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2,682 results on '"Kangawa, Kenji"'

54. Retraction: Transcriptome analysis reveals a role for the endothelial ANP-GC-A signaling in interfering with pre-metastatic niche formation by solid cancers

Author

Nojiri, Takashi, primary, Arai, Miki, additional, Suzuki, Yutaka, additional, Kumazoe, Motofumi, additional, Tokudome, Takeshi, additional, Miura, Koichi, additional, Hino, Jun, additional, Hosoda, Hiroshi, additional, Miyazato, Mikiya, additional, Okumura, Meinoshin, additional, Kawaoka, Shinpei, additional, and Kangawa, Kenji, additional

Published
2022
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55. Utility of perinatal natriuretic peptide for predicting neonatal heart failure

Author

Miyoshi, Takekazu, primary, Hosoda, Hiroshi, additional, Miyake, Akira, additional, Sakaguchi, Heima, additional, Kitano, Masataka, additional, Kurosaki, Ken‐ichi, additional, Shiraishi, Isao, additional, Nakai, Michikazu, additional, Nishimura, Kunihiro, additional, Miyazato, Mikiya, additional, Kangawa, Kenji, additional, Yoshimatsu, Jun, additional, and Minamino, Naoto, additional

Published
2022
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63. Ghrelin protects the heart against ischemia-induced arrhythmias by preserving connexin-43 protein

Author

Soeki, Takeshi, Niki, Toshiyuki, Uematsu, Etsuko, Bando, Sachiko, Matsuura, Tomomi, Kusunose, Kenya, Ise, Takayuki, Ueda, Yuka, Tomita, Noriko, Yamaguchi, Koji, Koshiba, Kunihiko, Yagi, Shusuke, Fukuda, Daiju, Taketani, Yoshio, Iwase, Takashi, Yamada, Hirotsugu, Wakatsuki, Tetsuzo, Akaike, Masashi, Shimabukuro, Michio, Kishimoto, Ichiro, Kangawa, Kenji, and Sata, Masataka

Published
2013
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73. Inhibition of N-type Ca2+ channels ameliorates an imbalance in cardiac autonomic nerve activity and prevents lethal arrhythmias in mice with heart failure

Author

Yamada, Yuko, Kinoshita, Hideyuki, Kuwahara, Koichiro, Nakagawa, Yasuaki, Kuwabara, Yoshihiro, Minami, Takeya, Yamada, Chinatsu, Shibata, Junko, Nakao, Kazuhiro, Cho, Kosai, Arai, Yuji, Yasuno, Shinji, Nishikimi, Toshio, Ueshima, Kenji, Kamakura, Shiro, Nishida, Motohiro, Kiyonaka, Shigeki, Mori, Yasuo, Kimura, Takeshi, Kangawa, Kenji, and Nakao, Kazuwa

Published
2014
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85. A mouse model of ghrelinoma exhibited activated growth hormone-insulin-like growth factor I axis and glucose intolerance

Author

Iwakura, Hiroshi, Ariyasu, Hiroyuki, Li, Yushu, Kanamoto, Naotetsu, Bando, Mika, Yamada, Go, Hosoda, Hiroshi, Hosoda, Kiminori, Shimatsu, Akira, Nakao, Kazuwa, Kangawa, Kenji, and Akamizu, Takashi

Subjects
Animal models in research -- Usage, Ghrelin -- Research, Ghrelin -- Physiological aspects, Growth factors -- Research, Growth factors -- Physiological aspects, Glucose intolerance -- Research, Glucose intolerance -- Physiological aspects, Biological sciences
Abstract

