In 4 experiments (Experiments 1A, 1B, 3A, and 3B), inhibitory neighbor priming effects were observed for low-frequency targets primed by higher frequency Kanji word neighbors In contrast, there was a significant facilitation effect when targets were primed by Kanji nonword neighbors (Experiments 2 and 3). Significant facilitation was also observed when targets were primed by single constituent Kanji characters (Experiment
4). Taken together, these results suggest that lexical competition plays a role in the recognition of Kanji words, just as it does for words in alphabetic languages. However, in Kanji, and likely in other logographic languages, the effect of lexical competition appears to be counteracted by facilitory morphological priming due to the repetition of a morphological unit in the prime and target (i.e., in Kanji, each character represents a morpheme).”
“The GSK1838705A CACNA1F gene
encodes a member of the alpha-IF subunit find more family in the voltage-dependent calcium channel (Cav1.4) complex. Mutations in this gene result in incomplete congenital stationary night blindness (iCSNB2) in humans. And Cav1.4 mutation could affect the functions of the skeletal muscle. This study investigated the role of Cacna1f mutations in alteration of the skeletal muscle functions in a Cacna1f mutation rat model (Cacna1f(CSNB2) rat). We found that the muscle endurance behaviors of Cacna1f(CSNB2) rats were significantly lower than those of the wild-type rats. The high-frequency fatigue resistance of the soleus muscle was decreased in Cacna1f(CSNB2) rats under continuous tetanic stimulation. The expression levels of the syntaxin (SYN) proteins in the
soleus of the Cacna1f(CSNB2) rats were lower than those of wild-type rats. SYN was expressed in the soleus muscle, but not in the extensor GANT61 supplier digitorum longus. The Ca(v)1.4 protein was not detected in the skeletal muscle of Cacna1f(CSNB2) rats. The Cacna1f mRNA level in the soleus of Cacna1f(CSNB2) rats was decreased compared with that in wild-type rats. This study demonstrated for the first time that the Cacna1f mutation reduces the function of slow-twitch skeletal muscle. And it also demonstrated that the Cacna1f gene affects synapse-associated protein expression, which may block the signal transmission in synaptic connectivity of the retina and skeletal muscle in Cacna1f-mutant rats. (C) 2015 Elsevier B.V. All rights reserved.”
“Somitogenesis is thought to be controlled by a segmentation clock, which consists of molecular oscillators in the Wnt3a, Fgf8 and Notch pathways. Using conditional alleles of Ctnnb1 (beta-catenin), we show that the canonical Wnt3a/beta-catenin pathway is necessary for molecular oscillations in all three signaling pathways but does not function as an integral component of the oscillator.