The complete mitochondrial genome of soft coral Ofwegen and Benayahu, 2012 (Octocorallia: Alcyonacea): the analysis of mitogenome organization and phylogeny.

The complete mitochondrial genome of was sequenced and analyzed using next-generation sequencing. The present mitochondrial genome was 18730 bp in length, containing 14 protein-coding genes (PCGs) (-.-, , , , , and ), two ribosomal genes (s) ( and ), and one transfer gene ().

Half-sandwich rare-earth metal complexes bearing a CMe-CH-o-CHNMe ligand: synthesis, characterization and catalytic properties for isoprene, 1-hexene and MMA polymerization.

A new ortho-dimethylaminomethylphenyl-tetramethylcyclopentadienyl ligand CMeH-CH-o-CHNMe (HL) and a series of rare-earth metal complexes bearing this ligand were synthesized. Of these complexes, two binuclear alkyl complexes [(CMe-CH-o-CHN(Me)CH-μ)Ln(CHSiMe)] (Ln = Sc (1a) and Y (1b)) were obtained from the alkane elimination reaction of the free ligand with Ln(CHSiMe)(THF), followed by an intramolecular C-H activation process of a NMe group in the ligand with a CHSiMe group, two binuclear dichloro complexes (CMe-CH-o-CHNMe)YCl[LiCl(THF)] (2a) and [(CMe-CH-o-CHNMe)LuCl(μ-Cl)] (2b) were synthesized by the reaction of anhydrous yttrium or lutetium trichloride with the lithium salt of the ligand LiL, and the binuclear bis(borohydrido) complexes [(CMe-CH-o-CHNMe)Ln(μ-BH)BH] (Ln = Sm (3a) and Nd (3b)) were synthesized by the reaction of Ln(BH)(THF) (Ln = Sm and Nd) with the lithium salt of the ligand. The molecular structures of all complexes 1a, 1b, 2a, 2b, 3a and 3b were determined by single-crystal X-ray crystallography.

The complete mitochondrial genome of soft coral (Cnidaria: Anthozoa) using next-generation sequencing.

The complete mitochondrial genome of was completed using next-generation sequencing (NGS) method. The mitochondrial genome is a circular molecule of 18,508 bp in length, containing 14 protein-coding genes, two ribosomal RNA genes and one transfer RNA gene (Met-tRNA). The base composition is 30.

Titanium and zirconium complexes bearing new tridentate [OSO] bisphenolato-based ligands: synthesis, characterization and catalytic properties for alkene polymerization.

A number of new sulfur-bridged tridentate [OSO] bisphenolato-based ligand precursors S(2-CH2-4-tBu-6-R-C6H2OH)2 [R = CMe3 (H2L1), CMe2Ph (H2L2), CMePh2 (H2L3), CPh3 (H2L4), and C(p-Tol)3 (H2L5)] were synthesized by reactions of Na2S·9H2O with 2 eq. of the corresponding 2-(bromomethyl)-4-(tert-butyl)-6-R-phenol. Their neutral titanium complexes [S(2-CH2-4-tBu-6-R-C6H2O)2]TiCl2 [R = CMe3 (1), CMe2Ph (2), CMePh2 (3), CPh3 (4), and C(p-Tol)3 (5)] were synthesized in high yields by direct HCl-elimination reactions of TiCl4 with the corresponding ligand precursors in toluene.

Synthesis and characterization of chromium complexes 2-MeCpCHCH(R)NHCrCl and their catalytic properties in ethylene homo- and co-polymerization.

A series of new half-sandwich secondary amine-coordinated dichlorochromium complexes chelated by 2-(tetramethylcyclopentadienyl)benzylamine ligands, 2-Me4CpC6H4CH2(R)NHCrCl2 [R = iPr (1), Cy (2), Ph (3), 4-MePh (4), 2,6-Me2Ph (5), 2,6-Et2Ph (6)], have been synthesized from the reactions of CrCl3(THF)3 with the dilithium salts of the corresponding ligands in THF, followed by the addition of 1/2 eq. of H2O to the reaction mixtures. The isolated yields of the chromium complexes were found to increase with the increase in the amount of H2O introduced and reach the highest values (66-76%) when 1/2 eq.