Ghrelin is a stomach-derived peptide that has growth hormone-stimulating and orexigenic activities. Although there have been several reports of ghrelinoma cases, only a few cases have elevated circulating ghrelin levels, hampering the investigation of pathophysiological features of ghrelinoma and chronic effects of ghrelin excess. Furthermore, standard transgenic technique has resulted in desacyl ghrelin production only because of the limited tissue expression of ghrelin O-acyltransferase, which mediates acylation of ghrelin. Accordingly, we attempted to create ghrelin promoter SV40 T-antigen transgenic (GP-Tag Tg) mice, in which ghrelin-producing cells continued to proliferate and finally developed into ghrelinoma. Adult GP-Tag Tg mice showed elevated plasma ghrelin levels with preserved physiological regulation. Adult GP-Tag Tg mice with increased plasma ghrelin levels exhibited elevated IGF-I levels despite poor nutrition. Although basal growth hormone levels were not changed, those after growth hormone-releasing hormone injection tended to be higher. These results indicate that chronic elevation of ghrelin activates GH-IGF-I axis. In addition, GP-Tag Tg mice demonstrated glucose intolerance. Insulin secretion by glucose tolerance tests was significantly attenuated in GP-Tag Tg, whereas insulin sensitivity determined by insulin tolerance tests was preserved, indicating that chronic elevation of ghrelin suppresses insulin secretion and leads to glucose intorelance. Thus, we successfully generated a Tg model of ghrelinoma, which is a good tool to investigate chronic effects of ghrelin excess. Moreover, their characteristic features could be a hint on ghrelinoma. ghrelin; glucose metabolism

Published
2009

88. Ghrelin suppresses cardiac sympathetic activity and prevents early left ventricular remodeling in rats with myocardial infarction

Author

Soeki, Takeshi, Kishimoto, Ichiro, Schwenke, Daryl O., Tokudome, Takeshi, Horio, Takeshi, Yoshida, Morikatsu, Hosoda, Hiroshi, and Kangawa, Kenji

Subjects
Ghrelin -- Research, Heart attack -- Research, Cardiac glycosides -- Research, Cardiotonic agents -- Research, Reperfusion injury -- Research, Cardiovascular research, Biological sciences
Abstract

A recent study suggests that exogenous ghrelin administration might decrease renal sympathetic nerve activity in conscious rabbits. In the present study, we investigated whether ghrelin administration would attenuate left ventricular (LV) remodeling following myocardial infarction (MI) via the suppression of cardiac sympathetic activity. Ghrelin (100 [micro]g/kg sc, twice daily, n = 15) or saline (n = 15) were administered for 2 wk from the day after MI operation in Sprague-Dawley rats. The effects of ghrelin on cardiac remodeling were evaluated by echocardiographic, hemodynamic, histopathological, and gene analysis. In addition, before and after ghrelin (100 [micro]g/kg sc, n = 6) was administered in conscious rats with MI, the autonomic nervous function was investigated by power spectral analysis obtained by a telemetry system. In ghrelin-treated rats, LV enlargement induced by MI was significantly attenuated compared with saline-treated rats. In addition, there was a substantial decrease in LV end-diastolic pressure and increases in the peak rate of the rise and fall of LV pressure in ghrelin-treated MI rats compared with saline-treated MI rats. Furthermore, ghrelin attenuated an increase in morphometrical collagen volume fraction in the noninfarct region, which was accompanied by the suppression of collagen I and III mRNA levels. Importantly, a 2-wk administration of ghrelin dramatically suppressed the MI-induced increase in heart rate and plasma norepinephrine concentration to the similar levels as in sham-operated controls. Moreover, acute administration of ghrelin to MI rats decreased the ratio of the low-to-high frequency spectra of heart rate variability (P < 0.01). In conclusion, these data suggest the potential usefulness of ghrelin as a new cardioprotective hormone early after MI. autonomic nervous function; infarction; peptide hormones

Published
2008

89. The GPCR modulator protein RAMP2 is essential for angiogenesis and vascular integrity

Author

Ichikawa-Shindo, Yuka, Sakurai, Takayuki, Kamiyoshi, Akiko, Kawate, Hisaka, Iinuma, Nobuyoshi, Yoshizawa, Takahiro, Koyama, Teruhide, Fukuchi, Junichi, Iimuro, Satoshi, Moriyama, Nobuo, Kawakami, Hayato, Murata, Toshinori, Kangawa, Kenji, Nagai, Ryozo, and Shindo, Takayuki

