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1. Tyrosine levels are associated with insulin resistance in patients with nonalcoholic fatty liver disease

Author

Kawanaka M, Nishino K, Oka T, Urata N, Nakamura J, Suehiro M, Kawamoto H, Chiba Y, and Yamada G

Subjects
Diseases of the digestive system. Gastroenterology, RC799-869
Abstract

Miwa Kawanaka,1 Ken Nishino,1 Takahito Oka,1 Noriyo Urata,1 Jun Nakamura,1 Mitsuhiko Suehiro,1 Hirofumi Kawamoto,1 Yasutaka Chiba,2 Gotaro Yamada1 1Department of General Internal Medicine 2, Kawasaki Hospital, Kawasaki Medical School, Okayama, Japan; 2Clinical Research Center, Kinki University Hospital, Sayama, Japan Objective: Amino acid imbalance is often found in patients with cirrhosis, and this imbalance is associated with insulin resistance. However, the mechanism underlying the relationship between amino acid imbalance and insulin resistance remains unclear. We evaluated serum amino acid concentrations in patients with nonalcoholic fatty liver disease to determine if any of the levels of amino acids were associated with the biochemical markers and fibrosis stage of nonalcoholic steatohepatitis (NASH). Methods: In 137 patients with nonalcoholic fatty liver disease who underwent liver biopsy, plasma levels of branched-chain amino acid (BCAA), tyrosine (Tyr), and the BCAA-to-Tyr ratio values were determined using mass spectroscopy. These values were then assessed for associations with fibrosis stage, anthropometric markers (age, sex, and body mass index), biochemical markers (alanine aminotransferase, aspartate aminotransferase, γ-glutamyl transpeptidase, albumin, platelet count, total cholesterol, triglycerides, low-density lipoprotein cholesterol, and glycosylated hemoglobin), and relevant disease-specific biomarkers (homeostasis model assessment of insulin resistance [HOMA-IR], serum iron, ferritin, leptin, adiponectin, high-sensitivity C-reactive protein, and hyaluronic acid). Results: Serum albumin levels, plasma BCAA levels, and BCAA-to-Tyr ratio values were negatively associated with the fibrosis stage. In contrast, Tyr levels increased with increasing fibrotic staging. Tyr levels were also correlated with HOMA-IR results. Conclusion: Plasma BCAA levels in patients with NASH decreased with increasing liver fibrosis, while Tyr levels increased with increasing fibrotic stage. These results suggest that amino acid imbalance and insulin resistance are intimately involved in a complex pathogenic mechanism for NASH. Keywords: nonalcoholic steatohepatitis, amino acid imbalance, branched-chain amino acids, branched-chain amino acid-to-tyrosine ratio (BTR)

Published
2015

2. Treatment of nonalcoholic steatohepatitis with vitamins E and C: a pilot study

Author

Kawanaka M, Nishino K, Nakamura J, Suehiro M, Goto D, Urata N, Oka T, Kawamoto H, Nakamura H, Yodoi J, Hino K, and Yamada G

Subjects
Diseases of the digestive system. Gastroenterology, RC799-869
Abstract

Miwa Kawanaka,1 Ken Nishino,1 Jun Nakamura,1 Mitsuhiko Suehiro,1 Daisuke Goto,1 Noriyo Urata,1 Takahito Oka,1 Hirofumi Kawamoto,1 Hajime Nakamura,2 Junji Yodoi,3 Keisuke Hino,4 Gotaro Yamada11Department of Internal Medicine 2, Kawasaki Hospital, Kawasaki Medical School, Okayama, 2Department of Experimental Therapeutics, Translational Research Center, Kyoto University Hospital, Kyoto, 3Department of Biological Responses, Institute for Virus Research, Kyoto University, Kyoto, 4Department of Hepatology and Pancreatology, Kawasaki Medical School, Okayama, JapanBackground: Nonalcoholic steatohepatitis (NASH) is a common liver disease that can progress to cirrhosis. Oxidative stress is one of the central mechanisms causing hepatocellular injury in the disease. In this study, antioxidant therapy using both vitamins C and E was conducted in patients with NASH.Methods: Vitamin E 300 mg/day and vitamin C 300 mg/day were administered orally to 23 patients with NASH for 12 months. Body mass index was measured during therapy. Serum levels of alanine aminotransferase, thioredoxin (an oxidative stress marker), and high-sensitivity C-reactive protein were measured before treatment and after 12 months in all patients. Ten of the 23 patients underwent liver biopsy before and after treatment.Results: Body mass index remained unchanged during treatment with vitamins C and E. Serum alanine aminotransferase, thioredoxin, and high-sensitivity C-reactive protein levels were decreased significantly at 12 months compared with pretreatment. Liver biopsies showed improved necroinflammatory activity in eight cases and improved fibrosis staging in 4.Conclusion: Serum alanine aminotransferase, thioredoxin, and high-sensitivity C-reactive protein levels, and liver histology were clearly improved with vitamin C and E therapy. These findings suggest that combination therapy using these vitamins may be useful in patients with NASH to minimize damage from oxidative stress and slow the processes leading to cirrhosis.Keywords: vitamin E, vitamin C, nonalcoholic steatohepatitis, oxidative stress

