Metal-Insulator Transition and Emergent Gapped Phase in the Surface-Doped 2D Semiconductor 2H-MoTe_{2}.

Artificially created two-dimensional (2D) interfaces or structures are ideal for seeking exotic phase transitions due to their highly tunable carrier density and interfacially enhanced many-body interactions. Here, we report the discovery of a metal-insulator transition (MIT) and an emergent gapped phase in the metal-semiconductor interface that is created in 2H-MoTe_{2} via alkali-metal deposition. Using angle-resolved photoemission spectroscopy, we found that the electron-phonon coupling is strong at the interface as characterized by a clear observation of replica shake-off bands. Such strong electron-phonon coupling interplays with disorder scattering, leading to an Anderson localization of polarons which could explain the MIT. The domelike emergent gapped phase could then be attributed to a polaron extended state or phonon-mediated superconductivity. Our results demonstrate the capability of alkali-metal deposition as an effective method to enhance the many-body interactions in 2D semiconductors. The surface-doped 2H-MoTe_{2} is a promising candidate for realizing polaronic insulator and high-T_{c} superconductivity.

Band insulator to Mott insulator transition in 1T-TaS2.

1T-TaS2 undergoes successive phase transitions upon cooling and eventually enters an insulating state of mysterious origin. Some consider this state to be a band insulator with interlayer stacking order, yet others attribute it to Mott physics that support a quantum spin liquid state. Here, we determine the electronic and structural properties of 1T-TaS2 using angle-resolved photoemission spectroscopy and X-Ray diffraction. At low temperatures, the 2π/2c-periodic band dispersion, along with half-integer-indexed diffraction peaks along the c axis, unambiguously indicates that the ground state of 1T-TaS2 is a band insulator with interlayer dimerization. Upon heating, however, the system undergoes a transition into a Mott insulating state, which only exists in a narrow temperature window. Our results refute the idea of searching for quantum magnetism in 1T-TaS2 only at low temperatures, and highlight the competition between on-site Coulomb repulsion and interlayer hopping as a crucial aspect for understanding the material's electronic properties.

Isostructural Spin-Density-Wave and Superconducting Gap Anisotropies in Iron-Arsenide Superconductors.

When passing through a phase transition, electronic system saves energy by opening energy gaps at the Fermi level. Delineating the energy gap anisotropy provides insights into the origin of the interactions that drive the phase transition. Here, we report the angle-resolved photoemission spectroscopy (ARPES) study on the detailed gap anisotropies in both the tetragonal magnetic and superconducting phases in Sr_{1-x}Na_{x}Fe_{2}As_{2}. First, we found that the spin-density-wave (SDW) gap is strongly anisotropic in the tetragonal magnetic phase. The gap magnitude correlates with the orbital character of Fermi surface closely. Second, we found that the SDW gap anisotropy is isostructural to the superconducting gap anisotropy regarding to the angular dependence, gap minima locations, and relative gap magnitudes. Our results indicate that the superconducting pairing interaction and magnetic interaction share the same origin. The intraorbital scattering plays an important role in constructing these interactions resulting in the orbital-selective magnetism and superconductivity in iron-based superconductors.

MiR-135b-5p inhibits the progression of malignant melanoma cells by targeting RBX1.

OBJECTIVE: The aim of this study was to investigate the potential effects of microRNA-135b-5p (miR-135b) on the development of malignant melanoma (MM) and the relevant mechanism. PATIENTS AND METHODS: The expression level of miR-135b in MM tissues and cells was detected by quantitative Real Time-Polymerase Chain Reaction (qRT-PCR). Online prediction software and luciferase reporter assays were used to predict and verify the possible target of miR-135b, respectively. Furthermore, the effects of the miR-135b on MM A375 cells were determined by Western blotting, MTT, and transwell assays. RESULTS: MiR-135b was significantly down-regulated in MM. RING-box protein 1 (RBX1) was verified as a direct target of miR-135b. Subsequent experiments showed that down-regulation of RBX1 resulted from miR-135b up-regulation could significantly inhibit the proliferation, invasion, and migration abilities of MM cells. CONCLUSIONS: MiR-135b inhibited the progression of MM by targeting RBX1. Our findings revealed that miR-135b/RBX1 might be a potential therapeutic target for the treatment of MM.