Subjects
Proteins -- Research, Proteins -- Physiological aspects, Cardiovascular diseases -- Research, Cardiovascular diseases -- Physiological aspects, Peptides -- Research, Peptides -- Physiological aspects
Abstract

Adrenomedullin (AM) is a peptide involved both in the pathogenesis of cardiovascular diseases and in circulatory homeostasis. The high-affinity AM receptor is composed of receptor activity--modifying protein 2 or 3 (RAMP2 or -3) and the GPCR calcitonin receptor--like receptor. Testing our hypothesis that RAMP2 is a key determinant of the effects of AM on the vasculature, we generated and analyzed mice lacking RAMP2. Similar to AM-/- embryos, RAMP2-/- embryos died in utero at midgestation due to vascular fragility that led to severe edema and hemorrhage. Vascular ECs in RAMP2-/- embryos were severely deformed and detached from the basement membrane. In addition, the abnormally thin arterial walls of these mice had a severe disruption of their typically multilayer structure. Expression of tight junction, adherence junction, and basement membrane molecules by ECs was diminished in Ramp2-/- embryos, leading to paracellular leakage and likely contributing to the severe edema observed. In adult Ramp2+/- mice, reduced RAMP2 expression led to vascular hyperpermeability and impaired neovascularization. Conversely, ECs overexpressing RAMP2 had enhanced capillary formation, firmer tight junctions, and reduced vascular permeability. Our findings in human cells and in mice demonstrate that RAMP2 is a key determinant of the effects of AM on the vasculature and is essential for angiogenesis and vascular integrity., Introduction Many vasoactive substances play critical roles in the maintenance of cardiovascular homeostasis; moreover, imbalances among these substances have been implicated in the pathogenesis of various cardiovascular diseases. Among these, [...]

Published
2008

94. Expression of CCN1 (CYR61) in developing, normal, and diseased human kidney

Author

Sawai, Kazutomo, Mukoyama, Masashi, Mori, Kiyoshi, Kasahara, Masato, Koshikawa, Masao, Yokoi, Hideki, Yoshioka, Tetsuro, Ogawa, Yoshihisa, Sugawara, Akira, Nishiyama, Hiroyuki, Yamada, Shigehito, Kuwahara, Takashi, Saleem, Moin A., Shiota, Kohei, Ogawa, Osamu, Miyazato, Mikiya, Kangawa, Kenji, and Nakao, Kazuwa

Subjects
Kidneys -- Medical examination, Epithelial cells -- Properties, Cell physiology -- Research, Protein research, Biological sciences
Abstract

CCN1 (cysteine-rich protein 61; Cyr61) is an extracellular matrix-associated signaling molecule that functions in cell migration, adhesion, and differentiation. We previously reported that CCN1 is induced at podocytes in rat anti-Thy-1 glomerulonephritis, a well-known model of reversible glomerular injury, but its expression and significance in the human kidney remain totally unknown (Sawai K, Mori K, Mukoyama M, Sugawara A, Suganami T, Koshikawa M, Yahata K, Makino H, Nagae T, Fujinaga Y, Yokoi H, Yoshioka T, Yoshimoto A, Tanaka I, Nakao K. J Am Soc Nephrol 14:1154-1163, 2003). Here we report that, in the human kidney, CCN1 expression was confined to podocytes in normal adult and embryonic glomeruli from the capillary loop stage. Podocyte CCNI expression was decreased in IgA nephropathy, diabetic nephropathy, and membranous nephropathy, whereas it remained unchanged in minimal change disease and focal segmental glomerulosclerosis. Downregulation of CCN1 was significantly greater in diseased kidneys with severe mesangial expansion. CCN1 protein was also localized in the thick ascending limb of Henle's loop, distal and proximal tubules, and collecting ducts, which was not altered in diseased kidneys. In vitro, recombinant CCN1 protein enhanced endothelial cell adhesion, whereas it prominently inhibited mesangial cell adhesion. CCN1 also completely suppressed mesangial cell migration, suggesting its role as a mesangial-repellent factor. In cultured podocytes, CCN1 markedly induced the expression of cyclin-dependent kinase inhibitor [p27.sup.Kip1] as well as synaptopodin in a dose-dependent manner and suppressed podocyte migration. These data indicate that CCN1 is expressed in podocytes, can act on glomerular cells to modulate glomerular remodeling, and is downregulated in diseased kidneys, suggesting that impairment of CCN1 expression in podocytes may contribute to the progression of glomerular disease with mesangial expansion. podocyte; glomerular visceral epithelial cell; cysteine-rich protein 61; mesangial cell; synaptopodin

