Regular modes in rotating stars

Despite more and more observational data, stellar acoustic oscillation modes are not well understood as soon as rotation cannot be treated perturbatively. In a way similar to semiclassical theory in quantum physics, we use acoustic ray dynamics to build an asymptotic theory for the subset of regular modes which are the easiest to observe and identify. Comparisons with 2D numerical simulations of oscillations in polytropic stars show that both the frequency and amplitude distributions of these modes can accurately be described by an asymptotic theory for almost all rotation rates. The spectra are mainly characterized by two quantum numbers; their extraction from observed spectra should enable one to obtain information about stellar interiors.Comment: 5 pages, 4 figures, discussion adde

Prevalence of generalised joint hypermobility in school-aged children from east-central European region

Background: There is no literature regarding joint mobility in children of the Central and Eastern Europe. Studies describing clinical characteristics and functional outcomes are still needed. The aim of this study was to assess the prevalence of generalised joint hypermobility (GJH) in the group of school-aged children from Vilnius, the capital city of Lithuania, in relation to different cut-off values of the Beighton score (BS), and to identify possible patients with joint hypermobility syndrome. Materials and methods: The representative sample of this study was calculated to be 760 subjects. A total of 778 children from different schools were screened for the mobility of joints. The medical examination included an assessment of joints’ hypermobility according to the BS. The presence of specific signs (marfanoid habitus, antimongoloid slant and drooping eyelids) was assessed additionally. Parents of all involved children were asked to answer the questions developed based on the Brighton criteria regarding the medical history of children. Results: The prevalence of GJH in school-aged children from Vilnius, depending on the BS cut-off value, was 19.2% (BS ≥ 4), 9.5% (BS ≥ 5) or 5.7% (BS ≥ 6). The increased range of mobility was most frequently detected in thumbs of school- -aged children. The frequency of hyperextension > 10o in knees was 7- to 8-fold lower than the frequency of hyperextension > 10o in a passive opposition of the thumb. The evaluation results were similar on the left and right sides in 87.4% cases of thumb opposition, 90.1% cases of hyperextension of 5th finger, 87.9% cases of elbow manoeuvres, and 94.8% attempts to hyperextend knee. Conclusions: The prevalence of GJH in school-aged children from Vilnius depends on the BS cut-off value and ranges from 5.7% to 19.2%.

Molecular Basis of Calmodulin Binding to Cardiac Muscle Ca 2 + Release Channel (Ryanodine Receptor)

Calmodulin (CaM) is a ubiquitous Ca2+-binding protein that regulates the ryanodine receptors (RyRs) by direct binding. CaM inhibits the skeletal muscle ryanodine receptor (RyR1) and cardiac muscle receptor (RyR2) at >1 microm Ca2+ but activates RyR1 and inhibits RyR2 at <1 microm Ca2+. Here we tested whether CaM regulates RyR2 by binding to a highly conserved site identified previously in RyR1. Deletion of RyR2 amino acid residues 3583-3603 resulted in background [35S]CaM binding levels. In single channel measurements, deletion of the putative CaM binding site eliminated CaM inhibition of RyR2 at Ca2+ concentrations below and above 1 microm. Five RyR2 single or double mutants in the CaM binding region (W3587A, L3591D, F3603A, W3587A/L3591D, L3591D/F3603A) eliminated or greatly reduced [35S]CaM binding and inhibition of single channel activities by CaM depending on the Ca2+ concentration. An RyR2 mutant, which assessed the effects of 4 amino acid residues that differ between RyR1 and RyR2 in or flanking the CaM binding domain, bound [35S]CaM and was inhibited by CaM, essentially identical to wild type (WT)-RyR2. Three RyR1 mutants (W3620A, L3624D, F3636A) showed responses to CaM that differed from corresponding mutations in RyR2. The results indicate that CaM regulates RyR1 and RyR2 by binding to a single, highly conserved CaM binding site and that other RyR type-specific sites are likely responsible for the differential functional regulation of RyR1 and RyR2 by CaM

