(1,2-Dicarba-closo-dodeca­boran­yl)trimethyl­methanaminium iodide

The title compound, [1-(CH3)3NCH2-1,2-C2B10H11]+·I− or C6H22B10N+·I−, was obtained by the reaction of (1,2-dicarba-closo-dodeca­boran­yl)dimethyl­methanamine with methyl iodide. The asymmetric unit contains two iodide anions and two (o-carboran­yl)tetra­methyl­ammonium cations. The bond lengths and angles in the carborane cage are within normal ranges, but the N—Cmethyl­ene—Ccage angle is very large [120.2 (2)°] because of repulsion between the carborane and tetra­methyl­ammonium units. In the crystal, ions are linked through C—H⋯I hydrogen bonds

The Rhizome Mixture of Anemarrhena asphodeloides

We investigated the effect of DWac on the gut microbiota composition in mice with 2,3,6-trinitrobenzenesulfonic acid- (TNBS-) induced colitis. Treatment with DWac restored TNBS-disturbed gut microbiota composition and attenuated TNBS-induced colitis. Moreover, we examined the effect of DWac in mice with mesalazine-resistant colitis (MRC). Intrarectal injection of TNBS in MRC mice caused severe colitis, as well as colon shortening, edema, and increased myeloperoxidase activity. Treatment with mesalazine (30 mg/kg) did not attenuate TNBS-induced colitis in MRC mice, whereas treatment with DWac (30 mg/kg) significantly attenuated TNBS-induced colitis. Moreover, treatment with the mixture of mesalazine (15 mg/kg) and DWac (15 mg/kg) additively attenuated colitis in MRC mice. Treatment with DWac and its mixture with mesalazine inhibited TNBS-induced activation of NF-κB and expression of M1 macrophage markers but increased TNBS-suppressed expression of M2 macrophage markers. Furthermore, these inhibited TNBS-induced T-bet, RORγt, TNF-α, and IL-17 expression but increased TNBS-suppressed Foxp3 and IL-10 expression. However, Th2 cell differentiation and GATA3 and IL-5 expression were not affected. These findings suggest that DWac can ameliorate MRC by increasing the polarization of M2 macrophage and correcting the disturbance of gut microbiota and Th1/Th17/Treg, as well as additively attenuating MRC along with mesalazine

trans-{1,8-Bis[(R)-α-methyl­benz­yl]-1,3,6,8,10,13-hexa­azacyclo­tetra­deca­ne}dithio­cyanato­nickel(II)

The title compound, [Ni(NCS)2(C24H38N6)], is a thio­cyanate-coordinated aza­macrocyclic nickel(II) complex. There are two independent mol­ecules in the asymmetric unit and their bond lengths and angles are similar. Both Ni atoms have a tetra­gonally distorted octa­hedral geometry, in which the NiII ion is coordinated by the four secondary N atoms of the aza­macrocyclic ligand and by two N atoms of the thio­cyanate ions. The average equatorial Ni—N bond lengths are shorter than the average axial Ni—N bond lengths [2.071 (1) and 2.115 (2) Å, respectively]. N—H⋯S hydrogen-bonding inter­actions between a secondary amine N atom and the adjacent thio­cyanate ion leads to a polymeric chain along [100]

Palladium Catalysts for Dehydrogenation of Ammonia Borane with Preferential B−H Activation

Cationic Pd(II) complexes catalyzed the dehydrogenation of ammonia borane in the most efficient manner with the release of 2.0 equiv of H_2 in less than 60 s at 25 °C. Most of the hydrogen atoms were obtained from the boron atom of the ammonia borane. The first step of the dehydrogenation reaction was elaborated using density functional theory calculations

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)

Enhanced cardiac expression of two isoforms of matrix metalloproteinase-2 in experimental diabetes mellitus.

BackgroundDiabetic cardiomyopathy (DM CMP) is defined as cardiomyocyte damage and ventricular dysfunction directly associated with diabetes independent of concomitant coronary artery disease or hypertension. Matrix metalloproteinases (MMPs), especially MMP-2, have been reported to underlie the pathogenesis of DM CMP by increasing extracellular collagen content.PurposeWe hypothesized that two discrete MMP-2 isoforms (full length MMP-2, FL-MMP-2; N-terminal truncated MMP-2, NTT-MMP-2) are induced by high glucose stimulation in vitro and in an experimental diabetic heart model.MethodsRat cardiomyoblasts (H9C2 cells) were examined to determine whether high glucose can induce the expression of the two isoforms of MMP-2. For the in vivo study, we used the streptozotocin-induced DM mouse heart model and age-matched controls. The changes of each MMP-2 isoform expression in the diabetic mice hearts were determined using quantitative real-time polymerase chain reaction (qRT-PCR). Immunohistochemical stains were conducted to identify the location and patterns of MMP-2 isoform expression. Echocardiography was performed to compare and analyze the changes in cardiac function induced by diabetes.ResultsQuantitative RT-PCR and immunofluorescence staining showed that the two MMP-2 isoforms were strongly induced by high glucose stimulation in H9C2 cells. Although no definite histologic features of diabetic cardiomyopathy were observed in diabetic mice hearts, left ventricular systolic dysfunction was determined by echocardiography. Quantitative RT-PCR and IHC staining showed this abnormal cardiac function was accompanied with the increases in the mRNA levels of the two isoforms of MMP-2 and related to intracellular localization.ConclusionTwo isoforms of MMP-2 were induced by high glucose stimulation in vitro and in a Type 1 DM mouse heart model. Further study is required to examine the role of these isoforms in DM CMP

trans-{1,8-Bis[(S)-1-phenyl­eth­yl]-1,3,6,8,10,13-hexa­aza­cyclo­tetra­deca­ne}bis(thio­cyanato­-κN)copper(II)

In the title thio­cyanate-coordinated aza-macrocyclic copper(II) complex, [Cu(NCS)2(C24H38N6)], the CuII atom is coordinated by the four secondary N atoms of the aza-macrocyclic ligand and by the two N atoms of the thio­cyanate ions in a tetra­gonally distorted octa­hedral geometry. The average equatorial Cu—N bond length is shorter than the average axial Cu—N bond length [2.010 (2) and 2.528 (4) Å, respectively]. An N—H⋯N hydrogen-bonding inter­action between the secondary amine N atom and the adjacent thio­cyanate ion leads to a polymeric chain along the a axis