Recast and Elicitation: The Effectiveness of Corrective Feedback on Japanese Language Learners

This paper examines the effectiveness of corrective feedback on learners of the Japanese language. The current study had a total of 25 students who agreed to participate, consisting of both advanced and intermediate levels. There are six main types of corrective feedback established and defined by Lyster and Ranta (1997), this study focused on two particular types, recast (a category of implicit) and elicitation (a category of prompt). Comparing a particular feedback or a category of feedback with another has been one of the ongoing topics in the field of second language (L2) learning. The present study is intended to examine which feedback works better for the learners in terms of repairing their mistakes and to investigate which learner group shows a better effect on each feedback. The results suggest that elicitation is more beneficial to L2 learners than recast in reformulating their utterance. The reason for this is likely that elicitation is not as implicit as recast; thus, the learners had a better opportunity to notice elicitation that was given when they made a mistake. Interestingly, this outcome also provided a comparison between the advanced and intermediate groups. Both repaired their mistakes more after elicitation was given, but the advanced group did better. Since each group displayed almost the same moderate rate of repairing for recast, what truly differentiated one group from the other was elicitation. This result suggests that learners who have more knowledge of the target language will benefit from elicitation

Identification of Qk as a Glial Precursor Cell Marker that Governs the Fate Specification of Neural Stem Cells to a Glial Cell Lineage

神経幹細胞の運命を決める分子を発見 --脳形成機構の解明と脳腫瘍や精神疾患の治療法に期待--. 京都大学プレスリリース. 2020-09-28.During brain development, neural stem cells (NSCs) initially produce neurons and change their fate to generate glias. While the regulation of neurogenesis is well characterized, specific markers for glial precursor cells (GPCs) and the master regulators for gliogenesis remain unidentified. Accumulating evidence suggests that RNA-binding proteins (RBPs) have significant roles in neuronal development and function, as they comprehensively regulate the expression of target genes in a cell-type-specific manner. We systematically investigated the expression profiles of 1, 436 murine RBPs in the developing mouse brain and identified quaking (Qk) as a marker of the putative GPC population. Functional analysis of the NSC-specific Qk-null mutant mouse revealed the key role of Qk in astrocyte and oligodendrocyte generation and differentiation from NSCs. Mechanistically, Qk upregulates gliogenic genes via quaking response elements in their 3′ untranslated regions. These results provide crucial directions for identifying GPCs and deciphering the regulatory mechanisms of gliogenesis from NSCs

新生豚にみられた先天性過骨症

先天性過骨症は，前肢の硬化・腫脹を特徴とする新生豚の稀な疾患である。本疾患は常染色体の劣性遺伝によるものと考えられているが，原因や発生機序は明らかにされていない。病変部は四肢に限局し，橈骨・尺骨で顕著である。我々は分娩直後に死亡した雌の子豚に前肢の硬化・腫脹を認め，病理学的に先天性過骨症と診断した。組織学的に腫脹していた橈骨・尺骨では線維性骨梁が皮質骨表面から放射状に伸長し，周囲骨格筋は変性・萎縮し，線維化していた。後肢やその他臓器には著変はみられなかった。鑑別診断として，先天性筋症と肺性肥大性骨症が挙げられるが，前者は本例の病変が骨に主座し筋原線維の一次性構造異常がないことから，また後者は造骨形態や胸腔内に腫瘤病変がないことから否定された。Congenital hyperostosis is a rare disease of newborn pigs, characterized by thickening and sclerosis of the forelimbs. It has been suspected that it is inherited as an autosomal recessive trait, but the pathogenesis of the bone abnormalities has not been clarified. The lesions are characteristically localized in the limbs, and the radius and ulna are the most severely affected. We examined a female piglet who died right after delivery; the piglet showed thickening and sclerosis of the forelimbs, and the bone lesions were diagnosed as congenital hyperostosis. Histologically, fibrous trabecular bone proliferated radially and extended out from the surface of cortical bone of the swollen radius and ulna. The skeletal muscles around the bones showed degeneration and atrophy with fibrosis. No lesions were found in other bones and organs. For the differential diagnosis, congenital myopathy and pulmonary hypertrophic osteopathy were considered, but myopathy was excluded because of the lesion distribution and the absence of a primary structural abnormality of myofibrils, while pulmonary hypertrophic osteopathy was also excluded because of the different form of osteogenesis and the absence of a tumor in the thoracic cavity

