English read by Japanese phonetic corpus: an interim report

The primary purpose of this paper is to explain the procedure of developing the English Read by Japanese Phonetic Corpus. A series of preliminary studies (Makino 2007, 2008, 2009) made it clear that a phonetically-transcribed computerized corpus of Japanese speakers’ English speech was worth making. Because corpus studies on L2 pronunciation have been very rare, we intend to fill this gap. For the corpus building, the 1,902 sentence files in the English Read by Japanese speech database scored for their individual sounds by American English teachers trained in phonetics in Minematsu, et al. (2002b) have been chosen. The files were pre-processed with the Penn Phonetics Lab Forced Aligner to generate Praat TextGrids where target English words and phonemes were forced-aligned to the speech files. Two additional tiers (actual phones and substitutions) were added to those TextGrids, the actual phones were manually transcribed and the other tiers were aligned to that tier. Then the TextGrids were imported to ELAN, which has a much better searching functionality. So far, fewer than 10% of the files have been completed and the corpus-building is still in its initial stage. The secondary purpose of this paper is to report on some findings from the small part of the corpus that has been completed. Although it is still premature to talk of any tendency in the corpus, it is worth noting that we have found evidence of phenomena which are not readily predicted from L1 phonological transfer, such as the spirantization of voiceless plosives, which is not considered normal in the pronunciation of Japanese

Sound feature interference between two second languages: An expansion of the feature hypothesis to the multilingual situation in SLA

Proceedings of the 37th Annual Meeting of the Berkeley Linguistics Society (2013), pp. 18-3

中国語・日本語バイリンガルによる英語の破裂音知覚と生成

学位の種別: 課程博士審査委員会委員 : （主査）東京大学准教授 グレノン イザベル, 東京大学教授 田中 伸一, 東京大学教授 ガリー トム, 東京大学准教授 広瀬 友紀, 早稲田大学准教授 シェファード クリスUniversity of Tokyo(東京大学

Relationship between lymph node metastasis and E-cadherin expression in submucosal invasive gastric carcinomas with gastric-phenotype

Background : Recent advances in immunohistochemical staining have led to the proposition of a classification of gastric carcinomas based on cellular phenotypes, and the degree of biological malignancy of gastric-phenotype carcinomas has attracted particular attention. Subjects and Methods : One hundred and seven submucosal (SM) invasive carcinomas encountered in our center were examined for their histological type, cellular phenotype, and E-cadherin expression status to clarify their relationships with lymph node metastasis. Results : Eleven (10.3%) of 107 SM gastric carcinomas were lymph node metastasis-positive. Gastric-phenotype carcinomas accounted for 20.6%, with a lymph node metastasis rate of 27.3% (6/22), which was significantly higher (p<0.05) than those of intestinal-phenotype carcinomas (5.9%) and mixed-phenotype carcinomas (2.9%). In terms of E-cadherin expression, only carcinomas with reduced E-cadherin expression showed lymph node metastasis at a rate significantly higher than that of carcinomas with normal E-cadherin expression (p<0.05). The lymph node metastasis rate (46.2%) of gastric-phenotype carcinomas with reduced E-cadherin expression was significantly higher than those of carcinomas of other phenotypes (p<0.05). Conclusion : Since gastric-phenotype differentiated carcinomas with reduced E-cadherin expression have the potential for becoming undifferentiated, the risk of lymph node metastasis should be considered

Evaluation of serum amylase and gabexate mesilate with endoscopic papillary balloon dilatation

Gabexate mesilate (GM) relaxes the papilla of Vater in addition to inhibiting the several proteases. We evaluated whether prophylactic administration of GM would prevent the occurrence of acute pancreatitis in endoscopic papillary balloon dilation (EPBD). Nineteen patients with common bile duct stones were separated into two groups according to the admission year. The group A has been administered GM intravenously at 2mg/kg/hr after EPBD till six hours later, and the group B has been administered GM before fifteen minutes of EPBD till six hours later. The mean value of sphincter of Oddi (SO) basal and peak pressure in the group B was significantly lower than that in the group A, moreover the mean value of the pancreatic pressure in the group B was significantly lower than that in the group A. However two cases had mild acute pancreatitis in the group B. GM loosened SO and pancreatic duct pressure by direct stimulation of SO, although it could not have enough effect to prevent the acute pancreatitis in EPBD

Gastric cancer with autoimmune gastritis

Background: Autoimmune gastritis is known to be associated with neoplastic lesions but the relationship between autoimmunity and tumorigenesis have not been sufficiently clarified. The aim of this study is to assess the clinicopathological characteristics of gastric cancer cases associated with autoimmune gastritis. Methods: A total of 24 patients diagnosed as early gastric cancer with autoimmune gastritis were registered. Chart reviews with the data including age, gender, state of Helicobacter pylori infection, comorbidity, and concomitant gastric diseases were conducted. As for the characteristics of gastric cancer, location, size, morphological type, histopathology, invasion depth, and the presence of metachronous or simultaneous lesion were assessed. These data from autoimmune gastritis group were compared with those from 301 patients of early gastric cancer as a control group. Results: The gastric cancer associated with autoimmune gastritis was located in the upper, middle, and lower parts in 28.1%, 53.1%, and 18.8%, respectively. The morphological types are as follows: 0-I, 9.4%; 0-IIa, 28.1%; 0-IIb, 15.6%; 0-IIc, 46.9%; and 0-III, 0.0%. The mean tumor size was 21.8 mm. While 90.6% were confined to the mucosa, 9.4% showed submucosal invasion. The histological classifications are as follows: tub1, 50.0%; tub2, 15.6%; pap, 21.9%; sig, 9.4%; and por, 3.1%. More numbers of female, protruded types, larger tumor size, papillary tumor, and that in the upper location were observed in autoimmune gastritis group compared to control group. Conclusion: Early gastric cancer associated with autoimmune gastritis demonstrated different characteristics from those without autoimmune gastritis including variety of tumor morphologies and histological types with female dominancy