Published
2013

8. Adiposity and risk of decline in glomerular filtration rate : Meta-analysis of individual participant data in a global consortium

Author

Chang AR, Grams ME, Ballew SH, Bilo H, Correa A, Evans M, Gutierrez OM, Hosseinpanah F, Iseki K, Kenealy T, Klein B, Kronenberg F, Lee BJ, Li Y, Miura K, Navaneethan SD, Roderick PJ, Valdivielso JM, Visseren FLJ, Zhang L, Gansevoort RT, Hallan SI, Levey AS, Matsushita K, Shalev V, Woodward M, Astor B, Appel L, Greene T, Chen T, Chalmers J, Arima H, Perkovic V, Yatsuya H, Tamakoshi K, Hirakawa Y, Coresh J, Sang Y, Polkinghorne K, Chadban S, Atkins R, Levin A, Djurdjev O, Klein R, Lee K, Liu L, Zhao M, Wang F, Wang J, Tang M, Heine G, Emrich I, Zawada A, Bauer L, Nally J, Schold J, Shlipak M, Sarnak M, Katz R, Hiramoto J, Iso H, Yamagishi K, Umesawa M, Muraki I, Fukagawa M, Maruyama S, Hamano T, Hasegawa T, Fujii N, Jafar T, Hatcher J, Poulter N, Chaturvedi N, Wheeler D, Emberson J, Townend J, Landray M, Brenner H, Schöttker B, Saum KU, Rothenbacher D, Fox C, Hwang SJ, Köttgen A, Schneider MP, Eckardt KU, Green J, Kirchner HL, Ito S, Miyazaki M, Nakayama M, Yamada G, Cirillo M, Romundstad S, Øvrehus M, Langlo KA, Irie F, Sairenchi T, Rebholz CM, Young B, Boulware LE, Ishikawa S, Yano Y, Kotani K, Nakamura T, Jee SH, Kimm H, Mok Y, Chodick G, Wetzels JFM, Blankestijn PJ, van Zuilen AD, Bots M, Inker L, Peralta C, Kollerits B, Ritz E, Nitsch D, Fletcher A, Bottinger E, Nadkarni GN, Ellis SB, Nadukuru R, Fernandez E, Betriu A, Bermudez-Lopez M, Stengel B, Metzger M, Flamant M, Houillier P, Haymann JP, Froissart M, Ueshima H, Okayama A, Tanaka S, Okamura T, Elley CR, Collins JF, Drury PL, Ohkubo T, Asayama K, Metoki H, Kikuya M, Iseki C, Nelson RG, Knowler WC, Bakker SJL, Heerspink HJL, Brunskill N, Major R, Shepherd D, Medcalf J, Jassal SK, Bergstrom J, Ix JH, Barrett-Connor E, Kovesdy C, Kalantar-Zadeh K, Sumida K, Muntner P, Warnock D, Judd S, Panwar B, de Zeeuw D, Brenner B, Sedaghat S, Ikram MA, Hoorn EJ, Dehghan A, Wong TY, Sabanayagam C, Cheng CY, Banu R, Segelmark M, Stendahl M, Schön S, Tangri N, Sud M, Naimark D, Wen CP, Tsao CK, Tsai MK, Chen CH, Konta T, Hirayama A, Ichikawa K, Hadaegh F, Mirbolouk M, Azizi F, Solbu MD, Jenssen TG, Eriksen BO, Eggen AE, Lannfelt L, Larsson A, Ärnlöv J, Landman GWD, van Hateren KJJ, Kleefstra N, Chen J, Kwak L, Surapaneni A., Chang, Ar, Grams, Me, Ballew, Sh, Bilo, H, Correa, A, Evans, M, Gutierrez, Om, Hosseinpanah F, Iseki