Published
2007

95. Central control of bone remodeling by neuromedin U

Author

Sato, Shingo, Hanada, Reiko, Kimura, Ayako, Abe, Tomomi, Matsumoto, Takahiro, Iwasaki, Makiko, Inose, Hiroyuki, Ida, Takanori, Mieda, Michihiro, Takeuchi, Yasuhiro, Fukumoto, Seiji, Fujita, Toshiro, Kato, Shigeaki, Kangawa, Kenji, Kojima, Masayasu, Shinomiya, Ken-ichi, and Takeda, Shu

Abstract

Author(s): Shingo Sato [1]; Reiko Hanada [2]; Ayako Kimura [1]; Tomomi Abe [3]; Takahiro Matsumoto [4, 5]; Makiko Iwasaki [1]; Hiroyuki Inose [1]; Takanori Ida [2]; Michihiro Mieda [3]; Yasuhiro [...]

Published
2007
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96. Effects of ghrelin administration on decreased growth hormone status in obese animals

Author

Iwakura, Hiroshi, Akamizu, Takashi, Ariyasu, Hiroyuki, Irako, Taiga, Hosoda, Kiminori, Nakao, Kazuwa, and Kangawa, Kenji

Subjects
Obesity -- Research, Ghrelin -- Research, Somatotropin -- Research, Diabetes -- Research, Somatotropin -- Receptors, Biological sciences
Abstract

Obesity is characterized by markedly decreased ghrelin and growth hormone (GH) secretion. Ghrelin is a GH-stimulating, stomach-derived peptide that also has orexigenic action. Ghrelin supplement may restore decreased GH secretion in obesity, but it may worsen obesity by its orexigenic action. To reveal effects of ghrelin administration on obese animals, we first examined acute GH and orexigenic responses to ghrelin in three different obese and/or diabetic mouse models: db/db mice, mice on a high-fat diet (HFD mice), and Akita mice for comparison. GH responses to ghrelin were significantly suppressed in db/db, HFD, and Akita mice. Food intake of db/db and Akita mice were basally higher, and further stimulation of food intake by ghrelin was suppressed. Pituitary GH secretagogue receptor mRNA levels in db/db and HFD mice were significantly decreased, which may partly contribute to decreased GH response to ghrelin in these mice. In Akita mice for comparison, decreased hypothalamic GH-releasing hormone (GHRH) mRNA levels may be responsible for decreased GH response, since maximum GH response to ghrelin needs GHRH. When ghrelin was injected into HFD mice with GHRH coadministrated, GH responses to ghrelin were significantly emphasized. HFD mice injected with low-dose ghrelin and GHRH for 10 days did not show weight gain. These results indicate that low-dose ghrelin and GHRH treatment may restore decreased GH secretion in obesity without worsening obesity. growth hormone secretagogue receptor; obesity; diabetes

Published
2007

97. Adrenomedullin ameliorates lipopolysaccharide-induced acute lung injury in rats

Author

Itoh, Takefumi, Obata, Hiroaki, Murakami, Shinsuke, Hamada, Kaoru, Kangawa, Kenji, Kimura, Hiroshi, and Nagaya, Noritoshi

Subjects
Apoptosis -- Observations, Inflammation -- Observations, Lungs -- Injuries, Rats -- Physiological aspects, Rattus -- Physiological aspects, Cells -- Permeability, Cells -- Evaluation, Biological sciences
Abstract

