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392 results on '"Tsukuda, K."'

1. Topic: Inguinal Hernia — Unsolved problem in the daily practice

Author

Yasuo, S., Kenichi, Y., Ueno, N., Arimoto, A., Hosono, M., Yoshikawa, T., Toyokawa, A., Kakeji, Y., Tsai, Y., Tsai, C., Sul, J., Lim, M., Park, J., Jang, C. E., Santilli, O., Tripoloni, D., Santilli, H., Nardelli, N., Greco, A., Estevez, M., Sakurai, S., Ryu, S., Cesana, G., Ciccarese, F., Uccelli, M., Grava, G., Castello, G., Carrieri, D., Legnani, G., Olmi, S., Naito, M., Yamamoto, H., Sawada, Y., Mandai, Y., Asano, H., Ino, H., Tsukuda, K., Nagahama, T., Ando, M., Ami, K., Arai, K., Miladinovic, M., Kitanovic, A., Lechner, M., Mayer, F., Meissnitzer, M., Fortsner, R., Öfner, D., Köhler, G., Jäger, T., Kumata, Y., Fukushima, R., Inaba, T., Yaguchi, Y., Horikawa, M., Ogawa, E., Katayama, T., Kumar, P. S., Unal, D., Caparlar, C., Akkaya, T., Mercan, U., Kulacoglu, H., Barreiro, J. Jorge, Baer, I. García, García, L. Solar, Cumplido, P. Lora, Florez, L. J. García, Muñiz, P. Fernandez, Fujino, K., Mita, K., Ohta, E., Takahashi, K., Hashimoto, M., Nagayasu, K., Murabayashi, R., Asakawa, H., Koizumi, K., Hayashi, G., Ito, H., Felberbauer, F., Strobl, S., Kristo, I., Riss, S., Prager, G., El Komy, H., El Gendi, A., Nabil, W., Karam, M., El Kayal, S., Chihara, N., Suzuki, H., Watanabe, M., Uchida, E., Chen, T., Wang, J., Wang, H., Bouchiba, N., Elbakary, T., Ramadan, A., Elakkad, M., Berney, C., Vlasov, V., Babii, I., Pidmurnyak, O., Prystupa, M., Asakage, N., Molinari, P., Contino, E., Guzzetti, L., Oggioni, M., Sambuco, M., Berselli, M., Farassino, L., Cocozza, E., Crespi, A., Ambrosoli, A., and Zhao, Y.

Published
2015
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10. Aberrant Methylation of p21 Gene in Lung Cancer and Malignant Pleural Mesothelioma

Author

Teramen, H., Tsukuda, K., Tanaka, N., Ueno, T., Kubo, T., Ando, M., Junichi Soh, Asano, H., Pass, H. I., Toyooka, S., and Miyoshi, S.

Subjects
Cyclin-Dependent Kinase Inhibitor p21, Male, Lung Neoplasms, p21, Pleural Neoplasms, Cell Line, respiratory tract diseases, Gene Expression Regulation, Neoplastic, lung cancer, mesothelioma, Humans, Female, RNA, Messenger, methylation, Aged
Abstract

Suppression of p21 has been implicated in the genesis and progression of many human malignancies. DNA methylation is an important mechanism of gene silencing in human malignancies. In this study, we examined the expression status and aberrant methylaion of p21 in lung cancers and malignant pleural mesotheliomas (MPM). We used 12 small cell lung cancer (SCLC) cell lines, 13 non-small cell lung cancer (NSCLC) cell lines, 50 primary NSCLCs, 6 MPM cell lines and 10 primary MPMs. The expression and methylation of p21 was examined by reverse transcription-PCR (RT-PCR), Western blotting and methylation-specific PCR (MSP) assay. Loss of p21 protein expression was observed in 7 SCLC cell lines (58.3%), 5 NSCLC cell lines (38.5%) and 3 MPM cell lines (50%) while mRNA expression was lost in 2 SCLC cell lines (16.7%), 2 NSCLC cell lines (15.4%) and none of the MPM cell lines. Aberrant methylation of p21 was found in 8.3% of SCLC cell lines, 30.2% of NSCLCs and 6.3% of MPMs. Among primary NSCLCs, methylation in adenocarcinomas was significantly more frequent than in squamous cell carcinomas. Loss of p21 expression was frequently observed in lung cancers and MPMs and aberrant methylation was one of the mechanisms of suppression of p21, especially in NSCLCs.