K, Kenealy, T, Klein, B, Kronenberg, F, Lee, Bj, Li, Y, Miura, K, Navaneethan, Sd, Roderick, Pj, Valdivielso, Jm, Visseren, Flj, Zhang, L, Gansevoort, Rt, Hallan, Si, Levey, A, Matsushita, K, Shalev, V, Woodward, M, Astor, B, Appel, L, Greene, T, Chen, T, Chalmers, J, Arima, H, Perkovic, V, Yatsuya, H, Tamakoshi, K, Hirakawa, Y, Coresh, J, Sang, Y, Polkinghorne, K, Chadban, S, Atkins, R, Levin, A, Djurdjev, O, Klein, R, Lee, K, Liu, L, Zhao, M, Wang, F, Wang, J, Tang, M, Heine, G, Emrich, I, Zawada, A, Bauer, L, Nally, J, Schold, J, Shlipak, M, Sarnak, M, Katz, R, Hiramoto, J, Iso, H, Yamagishi, K, Umesawa, M, Muraki, I, Fukagawa, M, Maruyama, S, Hamano, T, Hasegawa, T, Fujii, N, Jafar, T, Hatcher, J, Poulter, N, Chaturvedi, N, Wheeler, D, Emberson, J, Townend, J, Landray, M, Brenner, H, Schöttker, B, Saum, Ku, Rothenbacher, D, Fox, C, Hwang, Sj, Köttgen, A, Schneider, Mp, Eckardt, Ku, Green, J, Kirchner, Hl, Ito, S, Miyazaki, M, Nakayama, M, Yamada, G, Cirillo, M, Romundstad, S, Øvrehus, M, Langlo, Ka, Irie, F, Sairenchi, T, Rebholz, Cm, Young, B, Boulware, Le, Ishikawa, S, Yano, Y, Kotani, K, Nakamura, T, Jee, Sh, Kimm, H, Mok, Y, Chodick, G, Wetzels, Jfm, Blankestijn, Pj, van Zuilen, Ad, Bots, M, Inker, L, Peralta, C, Kollerits, B, Ritz, E, Nitsch, D, Fletcher, A, Bottinger, E, Nadkarni, Gn, Ellis, Sb, Nadukuru, R, Fernandez, E, Betriu, A, Bermudez-Lopez, M, Stengel, B, Metzger, M, Flamant, M, Houillier, P, Haymann, Jp, Froissart, M, Ueshima, H, Okayama, A, Tanaka, S, Okamura, T, Elley, Cr, Collins, Jf, Drury, Pl, Ohkubo, T, Asayama, K, Metoki, H, Kikuya, M, Iseki, C, Nelson, Rg, Knowler, Wc, Bakker, Sjl, Heerspink, Hjl, Brunskill, N, Major, R, Shepherd, D, Medcalf, J, Jassal, Sk, Bergstrom, J, Ix, Jh, Barrett-Connor, E, Kovesdy, C, Kalantar-Zadeh, K, Sumida, K, Muntner, P, Warnock, D, Judd, S, Panwar, B, de Zeeuw, D, Brenner, B, Sedaghat, S, Ikram, Ma, Hoorn, Ej, Dehghan, A, Wong, Ty, Sabanayagam, C, Cheng, Cy, Banu, R, Segelmark, M, Stendahl, M, Schön, S, Tangri, N, Sud, M, Naimark, D, Wen, Cp, Tsao, Ck, Tsai, Mk, Chen, Ch, Konta, T, Hirayama, A, Ichikawa, K, Hadaegh, F, Mirbolouk, M, Azizi, F, Solbu, Md, Jenssen, Tg, Eriksen, Bo, Eggen, Ae, Lannfelt, L, Larsson, A, Ärnlöv, J, Landman, Gwd, van Hateren, Kjj, Kleefstra, N, Chen, J, Kwak, L, Surapaneni, A., Lifestyle Medicine (LM), Cardiovascular Centre (CVC), Groningen Kidney Center (GKC), Groningen Institute for Organ Transplantation (GIOT), Real World Studies in PharmacoEpidemiology, -Genetics, -Economics and -Therapy (PEGET), Asayama, Kei, and Sedaghat, SeyyedMah

