Where is the pseudoscalar glueball ?

The pseudoscalar mesons with the masses higher than 1 GeV are assumed to belong to the meson decuplet including the glueball as the basis state supplementing the standard $SU(3)_F$ nonet of light $q\bar{q}$ states $(u,d,s)$. The decuplet is investigated by means of an algebraic approach based on hypothesis of vanishing the exotic $SU(3)_F$ commutators of "charges" and their time derivatives. These commutators result in a system of equations determining contents of the isoscalar octet state in the physical isoscalar mesons as well as the mass formula including all masses of the decuplet: $\pi(1300)$, K(1460), $\eta(1295)$, $\eta(1405)$ and $\eta(1475)$. The physical isoscalar mesons $\eta_i$, are expressed as superpositions of the "ideal" $q\bar{q}$ states ($N$ and $S$) and the glueball $G$ with the mixing coefficient matrix following from the exotic commutator restrictions. Among four one-parameter families of the calculated mixing matrix (numerous solutions result from bad quality of data on the $\pi(1300)$ and K(1460) masses) there is one family attributing the glueball-dominant composition to the $\eta(1405)$ meson. Similarity between the pseudoscalar and scalar decuplets, analogy between the whole spectra of the $0^{-+}$ and $0^{++}$ mesons and affinity of the glueball with excited $q\bar{q}$ states are also noticed.Comment: 18 pp., 2. figs., 2 tabs.; Published version. One of the authors withdraws his nam

Beyond homozygosity mapping: family-control analysis based on Hamming distance for prioritizing variants in exome sequencing

A major challenge in current exome sequencing in autosomal recessive (AR) families is the lack of an effective method to prioritize single-nucleotide variants (SNVs). AR families are generally too small for linkage analysis, and length of homozygous regions is unreliable for identification of causative variants. Various common filtering steps usually result in a list of candidate variants that cannot be narrowed down further or ranked. To prioritize shortlisted SNVs we consider each homozygous candidate variant together with a set of SNVs flanking it. We compare the resulting array of genotypes between an affected family member and a number of control individuals and argue that, in a family, differences between family member and controls should be larger for a pathogenic variant and SNVs flanking it than for a random variant. We assess differences between arrays in two individuals by the Hamming distance and develop a suitable test statistic, which is expected to be large for a causative variant and flanking SNVs. We prioritize candidate variants based on this statistic and applied our approach to six patients with known pathogenic variants and found these to be in the top 2 to 10 percentiles of ranks

Raising Bi-O bands above the Fermi energy level of hole-doped Bi2_2Sr2_2CaCu2_2O8+δ_{8+\delta} and other cuprate superconductors

The Fermi surface (FS) of Bi$_2$Sr$_2$CaCu$_2$O$_{8+\delta}$ (Bi2212) predicted by band theory displays Bi-related pockets around the $(\pi,0)$ point, which have never been observed experimentally. We show that when the effects of hole doping either by substituting Pb for Bi or by adding excess O in Bi2212 are included, the Bi-O bands are lifted above the Fermi energy ($E_F$) and the resulting first-principles FS is in remarkable accord with measurements. With decreasing hole-doping the Bi-O bands drop below $E_F$ and the system self-dopes below a critical hole concentration. Computations on other Bi- as well as Tl- and Hg-based compounds indicate that lifting of the cation-derived band with hole doping is a general property of the electronic structures of the cuprates.Comment: 4 pages, 4 figures; PRL (2006, in press

Pulmonary arterial hypertension: a current review of pharmacological management

Pulmonary hypertension (PHTN) is a rare and devastating disease characterized by progressive increases in pulmonary arterial pressure and pulmonary vascular resistance, which eventually leads to right ventricular failure and death. At present there is no cure for pulmonary arterial hypertension (PAH); however over the past decade targeted pharmaceutical options have become available for the treatment of PAH. Prior to evaluation for therapeutic options a definitive diagnosis of pulmonary arterial hypertension must be made via comprehensive physical exam and definitive diagnostic testing. Screening test of choice remains echocardiography and gold standard for definitive diagnosis is right heart catheterization. Once the establishment of a diagnosis of PAH is made therapeutic options may be a possibility based on a diagnostic algorithm and disease severity of the PAH patient. There are different classes of medications available with different mechanisms of actions which net a vasodilatory effect and improve exercise tolerance, quality of life as well and survival