infected mice had widespread necrotic debris, but the spleens lacked necrosis and displayed neutrophilia. In contrast, the lungs of wild-type-infected mice had nominal necrosis, but the spleens had widespread necrosis. These data indicate that murine death caused by wild-type strains occurs by a mechanism different from that by which the mutant strains kill mice. Mice immunized with these mutant strains displayed >10-fold protective effects against virulent type A F. tularensis challenge

    Dust extinction and X-ray emission from the star burst galaxy NGC 1482

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    We present the results based on multiwavelength imaging observations of the prominent dust lane starburst galaxy NGC 1482 aimed to investigate the extinction properties of dust existing in the extreme environment. (B-V) colour-index map derived for the starburst galaxy NGC 1482 confirms two prominent dust lanes running along its optical major axis and are found to extend up to \sim 11 kpc. In addition to the main lanes, several filamentary structures of dust originating from the central starburst are also evident. Though, the dust is surrounded by exotic environment, the average extinction curve derived for this target galaxy is compatible with the Galactic curve, with RV =3.05, and imply that the dust grains responsible for the optical extinction in the target galaxy are not really different than the canonical grains in the Milky Way. Our estimate of total dust content of NGC 1482 assuming screening effect of dust is \sim 2.7 \times 10^5 Msun, and provide lower limit due to the fact that our method is not sensitive to the intermix component of dust. Comparison of the observed dust in the galaxy with that supplied by the SNe to the ISM, imply that this supply is not sufficient to account for the observed dust and hence point towards the origin of dust in this galaxy through a merger like event. Our multiband imaging analysis reveals a qualitative physical correspondence between the morphologies of the dust and H{\alpha} emission lines as well as diffuse X-ray emission in this galaxy. continue.... for more detail please see in pdf file.Comment: 22 pages, 11 Figures. Accepted for publication in New Astronom

    Dysfunction of the Heteromeric KV7.3/KV7.5 Potassium Channel is Associated with Autism Spectrum Disorders

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    Heterozygous mutations in the KCNQ3 gene on chromosome 8q24 encoding the voltage-gated potassium channel KV7.3 subunit have previously been associated with rolandic epilepsy and idiopathic generalized epilepsy (IGE) including benign neonatal convulsions. We identified a de novo t(3;8) (q21;q24) translocation truncating KCNQ3 in a boy with childhood autism. In addition, we identified a c.1720C > T [p.P574S] nucleotide change in three unrelated individuals with childhood autism and no history of convulsions. This nucleotide change was previously reported in patients with rolandic epilepsy or IGE and has now been annotated as a very rare SNP (rs74582884) in dbSNP. The p.P574S KV7.3 variant significantly reduced potassium current amplitude in Xenopus laevis oocytes when co-expressed with KV7.5 but not with KV7.2 or KV7.4. The nucleotide change did not affect trafficking of heteromeric mutant KV7.3/2, KV7.3/4, or KV7.3/5 channels in HEK 293 cells or primary rat hippocampal neurons. Our results suggest that dysfunction of the heteromeric KV7.3/5 channel is implicated in the pathogenesis of some forms of autism spectrum disorders, epilepsy, and possibly other psychiatric disorders and therefore, KCNQ3 and KCNQ5 are suggested as candidate genes for these disorders
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