Subjects
CHRONIC KIDNEY-DISEASE, Male, 030232 urology & nephrology, 030204 cardiovascular system & hematology, OBESITY PARADOX, Body Mass Index, BMI, eGFR, CKD-PC, Cohort Studies, 0302 clinical medicine, Risk Factors, Urologi och njurmedicin, Medicine, ALL-CAUSE MORTALITY, Adiposity, 2. Zero hunger, Aged, 80 and over, Medicine(all), education.field_of_study, Hazard ratio, ASSOCIATION, General Medicine, Middle Aged, 3. Good health, Cohort, Female, Waist Circumference, Life Sciences & Biomedicine, WAIST CIRCUMFERENCE, Obesity paradox, Glomerular Filtration Rate, Adult, Waist, Population, Renal function, 03 medical and health sciences, Medicine, General & Internal, General & Internal Medicine, CKD, Urology and Nephrology, Humans, Mortality, education, Aged, Science & Technology, business.industry, Research, medicine.disease, Body Height, BODY-MASS INDEX, Kidney Failure, Chronic, WEIGHT, Renal disorders Radboud Institute for Health Sciences [Radboudumc 11], business, Body mass index, Demography, Kidney disease
Abstract

ObjectiveTo evaluate the associations between adiposity measures (body mass index, waist circumference, and waist-to-height ratio) with decline in glomerular filtration rate (GFR) and with all cause mortality.DesignIndividual participant data meta-analysis.SettingCohorts from 40 countries with data collected between 1970 and 2017.ParticipantsAdults in 39 general population cohorts (n=5 459 014), of which 21 (n=594 496) had data on waist circumference; six cohorts with high cardiovascular risk (n=84 417); and 18 cohorts with chronic kidney disease (n=91 607).Main outcome measuresGFR decline (estimated GFR decline ≥40%, initiation of kidney replacement therapy or estimated GFR 2) and all cause mortality.ResultsOver a mean follow-up of eight years, 246 607 (5.6%) individuals in the general population cohorts had GFR decline (18 118 (0.4%) end stage kidney disease events) and 782 329 (14.7%) died. Adjusting for age, sex, race, and current smoking, the hazard ratios for GFR decline comparing body mass indices 30, 35, and 40 with body mass index 25 were 1.18 (95% confidence interval 1.09 to 1.27), 1.69 (1.51 to 1.89), and 2.02 (1.80 to 2.27), respectively. Results were similar in all subgroups of estimated GFR. Associations weakened after adjustment for additional comorbidities, with respective hazard ratios of 1.03 (0.95 to 1.11), 1.28 (1.14 to 1.44), and 1.46 (1.28 to 1.67). The association between body mass index and death was J shaped, with the lowest risk at body mass index of 25. In the cohorts with high cardiovascular risk and chronic kidney disease (mean follow-up of six and four years, respectively), risk associations between higher body mass index and GFR decline were weaker than in the general population, and the association between body mass index and death was also J shaped, with the lowest risk between body mass index 25 and 30. In all cohort types, associations between higher waist circumference and higher waist-to-height ratio with GFR decline were similar to that of body mass index; however, increased risk of death was not associated with lower waist circumference or waist-to-height ratio, as was seen with body mass index.ConclusionsElevated body mass index, waist circumference, and waist-to-height ratio are independent risk factors for GFR decline and death in individuals who have normal or reduced levels of estimated GFR.

Published
2019

10. Benefit of interferon therapy in hepatocellular carcinoma prevention for individual patients with chronic hepatitis C

Author

Yoshida, H., Tateishi, R., Arakawa, Y., Sata, M., Fujiyama, S., Nishiguchi, S., Ishibashi, H., Yamada, G., Yokosuka, O., Shiratori, Y., and Omata, M.

Subjects
Health
Abstract

Gut 2004;53:425-430. doi: 10.1136/gut.2003.030353 Background: An increase in the incidence of hepatocellular carcinoma (HCC) in Japan since the 1980s suggests an imminent outbreak in other countries where viral spread occurred [...]

Published
2004

11. One-to-one internal resonance of symmetric crossply laminated shallow shells

Author

Abe, A., Kobayashi, Y., and Yamada, G.

Subjects
Resonance -- Models, Materials -- Dynamic testing, Nonlinear mechanics -- Analysis, Science and technology
Abstract

This paper presents the response of symmetric crossply laminated shallow shells with an internal resonance [omega.sub.2] [approximately equal to] [omega.sub.3] where [omega.sub.3] and [omega.sub.3] are the linear natural frequencies of the asymmetric vibration modes (2,1) and (1,2), respectively. Galerkin's procedure is applied to the nonlinear governing equations for the shells based on the yon Karman-type geometric nonlinear theory and the first-order shear deformation theory, and the shooting method is used to obtain the steady-state response when a driving frequency [OMEGA] is near [omega.sub.2]. In order to take into account the influence of quadratic nonlinearities, the displacement functions of the shells are approximated by the eigenfunctions for the linear vibration mode (1,1) in addition to the ones for the modes (2,1) and (1,2). This approximation overcomes the shortcomings in Galerkin's procedure. In the numerical examples, the effect of the (1,1) mode on the primary resonance of the (2,1) mode is examined in detail, which allows us to conclude that the consideration of the (1,1) mode is indispensable for analyzing nonlinear vibrations of asymmetric vibration modes of shells. [DOI: 10.1115/1.1356416]

Published
2001

14. External Genitalia Development

Author

Suzuki, K, primary, Nishida, H, additional, Ohta, S, additional, Satoh, Y, additional, Xu, Y, additional, Zhang, Y, additional, Wada, Y, additional, Ogino, Y, additional, Nakagata, N, additional, Ohba, T, additional, and Yamada, G, additional

Published
2005
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17. Analytical method for vibration of angle-ply cylindrical shells having arbitrary edges

Author

Narita, Y., Ohta, Y., Yamada, G., and Kobayashi, Y.

Subjects
Composite materials -- Research, Airframes -- Research, Aerospace and defense industries, Business
Abstract

A numerical method for investigating free vibration characteristics of angle-ply cylindrical shells was evaluated. The dimensions of cylindrical shell model having arbitrary edges were obtained and the numerical approach was applied to determine the material's properties with regard to stress and strain. The frequency equation was derived using the Ritz method. Results indicated that the method can be useful in dynamic behavior analyses of composite shell structures.