Exome sequencing of senescence-accelerated mice (SAM) reveals deleterious mutations in degenerative disease-causing genes

Background: Senescence-accelerated mice (SAM) are a series of mouse strains originally derived from unexpected crosses between AKR/J and unknown mice, from which phenotypically distinct senescence-prone (SAMP) and -resistant (SAMR) inbred strains were subsequently established. Although SAMP strains have been widely used for aging research focusing on their short life spans and various age-related phenotypes, such as immune dysfunction, osteoporosis, and brain atrophy, the responsible gene mutations have not yet been fully elucidated. Results: To identify mutations specific to SAMP strains, we performed whole exome sequencing of 6 SAMP and 3 SAMR strains. This analysis revealed 32,019 to 38,925 single-nucleotide variants in the coding region of each SAM strain. We detected Ogg1 p.R304W and Mbd4 p.D129N deleterious mutations in all 6 of the SAMP strains but not in the SAMR or AKR/J strains. Moreover, we extracted 31 SAMP-specific novel deleterious mutations. In all SAMP strains except SAMP8, we detected a p.R473W missense mutation in the Ldb3 gene, which has been associated with myofibrillar myopathy. In 3 SAMP strains (SAMP3, SAMP10, and SAMP11), we identified a p.R167C missense mutation in the Prx gene, in which mutations causing hereditary motor and sensory neuropathy (Dejerine-Sottas syndrome) have been identified. In SAMP6 we detected a p.S540fs frame-shift mutation in the Il4ra gene, a mutation potentially causative of ulcerative colitis and osteoporosis. Conclusions: Our data indicate that different combinations of mutations in disease-causing genes may be responsible for the various phenotypes of SAMP strains.ArticleBMC GENOMICS. 14:248 (2013)journal articl

Molecular Hydrogen as an Emerging Therapeutic Medical Gas for Neurodegenerative and Other Diseases

Effects of molecular hydrogen on various diseases have been documented for 63 disease models and human diseases in the past four and a half years. Most studies have been performed on rodents including two models of Parkinson's disease and three models of Alzheimer's disease. Prominent effects are observed especially in oxidative stress-mediated diseases including neonatal cerebral hypoxia; Parkinson's disease; ischemia/reperfusion of spinal cord, heart, lung, liver, kidney, and intestine; transplantation of lung, heart, kidney, and intestine. Six human diseases have been studied to date: diabetes mellitus type 2, metabolic syndrome, hemodialysis, inflammatory and mitochondrial myopathies, brain stem infarction, and radiation-induced adverse effects. Two enigmas, however, remain to be solved. First, no dose-response effect is observed. Rodents and humans are able to take a small amount of hydrogen by drinking hydrogen-rich water, but marked effects are observed. Second, intestinal bacteria in humans and rodents produce a large amount of hydrogen, but an addition of a small amount of hydrogen exhibits marked effects. Further studies are required to elucidate molecular bases of prominent hydrogen effects and to determine the optimal frequency, amount, and method of hydrogen administration for each human disease

Secreted Signaling Molecules at the Neuromuscular Junction in Physiology and Pathology