Clinicopathological evaluation of biological behavior of submucosal invasive gastric carcinomas : relationship among lymph node metastasis, mucin phenotype and proliferative activity

Background : Gastric carcinomas have been classified into the differentiated and undifferentiated type, on the basis of its tendency to gland formation. As a result of recent advances in mucin histochemistry, mucin phenotypes of gastric carcinomas have been investigated. However, no consensus on the evaluation of the grade of malignancy of early gastric carcinomas regarding mucin phenotype expression has developed. To address this issue, we evaluated the lymph node metastasis rate and proliferative activity of a submucosal invasive (sm) gastric carcinoma according to mucin phenotype expression. Methods : In resected surgical specimens from 108 patients with a single sm gastric carcinoma, the association between clinicopathological factors and lymph node metastasis was evaluated. In all cases, immunohistochemical staining with human gastric mucin, Muc-2, and CD10 and mucin histochemical staining by paradoxical concanavalin A staining were performed. The mucin phenotypes were classified into gastric-type (G-type), intestinal-type (I-type), mixed gastric and intestinal type (M-type), or a lack of mucin (LOM), using these as markers. To evaluate the cell proliferative activity of the gastric carcinoma, proliferating cell nuclear antigen (PCNA) staining was also performed. Results : The rate of lymph node metastasis was higher for G-type sm carcinomas. A multivariate analysis showed that the G-type and lymphatic invasion were independent factors of lymph node metastasis. However, the PCNA-labeling index (PCNA-LI) was low for G-type carcinomas irrespective of the presence or absence of lymph node metastasis. In I-type carcinomas, PCNA-LI was significantly higher in cases that were positive for lymph node metastasis than in negative cases. Conclusion : G-type and lymphatic invasion are independent risk factors for lymph node metastasis of an sm gastric carcinoma, and proliferative activity may be a significant parameter for lymph node metastasis in cases with I-type carcinomas

Inhibition of c-Jun NH2-terminal kinase activity improves ischemia/reperfusion injury in rat lungs

Although c-Jun NH 2 -terminal kinase (JNK) has been implicated in the pathogenesis of transplantation-induced ischemia/reperfusion (I/R) injury in various organs, its significance in lung transplantation has not been conclusively elucidated. We therefore attempted to measure the transitional changes in JNK and AP-1 activities in I/R-injured lungs. Subsequently, we assessed the effects of JNK inhibition by the three agents including SP600125 on the degree of lung injury assessed by means of various biological markers in bronchoalveolar lavage fluid and histological examination including detection of apoptosis. In addition, we evaluated the changes in p38, extracellular signal-regulated kinase, and NF-B-DNA binding activity. I/R injury was established in the isolated rat lung preserved in modified Euro-Collins solution at 4°C for 4 h followed by reperfusion at 37°C for 3 h. We found that AP-1 was transiently activated during ischemia but showed sustained activation during reperfusion, leading to significant lung injury and apoptosis. The change in AP-1 was generally in parallel with that of JNK, which was activated in epithelial cells (bronchial and alveolar), alveolar macrophages, and smooth muscle cells (bronchial and vascular) on immunohistochemical examination. The change in NF-B qualitatively differed from that of AP-1. Protein leakage, release of lactate dehydrogenase and TNF-␣ into bronchoalveolar lavage fluid, and lung injury were improved, and apoptosis was suppressed by JNK inhibition. In conclusion, JNK plays a pivotal role in mediating lung injury caused by I/R. Therefore, inhibition of JNK activity has potential as an effective therapeutic strategy for preventing I/R injury during lung transplantation

Quantitative antisense screening and optimization for exon 51 skipping in Duchenne muscular dystrophy

International audienceDuchenne muscular dystrophy (DMD), the most common lethal genetic disorder, is caused by mutations in the dystrophin (DMD) gene. Exon skipping is a therapeutic approach that uses antisense oligonucleotides (AOs) to modulate splicing and restore the reading frame, leading to truncated, yet functional protein expression. In 2016, the US Food and Drug Administration (FDA) conditionally approved the first phosphorodiamidate morpholino oligomer (morpholino)-based AO drug, eteplirsen, developed for DMD exon 51 skipping. Eteplirsen remains controversial with insufficient evidence of its therapeutic effect in patients. We recently developed an in silico tool to design antisense morpholino sequences for exon skipping. Here, we designed morpholino AOs targeting DMD exon 51 using the in silico tool and quantitatively evaluated the effects in immortalized DMD muscle cells in vitro. To our surprise, most of the newly designed morpholinos induced exon 51 skipping more efficiently compared with the eteplirsen sequence. The efficacy of exon 51 skipping and rescue of dystrophin protein expression were increased by up to more than 12-fold and 7-fold, respectively, compared with the eteplirsen sequence. Significant in vivo efficacy of the most effective morpholino, determined in vitro, was confirmed in mice carrying the human DMD gene. These findings underscore the importance of AO sequence optimization for exon skipping