Published
1992

19. Disruption of eyelid and cornea morphogenesis by epithelial β-catenin gain-of-function

Author

Mizoguchi, S., Suzuki, K., Zhang, J., Yamanaka, O., Chia-yang Liu, Okada, Y., Miyajima, M., Kokado, M., Kao, W. W. Y., Yamada, G., and Saika, S.

Subjects
Epithelial-Mesenchymal Transition, Eyelids, Cell Differentiation, Gestational Age, Mice, Transgenic, eye diseases, Epithelium, Mice, Mutant Strains, Cornea, Mice, Pregnancy, Mutation, Morphogenesis, Animals, Keratin-5, Female, sense organs, Promoter Regions, Genetic, beta Catenin, Research Article, Cell Proliferation, Signal Transduction
Abstract

Purpose To examine the developmental pathobiology of the eyelid and the cornea caused by epithelial β-catenin gain-of-function (gof) during mouse embryogenesis. Methods Compound mutant mice (Ctnnb1GOFOSE, gof of β-catenin in the epidermis and the ocular surface epithelium) were generated by time-mating keratin 5-promoter-Cre recombinase (Krt5-Cre) and Ctnnb1fE3/WT (floxed exon 3 of Ctnnb1) mice. Eyes obtained from wild-type (WT) and mutant embryos at various gestation stages until E18.5 were examined with histology and immunohistochemistry. The ultrastructure of the ocular tissues of the E18.5 embryos was also examined. Results Expression of the gof-β-catenin mutant protein in the epidermis severely impaired eyelid morphogenesis at E15.5, E17.5, and E18.5. The mutant stroma exhibited impaired keratocyte differentiation with accelerated cell proliferation and reduction in the accumulation of collagen type I. The mutant embryos also showed hyperproliferative nodules in the ocular surface epithelia with anomaly of cornea-type epithelial differentiation and the absence of the epithelial basement membrane. Conclusions Expression of the gof-β-catenin mutant protein in basal epithelial cells disrupts eyelid and cornea morphogenesis during mouse embryonic development due to the perturbation of cell proliferation and differentiation of the epithelium and the neural crest-derived mesenchyme.

Published
2015

26. ISL1 is a major susceptibility gene for classic bladder exstrophy and a regulator of urinary tract development

Author

Zhang, R., Knapp, M., Suzuki, K., Kajioka, D., Schmidt, J.M., Winkler, J., Yilmaz, O., Pleschka, M., Cao, J., Kockum, C.C., Barker, G., Holmdahl, G., Beaman, G., Keene, D., Woolf, A.S., Cervellione, R.M., Cheng, W., Wilkins, S., Gearhart, J.P., Sirchia, F., Grazia, M. Di, Ebert, A.K., Rosch, W., Ellinger, J., Jenetzky, E., Zwink, N., Feitz, W.F.J., Marcelis, C.L., Schumacher, J., Martinon-Torres, F., Hibberd, M.L., Khor, C.C., Heilmann-Heimbach, S., Barth, S., Boyadjiev, S.A., Brusco, A., Ludwig, M., Newman, W., Nordenskjold, A., Yamada, G., Odermatt, B., Reutter, H., Zhang, R., Knapp, M., Suzuki, K., Kajioka, D., Schmidt, J.M., Winkler, J., Yilmaz, O., Pleschka, M., Cao, J., Kockum, C.C., Barker, G., Holmdahl, G., Beaman, G., Keene, D., Woolf, A.S., Cervellione, R.M., Cheng, W., Wilkins, S., Gearhart, J.P., Sirchia, F., Grazia, M. Di, Ebert, A.K., Rosch, W., Ellinger, J., Jenetzky, E., Zwink, N., Feitz, W.F.J., Marcelis, C.L., Schumacher, J., Martinon-Torres, F., Hibberd, M.L., Khor, C.C., Heilmann-Heimbach, S., Barth, S., Boyadjiev, S.A., Brusco, A., Ludwig, M., Newman, W., Nordenskjold, A., Yamada, G., Odermatt, B., and Reutter, H.

Abstract

Contains fulltext : 173200.pdf (publisher's version ) (Open Access), Previously genome-wide association methods in patients with classic bladder exstrophy (CBE) found association with ISL1, a master control gene expressed in pericloacal mesenchyme. This study sought to further explore the genetics in a larger set of patients following-up on the most promising genomic regions previously reported. Genotypes of 12 markers obtained from 268 CBE patients of Australian, British, German Italian, Spanish and Swedish origin and 1,354 ethnically matched controls and from 92 CBE case-parent trios from North America were analysed. Only marker rs6874700 at the ISL1 locus showed association (p = 2.22 x 10-08). A meta-analysis of rs6874700 of our previous and present study showed a p value of 9.2 x 10-19. Developmental biology models were used to clarify the location of ISL1 activity in the forming urinary tract. Genetic lineage analysis of Isl1-expressing cells by the lineage tracer mouse model showed Isl1-expressing cells in the urinary tract of mouse embryos at E10.5 and distributed in the bladder at E15.5. Expression of isl1 in zebrafish larvae staged 48 hpf was detected in a small region of the developing pronephros. Our study supports ISL1 as a major susceptibility gene for CBE and as a regulator of urinary tract development.