Adrenomedullin (AM), an endogenous peptide, has been shown to have a variety of protective effects on the cardiovascular system. However, the effect of AM on acute lung injury remains unknown. Accordingly, we investigated whether AM infusion ameliorates lipopolysaccharide (LPS)-induced acute lung injury in rats. Rats were randomized to receive continuous intravenous infusion of AM (0.1 [micro]g*[kg.sup.-1]*[min.sup.-1]) or vehicle through a microosmotic pump. The animals were intratracheally injected with either LPS (1 mg/kg) or saline. At 6 and 18 h after intratracheal instillation, we performed histological examination and bronchoalveolar lavage and assessed the lung wet/dry weight ratio as an index of acute lung injury. Then we measured the numbers of total cells and neutrophils and the levels of tumor necrosis factor (TNF)-[alpha] and cytokine-induced neutrophil chemoattractant (CINC) in bronchoalveolar lavage fluid (BALF). In addition, we evaluated BALF total protein and albumin levels as indexes of lung permeability. LPS instillation caused severe acute lung injury, as indicated by the histological findings and the lung wet/dry weight ratio. However, AM infusion attenuated these LPS-induced abnormalities. AM decreased the numbers of total cells and neutrophils and the levels of TNF-[alpha] and CINC in BALF. AM also reduced BALF total protein and albumin levels. In addition, AM significantly suppressed apoptosis of alveolar wall cells as indicated by cleaved caspase-3 staining. In conclusion, continuous infusion of AM ameliorated LPS-induced acute lung injury in rats. This beneficial effect of AM on acute lung injury may be mediated by inhibition of inflammation, hyperpermeability, and alveolar wall cell apoptosis. apoptosis; hyperpermeability; inflammation

Published
2007

98. [beta]-Defensin overexpression induces progressive muscle degeneration in mice

Author

Yamaguchi, Yasuhiro, Nagase, Takahide, Tomita, Tetsuji, Nakamura, Kyoko, Fukuhara, Shigetomo, Amano, Tomokazu, Yamamoto, Hiroshi, Ide, Yukie, Suzuki, Misao, Teramoto, Shinji, Asano, Tomoichiro, Kangawa, Kenji, Nakagata, Naomi, Ouchi, Yasuyoshi, and Kurihara, Hiroki

Subjects
Muscular dystrophy -- Diagnosis, Immunity -- Analysis, Peptides -- Properties, Muscles -- Physiological aspects, Biological sciences
Abstract

Defensins comprise a family of cationic antimicrobial peptides characterized by conserved cysteine residues. They are produced in various organs including skeletal muscle and are identified as key elements in the host defense system as potent effectors. At the same time, defensins have potential roles in the regulation of inflammation and, furthermore, can exert cytotoxic effects on several mammalian cells. Here, we developed transgenic mice overexpressing mouse [beta]-defensin-6 to explore the pathophysiological roles of the defensin family as a novel mediator of inflammatory tissue injury. Unexpectedly, the transgenic mice showed short lifespan, poor growth, and progressive myofiber degeneration with functional muscle impairment, predominant centronucleated myofibers, and elevated serum creatine kinase activity, as seen in human muscular dystrophy. Furthermore, some of the transgenic myofibers showed I[kappa]B[alpha] accumulation, which would be related to the myofiber apoptosis of limb-girdle muscular dystrophy type 2A. The present findings may unravel a concealed linkage between the innate immune system and the pathophysiology of degenerative diseases. muscular dystrophy; innate immunity; NF-[kappa]B doi:10.1152/ajpcell.00295.2006

Published
2007

99. Ghrelin

Author

Kojima, Masayasu, primary, Nakamura, Yuki, additional, Sato, Takahiro, additional, and Kangawa, Kenji, additional

Published
2013
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100. Contributors

