RESUMEN
Nickel-catalyzed carbonylation of alkenes is a stereoselective and regioselective method for the synthesis of amide compounds. Theoretical predictions with density functional theory calculations revealed the mechanism and origin of stereoselectivity and regioselectivity for the nickel-catalyzed carbonylation of norbornene. The carbonylation reaction proceeds through oxidative addition, migration insertion of alkenes, and subsequent reduction elimination to afford cis-carbonylation product. The C-N bond activation of amides is unfavorable because the oxidative addition ability of the C-C bond is stronger than that of the C-N bond. The determining step of stereoselectivity is the migratory insertion of the strained olefin. The structural analysis shows that steroselectivity is controlled by the steric hindrance of methyl groups to olefins and substituents to IMes in ligands.
RESUMEN
The Ni-catalyzed alkylboration of endocyclic olefins is a stereo- and regioselective approach for the synthesis of boron-containing compounds. We report a detailed density functional theory (DFT) study to elucidate the mechanism and origins of the stereo-, chemo-, and regioselectivity of alkylboration of endocyclic olefins enabled by nickel catalysis. The alkylboration proceeds via the migratory insertion of alkenes, ß-H elimination of the Ni(II) complex, subsequent migratory insertion leading to a new Ni(II) complex, combined with an alkyl radical, and reductive eliminations. The electronic effects of the endocyclic olefins synergistically control the regioselectivity toward the C1- and C2-position boration. In C1-position boration, a more electron-deficient carbon atom tends to combine with an electron-rich -Bpin group and leads to C1-position boration products. The stereoselectivity is influenced by the solvent effect, and the interaction between the substrate and Ni-catalyzed groups, the low-polarity solvent 1,4-dioxane, and a favorable steric hindrance effect result in the cis-alkylboration product. Chemoselectivity toward 1,3-alkylboration results from the steric hindrance effects of the -Bpin group.
RESUMEN
We report the complete mitochondrial genome of Rhinogobius lentiginis, which was found to be a circular molecule of 16,633 bp in length and included 13 protein-coding genes (PCGs), 2 rRNA genes, 22 tRNA genes, and a non-coding control region. The overall base composition was 28.44% A, 26.21% T, 16.33% G, and 29.02% C. Phylogenetic analyses using maximum-likelihood and Bayesian inference methods revealed a close genome relationship among R. lentiginis, R. niger, R. shennongensis and R. maculagenys. The complete mitogenome of R. lentiginis will provide a valuable resource for species classification and conservation.
RESUMEN
Danio roseus, collected from Gadu River in Yingjiang area, Yunnan Province, China, had been sequenced on Illumina HiSeq platform with 16523 bp in length, which included 37 genes encoding 13 proteins-coding genes (PCGs), 22 tRNAs, 2 rRNAs and a displacement loop region. The proportion of nucleotides in mitochondrial genome was T (28.7%), C (23.2%), A (32.3%), G (15.8%) with an AT bias of 61%. Maximum-Likelihood phylogenetic tree was reconstructed using concatenated mitochondrial protein-coding genes of D. roseus and other 12 fishes. The result of phylogenetic analysis supported the consanguineous relationship among D. roseus, D. rerio, D. nigrofasciatus and D. dangila.
RESUMEN
Increasing evidences approve the long-term analgesia effects of intrathecal lidocaine in patients with chronic pain and in animal peripheral nerve injury models, but the underlying mechanism remains elusive. Previous evidences suggest that the activation of the p38 MAPK signaling pathway in hyperactive microglia in the dorsal horn of spinal cord involves in nerve injury-induced neuropathic pain. In this study, we demonstrate that attenuating phosphorylation of p38 MAPK in the activated microglia of spinal cord, at least partly, is the mechanism of intrathecal lidocaine reversing established tactile allodynia in chronic constriction injury model of rats. This finding not only provides a new insight into the mechanisms underlying long-term therapeutic effects of lidocaine on neuropathic pain, but also reveals one more specific drug target for analgesia.