Published
2017

27. Cognitive and non-cognitive skills and wages: the role of latent abilities on the gender wage gap in Peru

Author

Lavado, P, Velarde, L, and Yamada, G

Subjects
Cognition, Latin America, Labour economics, Gender, Psychology, Children and youth, Poverty
Abstract

Recently there has been growing interest in the relationship between cognitive and non-cognitive abilities and labour market outcomes. A large literature provides evidence on the positive connection between cognitive test scores and higher wages. Fewer and newer papers have explored the correlation between non cognitive test scores and wages. However, attention is focused on developed countries. Test scores suffer two limitations. First, they can be considered outcomes of the schooling level and latent (unobserved) cognitive and non-cognitive abilities. Second, they are potentially measured with error. The main objective of this paper is to identify latent abilities and explore their role in the gender wage gap in a developing country: Peru. The main identification strategy relies on exploiting panel data information on test scores and arguing that time dependence across measures is due to latent abilities. We exploit two databases Young Lives Study (YL) and the Peruvian Skills and Labor Market Survey (ENHAB). Young Lives has panel data information on test scores and ENHAB has information on test scores and wages. Results show that even though when accounting for measured abilities differences in non-cognitive abilities seem irrelevant, when accounting for differences in actual latent ability non cognitive abilities account for important inter-gender differences in the endowment and returns of abilities. Moreover, inter-gender differences in latent abilities play an important role not only in wage profiles, but in schooling, employment and occupation decisions.

Published
2016

28. Stiripentol for the treatment of super-refractory status epilepticus with cross-sensitivity

Author

Uchida, Y., primary, Terada, K., additional, Adachi, K., additional, Madokoro, Y., additional, Yamada, G., additional, Kondo, Y., additional, Fujioka, T., additional, Mizuno, M., additional, Kawashima, S., additional, Toyoda, T., additional, Oomura, M., additional, Ueki, Y., additional, Okita, K., additional, Kato, D., additional, and Matsukawa, N., additional

Published
2017
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31. Molecular analysis of murine external genitalia formation: control of morphogenesis of genital tubercle by shh and Fgf system

Author

YAMADA, G.

Subjects
Zoological research -- Analysis, Reproductive organs -- Genetic aspects, Zoology and wildlife conservation
Abstract

Recent gene KO studies have suggested that the developmental process of the anlage, the genital tubercle (GT), has much in common with those of limb buds. However, except for some previous genetic studies, systematic approach on several regulatory molecules during GT formation has not been performed. The shh and fibroblast growth factor (Fgf) genes have been postulated as regulating several downstream genes during organogenesis. The Fgf8 gene was expressed in the distal urethral plate epithelium of the GT along with other marker genes expressed in the mesenchyme. The Shh gene was found to be expressed in the urethral plate epithelium. The urogenital expression of the Shh gene was also reported by Bitgood and McMahon. To functionally analyze the role of the FGF and shh system during GT formation, an in vitro organ culture system was utilized. It was suggested that the distal urethral plate epithelium of GT, the Fgf8 gene expressing region, regulates the outgrowth of GT. The region was thus suggested as a candidate region for the signaling center during GT development. Ectopic application of FGF8 beads to the murine GT induced mesenchymal gene expression, and also promoted the outgrowth of the GT. Experiments utilizing anti-FGF neutralizing antibody suggested a growth-promoting role for FGF protein(s) in GT outgrowth. In contrast, the Fgf10 gene appears not to be primarily essential for initial outgrowth of GT despite its vital role during limb bud formation. Rather, the abnormal external genitalia development of Fgf10 mutant perinatal mice suggested the importance of the Fgf10 gene in the development of the glans penis and the glans clitoridis. Our recent analysis on FGF and shh system will be presented. These data are expected to contribute elucidating 'a model plan' for organogenesis of external genitalia and other organs such as limbs.