Published
2011

16. Insulin Secretion from Isolated Rat Islets Induced by the Novel Hypoglycemic Agent A-4166, a Derivative of D-Phenylalanine

Author

Oka Y, Tsukuda K, Kikuchi M, Sakurada M, and Niki I

Subjects
Male, Potassium Channels, Receptors, Drug, Endocrinology, Diabetes and Metabolism, medicine.medical_treatment, Clinical Biochemistry, Nateglinide, Sulfonylurea Receptors, Biochemistry, Rats, Sprague-Dawley, chemistry.chemical_compound, Endocrinology, Glyburide, Insulin Secretion, Insulin, geography.geographical_feature_category, Stereoisomerism, General Medicine, Islet, Somatostatin, Protein Binding, medicine.drug, medicine.medical_specialty, Epinephrine, Phenylalanine, Tolbutamide, Biological Availability, chemistry.chemical_element, Calcium, Cell Line, Islets of Langerhans, D-Phenylalanine, Cyclohexanes, In vivo, Internal medicine, medicine, Diazoxide, Animals, Hypoglycemic Agents, Potassium Channels, Inwardly Rectifying, geography, Biochemistry (medical), Rubidium, Rats, Glucose, L-Glucose, chemistry, ATP-Binding Cassette Transporters
Abstract

A derivative of D-phenylalanine, A-4166, reportedly evokes a more rapid and short-lived hypoglycemic action in vivo than any of the currently available sulfonylureas. This novel oral hypoglycemic agent is structurally different from sulfonylureas. Therefore, studies were designed to elucidate the mechanisms by which A-4166 stimulates insulin secretion. Insulin release from incubated or perifused rat islets was dose-dependently stimulated by 10 to 200 mumol/l A-4166, in the presence of 2.8 mmol/l glucose. Both A-4166 and tolbutamide evoke a prompt rise in insulin secretion followed by a sustained gradually decreasing release from perfused islets in the presence of low glucose, although A-4166 appeared to be more sensitive than tolbutamide to subthreshold glucose concentration. Diazoxide abolished the initial release and blunted sustained release. Removing calcium from the perifusate abolished insulin release within 15 minutes. A-4166 inhibited [3H]-glibenclamide binding to HIT cell membranes and 86Rb efflux from ATP-depleted or diazoxide-treated cells. These results suggest that the insulin release induced by A-4166 is relevant to this agent occupying the tolbutamide binding sites. Therefore, one possible mechanism accounting for the more rapid and short-lived hypoglycemic action of A-4166 in vivo, as compared with tolbutamide, may involve the reported differences in the bioavailability of A-4166.

Published
1998

17. Silenced expression of NFKBIA in lung adenocarcinoma patients with a never-smoking history

Author

Furukawa, M., Junichi Soh, Yamamoto, H., Ichimura, K., Shien, K., Maki, Y., Muraoka, T., Tanaka, N., Ueno, T., Asano, H., Tsukuda, K., Toyooka, S., and Miyoshi, S.

