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To preserve some invariant properties of the original differential equation is an important criterion to judge the success of a numerical simulation. In this paper, we construct, analyze and numerically validate a class of momentum-preserving finite difference methods for the Korteweg-de Vries equation. The proposed schemes can conserve the discrete momentum to machine precision. Numerical experiments reveal that the phase and amplitude errors, after long time simulation, are well controlled due to the momentum-preserving property. Besides, the numerical results show that the numerical errors grow only linearly as a function of time. [ABSTRACT FROM AUTHOR]

Many ion channel genes have been associated with human genetic pain disorders. Here we report two large Chinese families with autosomal-dominant episodic pain. We performed a genome-wide linkage scan with microsatellite markers after excluding mutations in three known genes (SCN9A, SCN10A, and TRPA1) that cause similar pain syndrome to our findings, and we mapped the genetic locus to a 7.81 Mb region on chromosome 3p22.3–p21.32. By using whole-exome sequencing followed by conventional Sanger sequencing, we identified two missense mutations in the gene encoding voltage-gated sodium channel Nav1.9 (SCN11A): c.673C>T (p.Arg225Cys) and c.2423C>G (p.Ala808Gly) (one in each family). Each mutation showed a perfect cosegregation with the pain phenotype in the corresponding family, and neither of them was detected in 1,021 normal individuals. Both missense mutations were predicted to change a highly conserved amino acid residue of the human Nav1.9 channel. We expressed the two SCN11A mutants in mouse dorsal root ganglion (DRG) neurons and showed that both mutations enhanced the channel’s electrical activities and induced hyperexcitablity of DRG neurons. Taken together, our results suggest that gain-of-function mutations in SCN11A can be causative of an autosomal-dominant episodic pain disorder. [Copyright &y& Elsevier]

The article discusses the findings of a study to determine the separability of two types of exocytosis. It notes the function of Ca2+-regulated exocytosis the somata of dorsal root ganglions (DRG) in neurotransmitter and hormone release. The experiment cites the use of electrical stimulation to confirm the presence of distinct exocytosis and vesicle pools within DRG neurons without any effect on Ca2+ -independent but voltage-dependent secretion (CVIDS) exocytosis.