Dehydrogenation of ammonia-borane by cationic Pd(II) and Ni(II) complexes in a nitromethane medium: hydrogen release and spent fuel characterization

A highly electrophilic cationic PdII complex, [Pd(MeCN)_4][BF_4]_2 (1), brings about the preferential activation of the B–H bond in ammonia-borane (NH3·BH3, AB). At room temperature, the reaction between 1 in CH_3NO_2 and AB in tetraglyme leads to Pd nanoparticles and formation of spent fuels of the general formula MeNH_xBO_y as reaction byproducts, while 2 equiv. of H_2 is efficiently released per AB equiv. at room temperature within 60 seconds. For a mechanistic understanding of dehydrogenation by 1, the chemical structures of spent fuels were intensely characterized by a series of analyses such as elemental analysis (EA), X-ray photoelectron spectroscopy (XPS), solid state magic-angle-spinning (MAS) NMR spectra (^2H, ^(13)C, ^(15)N, and ^(11)B), and cross polarization (CP) MAS methods. During AB dehydrogenation, the involvement of MeNO2 in the spent fuels showed that the mechanism of dehydrogenation catalyzed by 1 is different from that found in the previously reported results. This AB dehydrogenation derived from MeNO_2 is supported by a subsequent digestion experiment of the AB spent fuel: B(OMe)_3 and N-methylhydroxylamine ([Me(OH)N]_2CH_2), which are formed by the methanolysis of the AB spent fuel (MeNH_xBO_y), were identified by means of ^(11)B NMR and single crystal structural analysis, respectively. A similar catalytic behavior was also observed in the AB dehydrogenation catalyzed by a nickel catalyst, [Ni(MeCN)_6][BF_4]_2 (2)

N-(3,4-Difluoro­phen­yl)-2-(3,4-dimethoxy­phen­yl)acetamide

In the title amide, C16H15F2NO3, the dihedral angle between the benzene rings is 53.7 (1)°. Mol­ecules are linked in the crystal structure by an inter­molecular N—H⋯O hydrogen bond involving N—H and C=O functionalities of the amide group. A one-dimensional network is thus formed along the [001] direction. No significant inter­chain contacts are observed

Deep Seawater flow Characteristics Around the Manganese Nodule Collecting Device

AbstractFlow field characteristics with outflow discharge from a collecting device in deep seawater while gathering manganese nodules have been analyzed by CFD. Numerical model is used for the analysis with CFD program of FLUENT. It is assumed that the collecting device is 4.5×5.4×6.7m with outflow speed = 1.75 m/s and the current speed = 0.1m/s.Overall seawater flow field characteristics are largely influenced by the outflow discharge from the collecting device and manganese nodule particle behavior. The outflow discharge effect reaches to about few times of the collecting device in back. As simulation results, flow velocity and streamline distributions are compared including turbulence kinetic energyvariation. This study will be useful for optimal design for manganese nodule collecting device system in deep sea

Diosgenin Induces Apoptosis in HepG2 Cells through Generation of Reactive Oxygen Species and Mitochondrial Pathway

Diosgenin, a naturally occurring steroid saponin found abundantly in legumes and yams, is a precursor of various synthetic steroidal drugs. Diosgenin is studied for the mechanism of its action in apoptotic pathway in human hepatocellular carcinoma cells. Based on DAPI staining, diosgenin-treated cells manifested nuclear shrinkage, condensation, and fragmentation. Treatment of HepG2 cells with 40 μM diosgenin resulted in activation of the caspase-3, -8, -9 and cleavage of poly-ADP-ribose polymerase (PARP) and the release of cytochrome c. In the upstream, diosgenin increased the expression of Bax, decreased the expression of Bid and Bcl-2, and augmented the Bax/Bcl-2 ratio. Diosgenin-induced, dose-dependent induction of apoptosis was accompanied by sustained phosphorylation of JNK, p38 MAPK and apoptosis signal-regulating kinase (ASK)-1, as well as generation of the ROS. NAC administration, a scavenger of ROS, reversed diosgene-induced cell death. These results suggest that diosgenin-induced apoptosis in HepG2 cells through Bcl-2 protein family-mediated mitochndria/caspase-3-dependent pathway. Also, diosgenin strongly generated ROS and this oxidative stress might induce apoptosis through activation of ASK1, which are critical upstream signals for JNK/p38 MAPK activation in HepG2 cancer cells