Different Regions in Skeletal and Cardiac Muscle Ryanodine Receptors Are Involved in Transducing the Functional Effects of Calmodulin

Calmodulin (CaM) inhibits the skeletal muscle ryanodine receptor-1 (RyR1) and cardiac muscle RyR2 at micromolar Ca(2+) but activates RyR1 and inhibits RyR2 at submicromolar Ca(2+) by binding to a single, highly conserved CaM-binding site. To identify regions responsible for the differential regulation of RyR1 and RyR2 by CaM, we generated chimeras encompassing and flanking the CaM-binding domain. We found that the exchange of the N- and C-terminal flanking regions differentially affected RyR1 and RyR2. A RyR1/RyR2 chimera with an N-terminal flanking RyR2 substitution (RyR2 amino acid (aa) 3537-3579) was activated by CaM in single channel measurements at both submicromolar and micromolar Ca(2+). A RyR2/RyR1 chimera with a C-terminal flanking the 86-amino acid RyR1 substitution (RyR1 aa 3640-3725) bound (35)S-CaM but was not inhibited by CaM at submicromolar Ca(2+). In this region, five non-conserved amino acid residues (RyR1 aa 3680 and 3682-3685 and RyR2 aa 3647 and 3649-3652) differentially affect RyR helical probability. Substitution of the five amino acid residues in RyR1 with those of RyR2 showed responses to CaM comparable with wild type RyR1. In contrast, substitution of the five amino acid residues in RyR2 with those of RyR1 showed loss of CaM inhibition, whereas substitution of the five RyR2 sequence residues in the RyR2 chimera containing the RyR1 calmodulin-binding domain and C-flanking sequence restored wild type RyR2 inhibition by CaM at submicromolar Ca(2+). The results suggest that different regions are involved in CaM modulation of RyR1 and RyR2. They further suggest that five non-conserved amino acids in the C-terminal region flanking the CaM-binding domain have a key role in CaM inhibition of RyR2

Motivations and barriers to prosthesis users participation in physical activity, exercise and sport : a review of the literature

The UK will host the Paralympics in 2012 and the Commonwealth Games in 2014 showcasing the talents of elite athletes and aiming to inspire the population to become involved. However, low levels of physical activity (PA) are prevalent: only 40% of men and 28% of women meet the minimum UK recommendations. The limb absent population is no exception. To determine if people with limb amputations are participating in physical activity and sport; whether post-amputation activity levels match pre-amputation levels; and if there are motivations and barriers to participation. Study design: Literature review Five reviewers systematically search of peer reviewed and gray literature in seven bibliographic databases and the Cochrane Library. Results: Following rigorous elimination, 12 articles were finally included in the review and critically appraised. Four themes were identified: components, rehabilitation outcomes, body image and motivations and barriers to participation. People with limb absence are not participating in PA conducive to health benefits, and only a minority participate in exercise and sports. Participation following amputation does not mirror that of pre-amputation levels, and more barriers than motivations exist to adopting and maintaining a physically active lifestyle. This literature review aims to inform those involved in rehabilitation and ongoing care of those with limb absence about what motivates or precludes their participation in physical activity, exercise and sport. Such knowledge could be applied to improving health and well being in this population

Inhibition of CaMKII Does Not Attenuate Cardiac Hypertrophy in Mice with Dysfunctional Ryanodine Receptor

