Let $\alpha $ be a totally positive algebraic integer of degree d, with conjugates $\alpha _1=\alpha , \alpha _2, \ldots , \alpha _d$ . The absolute $S_k$ -measure of $\alpha $ is defined by $s_k(\alpha )= d^{-1} \sum _{i=1}^{d}\alpha _i^k$ . We compute the lower bounds $\upsilon _k$ of $s_k(\alpha )$ for each integer in the range $2\leq k \leq 15$ and give a conjecture on the results for integers $k>15$ . Then we derive the lower bounds of $s_k(\alpha )$ for all real numbers $k>2$ . Our computation is based on an improvement in the application of the LLL algorithm and analysis of the polynomials in the explicit auxiliary functions.

The rhoptry kinase 18 of Toxoplasma gondii (TgROP18) has been identified as a key virulence factor that allows the parasite to escape from host immune defences and promotes its proliferation in host cells. Although much research is focused on the interaction between host cells and TgROP18, the development of monoclonal antibodies (mAbs) against TgROP18 has not been reported till date. To produce mAbs targeting TgROP18, two hybridomas secreting mAbs against TgROP18, designated as A1 and T2, were generated using cell fusion technology. The subtypes of the A1 and T2 mAbs were identified as IgG3 λ and IgM κ, and peptide scanning revealed that the core sequences of the antigenic epitopes were 180LRAQRRRSELVFE192 and 351NYFLLMMRAEADM363, respectively. The T2 mAb specifically reacted with both T. gondii type I and Chinese I, but not with T. gondii type II, Plasmodium falciparum or Schistosoma japonicum. Finally, the sequences of heavy chain and light chain complementarity-determining regions of T2 were amplified, cloned and characterized, making the modification of the mAb feasible in the future. The development of mAbs against TgROP18 would aid the investigation of the molecular mechanisms underlying the modulation of host cellular functions by TgROP18, and in the development of strategies to diagnose and treat Toxoplasmosis.

The rugose corals described in this study were collected from the Gyanyima section in the Ngari region of southwestern Tibet (Xizang) and are assigned to three genera and 11 species, including a new genus and seven new species: Waagenophyllum (Waagenophyllum) ngariense He, 1990; W. (W.) elegantulum He in Luo et al., 1989; W. (W.) minutum Zhao, 1981; W. (W.) tachtabulasicum Ilyina, 1997; W. (W.) gyanyimaense n. sp., W. (W.) intermedium n. sp., Waagenophyllum (Liangshanophyllum) clisicolumellum n. sp., Ipciphyllum naoticum n. sp., I. floricolumellum n. sp., I. zandaense n. sp., and Gyanyimaphyllum crassiseptatum n. gen. n. sp. Ontogeny and intraspecific variation are given special attention when describing and discussing these taxa. Coral reefs, with Waagenophyllum as the major skeletal reef builder, occur in several horizons in the uppermost part of the section. The accompanying foraminifers indicate the rugose coral fauna is a late Permian Changhsingian age. Therefore, this is possibly one of the latest Permian rugose coral reefs in the world known up to now.

UUID: http://zoobank.org/b9e621cb-197d-4208-8267-14d62f382a1b

Toxoplasma gondii is a major cause of congenital brain disease; however, the underlying mechanism of neuropathogenesis in brain toxoplasmosis remains elusive. To explore the role of T. gondii in the development of neural stem cells (NSCs), NSCs were isolated from GD14 embryos of ICR mice and were co-cultured with tachyzoites of T. gondii RH strain. We found that apoptosis levels of the NSCs co-cultured with 1×106 RH tachyzoites for 24 and 48 h significantly increased in a dose-dependent manner, as compared with the control. Western blotting analysis displayed that the protein level of C/EBP homologous protein (CHOP) was up-regulated, and caspase-12 and c-Jun N-terminal kinase (JNK) were activated in the NSCs co-cultured with the parasites. Pretreatment with endoplasmic reticulum stress (ERS) inhibitor (TUDCA) and caspase-12 inhibitor (Z-ATAD-FMK) inhibited the expression or activation of the key molecules involved in the ERS-mediated apoptotic pathway, and subsequently decreased the apoptosis levels of the NSCs induced by the T. gondii. The findings here highlight that T. gondii induced apoptosis of the NSCs through the ERS signal pathway via activation of CHOP, caspase-12 and JNK, which may constitute a potential molecular mechanism responsible for the cognitive disturbance in neurological disorders of T. gondii.

We investigated the persistent luminescence in europium-doped LiBaPO4. The persistent phosphors were synthesized via solid-state reaction method under mild reducing atmosphere. Its properties were investigated by x-ray diffraction, diffuse reflectance, photoluminescence, persistent luminescence, and thermoluminescence spectra. Under UV irradiation, broad-band persistent luminescence peaked at ∼470 nm was observed in the phosphors at room temperature. The effects of Eu2+ concentration on the persistent luminescence of LiBaPO4:Eu2+ were discussed. An energy level scheme was constructed to convey reasonable trapping and detrapping processes in the material.

A novel Ba2MgMoO6:Eu3+ orange-red phosphor was synthesized by the Pechini method and characterized by x-ray diffraction. Photoluminescence properties of BaMgMoO6:Eu3+ phosphors have been represented in the excitation and emission spectra. The charge transfer (CT) band of Ba2MgMoO6 host is situated at near-ultraviolet (UV) region, whose central wave length and bandwidth are 394 and 80 nm, respectively. And it matches well the emission wave length from near-UV light emitting diodes (LEDs). The most intensive emission of 5D0 → 7F1 (598 nm) of Eu3+ in Ba2MgMoO6:Eu3+ is much narrow with a full width at half-maximum less than 2 nm under excitation with either CT band or 394 nm. And a low concentration quenching occurs in Ba2MgMoO6:Eu3+, and the optimal doping concentration is about 0.05. The mechanism of charge and energy transfer from Ba2MgMoO6 host to Eu3+ is proposed and analyzed on the basis of its crystal structure. In a word, Ba2MgMoO6:Eu3+ may be a promising orange-red component for near UV white LEDs.

Quantitative trait loci (QTLs) mapping often results in data on a number of traits that have well-established causal relationships. Many multi-trait QTL mapping methods that account for correlation among the multiple traits have been developed to improve the statistical power and the precision of QTL parameter estimation. However, none of these methods are capable of incorporating the causal structure among the traits. Consequently, genetic functions of the QTL may not be fully understood. In this paper, we developed a Bayesian multiple QTL mapping method for causally related traits using a mixture structural equation model (SEM), which allows researchers to decompose QTL effects into direct, indirect and total effects. Parameters are estimated based on their marginal posterior distribution. The posterior distributions of parameters are estimated using Markov Chain Monte Carlo methods such as the Gibbs sampler and the Metropolis–Hasting algorithm. The number of QTLs affecting traits is determined by the Bayes factor. The performance of the proposed method is evaluated by simulation study and applied to data from a wheat experiment. Compared with single trait Bayesian analysis, our proposed method not only improved the statistical power of QTL detection, accuracy and precision of parameter estimates but also provided important insight into how genes regulate traits directly and indirectly by fitting a more biologically sensible model.