Angular dependence of the bulk nucleation field Hc2 of aligned MgB2 crystallites

The angular dependence of the bulk nucleation field of a sample made of aligned MgB2 crystallites was obtained using dc magnetization and ac susceptibility measurements. A good fitting of the data by the three-dimensional anisotropic Ginzburg-Landau theory attests to the bulk nature of the critical field H-c2. We found a mass anisotropy ratio epsilon2 approximate to0.39 that implies an anisotropy of the Fermi velocity, with a ratio of 1.6 between the in-plane and perpendicular directions, if an isotropic gap energy is assumed. For an s-wave anisotropic gap this ratio could increase to 2.5. Besides the fundamental implications of this result, it also implies the use of texturization techniques to optimize the critical current in wires and other polycrystalline forms of MgB2.641

Mapping the genetic architecture of gene expression in human liver

Genetic variants that are associated with common human diseases do not lead directly to disease, but instead act on intermediate, molecular phenotypes that in turn induce changes in higher-order disease traits. Therefore, identifying the molecular phenotypes that vary in response to changes in DNA and that also associate with changes in disease traits has the potential to provide the functional information required to not only identify and validate the susceptibility genes that are directly affected by changes in DNA, but also to understand the molecular networks in which such genes operate and how changes in these networks lead to changes in disease traits. Toward that end, we profiled more than 39,000 transcripts and we genotyped 782,476 unique single nucleotide polymorphisms (SNPs) in more than 400 human liver samples to characterize the genetic architecture of gene expression in the human liver, a metabolically active tissue that is important in a number of common human diseases, including obesity, diabetes, and atherosclerosis. This genome-wide association study of gene expression resulted in the detection of more than 6,000 associations between SNP genotypes and liver gene expression traits, where many of the corresponding genes identified have already been implicated in a number of human diseases. The utility of these data for elucidating the causes of common human diseases is demonstrated by integrating them with genotypic and expression data from other human and mouse populations. This provides much-needed functional support for the candidate susceptibility genes being identified at a growing number of genetic loci that have been identified as key drivers of disease from genome-wide association studies of disease. By using an integrative genomics approach, we highlight how the gene RPS26 and not ERBB3 is supported by our data as the most likely susceptibility gene for a novel type 1 diabetes locus recently identified in a large-scale, genome-wide association study. We also identify SORT1 and CELSR2 as candidate susceptibility genes for a locus recently associated with coronary artery disease and plasma low-density lipoprotein cholesterol levels in the process. © 2008 Schadt et al

PENGARUH PEMBIAYAAN BERMASALAH MUDHARABAH DAN PEMBIAYAAN BERMASALAH MUSYARAKAH TERHADAP PROFITABILITAS (Studi pada Bank Umum Syariah yang terdaftar di OJK Periode 2013-2017)

ABSTRAK Penelitian ini bertujuan untuk meneliti secara empiris mengenai Pengaruh Pembiayaan Bermasalah Mudharabah dan Pembiayaan Bermasalah Musyarakah terhadap Profitabilitas pada Bank Umum Syariah yang terdaftar di Otoritas Jasa Keuangan (OJK) periode 2013-2017. Penelitian ini merupakan replikasi dari penelitian sebelumnya Sri Mulyaningsih dan Iwan Fakhrudin (2016). Metode yang digunakan dalam penelitian ini adalah metode deskriptif dan verifikatif dengan menggunakan data sekunder yang diperoleh dari website Otoritas Jasa Keuangan (OJK).Pengambilan sampel dalam penelitian ini menggunakan sampel purposive sampling sehingga memperoleh 8 Bank Umum Syariah. Pengujian hipotesis penelitian menggunakan statistik uji hipotesis. Untuk mengetahui besarnya pengaruh pembiayaan bermasalah mudharabah dan pembiayaan bermasalah musyarakah digunakan analisis regresi linear berganda, analisis korelasi, analisis koefisien determinasi, uji hipotesis parsial serta ujia hipotesis simultan. Hasil dari penelitian yang telah dilakukan dengan menggunakan analisis regresi linear berganda menunjukkan bahwa secara parsial pembiayaan bermasalah mudharabah dan pembiayaan bermasalah musyarakah berpengaruh secara signifikan terhadap profitabilitas. Hasil penelitian secara simultan menunjukan bahwa pembiayaan bermasalah mudharabah dan pembiayaan bermasalah musyarakah berpengaruh secara signifikan terhadap profitabilitas pada bank umum syariah yang terdaftar di Otoritas Jasa Keuangan periode 2013- 2017. Kata kunci : Pembiayaan Bermasalah, Mudharabah, Musyarakah, Profitabilitas, ROE