Signal transduction at the neuromuscular junction (NMJ) is affected in many human diseases, including congenital myasthenic syndromes (CMS), myasthenia gravis, Lambert–Eaton myasthenic syndrome, Isaacs’ syndrome, Schwartz–Jampel syndrome, Fukuyama-type congenital muscular dystrophy, amyotrophic lateral sclerosis, and sarcopenia. The NMJ is a prototypic cholinergic synapse between the motor neuron and the skeletal muscle. Synaptogenesis of the NMJ has been extensively studied, which has also been extrapolated to further understand synapse formation in the central nervous system. Studies of genetically engineered mice have disclosed crucial roles of secreted molecules in the development and maintenance of the NMJ. In this review, we focus on the secreted signaling molecules which regulate the clustering of acetylcholine receptors (AChRs) at the NMJ. We first discuss the signaling pathway comprised of neural agrin and its receptors, low-density lipoprotein receptor-related protein 4 (Lrp4) and muscle-specific receptor tyrosine kinase (MuSK). This pathway drives the clustering of acetylcholine receptors (AChRs) to ensure efficient signal transduction at the NMJ. We also discuss three secreted molecules (Rspo2, Fgf18, and connective tissue growth factor (Ctgf)) that we recently identified in the Wnt/β-catenin and fibroblast growth factors (FGF) signaling pathways. The three secreted molecules facilitate the clustering of AChRs by enhancing the agrin-Lrp4-MuSK signaling pathway

Secreted Signaling Molecules at the Neuromuscular Junction in Physiology and Pathology

Signal transduction at the neuromuscular junction (NMJ) is affected in many human diseases, including congenital myasthenic syndromes (CMS), myasthenia gravis, Lambert–Eaton myasthenic syndrome, Isaacs’ syndrome, Schwartz–Jampel syndrome, Fukuyama-type congenital muscular dystrophy, amyotrophic lateral sclerosis, and sarcopenia. The NMJ is a prototypic cholinergic synapse between the motor neuron and the skeletal muscle. Synaptogenesis of the NMJ has been extensively studied, which has also been extrapolated to further understand synapse formation in the central nervous system. Studies of genetically engineered mice have disclosed crucial roles of secreted molecules in the development and maintenance of the NMJ. In this review, we focus on the secreted signaling molecules which regulate the clustering of acetylcholine receptors (AChRs) at the NMJ. We first discuss the signaling pathway comprised of neural agrin and its receptors, low-density lipoprotein receptor-related protein 4 (Lrp4) and muscle-specific receptor tyrosine kinase (MuSK). This pathway drives the clustering of acetylcholine receptors (AChRs) to ensure efficient signal transduction at the NMJ. We also discuss three secreted molecules (Rspo2, Fgf18, and connective tissue growth factor (Ctgf)) that we recently identified in the Wnt/β-catenin and fibroblast growth factors (FGF) signaling pathways. The three secreted molecules facilitate the clustering of AChRs by enhancing the agrin-Lrp4-MuSK signaling pathway

M (2012) Molecular hydrogen as an emerging therapeutic medical gas for neurodegenerative and other diseases. Oxid Med Cell Longev doi: 10.1155/2012/353152

Effects of molecular hydrogen on various diseases have been documented for 63 disease models and human diseases in the past four and a half years. Most studies have been performed on rodents including two models of Parkinson's disease and three models of Alzheimer's disease. Prominent effects are observed especially in oxidative stress-mediated diseases including neonatal cerebral hypoxia; Parkinson's disease; ischemia/reperfusion of spinal cord, heart, lung, liver, kidney, and intestine; transplantation of lung, heart, kidney, and intestine. Six human diseases have been studied to date: diabetes mellitus type 2, metabolic syndrome, hemodialysis, inflammatory and mitochondrial myopathies, brain stem infarction, and radiation-induced adverse effects. Two enigmas, however, remain to be solved. First, no dose-response effect is observed. Rodents and humans are able to take a small amount of hydrogen by drinking hydrogen-rich water, but marked effects are observed. Second, intestinal bacteria in humans and rodents produce a large amount of hydrogen, but an addition of a small amount of hydrogen exhibits marked effects. Further studies are required to elucidate molecular bases of prominent hydrogen effects and to determine the optimal frequency, amount, and method of hydrogen administration for each human disease