[Research on Hemorheology in Rats with Acute Hyperuricemia].

Hyperuricemia is a risk factor for various diseases, but knowledge on acute hyperuricemia is still not sufficient. The present study was aimed to investigate the effect of acute hyperuricemia on red blood cells from hemorheological point of view, and to provide the reference for clinical treatment. The rats were gavaged with 500 mg/kg hypoxanthine and intraperitoneally injected with 100 mg/kg oxonate to induce the model of acute hyperuricemia.

Involvement of heat shock protein 27 in the susceptibility of KT human breast cancer cells to UVC and interferon lethality.

Revealing the key molecules regulating the stress-response pathways in human cells is an intriguing problem. Chaperones, such as glucose-regulated protein 78 (GRP78) and heat shock protein 27 (HSP27), are important molecules for protecting the viability of human cells; however, it remains to be further clarified whether the molecules differentially modulate cellular responses to various types of stressors, such as DNA-damaging ultraviolet ray C (principally 254-nm wavelength, UVC) and cytocidal cytokine interferons. In the present study, the human breast cancer cell lines KT and MCF-7 were examined for GRP78 and HSP27 expression following exposure to UVC and human interferon-β (HuIFN-β).

Extracellular recombinant annexin II confers UVC-radiation resistance and increases the Bcl-xL to Bax protein ratios in human UVC-radiation-sensitive cells.

In this study, we found that refractoriness to ultraviolet (UVC) light-induced cell death was increased in UVC-radiation-sensitive cells derived from Cockayne syndrome patients when the cells were precultured in medium supplemented with recombinant annexin II (rANX II). In CS3BES cells, an immortal cell line derived from Cockayne syndrome patients, the rANX II supplementation-induced UVC-radiation resistance was suppressed by treatment with an anti-annexin II antibody and EGTA. The amount of biotinylated annexin II on the cell surface increased in the rANX II-supplemented cells but did not increase in the cells that were cotreated with rANX II and EGTA.

UVC mutagenicity is suppressed in Japanese miso-treated human RSa cells, possibly via GRP78 expression.

Little is known about the ability of miso, to modulate mutability in human cells. We have observed increased levels of glucose-regulated protein 78 (GRP78) expression in association with suppression of mutation in human RSa cells irradiated with ultraviolet C (UVC). Here we examined to determine whether miso treatment results in increased GRP78 expression and suppression of UVC mutagenicity in RSa cells.

The roles of HSP27 and annexin II in resistance to UVC-induced cell death: comparative studies of the human UVC-sensitive and -resistant cell lines RSa and APr-1.

We have reported that heat shock protein 27 (HSP27) and annexin II are involved in the protection of human cells against UVC-induced cell death. In this study we tried to confirm the combined roles of HSP27 and annexin II in cell death after UVC irradiation. In RSa cells with sensitivity to UVC, expression of annexin II decreased after UVC irradiation, but not in AP(r)-1 cells with increased resistance to UVC.

Annexin II, a novel HSP27-interacted protein, is involved in resistance to UVC-induced cell death in human APr-1 cells.

Heat shock protein 27 (HSP27) is implicated in diverse biologic functions as a molecular chaperone. We found that HSP27 is involved in the protection of human cells against UVC lethality. To elucidate the molecular mechanisms underlying UVC resistance, we searched for HSP27-interacted proteins related to resistance in UVC-resistant human cells, APr-1.

Leupeptin-sensitive proteases involved in cell survival after X-ray irradiation in human RSa cells.

Proteases have received attention as important cellular components responsible for stress response in human cells. However, little is known about the role of proteases in the early steps of cell response after X-ray irradiation. In the present study, we first searched for proteases whose activity levels are changed soon after X-ray irradiation in human RSa cells with a high sensitivity to X-ray cell-killing.