Author

Aalen, Reidunn B., primary, Abdel-Wahab, Yasser H.A., additional, Adams, Michael E., additional, Adan, Roger A.H., additional, Ahima, Rexford S., additional, Ahmed, Naima, additional, Al-Massadi, Omar, additional, Altstein, Miriam, additional, Anouar, Youssef, additional, Anselmi, Laura, additional, Ansorge, Siegfried, additional, Antcheva, Nikolinka, additional, Antonova-Koch, Yevgeniya, additional, Appel, Jon R., additional, Arik, Anam J., additional, Arter, Alison L., additional, Arvan, Peter, additional, Ashkenazi, Avraham, additional, Baas, P.W., additional, Bado, André, additional, Baird, Andrew, additional, Baiula, Monica, additional, Bakaletz, Lauren O., additional, Bakken, Earl E., additional, Balaskó, Márta, additional, Baldwin, Graham S., additional, Banks, William A., additional, Barra, Donatella, additional, Barson, Jessica R., additional, Basille, Magali, additional, Bauer, Natalie N., additional, Bedini, Andrea, additional, Beeton, Christine, additional, Begley, David J., additional, Beinfeld, Margery C., additional, Bendena, William G., additional, Benoit, Stephen C., additional, Bentov, Itay, additional, Bern, Howard, additional, Bierbaum, Gabriele, additional, Billington, Charles J., additional, Blasiak, Anna, additional, Block, Norman L., additional, Bloom, Stephen. R., additional, Bonney, Iwona, additional, Bowie, John H., additional, Boyd, Sunny K., additional, Brain, Susan D., additional, Brede, Dag A., additional, Broeck, Jozef Vanden, additional, Brown, Kelly L., additional, Brown, Mark R., additional, Bugni, James M., additional, Bundgaard, Jens R., additional, Burel, Delphine, additional, Butenko, Melinka A., additional, Call, Melissa J., additional, Calò, Girolamo, additional, Campbell, Duncan John, additional, Carlsson, Anna, additional, Carr, Daniel B., additional, Carraway, Robert E., additional, Carreira, Marcos C., additional, Casanueva, Felipe F., additional, Cassella, Sarah N., additional, Casson, Stuart A., additional, Castaño, Justo P., additional, Cebrat, Marek, additional, Chappe, Valerie, additional, Chatenet, David, additional, Chen, Keqiang, additional, Chen, Chen, additional, Chen, Longchuan, additional, Chen, Duan, additional, Cheng, Carrie Y.Y., additional, Cho, Sung Ki, additional, Chow, Billy K.C., additional, Christopoulos, Arthur, additional, Chu, Shijian, additional, Clarke, Iain J., additional, Coast, Geoffrey M., additional, Compere, Vincent, additional, Concepcion, Gisela P., additional, Cone, Roger D., additional, Conlon, J. Michael, additional, Cornélissen, Germaine, additional, Courel, Maité, additional, Couture, Réjean, additional, Cramer, W.A., additional, Croft, Nathan P., additional, Crujeiras, Ana B., additional, Cuttitta, Frank, additional, Cynis, Holger, additional, D’Acquisto, F., additional, Davis, Jon F., additional, Davis, Thomas P., additional, de La Serre, Claire Barbier, additional, de Lartigue, Guillaume, additional, de Lecea, Luis, additional, de Oliveira Santos, Marcelo, additional, De Waard, Michel, additional, Bolette Hartmann, Carolyn F. Deacon, additional, Delestre, Charlène, additional, Delgado, Mario, additional, Demuth, Hans-Ulrich, additional, Deng, Xiaoming, additional, Dharmawardhana, Palitha, additional, Di Cosmo, Anna, additional, Dias, Simoni Campos, additional, Dickerson, Jonathan W., additional, Diep, Dzung B., additional, Dircksen, H., additional, Dischinger, Jasmin, additional, do Rego, Jean-Claude, additional, Dobner, Paul R., additional, Dockray, Graham J., additional, Dores, Robert