Peripheral nervous system manifestations in a Sandhoff disease mouse model: nerve conduction, myelin structure, lipid analysis

<p>Abstract</p> <p>Background</p> <p>Sandhoff disease is an inherited lysosomal storage disease caused by a mutation in the gene for the β-subunit (<it>Hexb </it>gene) of β-hexosaminidase A (αβ) and B (ββ). The β-subunit together with the GM2 activator protein catabolize ganglioside GM2. This enzyme deficiency results in GM2 accumulation primarily in the central nervous system. To investigate how abnormal GM2 catabolism affects the peripheral nervous system in a mouse model of Sandhoff disease (<it>Hexb-/-</it>), we examined the electrophysiology of dissected sciatic nerves, structure of central and peripheral myelin, and lipid composition of the peripheral nervous system.</p> <p>Results</p> <p>We detected no significant difference in signal impulse conduction velocity or any consistent change in the frequency-dependent conduction slowing and failure between freshly dissected sciatic nerves from the <it>Hexb</it>+/- and <it>Hexb</it>-/- mice. The low-angle x-ray diffraction patterns from freshly dissected sciatic and optic nerves of <it>Hexb</it>+/- and <it>Hexb</it>-/- mice showed normal myelin periods; however, <it>Hexb</it>-/- mice displayed a ~10% decrease in the relative amount of compact optic nerve myelin, which is consistent with the previously established reduction in myelin-enriched lipids (cerebrosides and sulfatides) in brains of <it>Hexb-/- </it>mice. Finally, analysis of lipid composition revealed that GM2 content was present in the sciatic nerve of the <it>Hexb</it>-/- mice (undetectable in <it>Hexb</it>+/-).</p> <p>Conclusion</p> <p>Our findings demonstrate the absence of significant functional, structural, or compositional abnormalities in the peripheral nervous system of the murine model for Sandhoff disease, but do show the potential value of integrating multiple techniques to evaluate myelin structure and function in nervous system disorders.</p

Long-term (trophic) purinergic signalling: purinoceptors control cell proliferation, differentiation and death

The purinergic signalling system, which uses purines and pyrimidines as chemical transmitters, and purinoceptors as effectors, is deeply rooted in evolution and development and is a pivotal factor in cell communication. The ATP and its derivatives function as a 'danger signal' in the most primitive forms of life. Purinoceptors are extraordinarily widely distributed in all cell types and tissues and they are involved in the regulation of an even more extraordinary number of biological processes. In addition to fast purinergic signalling in neurotransmission, neuromodulation and secretion, there is long-term (trophic) purinergic signalling involving cell proliferation, differentiation, motility and death in the development and regeneration of most systems of the body. In this article, we focus on the latter in the immune/defence system, in stratified epithelia in visceral organs and skin, embryological development, bone formation and resorption, as well as in cancer. Cell Death and Disease (2010) 1, e9; doi:10.1038/cddis.2009.11; published online 14 January 201

Cluster Lenses

Clusters of galaxies are the most recently assembled, massive, bound structures in the Universe. As predicted by General Relativity, given their masses, clusters strongly deform space-time in their vicinity. Clusters act as some of the most powerful gravitational lenses in the Universe. Light rays traversing through clusters from distant sources are hence deflected, and the resulting images of these distant objects therefore appear distorted and magnified. Lensing by clusters occurs in two regimes, each with unique observational signatures. The strong lensing regime is characterized by effects readily seen by eye, namely, the production of giant arcs, multiple-images, and arclets. The weak lensing regime is characterized by small deformations in the shapes of background galaxies only detectable statistically. Cluster lenses have been exploited successfully to address several important current questions in cosmology: (i) the study of the lens(es) - understanding cluster mass distributions and issues pertaining to cluster formation and evolution, as well as constraining the nature of dark matter; (ii) the study of the lensed objects - probing the properties of the background lensed galaxy population - which is statistically at higher redshifts and of lower intrinsic luminosity thus enabling the probing of galaxy formation at the earliest times right up to the Dark Ages; and (iii) the study of the geometry of the Universe - as the strength of lensing depends on the ratios of angular diameter distances between the lens, source and observer, lens deflections are sensitive to the value of cosmological parameters and offer a powerful geometric tool to probe Dark Energy. In this review, we present the basics of cluster lensing and provide a current status report of the field.Comment: About 120 pages - Published in Open Access at: http://www.springerlink.com/content/j183018170485723/ . arXiv admin note: text overlap with arXiv:astro-ph/0504478 and arXiv:1003.3674 by other author

