Pressure dependence of upper critical fields in FeSe single crystals

We investigate the pressure dependence of the upper critical fields ({\mu}$_0$$H$$_{c2}$) for FeSe single crystals with pressure up to 2.57 GPa. The superconducting (SC) properties show a disparate behavior across a critical pressure where the pressure-induced antiferromagnetic phase coexists with superconductivity. The magnetoresistance for $H//ab$ and $H//c$ is very different: for $H//c$, magnetic field induces and enhances a hump in the resistivity close to the $T_c$ for pressures higher than 1.2 GPa, while it is absent for $H//ab$. Since the measured {\mu}$_0$$H$$_{c2}$ for FeSe samples is smaller than the orbital limited upper critical field ($H$$^{orb}$$_{c2}$) estimated by the Werthamer Helfand and Hohenberg (WHH) model, the Maki parameter ({\alpha}) related to Pauli spin-paramagnetic effects is additionally considered to describe the temperature dependence of {\mu}$_0$$H$$_{c2}$($T$). Interestingly, the {\alpha} value is hardly affected by pressure for $H//ab$, while it strongly increases with pressure for $H//c$. The pressure evolution of the {\mu}$_0$$H$$_{c2}$(0)s for the FeSe single crystals is found to be almost similar to that of $T_c$($P$), suggesting that the pressure-induced magnetic order adversely affects the upper critical fields as well as the SC transition temperature.Comment: 23 pages, 6 figures, 1 tabl

Single Spin Asymmetry Scaling in the Forward Rapidity Region at RHIC

We investigate the scaling properties in inclusive hadron production and the associated single transverse spin asymmetry in the forward rapidity region at RHIC. We find that the spin-averaged experimental data in both $pp$ and $dAu$ collisions demonstrates a transverse-momentum-dependent geometric scaling. We introduce the transverse momentum dependent Collins fragmentation function to study the scaling of the single transverse spin asymmetries. The general feature of the scaling analysis is consistent with the experimental observations, in particular, for the transverse momentum dependence of the spin asymmetries at RHIC energy. We further propose to probe the saturation scale of nucleus by measuring the spin asymmetry normalized by that in $pp$ scattering at low transverse momentum.Comment: 13 pages, 4 figure

Molecular Etiology of Hearing Impairment in Inner Mongolia: mutations in SLC26A4 gene and relevant phenotype analysis

<p>Abstract</p> <p>Background</p> <p>The molecular etiology of hearing impairment in Chinese has not been thoroughly investigated. Study of <it>GJB2 </it>gene revealed that 30.4% of the patients with hearing loss in Inner Mongolia carried <it>GJB2 </it>mutations. The <it>SLC26A4 </it>gene mutations and relevant phenotype are analyzed in this study.</p> <p>Methods</p> <p>One hundred and thirty-five deaf patients were included. The coding exons of <it>SLC26A4 </it>gene were sequence analyzed in 111 patients, not including 22 patients carrying bi-allelic <it>GJB2 </it>mutations or one patient carrying a known <it>GJB2 </it>dominant mutation as well as one patient with <it>mtDNA </it>1555A>G mutation. All patients with <it>SLC26A4 </it>mutations or variants were subjected to high resolution temporal bone CT scan and those with confirmed enlarged vestibular aqueduct and/or other inner ear malformation were then given further ultrasound scan of thyroid and thyroid hormone assays.</p> <p>Results</p> <p>Twenty-six patients (19.26%, 26/135) were found carrying <it>SLC26A4 </it>mutation. Among them, 17 patients with bi-allelic <it>SLC26A4 </it>mutations were all confirmed to have EVA or other inner ear malformation by CT scan. Nine patients were heterozygous for one <it>SLC26A4 </it>mutation, including 3 confirmed to be EVA or EVA and Mondini dysplasia by CT scan. The most common mutation, IVS7-2A>G, accounted for 58.14% (25/43) of all <it>SLC26A4 </it>mutant alleles. The shape and function of thyroid were confirmed to be normal by thyroid ultrasound scan and thyroid hormone assays in 19 of the 20 patients with EVA or other inner ear malformation except one who had cystoid change in the right side of thyroid. No Pendred syndrome was diagnosed.</p> <p>Conclusion</p> <p>In Inner Mongolia, China, mutations in <it>SLC26A4 </it>gene account for about 12.6% (17/135) of the patients with hearing loss. Together with <it>GJB2 </it>(23/135), <it>SLC26A4 </it>are the two most commonly mutated genes causing deafness in this region. Pendred syndrome is not detected in this deaf population. We established a new strategy that detects <it>SLC26A4 </it>mutations prior to the temporal bone CT scan to find EVA and inner ear malformation patients. This model has a unique advantage in epidemiologic study of large deaf population.</p

Enhanced critical current density in the pressure-induced magnetic state of the high-temperature superconductor FeSe

We investigate the relation of the critical current density (Jc) and the remarkably increased superconducting transition temperature (Tc) for the FeSe single crystals under pressures up to 2.43 GPa, where the Tc is increased by ~8 K/GPa. The critical current density corresponding to the free flux flow is monotonically enhanced by pressure which is due to the increase in Tc, whereas the depinning critical current density at which the vortex starts to move is more influenced by the pressure-induced magnetic state compared to the increase of Tc. Unlike other high-Tc superconductors, FeSe is not magnetic, but superconducting at ambient pressure. Above a critical pressure where magnetic state is induced and coexists with superconductivity, the depinning Jc abruptly increases even though the increase of the zero-resistivity Tc is negligible, directly indicating that the flux pinning property compared to the Tc enhancement is a more crucial factor for an achievement of a large Jc. In addition, the sharp increase in Jc in the coexisting superconducting phase of FeSe demonstrates that vortices can be effectively trapped by the competing antiferromagnetic order, even though its antagonistic nature against superconductivity is well documented. These results provide new guidance toward technological applications of high-temperature superconductors.Comment: 24pages, 8 figure

Polymorphisms in Apoptosis-Related Genes and TP53 Mutations in Non-Small Cell Lung Cancer

Apoptosis plays an essential role in the elimination of mutated or transformed cells from the body. Therefore, polymorphisms of apoptosis-related genes may lead to an alteration in apoptotic capacity, thereby affecting the occurrence of TP53 mutations in lung cancer. We investigated the relationship between potentially functional polymorphisms of apoptosis-related genes and TP53 mutations in non-small cell lung cancer (NSCLC). Twenty-seven single nucleotide polymorphisms in 20 apoptosis-related genes were genotyped by a sequenome mass spectrometry-based genotyping assay in 173 NSCLCs and the associations with TP53 mutations in the entire coding exons (exons 2-11), including splicing sites of the gene, were analyzed. None of the 27 polymorphisms was significantly associated with the occurrence of TP53 mutations. This suggests that apoptosis-related genes may not play an important role in the occurrence of TP53 mutations in lung cancer