M., additional, Ducroc, Robert, additional, Dudek, Nadine L., additional, Dumont, Yvan, additional, Duraffourd, Celine, additional, Duterte-Boucher, Dominique, additional, Eberlé, Alex N., additional, Egleton, Richard D., additional, Eipper, Betty A., additional, Engel, Jorg B., additional, Englander, Ella W., additional, Epelbaum, Jacques, additional, Erlanson-Albertsson, Charlotte, additional, Evangelista, S., additional, Fagan, Karen A., additional, Farber, Joshua M., additional, Farkasfalvi, Klára, additional, Fekete, Csaba, additional, Flatt, Peter R., additional, Flower, R.J., additional, Forssmann, Wolf-Georg, additional, Fournier, Alain, additional, Foy, Kevin Chu, additional, Franco, Octávio Luiz, additional, Frenkel, Dan, additional, Fricker, Lloyd D., additional, de la Fuente-Núñez, César, additional, Fukuda, Hiroo, additional, Gäde, Gerd, additional, Galas, Ludovic, additional, Gallagher, Patricia E., additional, Gandolfo, Pierrick, additional, Garcia-Espinosa, Maria A., additional, García-Sanmartín, Josune, additional, Geary, Nori, additional, Geng, Hua, additional, Germano, Patrizia M., additional, Goetze, Jens P., additional, Gonzalez, Alexis A., additional, Gonzalez, Ana, additional, Gosnell, Blake A., additional, Goto, Katsutoshi, additional, Gourcerol, Guillaume, additional, Gozes, I., additional, Gracia-Navarro, Francisco, additional, Grayson, Bernadette E., additional, Greeley, George H., additional, Greenwald-Yarnell, Megan, additional, Gressens, Pierre, additional, Grider, John R., additional, Grünewald, Jan, additional, Guerreiro, Juliano R., additional, Guerrini, Remo, additional, Guida, Filomena, additional, Guilhaudis, Laure, additional, Guilmeau, Sandra, additional, Gundlach, Andrew L., additional, Gutkowska, Jolanta, additional, Hackbarth, Clifton, additional, Haim Ohana, Y., additional, Halberg, Franz, additional, Hallberg, Mathias, additional, Hamidi, Sayyed A., additional, Han, Song, additional, Han, Ji-Sheng, additional, Hancock, Robert E.W., additional, Haque, Samer-ul, additional, Hara-Nishimura, Ikuko, additional, Hariton, Aliza, additional, Hartsock, Wendy J., additional, Harvey, Alan L., additional, Hasunuma, Itaru, additional, Henning, Robert J., additional, Heppner, Kristy M., additional, Hertweck, Kate L., additional, Herzog, Herbert, additional, Higashiyama, Tetsuya, additional, Hinuma, Shuji, additional, Hippenstiel, Stefan, additional, Hirakawa, Yuki, additional, Hirose, Shuichi, additional, Hirsch, Jochen R., additional, Hocke, Andreas C., additional, Hodges, Robert S., additional, Hoffmann, Werner, additional, Hökfelt, Tomas, additional, Holst, Jens Juul, additional, Holzer, Peter, additional, Horodyski, Frank M., additional, Hosoda, Hiroshi, additional, Hou, Xiaowen, additional, Huffaker, Alisa, additional, Iijima, Norio, additional, Ikeuchi, Momoko, additional, Imperial, Julita S., additional, Improta, Giovanna, additional, Inui, Akio, additional, Irwin, Nigel, additional, Ishii, Munehiro, additional, Iturrioz, Xavier, additional, Ivanisevic, Ljubica, additional, Iwao, Hiroshi, additional, Iwata, Takeo, additional, Izumi, Yasukatsu, additional, Izumiyama, Hajime, additional, Jankowski, Marek, additional, Janssen, Tom, additional, Jégou, Sylvie, additional, Jensen, Robert T., additional, Jethwa, Preeti H., additional, Johannessen, Helene, additional, Johanson, Conrad, additional, Judkowski, Valeria, additional, Kaczmarek, Przemyslaw, additional, Kageyama, Haruaki, additional, Kakimoto, Tatsuo, additional, Kang, Ki Sung, additional, Kangawa, Kenji, additional, Kastin, Abba