Co(II) and Ni(II) complexes based on anthraquinone-1,4,5,8-tetracarboxylic acid (H4AQTC): canted antiferromagnetism and slow magnetization relaxation in {[Co2(AQTC)(H2O)6]·6H2O}.

Three coordination polymers {[Co2(AQTC)(H2O)6]·6H2O}n (1), {[M2(AQTC)(bpym)(H2O)6]·6H2O}n (M = Co(2), Ni(3)) have been synthesized and structurally characterized, where H4AQTC is anthraquinone-1,4,5,8-tetracarboxylic acid and bpym is 2,2'-bipyrimidine. Complex 1 features a 3-D structure, where layers of Co2(AQTC) are cross-linked by Co-H2O chains. Complexes 2 and 3 are isostructural and display 1-D chain structures. The chains are connected through hydrogen-bonding interactions to form 3-D supramolecular structures. Magnetic properties of these complexes are investigated. Compound 1 shows canted antiferromagnetism and slow relaxation below 4.0 K. For complexes 2 and 3, dominant antiferromagnetic interactions are observed. The luminescent properties of the three complexes are investigated as well.

Poly[[bis-{µ2-1,2-bis-[(1H-imidazol-1-yl)meth-yl]benzene}(µ4-9,10-dioxo-9,10-dihydro-anthracene-1,4,5,8-tetra-carbox-yl-ato)dicobalt(II)] dihydrate].

The title complex, {[Co2(C18H4O10)(C14H14N4)2]·2H2O} n was synthesized from CoCl2·6H2O, 9,10-dioxo-9,10-dihydro-anthracene-1,4,5,8-tetra-carb-oxy-lic acid (H4AQTC) and 1,2-bis-[(1H-imidazol-1-yl)meth-yl]benzene (o-bix) in water. The anthraquinone unit is located about a crystallographic center of inversion. Each asymmetric unit therefore contains one Co(II) atom and one o-bix ligand, as well as half an AQTC(4-) ligand and an additional solvent water mol-ecule. The Co(II) ions are tetra-hedrally surrounded by two O atoms from two AQTC(4-) anions and by two N atoms from two o-bix ligands, forming a two-dimensional coordination polymer. The solvent water mol-ecules are connected to the carboxyl-ate groups by O-H⋯O hydrogen bonds. Additional weak C-H⋯O hydrogen bonds are observed in the crystal structure.

[Activity of bilateral posterior cricoarytenoid muscle satellite cell after denervation or reinnervation with ansa in dogs].

OBJECTIVE: To investigate the activity of bilateral posterior cricoarytenoid muscle satellite cell after denervation or reinnervation with ansa cervicalis. METHODS: Twenty four dogs were randomly divided into 3 groups. The bilateral laryngeal recurrent nerves were cut in group one in all dogs. The bilateral laryngeal recurrent nerves were anastomosed with ansa cervicalis after incision in group two in all dogs. The dogs in group three were used as control. Nine weeks after surgery, the electromyography was used to test the regeneration of the nerve. The posterior cricoarytenoid muscles biopsy were collected. The expression of mRNA of Myogenin, Myf5, and Pax7 was assayed by realtime RT-PCR after total RNA isolation. RESULTS: Two dogs died after surgery in incision and anastomose group. The electromyography suggested that the RLN of all dogs had denervated in the incision group and had reinnervated in the anastomose group after 9 weeks. Myogenin mRNA from RLN incision dogs PCA muscles had greater expression versus controls (Z = 1.42, P < 0.01) or anastomosed dogs (Z = 1.38, P < 0.01). Myf5 mRNA expression from RLN incision dogs PCA muscles had significant increase versus control dogs (Z = 1.66, P < 0.01) or anastomosed dogs (Z = 1.69, P < 0.01). Pax7 mRNA expression from RNL incision dogs had significant increase compared with control (Z = 1.66, P < 0.01) or anastomosed animals (Z = 1.42, P < 0.05). There was no significant difference in Myogenin (Z = 1.34, P > 0.05), Myf5 (Z = 0.54, P > 0.05) and Pax (Z = 0.54, P > 0.05) mRNA expression between controls and anastomosed animals. CONCLUSIONS: The bilateral denervation of RLN cause significantly increasing in dog PCA muscle satellite cell proliferation and differentiation. The bilateral reinnervation of RLN cause PCA muscle satellite cell come back nonproliferative, quiescent state in dog.