Logarithmic correction in the deformed AdS5{\rm AdS}_5 model to produce the heavy quark potential and QCD beta function

We stude the \textit{holographic} QCD model which contains a quadratic term $-\sigma z^2$ and a logarithmic term $-c_0\log[(z_{IR}-z)/z_{IR}]$ with an explicit infrared cut-off $z_{IR}$ in the deformed ${\rm AdS}_5$ warp factor. We investigate the heavy quark potential for three cases, i.e, with only quadratic correction, with both quadratic and logarithmic corrections and with only logarithmic correction. We solve the dilaton field and dilation potential from the Einstein equation, and investigate the corresponding beta function in the G{\"u}rsoy -Kiritsis-Nitti (GKN) framework. Our studies show that in the case with only quadratic correction, a negative $\sigma$ or the Andreev-Zakharov model is favored to fit the heavy quark potential and to produce the QCD beta-function at 2-loop level, however, the dilaton potential is unbounded in infrared regime. One interesting observing for the case of positive $\sigma$, or the soft-wall ${\rm AdS}_5$ model is that the corresponding beta-function exists an infrared fixed point. In the case with only logarithmic correction, the heavy quark Cornell potential can be fitted very well, the corresponding beta-function agrees with the QCD beta-function at 2-loop level reasonably well, and the dilaton potential is bounded from below in infrared. At the end, we propose a more compact model which has only logarithmic correction in the deformed warp factor and has less free parameters.Comment: 24 pages, 16 figure

q-Deformation of W(2,2) Lie algebra associated with quantum groups

An explicit realization of the W(2,2) Lie algebra is presented using the famous bosonic and fermionic oscillators in physics, which is then used to construct the q-deformation of this Lie algebra. Furthermore, the quantum group structures on the q-deformation of this Lie algebra are completely determined.Comment: 12 page

SETD3 is an actin histidine methyltransferase that prevents primary dystocia.

For more than 50 years, the methylation of mammalian actin at histidine 73 has been known to occur1. Despite the pervasiveness of His73 methylation, which we find is conserved in several model animals and plants, its function remains unclear and the enzyme that generates this modification is unknown. Here we identify SET domain protein 3 (SETD3) as the physiological actin His73 methyltransferase. Structural studies reveal that an extensive network of interactions clamps the actin peptide onto the surface of SETD3 to orient His73 correctly within the catalytic pocket and to facilitate methyl transfer. His73 methylation reduces the nucleotide-exchange rate on actin monomers and modestly accelerates the assembly of actin filaments. Mice that lack SETD3 show complete loss of actin His73 methylation in several tissues, and quantitative proteomics analysis shows that actin His73 methylation is the only detectable physiological substrate of SETD3. SETD3-deficient female mice have severely decreased litter sizes owing to primary maternal dystocia that is refractory to ecbolic induction agents. Furthermore, depletion of SETD3 impairs signal-induced contraction in primary human uterine smooth muscle cells. Together, our results identify a mammalian histidine methyltransferase and uncover a pivotal role for SETD3 and actin His73 methylation in the regulation of smooth muscle contractility. Our data also support the broader hypothesis that protein histidine methylation acts as a common regulatory mechanism

Differences and Similarities in the Clinicopathological Features of Pancreatic Neuroendocrine Tumors in China and the United States: A Multicenter Study

The presentation, pathology, and prognosis of pancreatic neuroendocrine tumors (PNETs) in Asian patients have not been studied in large cohorts. We hypothesized that the clinicopathological features of PNETs of Chinese patients might be different from those of US patients. The objectives of this study were to address whether PNETs in Chinese patients exhibit unique clinicopathological features and natural history, and can be graded and staged using the WHO/ENETS criteria. This is a retrospective review of medical records of patients with PNETs in multiple academic medical centers in China (7) and the United States (2). Tumor grading and staging were based on WHO/ENETS criteria. The clinicopathological features of PNETs of Chinese and US patients were compared. Univariate and multivariate analyses were performed to find associations between survival and patient demographics, tumor grade and stage, and other clinicopathological characteristics. A total of 977 (527 Chinese and 450 US) patients with PNETs were studied. In general, Chinese patients were younger than US patients (median age 46 vs 56 years). In Chinese patients, insulinomas were the most common (52.2%), followed by nonfunctional tumors (39.7%), whereas the order was reversed in US patients. Tumor grade distribution was similar in the 2 countries (G1: 57.5% vs 55.0%; G2: 38.5% vs 41.3%; and G3: 4.0% vs 3.7%). However, age, primary tumor size, primary tumor location, grade, and stage of subtypes of PNETs were significantly different between the 2 countries. The Chinese nonfunctional tumors were significantly larger than US ones (median size 4 vs 3 cm) and more frequently located in the head/neck region (54.9% vs 34.8%). The Chinese and US insulinomas were similar in size (median 1.5 cm) but the Chinese insulinomas relatively more frequently located in the head/neck region (48.3% vs 26.1%). Higher grade, advanced stage, metastasis, and larger primary tumor size were significantly associated with unfavorable survival in both countries. Several clinicopathological differences are found between Chinese and US PNETs but the PNETs of both countries follow a similar natural history. The WHO tumor grading and ENETS staging criteria are applicable to both Chinese and US patients

