Beschreibung: There are three independent CdII ions in the title complex, {[Cd3(C10H3O8)2(H2O)4]·4H2O}n, one of which is coordinated by four O atoms from three 5-carboxybenzene-1,2,4-tricarboxylate ligands and by two water molecules in a distorted octahedral geometry. The second CdII ion is coordinated by five O atoms from four 5-carboxybenzene-1,2,4-tricarboxylate ligands and by one water molecule also in a distorted octahedral geometry while the third CdII ion is coordinated by five O atoms from three 5-carboxybenzene-1,2,4-tricarboxylate ligands and by one water molecule in a highly distorted octahedral geometry. The 5-carboxybenzene-1,2,4-tricarboxylate ligands bridge the CdII ions, resulting in the formation of a three-dimensional structure. Intra- and intermolecular O—H...O hydrogen bonds are present throughout the three-dimensional structure.

Beschreibung: In the title complex, {[CaZn(C10H2O8)(H2O)2]·H2O}n, the ZnII ion is coordinated by four O atoms from four benzene-1,2,4,5-tetracarboxylate anions in a distorted tetrahedral geometry. The CaII ion is eight-coordinated by six O atoms from four benzene-1,2,4,5-tetracarboxylate anions and by two water molecules in a distorted square-antiprismatic geometry. The CaII and ZnII ions and the lattice water molecule are located on twofold rotation axes; the centroid of the benzene-1,2,4,5-tetracarboxylate anion is located on a centre of inversion. The μ8-bridging mode of the anion results in the formation of a three-dimensional structure with channels extending along [100] in which lattice water molecules are situated. Intermolecular O—H...O hydrogen bonds involving the coordinating and lattice water molecules as donors and the carboxylate O atoms and lattice water molecules as acceptors are present in the structure.

Beschreibung: In vitro experiments have shown that the upregulation of small-conductance Ca 2+ -activated K + (SK) channels in ventricular epicardial myocytes is responsible for spontaneous ventricular fibrillation (VF) in failing ventricles. However, the role of SK channels in regulating VF has not yet been described in in vivo acute myocardial infarction (AMI) animals. The present study determined the role of SK channels in regulating spontaneous sustained ventricular tachycardia (SVT) and VF, the inducibility of ventricular tachyarrhythmias, and the effect of inhibition of SK channels on spontaneous SVT/VF and electrical ventricular instability in AMI rats. AMI was induced by ligation of the left anterior descending coronary artery in anesthetized rats. Spontaneous SVT/VF was analyzed, and programmed electrical stimulation was performed to evaluate the inducibility of ventricular tachyarrhythmias, ventricular effective refractory period (VERP), and VF threshold (VFT). In AMI, the duration and episodes of spontaneous SVT/VF were increased, and the inducibility of ventricular tachyarrhythmias was elevated. Pretreatment in the AMI group with the SK channel blocker apamin or UCL-1684 significantly reduced SVT/VF and inducibility of ventricular tachyarrhythmias ( P 〈 0.05). Various doses of apamin (7.5, 22.5, 37.5, and 75.0 μg/kg iv) inhibited SVT/VF and the inducibility of ventricular tachyarrhythmias in a dose-dependent manner. Notably, no effects were observed in sham-operated controls. Additionally, VERP was shortened in AMI animals. Pretreatment in AMI animals with the SK channel blocker significantly prolonged VERP ( P 〈 0.05). No effects were observed in sham-operated controls. Furthermore, VFT was reduced in AMI animals, and block of SK channels increased VFT in AMI animals, but, again, this was without effect in sham-operated controls. Finally, the monophasic action potential duration at 90% repolarization (MAPD 90 ) was examined in the myocardial infarcted (MI) and nonmyocardial infarcted areas (NMI) of the left ventricular epicardium. Electrophysiology recordings showed that MAPD 90 in the MI area was shortened in AMI animals, and pretreatment with SK channel blocker apamin or UCL-1684 significantly prolonged MAPD 90 ( P 〈 0.05) in the MI area but was without effect in the NMI area or in sham-operated controls. We conclude that the activation of SK channels may underlie the mechanisms of spontaneous SVT/VF and suseptibility to ventricular tachyarrhythmias in AMI. Inhibition of SK channels normalized the shortening of MAPD 90 in the MI area, which may contribute to the inhibitory effect on spontaneous SVT/VF and inducibility of ventricular tachyarrhythmias in AMI.

Beschreibung: Lemur tyrosine kinase 2 (LMTK2) is a novel membrane-anchored kinase reported to be involved in several normal and pathophysiological conditions, including endosomal membrane recycling, prostate cancer, and neurodegeneration. In this study, we have investigated the topology and orientation of LMTK2 within cellular membranes utilizing fluorescence protease protection. Appending the green fluorescent protein to either the amino or carboxyl terminus of LMTK2, we were able to determine which side of intracellular membrane these regions were located. Our results indicate that LMTK2 is an integral membrane protein in which both the amino and carboxyl termini are exposed to the cytoplasm. Moreover, this topology places the kinase active site within the cytoplasm.

Beschreibung: In the title complex, [Ni(C9H5O6)2(C11H10N4)2]·8H2O, the NiII ion exhibits site symmetry 2. It has a distorted octahedral coordination defined by two N atoms from two symmetry-related 1-[(1H-benzimidazol-1-yl)methyl]-1H-imidazole ligands and four O atoms from two symmetry-related 3,5-dicarboxybenzoate anions. In the crystal, the complex molecules and solvent water molecules are linked via O—H...O, O—H...N and N—H...O hydrogen bonds, forming a three-dimensional structure. There are also a number of C—H...O interactions present.