Effects of early-cleavage embryo transfer on in vitro fertilization-embryo transfer pregnancy outcomes.

PURPOSE: To observe the effects of early-cleavage embryo transfer (ET) on pregnancy outcomes in vitro fertilization-embryo transfer (IVF-ET). MATERIALS AND METHODS: The data of 6,548 two pro-nucleate (2PN) embryos and 968 patients who underwent IVF or intracytoplasmic sperm injection (ICSI) were analyzed. Of the 968 cycles, early-cleavage embryos were used in 432 cycles (early-cleavage group), late-cleavage embryos were used in 246 cycles (late-cleavage group), and both early and late-cleavage embryos were used in 290 cycles (mixed group). RESULTS: High-quality embryo rate was significantly higher in early-cleavage group than in late-cleavage group (82.74% vs 59.83%; p < 0.01). Both clinical pregnancy and implantation rates in IVF or ICSI were significantly higher in early-cleavage group than in late-cleavage group (all p < 0.01). In ICSI, both clinical pregnancy and implantation rates were significantly higher in mixed group than in late-cleavage group (all p < 0.05). CONCLUSION: Early-cleavage ET can improve pregnancy outcomes in IVF or ICSI.

Synthesis and antiprotozoal activities of some new triazine derivatives including a new antitrypanosomal agent: SIPI-1029.

Two series of compounds, 1,2-dihydro-2,2-dimethyl-4, 6-diamino-1-(omega-haloalkyloxy)-s-triazines and O, O'-bis (4, 6-diamino-1, 2-dihydro-2, 2-disubstituted-s-triazin-l-yl) alkanediols were synthesized and tested against Plasmodium berghei and Trypanosoma evansi in mice. Most title compounds showed good antimalarial activity and compounds IIc-e showed good antitrypanosomal effect. After further studies on pharmacology, toxicology, pharmacokinetics and efficacy on infected cattles compound IIe (SIPI-1029, T-46) was shown to be a new highly active antitrypanosomal agent with low toxicity and long half life in plasma.

[Synthesis and antimalarial as well as antitumor activities of 2,4-diamino-6-(N-methyl-substituted benzylamino) quinazolines].

Sixteen 2,4-diamino-6-(N-methyl-substituted benzylamino) quinazolines (I) were synthesized by two different methods. 2-Nitro-5-chloro-benzonitrile was treated with the appropriate N-methyl-substituted benzylamines and I was formed after reduction and cyclization. Another method was reductive methylation, i.e., 2,4-diamino-6-substituted benzylaminoquinazolines reacted with formaldehyde and sodium cyanoborohydride at pH 6.3. Suppressive therapeutic tests in mice infected with Plasmodium berghei showed that four (I6,7,10,16) out of these compounds suppressed all the parasites when administered orally at the dose of 5 mg/kg and produced more than 99% suppression at 2.5 mg/kg. Eight compounds (I1,2,4,5,8-10,15) were found to have antitumor effects against Leukemia cells in culture comparable with or superior to those of the positive control methotrexate.

[Synthesis and antimalarial as well as antitumor activities of 1-methyl-2,4-diamino-6-(N-methyl-substituted benzylamion) quinazolinium iodides].

Fourteen 1-methyl-2,4-diamino-6-(N-methyl-substituted benzylamino) quinazolinium iodides (II) were synthesized by treatment of 2,4-diamino-6-substituted benzylaminoquinazolines with methyl iodide. Three compounds (II4,7,10) were shown to produce 100% suppression on Plasmodium berghei in mice at oral dose of 20 mg/kg and II4 was found to inhibit twice as much as methotrexate on L1210 Leukemia cells in culture.