Uniqueness of near-horizon geometries of rotating extremal AdS(4) black holes

We consider stationary extremal black hole solutions of the Einstein-Maxwell equations with a negative cosmological constant in four dimensions. We determine all non-static axisymmetric near-horizon geometries (with non-toroidal horizon topology) and all static near-horizon geometries for black holes of this kind. This allows us to deduce that the most general near-horizon geometry of an asymptotically globally AdS(4) rotating extremal black hole, is the near-horizon limit of extremal Kerr-Newman-AdS(4). We also identify the subset of near-horizon geometries which are supersymmetric. Finally, we show which physical quantities of extremal black holes may be computed from the near-horizon limit alone, and point out a simple formula for the entropy of the known supersymmetric AdS(4) black hole. Analogous results are presented in the case of vanishing cosmological constant.Comment: 18 pages, Latex. v2: footnote added on pg. 12. v3: assumption of non-toroidal horizon topology made explicit, minor clarification

Loss-of-function mutations in Lysyl-tRNA synthetase cause various leukoencephalopathy phenotypes

Objective: To expand the clinical spectrum of lysyl-tRNA synthetase (KARS) gene–related diseases, which so far includes Charcot-Marie-Tooth disease, congenital visual impairment and microcephaly, and nonsyndromic hearing impairment. Methods: Whole-exome sequencing was performed on index patients from 4 unrelated families with leukoencephalopathy. Candidate pathogenic variants and their cosegregation were confirmed by Sanger sequencing. Effects of mutations on KARS protein function were examined by aminoacylation assays and yeast complementation assays. Results: Common clinical features of the patients in this study included impaired cognitive ability, seizure, hypotonia, ataxia, and abnormal brain imaging, suggesting that the CNS involvement is the main clinical presentation. Six previously unreported and 1 known KARS mutations were identified and cosegregated in these families. Two patients are compound heterozygous for missense mutations, 1 patient is homozygous for a missense mutation, and 1 patient harbored an insertion mutation and a missense mutation. Functional and structural analyses revealed that these mutations impair aminoacylation activity of lysyl-tRNA synthetase, indicating that de- fective KARS function is responsible for the phenotypes in these individuals. Conclusions: Our results demonstrate that patients with loss-of-function KARS mutations can manifest CNS disorders, thus broadening the phenotypic spectrum associated with KARS-related disease

Allelic based gene-gene interactions in rheumatoid arthritis

The detection of gene-gene interaction is an important approach to understand the etiology of rheumatoid arthritis (RA). The goal of this study is to identify gene-gene interaction of SNPs at the allelic level contributing to RA using real data sets (Problem 1) of North American Rheumatoid Arthritis Consortium (NARAC) provided by Genetic Analysis Workshop 16 (GAW16). We applied our novel method that can detect the interaction by a definition of nonrandom association of alleles that occurs when the contribution to RA of a particular allele inherited in one gene depends on a particular allele inherited at other unlinked genes. Starting with 639 single-nucleotide polymorphisms (SNPs) from 26 candidate genes, we identified ten two-way interacting genes and one case of three-way interacting genes. SNP rs2476601 on PTPN22 interacts with rs2306772 on SLC22A4, which interacts with rs881372 on TRAF1 and rs2900180 on C5, respectively. SNP rs2900180 on C5 interacts with rs2242720 on RUNX1, which interacts with rs881375 on TRAF1. Furthermore, rs2476601 on PTPN22 also interacts with three SNPs (rs2905325, rs1476482, and rs2106549) in linkage disequilibrium (LD) on IL6. The other three SNPs (rs2961280, rs2961283, and rs2905308) in LD on IL6 interact with two SNPs (rs477515 and rs2516049) on HLA-DRB1. SNPs rs660895 and rs532098 on HLA-DRB1 interact with rs2834779 and four SNPs in LD on RUNX1. Three-way interacting genes of rs10229203 on IL6, rs4816502 on RUNX1, and rs10818500 on C5 were also detected

Confront Holographic QCD with Regge Trajectories of vectors and axial-vectors

We derive the general 5-dimension metric structure of the $Dp-Dq$ system in type II superstring theory, and demonstrate the physical meaning of the parameters characterizing the 5-dimension metric structure of the \textit{holographic} QCD model by relating them to the parameters describing Regge trajectories. By matching the spectra of vector mesons $\rho_1$ with deformed $Dp-Dq$ soft-wall model, we find that the spectra of vector mesons $\rho_1$ can be described very well in the soft-wall $D3-Dq$ model, i.e, $AdS_5$ soft-wall model. We then investigate how well the $AdS_5$ soft-wall model can describe the Regge trajectory of axial-vector mesons $a_1$. We find that the constant component of the 5-dimension mass square of axial-vector mesons plays an efficient role to realize the chiral symmetry breaking in the vacuum, and a small negative $z^4$ correction in the 5-dimension mass square is helpful to realize the chiral symmetry restoration in high excitation states.Comment: 9 pages, 3 figure and 3 tables, one section adde