An equilibrium-conserving taxation scheme for income from capital

Under conditions of market equilibrium, the distribution of capital income follows a Pareto power law, with an exponent that characterizes the given equilibrium. Here, a simple taxation scheme is proposed such that the post-tax capital income distribution remains an equilibrium distribution, albeit with a different exponent. This taxation scheme is shown to be progressive, and its parameters can be simply derived from (i) the total amount of tax that will be levied, (ii) the threshold selected above which capital income will be taxed and (iii) the total amount of capital income. The latter can be obtained either by using Piketty's estimates of the capital/labor income ratio or by fitting the initial Pareto exponent. Both ways moreover provide a check on the amount of declared income from capital.Comment: 4 pages, 2 figure

Study of Radiative Leptonic D Meson Decays

We study the radiative leptonic $D$ meson decays of D^+_{(s)}\to \l^+\nu_{\l}\gamma (\l=e,\mu,\tau), $D^0\to \nu\bar{\nu}\gamma$ and D^0\to \l^+\l^-\gamma ($l=e,\mu$) within the light front quark model. In the standard model, we find that the decay branching ratios of $D^+_{(s)}\to e^+\nu_e\gamma$, $D^+_{(s)}\to\mu^+\nu_{\mu}\gamma$ and $D^+_{(s)}\to\tau^+\nu_{\tau}\gamma$ are $6.9\times 10^{-6}$ ($7.7\times 10^{-5}$), $2.5\times 10^{-5}$ ($2.6\times 10^{-4}$), and $6.0\times 10^{-6}$ ($3.2\times 10^{-4}$), and that of D^0\to\l^+\l^-\gamma (\l=e,\mu) and $D^0\to\nu\bar{\nu}\gamma$ are $6.3\times 10^{-11}$ and $2.7\times 10^{-16}$, respectively.Comment: 23 pages, 6 Figures, LaTex file, a reference added, to be published in Mod. Phys. Lett.

Expression and characterization of keratinase from Deinococcus gobiensis I-0

Keratin is a nonnutritious hard protein widely distributed in feather, wool, animal hoof, horn, and toenail. The disulfide bond interacts to form a dense structure of keratin, which is difficult to be degraded and utilized. Keratinase is a kind of enzymes that can destroy the dense structure of keratin to achieve the degradation, and has a good application prospect. In order to further tap the important gene resources of keratinase, improve its hydrolytic activity，and provide theoretical basis for industrial production, this experiment cloned a gene encoding keratinase from Deinococcus gobiensis I-0 isolated from Gobi desert of Xinjiang and named it as Kerdg. Prokaryotic expression vector pET-22B-Kerdg was constructed and then induced, expressed and purified in vitro, the optimal temperature and pH of the crude enzyme solution were determined through the hydrolysis activity to feathers. Results showed that the first 50 amino acids of N terminal had a great influence on the expression and purification of protein Kerdg. The crude enzyme solution of recombinant strain completely decomposed feathers in three days. The transparent circle on milk powder plate appeared more notable in crude enzyme solution of recombinant strain than that of empty strain. Kerdg adapted to a wide range of temperatures and pH，among which the optimal temperature was 60℃ and the optimal pH was 5.0. The Kerdg can degrade feathers and thus will have great application space in the future industrial production and treatment of waste feathers. Please click Additional Files below to see the full abstract

miR-638 suppresses cervical cancer progression by inhibiting NCAPG2 under the treatment of Tetrandrine

Background. The interaction of microRNA with Chinese herbal medicines is a promising therapeutic approach for prevention of cervical cancer. Methods. Western blotting or qRT-PCR were carried out to identify the expression of NCAPG2 and miR-638. A tetrandrine (TET) cell model was used to explore the effects of miR-638 and its target gene NCAPG2 using CCK-8, transwell, wound healing, and western blot assays. Furthermore, luciferase activity assay was conducted to measure the interaction among TET, NCAPG2 and miR-638. Results. Under TET treatment, Hela and SiHa cells exhibited repressed cell viability, migration, invasion, and epithelial-mesenchymal transition (EMT), and these effects were further enhanced by high expression of miR-638. In contrast, NCAPG2 expression was low in TET-treated cells and had an opposite effect to that of miR-638. Conclusion. We highlighted that miR-638 suppresses cervical cancer progression by inhibiting NCAPG2 under tetrandrine treatmen