Electrochemical synthesis based on electron as reagents provide a broad prospect for commodity chemical manufacturing. A direct one-step route from amino C-N bonds electrooxidation to nitrile C≡N bonds offer an alternative pathway for nitriles producting. However, this promising topic has not been fully explored whether the chemical bond reforming process or the performance optimization. Here we proposed a model of vacancies-rich Ni(OH)2 atomic layer to understand performance relationship with structure. By theory calculations, the vacancy-induced local electropositive site chemisorbs the N atom with lone pairs of electrons and then attack the corresponding N(sp3)-H, thus accelerating amino C-N bond activates dehydrogenation directly into nitrile C≡N bond. Vacancies-rich nanosheets exhibit up to 96.5% propionitrile selectivity at a moderately potential of 1.38 V. These findings will initiate a new pathway for triggering stubborn catalytic reaction in the chemicals industry.Axon guidance is a critical process in forming the connections between a neuron and its target. The growth cone steers the growing axon toward the appropriate direction by integrating extracellular guidance cues and initiating intracellular signal transduction pathways downstream of these cues. The growth cone generates these responses by remodeling its cytoskeletal components. Regulation of microtubule dynamics within the growth cone is important for making guidance decisions. TACC3, as a microtubule plus-end binding (EB) protein, modulates microtubule dynamics during axon outgrowth and guidance. We have previously shown that Xenopus laevis embryos depleted of TACC3 displayed spinal cord axon guidance defects, while TACC3-overexpressing spinal neurons showed increased resistance to Slit2-induced growth cone collapse.  https://www.selleckchem.com/products/bb-94.html  Tyrosine kinases play an important role in relaying guidance signals to downstream targets during pathfinding events via inducing tyrosine phosphorylation. Here, in order to investigate the mechanism behind TACC3-mediated axon guidance, we examined whether tyrosine residues that are present in TACC3 have any role in regulating TACC3's interaction with microtubules or during axon outgrowth and guidance behaviors. We find that the phosphorylatable tyrosines within the TACC domain are important for the microtubule plus-end tracking behavior of TACC3. Moreover, TACC domain phosphorylation impacts axon outgrowth dynamics such as growth length and growth persistency. Together, our results suggest that tyrosine phosphorylation of TACC3 affects TACC3's microtubule plus-end tracking behavior as well as its ability to mediate axon growth dynamics in cultured embryonic neural tube explants.Objective To evaluate safety and efficacy of trigone-involved Botox injections in comparison with trigone-sparing injections in refractory idiopathic overactive bladder (OAB). Materials and methods One hundred and three patients randomly received a 100-IU intradetrusal injection of Botox either sparing the trigone (52 patients) or involving the trigone (51 patients). Patients were prospectively evaluated at 1, 3, and 6 months. Efficacy was evaluated by 3-day voiding diaries, OAB symptom score (OABSS), and pressure flow study. Any complications were recorded. An ascending cystogram was done at 3 months for detection of vesicoureteral reflux. Urinary tract infection (UTI) was estimated on urine culture basis. Primary outcome was the difference of total OABSS at 3 months. Results The mean age ± SD was 34.3 ± 10 years (range 18-59 years). There was a reduction of episodes of all components of OAB in both groups in comparison with baseline by the end of the study but without significant difference between both groups. The trigonal-sparing group had less score of frequency compared with the trigonal-involved group throughout the study period (P 200 mL. There was a higher rate of UTI in the trigonal-involved group ranging from 5.6% up to 11.7% at each follow-up visit. No patient had reflux. Conclusion Trigone injections are not superior to trigone-sparing injections. On the contrary, the incidence of UTI and voiding difficulty were higher. The concept of reflux induced by trigonal injection has not been proven.Background X-linked Alport syndrome (XLAS) is a progressive, hereditary glomerular nephritis of variable severity caused by pathogenic COL4A5 variants. Currently, genetic testing is widely used for diagnosing XLAS; however, determining the pathogenicity of variants detected by such analyses can be difficult. Intronic variants or synonymous variants may cause inherited diseases by inducing aberrant splicing. Transcript analysis is necessary to confirm the pathogenicity of such variants, but it is sometimes difficult to extract mRNA directly from patient specimens. Methods In this study, we conducted in vitro splicing analysis using a hybrid minigene assay and specimens from three XLAS patients with synonymous variants causing aberrant splicing, including previously reported pathogenic mutations in the same codon. The variants were c.876 A>T (p.Gly292=), c.2358 A>G (p.Pro786=), and c.3906 A>G (p.Gln1302=). Results The results from our hybrid minigene assay were sufficient to predict splicing abnormalities; c.876 A>T cause 17-bp del and 35-bp del, c.2358 A>G cause exon 29 skipping, c.3906 A>G cause exon 42 skipping, which are very likely to cause pathogenicity. Further, patients carrying c.2358 A>G exhibited a mild phenotype that may have been associated with the presence of both normal and abnormally spliced transcripts. Conclusion The minigene system was shown to be a sensitive assay and a useful tool for investigating the pathogenicity of synonymous variants.Ionotropic glutamate receptors are ligand-gated ion channels governing neurotransmission in the central nervous system. Three major types of antagonists are known for the AMPA-type receptor GluA2 competitive, noncompetitive (i.e., negative allosteric modulators; NAMs) used for treatment of epilepsy, and uncompetitive antagonists. We here report a 4.65 Å resolution X-ray structure of GluA2, revealing that four molecules of the competitive antagonist ZK200775 and four molecules of the NAM GYKI53655 are capable of binding at the same time. Using negative stain electron microscopy, we show that GYKI53655 alone or ZK200775/GYKI53655 in combination predominantly results in compact receptor forms. The agonist AMPA provides a mixed population of compact and bulgy shapes of GluA2 not impacted by addition of GYKI53655. Taken together, this suggests that the two different mechanisms of antagonism that lead to channel closure are independent and that the distribution between bulgy and compact receptors primarily depends on the ligand bound in the glutamate binding site.