This account presents the diverse reactivity of nitridoruthenium() complexes with nucleophilic, electrophilic and oxidizing agents. [Ru VI (N)(L 1 )Cl] (1) [H 2 L 1 = 2,6-bis(2,2-diphenyl-2-hydroxyethyl)pyridine] reacted with excess phosphines such as PPh 3 , PPhMe 2 and dppe to give [Ru III (HL 1 )(PPh 3 )Cl 2 ] (2a), [Ru III (L 1 )(PPhMe 2 ) 2 Cl] (2b) and [Ru III (L 1 )(dppe)Cl] (2c), respectively. In the presence of py or Hpz, 1 was converted to [Ru III (L 1 )(py) 2 Cl] (3a) and [Ru III (L 1 )(Hpz) 3 ]Cl (3b), respectively. A dinuclear µ-nitridoruthenium complex, [Ru IV (L 1 )Cl 2 (µ-N)Ru VI (L 1 )-(C 8 H 10 N)Cl] (4), was obtained by treating 1 with 2,6-dimethylaniline. Based on X-ray crystallographic study, the compound is characterized by an unsymmetrical Ru-N᎐ ᎐ ᎐ Ru moiety with the measured Ru-N distances being 1.661(5) and 1.837(5) Å. Complex 1 reacted with dmf to give [Ru III (HL 1 )(dmf )Cl 2 ] (5) in 17% yield. Excess (Me 3 O)BF 4 reacted with 1 to give a dinuclear µ-OH ruthenium complex, [Ru 2 (N) 2 (L 1 ) 2 (OH)]PF 6 (6). The measured Ru-O (OH) distance is 1.984(3) Å and the average Ru-O-Ru angle was found to be 100.4(2)Њ. Other nitrido-metal complexes, [n-Bu 4 N]-[M VI (N)(L)] [L = L 2 and L 3 ; M = Os and Ru; H 4 L 2 = 1,2-dichloro-4,5-bis(2-hydroxybenzamido)benzene, H 4 L 3 = 1,2-bis(2-hydroxybenzamido)benzene], underwent ligand protonation to form [M VI (N)(HL)] complexes, which have been characterized by X-ray crystallography. Oxidation of [n-Bu 4 N][Os VI (N)(L 2 )] by PhI(OAc) 2 produced [n-Bu 4 N][Os VI (N)(L 2 O 2 )] ( 8) in 10% yield. X-ray structure analysis of 8 showed that the coordinated phenoxy moiety was converted to a benzoquinone moiety while the Os᎐ ᎐ ᎐ N group remained intact.

We unveiled the mechanism of how HPV employs Aurora kinase A (AurA) of host cells to exert its oncogenic capability synergistically. We systematically characterized the mode of interaction between E6-encoded by cancer-causing HPV and AurA.

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Objective To investigate the effect of water extract of Gastrodiae Rhizoma (GR) on the development of acquired temporal lobe epilepsy (TLE) and on regulating the expression of the mammalian target of rapamycin (mTOR) and semaphorin 3F (SEMA3F). Methods A pilocarpine‐induced status epilepticus (SE) model was adopted to precipitate injury in the limbic systems. GR and carbamazepine (CBZ) treatments were given to mice for 14 days prior to SE induction to demonstrate the antiepileptic effects and continued for 5 more days to illustrate the effects on histologic studies. Results Our results consolidated that GR treatment (92.1 minutes) could delay the SE onset in comparison with the control group (61.5 minutes, P = .041). Fewer mice had reached SE with GR treatment (41.7%) when compared with the control group (83.3%, P = .044). GR treatment (2.1 hours/mouse) could suppress the number of acute seizures in post‐SE survival mice when compared with the control group (4.5 hours/mouse, P < .001). The effects of GR treatment were elucidated with the mechanism of actions. GR treatment reduced the overexpression of mTOR (0.27 vs 0.67 AU/mg protein, P = .047). GR treatment increased the underexpression of SEMA3F (0.51 vs 0.16 µg/mg protein, P = .034). In the histochemical study of microtubule‐associated protein 2 (MAP2) staining, our results showed that GR prevented neuronal loss in the GR treatment group (64.8% positively stained pixel area) as compared with the control group (59%, P = .014) in the hippocampus. In glial fibrillary acidic protein (GFAP) staining, the severity of astrogliosis was mitigated by the GR treatment (4.1% positively stained pixel area) when compared to the control group (5.6%, P = .047) in the hippocampus. Significance These results provide preclinical evidence to support the use of GR, which could suppress acute seizures and relieve pathological changes in pilocarpine‐induced TLE mice. We demonstrated that the antiepileptic effects of GR could be accompanied by mTOR reduction and astrogliosis attenuation.