Accuracy and usefulness of BMI measures based on self-reported weight and height: findings from the NHANES & NHIS 2001-2006

<p>Abstract</p> <p>Background</p> <p>The Body Mass Index (BMI) based on self-reported height and weight ("self-reported BMI") in epidemiologic studies is subject to measurement error. However, because of the ease and efficiency in gathering height and weight information through interviews, it remains important to assess the extent of error present in self-reported BMI measures and to explore possible adjustment factors as well as valid uses of such self-reported measures.</p> <p>Methods</p> <p>Using the combined 2001-2006 data from the continuous National Health and Nutrition Examination Survey, discrepancies between BMI measures based on self-reported and physical height and weight measures are estimated and socio-demographic predictors of such discrepancies are identified. Employing adjustments derived from the socio-demographic predictors, the self-reported measures of height and weight in the 2001-2006 National Health Interview Survey are used for population estimates of overweight & obesity as well as the prediction of health risks associated with large BMI values. The analysis relies on two-way frequency tables as well as linear and logistic regression models. All point and variance estimates take into account the complex survey design of the studies involved.</p> <p>Results</p> <p>Self-reported BMI values tend to overestimate measured BMI values at the low end of the BMI scale (< 22) and underestimate BMI values at the high end, particularly at values > 28. The discrepancies also vary systematically with age (younger and older respondents underestimate their BMI more than respondents aged 42-55), gender and the ethnic/racial background of the respondents. BMI scores, adjusted for socio-demographic characteristics of the respondents, tend to narrow, but do not eliminate misclassification of obese people as merely overweight, but health risk estimates associated with variations in BMI values are virtually the same, whether based on self-report or measured BMI values.</p> <p>Conclusion</p> <p>BMI values based on self-reported height and weight, if corrected for biases associated with socio-demographic characteristics of the survey respondents, can be used to estimate health risks associated with variations in BMI, particularly when using parametric prediction models.</p

Functional Polymorphism of the Mu-Opioid Receptor Gene (OPRM1) Influences Reinforcement Learning in Humans

Previous reports on the functional effects (i.e., gain or loss of function), and phenotypic outcomes (e.g., changes in addiction vulnerability and stress response) of a commonly occurring functional single nucleotide polymorphism (SNP) of the mu-opioid receptor (OPRM1 A118G) have been inconsistent. Here we examine the effect of this polymorphism on implicit reward learning. We used a probabilistic signal detection task to determine whether this polymorphism impacts response bias to monetary reward in 63 healthy adult subjects: 51 AA homozygotes and 12 G allele carriers. OPRM1 AA homozygotes exhibited typical responding to the rewarded response—that is, their bias to the rewarded stimulus increased over time. However, OPRM1 G allele carriers exhibited a decline in response to the rewarded stimulus compared to the AA homozygotes. These results extend previous reports on the heritability of performance on this task by implicating a specific polymorphism. Through comparison with other studies using this task, we suggest a possible mechanism by which the OPRM1 polymorphism may confer reduced response to natural reward through a dopamine-mediated decrease during positive reinforcement learning

An Allosteric Mechanism for Switching between Parallel Tracks in Mammalian Sulfur Metabolism

Methionine (Met) is an essential amino acid that is needed for the synthesis of S-adenosylmethionine (AdoMet), the major biological methylating agent. Methionine used for AdoMet synthesis can be replenished via remethylation of homocysteine. Alternatively, homocysteine can be converted to cysteine via the transsulfuration pathway. Aberrations in methionine metabolism are associated with a number of complex diseases, including cancer, anemia, and neurodegenerative diseases. The concentration of methionine in blood and in organs is tightly regulated. Liver plays a key role in buffering blood methionine levels, and an interesting feature of its metabolism is that parallel tracks exist for the synthesis and utilization of AdoMet. To elucidate the molecular mechanism that controls metabolic fluxes in liver methionine metabolism, we have studied the dependencies of AdoMet concentration and methionine consumption rate on methionine concentration in native murine hepatocytes at physiologically relevant concentrations (40–400 µM). We find that both [AdoMet] and methionine consumption rates do not change gradually with an increase in [Met] but rise sharply (∼10-fold) in the narrow Met interval from 50 to 100 µM. Analysis of our experimental data using a mathematical model reveals that the sharp increase in [AdoMet] and the methionine consumption rate observed within the trigger zone are associated with metabolic switching from methionine conservation to disposal, regulated allosterically by switching between parallel pathways. This regulatory switch is triggered by [Met] and provides a mechanism for stabilization of methionine levels in blood over wide variations in dietary methionine intake