Subjects
Adult, Male, Lung Neoplasms, Oncogene Proteins, Fusion, Adenocarcinoma of Lung, Adenocarcinoma, Proto-Oncogene Proteins p21(ras), NF-KappaB Inhibitor alpha, Proto-Oncogene Proteins, Humans, Gene Silencing, Aged, Aged, 80 and over, never-smoker, Smoking, DNA Methylation, Middle Aged, nuclear factor of κ-light polypeptide gene enhancer in B cells inhibitor α, Immunohistochemistry, ErbB Receptors, lung cancer, Mutation, ras Proteins, Female, I-kappa B Proteins, epidermal growth factor receptor
Abstract

Nuclear factor of κ-light polypeptide gene enhancer in B cells inhibitor α (NFKBIA), which is a tumor suppressor gene, was found to be silenced in lung adenocarcinomas. We examined NFKBIA expression, mutations in the EGFR and K-ras genes, and EML4-ALK fusion in 101 resected lung adenocarcinoma samples from never-smokers. NFKBIA expression was evaluated using immunohistochemistry. NFKBIA expression was negative in 16 of the 101 samples (15.8%). EGFR and K-ras mutations and EML4-ALK fusion were detected in 61 (60.5%), 1 (1.0%), and 2 (2.0%) of the 101 samples, respectively, in a completely mutually exclusive manner. Negative NFKBIA expression was observed significantly more frequently among the tumors with none of the three genetic alterations compared to those with such alterations (p = 0.009). In addition, negative NFKBIA expression was significantly more frequent among the EGFR-wild type samples compared to the EGFR-mutant samples (p = 0.013). In conclusion, NFKBIA expression was silenced in adenocarcinomas without EGFR/K-ras mutations or EML4-ALK fusion, suggesting that the silencing of NFKBIA may play an important role in the carcinogenesis of adenocarcinomas independent of EGFR/K-ras mutations or EML4-ALK fusion.

Published
2013

18. Congenital heart disease with hypereosinophilic syndrome

Author

Tsukuda K, Y. Ootaki, Masahiro Yamaguchi, and Naoki Yoshimura

Subjects
Heart Defects, Congenital, congenital, hereditary, and neonatal diseases and abnormalities, medicine.medical_specialty, Heart disease, business.industry, Hypereosinophilic syndrome, Restrictive cardiomyopathy, Infant, Newborn, Tricuspid stenosis, medicine.disease, Cardiac surgery, Surgery, Stenosis, medicine.anatomical_structure, Ductus arteriosus, Internal medicine, Pediatrics, Perinatology and Child Health, Hypereosinophilic Syndrome, Patent foramen ovale, medicine, Cardiology, Humans, Female, Cardiology and Cardiovascular Medicine, business
Abstract

The idiopathic hypereosinophilic syndrome, common in adults, is a leukoproliferative disorder marked by a predilection to damage specific organs. This report describes a unique case of an infant with tricuspid stenosis, a hypoplastic right ventricle, severe pulmonary stenosis, patent ductus arteriosus, and a patent foramen ovale associated with hypereosinophilic syndrome. Although treatment with high-dose oral steroids failed to decrease the leukocyte counts, a right classic Blalock–Taussig shunt through a right thoracotomy resolved her cyanosis.

Published
2003

19. GENESIS: an extensible database management system

Author

Batory, D.S., Barnett, J.R., Garza, J.F., Smith, K.P., Tsukuda, K., Twichell, B.C., and Wise, T.E.

Subjects
Software Modification, DBMS, Software Architecture, New Technique, Application Development Software, Extensible Languages, Cost Benefit Analysis, System Design, Applications, Modeling
Published
1988

39. Human urinary macrophage colony-stimulating factor reduces the incidence and duration of febrile neutropenia and shortens the period required to finish three courses of intensive consolidation therapy in acute myeloid leukemia: a double-blind controlled study.

Author

Ohno, R, primary, Miyawaki, S, additional, Hatake, K, additional, Kuriyama, K, additional, Saito, K, additional, Kanamaru, A, additional, Kobayashi, T, additional, Kodera, Y, additional, Nishikawa, K, additional, Matsuda, S, additional, Yamada, O, additional, Omoto, E, additional, Takeyama, H, additional, Tsukuda, K, additional, Asou, N, additional, Tanimoto, M, additional, Shiozaki, H, additional, Tomonaga, M, additional, Masaoka, T, additional, Miura, Y, additional, Takaku, F, additional, Ohashi, Y, additional, and Motoyoshi, K, additional

Published
1997
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