J., additional, Kato, Johji, additional, Kaumaya, Pravin T.P., additional, Keep, Richard F., additional, Kem, William R., additional, Khomenko, Tetyana, additional, Kikuyama, Sakae, additional, Kim, Young-Joon, additional, Kimura, Sadao, additional, King, Ross, additional, Kiptoo, Paul, additional, Kishimoto, Ichiro, additional, Kitamura, Kazuo, additional, Kluczyk, Alicja, additional, Kobori, Hiroyuki, additional, Kodama, Yosuke, additional, Kojima, Masayasu, additional, Kondo, Yuki, additional, Körner, Meike, additional, Kosson, Piotr, additional, Kotz, Catherine M., additional, Krishnan, Bhavani, additional, Kulseng, Bård, additional, Kumpf, Robert, additional, Laburthe, Marc, additional, Lacaille, Hélène, additional, Ladenheim, Ellen E., additional, Ladram, Ali, additional, Laksitorini, Marlyn D., additional, Lambert, David G., additional, Lange, Angela B., additional, Langhans, Wolfgang, additional, Larauche, Muriel, additional, Larhammar, Dan, additional, Larráyoz, Ignacio M., additional, Lattanzi, Roberta, additional, Lechan, Ronald M., additional, Lefranc, Benjamin, additional, Leibowitz, Sarah F., additional, Lelièvre, Vincent, additional, Leprince, Jérôme, additional, Levine, Allen S., additional, Li, Qun, additional, Lifshitz, Veronica, additional, Lihrmann, Isabelle, additional, Chi-Jen Lin, James, additional, Lindberg, Iris, additional, Lindsey, Keith, additional, Lipkowski, Andrzej W., additional, Liron, T., additional, Liu, Junli, additional, Liu, Ying, additional, Liu, Min, additional, Llorens-Cortes, Catherine, additional, Loizidou, Marilena, additional, Lopez, C., additional, Lovejoy, David A., additional, Luca, Vincenzo, additional, Lutz, Thomas A., additional, Ma, Sherie, additional, Mains, Richard E., additional, Malagon, Maria M., additional, Malendowicz, Ludwik K., additional, Wan, Jennifer Man-Fan, additional, Mangoni, Maria Luisa, additional, Manigrasso, Michaele B, additional, Marahiel, Mohamed A., additional, Marco, Heather G., additional, Maric-Bilkan, Christine, additional, Marks, Nikki J., additional, Martin, Roland, additional, Martinez, Vicente, additional, Martínez, Alfredo, additional, Martinez-Fuentes, Antonio J., additional, Masler, Edward P., additional, Matsubayashi, Yoshikatsu, additional, Mattu, Harman S., additional, Maule, Aaron G., additional, McLaughlin, Patricia J., additional, McMurtry, Ivan F., additional, Meelkop, Ellen, additional, Mehdi, Saher, additional, Melchiorri, Pietro, additional, Millar, R.P., additional, Miller, Laurence J., additional, Miller, Miles, additional, Million, Mulugeta, additional, Minamino, Naoto, additional, Mittelman, M., additional, Miyauchi, Takashi, additional, Miyazato, Mikiya, additional, Mizoguchi, Hirokazu, additional, Mohme, Malte, additional, Montero-Hadjadje, Maité, additional, Moody, Terry W., additional, Mookherjee, Neeloffer, additional, Moran, Timothy H., additional, Morganstern, Irene, additional, Mori, Masatomo, additional, Morin, Fabrice, additional, Morris, John F., additional, Moura, Daniel S., additional, Mudge, Anna J., additional, Mul, Joram D., additional, Murthy, Karnam S., additional, Myers, Martin G., additional, Nachman, Ronald J., additional, Nahon, Jean-Louis, additional, Naithani, Sushma, additional, Nakada, Tomoaki, additional, Nakamachi, Tomoya, additional, Nakamura, Yuki, additional, Nalivaeva, Natalia N., additional, Nasrallah, June B., additional, Nässel, Dick R., additional, Navar, L. 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2013
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