In cardiac muscle, the release of calcium ions from the sarcoplasmic reticulum through ryanodine receptor ion channels (RyR2s) leads to muscle contraction. RyR2 is negatively regulated by calmodulin (CaM) and by phosphorylation of Ca2+/CaM-dependent protein kinase II (CaMKII). Substitution of three amino acid residues in the CaM binding domain of RyR2 (RyR2-W3587A/L3591D/F3603A, RyR2ADA) impairs inhibition of RyR2 by CaM and results in cardiac hypertrophy and early death of mice carrying the RyR2ADA mutation. To test the cellular function of CaMKII in cardiac hypertrophy, mutant mice were crossed with mice expressing the CaMKII inhibitory AC3-I peptide or the control AC3-C peptide in the myocardium. Inhibition of CaMKII by AC3-I modestly reduced CaMKII-dependent phosphorylation of RyR2 at Ser-2815 and markedly reduced CaMKII-dependent phosphorylation of SERCA2a regulatory subunit phospholamban at Thr-17. However the average life span and heart-to-body weight ratio of Ryr2ADA/ADA mice expressing the inhibitory peptide were not altered compared to control mice. In Ryr2ADA/ADA homozygous mice, AC3-I did not alter cardiac morphology, enhance cardiac function, improve sarcoplasmic reticulum Ca2+ handling, or suppress the expression of genes implicated in cardiac remodeling. The results suggest that CaMKII was not required for the rapid development of cardiac hypertrophy in Ryr2ADA/ADA mice

Selective Phosphonylation of 5′-Adenosine Monophosphate (5′-AMP) via Pyrophosphite [PPi(III)]

We describe here experiments which demonstrate the selective phospho-transfer from a plausibly prebiotic condensed phosphorus (P) salt, pyrophosphite [H2P2O52−; PPi(III)], to the phosphate group of 5′-adenosine mono phosphate (5′-AMP). We show further that this P-transfer process is accelerated both by divalent metal ions (M2+) and by organic co-factors such as acetate (AcO−). In this specific case of P-transfer from PPi(III) to 5′-AMP, we show a synergistic enhancement of transfer in the combined presence of M2+ & AcO−. Isotopic labelling studies demonstrate that hydrolysis of the phosphonylated 5′-AMP, [P(III)P(V)-5′-AMP], proceeds via nuceophilic attack of water at the Pi(III) terminus

Deletion of airway cilia results in noninflammatory bronchiectasis and hyperreactive airways

The mechanisms for the development of bronchiectasis and airway hyperreactivity have not been fully elucidated. Although genetic, acquired diseases and environmental influences may play a role, it is also possible that motile cilia can influence this disease process. We hypothesized that deletion of a key intraflagellar transport molecule, IFT88, in mature mice causes loss of cilia, resulting in airway remodeling. Airway cilia were deleted by knockout of IFT88, and airway remodeling and pulmonary function were evaluated. In IFT88− mice there was a substantial loss of airway cilia on respiratory epithelium. Three months after the deletion of cilia, there was clear evidence for bronchial remodeling that was not associated with inflammation or apparent defects in mucus clearance. There was evidence for airway epithelial cell hypertrophy and hyperplasia. IFT88− mice exhibited increased airway reactivity to a methacholine challenge and decreased ciliary beat frequency in the few remaining cells that possessed cilia. With deletion of respiratory cilia there was a marked increase in the number of club cells as seen by scanning electron microscopy. We suggest that airway remodeling may be exacerbated by the presence of club cells, since these cells are involved in airway repair. Club cells may be prevented from differentiating into respiratory epithelial cells because of a lack of IFT88 protein that is necessary to form a single nonmotile cilium. This monocilium is a prerequisite for these progenitor cells to transition into respiratory epithelial cells. In conclusion, motile cilia may play an important role in controlling airway structure and function

Topological Photonics

Topology is revolutionizing photonics, bringing with it new theoretical discoveries and a wealth of potential applications. This field was inspired by the discovery of topological insulators, in which interfacial electrons transport without dissipation even in the presence of impurities. Similarly, new optical mirrors of different wave-vector space topologies have been constructed to support new states of light propagating at their interfaces. These novel waveguides allow light to flow around large imperfections without back-reflection. The present review explains the underlying principles and highlights the major findings in photonic crystals, coupled resonators, metamaterials and quasicrystals.Comment: progress and review of an emerging field, 12 pages, 6 figures and 1 tabl