Published
2000

36. General Lectures-(II)

Author

Toriie, S., Nakajima, M., Kohli, Y., Takebayashi, M., Misaki, F., Kobayashi, A., Hashimoto, Y., Mitsuyoshi, Y., Ida, K., Kawai, K., Fujita, R., Kumura, F., Takahashi, M., Ohsawa, H., Hasegawa, Y., Kidokoro, T., Jojima, Y., Miyoshi, H., Okumura, Y., Yokouchi, A., Asano, H., Uehara, A., Oka, S., Saito, H., Yaginuma, M., Yamamoto, T., Asano, A., Nakamura, M., Okada, Y., Tomioka, T., Tamesue, N., Ikeda, S., Kunisaki, T., Emura, T., Yasumoto, M., Someya, N., Goto, A., Morokuma, K., Sakamoto, H., Kasaki, Y., Imamura, K., Amano, I., Iwanaga, K., Okugawa, N., Ninomiya, K., Yoshida, S., Okabe, N., Shimogawa, Y., Nakajima M., Ida, K., Akasaka, Y., Shimamoto, K., Misaki, F., Toriie, S., Tada, M., Sugawara, K., Chikayasu, I., Takeda, H., Kawai, K., Shibue, T., Yamaguchi, A., Osame, T., Shimada, K., Hori, M., Irisa, T., Miura, Y., Hanamure, B., Chuman, Y., Sato, H., Kizu, M., Kasugai, T., Kuno, N., Aoki, I., Nitta, Y., Machii, A., Murakami, Y., Aiso, Y., Kitahara, N., Yoshizawa, Y., Hishinuma, Y., Nao, Y., Ishiyama, K., Watanabe, M., Kimura, T., Hara, T., Sakaue, S., Shinoda, T., Ito, R., Hayashi, K., Sugie, H., Sekizawa, H., Nakamura, S., Kondo, J., Tanaka, E., Taniguchi, T., Kanayama, M., Koizumi, S., Watabiki, S., Ikeda, S., Tamura, K., Okada, Y., Arai, T., Saito, T., Tojo, S., Furuya, M., Hanaue, H., Ogoshi, K., Murohisa, B., Uchimura, M., Ishigaki, J., Waki, S., Nakafuji, H., Iida, F., Aratake, K., Nakano, T., Ono, N., Hara, I., Sassa, T., Takahashi, T., Inoue, J., Maruyama, Y., Mori, Y., Kawamura, T., Imai, F., Yorita, S., Saegusa, M., Ishihara, F., Asukata, I., Matsuda, M., Wakabayashi, K., Mitani, S., Sugahara, K., Ishikawa, K., Nakayoshi, A., Nakamoto, M., Kono, A., Oda, T., Sato, Y., Takahashi, T., Nagao, F., Nagano, M., Furusawa, T., Nakama, T., Itoh, H., Nishimura, M., Tsutsumi, K., Saito, H., Yoshida, K., Ito, H., Yoshimura, M., Yoshioka, K., Shimizu, T., Kuroda, C., Uchida, H., Ishida, O., Inoue, T., Hasegawa, S., Mitsusada, K., Kajiyama, Y., Matsuzawa, Y., Yokota, K., Hayashida, Y., Ikegudhi, S., Shida, S., Tsurumi, K., Ito, K., Kamiya, K., Takada, H., Ueno, S., Onda, M., Kojima, G., Shoji, E., Miyaji, M., Goto, K., Nitta, Y., Yazaki, Y., Ito, M., Kozuka, M., Tanabe, A., Murate, H., Takeuchi, T., Koshikawa, M., Kato, N., Maeda, K., Hayashi, K., Tsuru, T., Ooyama, I., Kukimoto, H., Nakashima, Y., Katsuki, T., Ueda, N., Kanno, T., Noda, A., Toda, Y., Hayakawa, T., Nakajima, S., Morishita, R., Furukawa, K., Ikeda, F., Fujii, M., Yamamoto, T., Wakisaka, G., Matasumoto, Y., Ono, H., Hirose, S., Kobayashi, K., Sawabu, N., Takeuchi, J., Kajikawa, K., Takada, A., Hirai, Y., Ohki, I., Sato, K., Tasaka, S., Sato, A., Aono, G., Kidokoro, T., Takezoe, K., Jojima, Y., Ohara, T., Soma, S., Ukawa, S., Yamaguchi, S., Shirahama, T., Sugiyama, K., Koyama, H., Haga, M., Arikawa, H., Toyokawa, H., Sato, R., Ueno, Y., Karasawa, Y., Onuma, H., Suzuki, H., Murakami, T., Yasui, A., Ichinose, Y., Hirase, Y., Okazaki, T., Takai, T., Watanabe, K., Kato, M., Yamada, M., Tsuji, T., Kunito, Y., Kobayashi, S., Udo, K., Iriyama, K., Sugiura, Y., Takahashi, Y., Kawamura, O., Ando, S., Hayashi, K., Tsuji, K., Yukawa, Y., Saito, N., Miyazawa, M., Imai, K., Tabayashi, T., Ito, H., Umehara, S., Watanabe, Y., Murai, S., Nukaga, A., Ishimatsu, N., Sotoyama, S., Abe, M., Hirai, K., Yoshida, K., Aoki, T., Nagao, F., Aoki, Y., Taniguchi, K., Wada, N., Tabuse, K., Yanagi, I., Tsuhada, K., Katsumi, M., Nakamura, K., Takemoto, K., Yamaura, Y., Karibe, N., Yamada, G., Ichikawa, H., Ogiwara, M., Matsushita, M., Kobayashi, I., Kusano, M., Yasuna, O., Hayashi, S., Yoshizumi, M., Kojima, Y., Matsubayashi, K., Yamamoto, T., Nishimura, R., Koga, M., Tachibana, M., Kurata, M., Suto, H., Ichinose, I., Ishizuka, K., Shimoda, M., Onai, M., Akiyama, T., Sekiguchi, T., Kobayashi, S., Matsuyoshi, M., Yonezawa, N., Kasamatsu, M., Yokota, Y., Toyoda, T., Uchimoto, I., Kanamoto, M., Fukai, Y., Sugawara, K., Katoh, M., Takebayashi, M., Mitsuyoshi, Y., Shimamoto, K., Nakamura, I., Tamura, M., Nishio, M., Mukaide, Y., Kuzumoto, Y., Ota, K., Yoshida, T., Sakamoto, A., Akiyama, T., Kaneko, S., Yanagida, M., Kishimoto, S., Miyaji, K., Shiraki, Y., Inoue, K., Tamada, T., Usui, T., Ohtsuka, K., Yamada, S., Fujishima, S., Tamiya, A., Saji, K., Ueda, A., Shiraki, Y., Inoue, K., Tamada, T., Usui, T., Ohtsuka, K., Yamada, S., Fujishima, S., Tamiya, A., Saji, K., Ueda, A., Yasutake, K., Irie, K., Ijiri, Y., Sato, H., Nishijima, H., Ogino, K., Okuno, T., Date, H., Yao, T., Koga, Y., Tomioka, T., Fuyuno, S., Okabe, H., Mitsui, H., Tamechika, Y., Masuda, N., Fujiwara, T., Sakimura, M., Okada, Y., Takamura, Y., Kono, T., Kurihara, M., Sumida, M., Izumi, T., Haraikawa, M., Hayakawa, H., Shirakabe, H., Yasui, A., Ushio, K., Okamoto, M., Noguchi, M., Kinoshita, A., Yamada, T., Ichikawa, H., Shimotori, K., Kudo, T., Mukaida, I., Ishikawa, H., Sato, K., Shirane, T., Kano, A., Suzuki, T., Tanaka, M., Iwanaga, T., Taniguchi, H., Inawashiro, M., Endo, N., Kawamura, T., Suzuki, Sh., Suzuki, H., Maki, T., Hayakawa, K., Ikezawa, H., Jao, C. C., Yamada, K., Nakamura, M., Tanaka, M., Maruyama, M., Nagasako, K., Oi, I., Kozu, T., Yamashita, K., Yokoyama, I., Endo, M., Takemoto, T., Nakayama, K., Hayakawa, R., Ishiguro, M., Nakano, H., Nakazawa, S., Tsuboi, Y., Yamase, H., Yamashita, T., Fujita, T., Ishikawa, Y., Ito, N., Mitsuno, T., Kanazawa, K., Yamashiro, M., Kubo, T., Iizuka, H., Watanabe, T., Sanada, M., Satoh, H., Shimada, H., Kusama, S., Ishikawa, K., Ikeda, K., Naramoto, J., Koga, M., Okazaki, Y., Nakamura, K., Kawamura, S., Fujimoto, S., Urayama, S., Matsuura, H., Sekitani, T., Sasayama, T., Nakagawa, K., Toyama, K., Nakagawa, S., Takada, T., Kusaka, K., Takaba, S., Satomura, A., Suzuki, T., Kawakami, Y., Watanabe, Y., Suzuki, H., Koike, T., Joh, S., Hara, T., Tamura, K., Kobayagawa, K., Hashimoto, T., Uemura, F., Fukui, O., Takahashi, M., Takasato, Y., Shirakawa, K., Hisamatsu, M., Saito, T., Ashizawa, S., Sakurane, Y., Miyamura, K., Sasaki, H., Katsumi, M., Ura, S., Emoto, M., Tatsumi, Y., Totsuka, Y., Chiba, N., Ozeki, M., Nakazawa, M., Takamura, S., Iida, F., Sawano, Y., Sugita, T., Funabiki, T., Watanabe, S., Moriya, T., Tomita, N., Nishida, K., Todo, A., Miyake, T., Suzaki, Y., Yamamoto, Y., Ariyoshi, J., Hajiro, K., Oishi, M., Yanagihara, K., Nakamura, A., Kuramata, H., Soeda, S., Kondo, N., Akashi, M., Hemmi, T., Kadono, H., Ito, T., Tsuchiya, R., Ikeda, Y., Futatsuki, K., Nomoto, S., Kino, I., Arai, M., Shimazu, H., Kobori, O., Ishikawa, K., Hiroshima, Y., Matsusaka, Y., Katase, K., Sakuma, Y., Murata, N., Komura, K., Ando, H., Ohara, K., Hayashi, A., Suzuki, M., Watanuki, T., Asano, T., Koide, N., Shiobara, M., Matsuo, N., Imai, K., Segawa, K., Nakazawa, S., Okabe, N., Kawai, K., Matsumoto, K., Shimada, H., Machida, K., Koizumi, Y., Hoshi, Y., Oi, M., Watanuki, T., Seki, H., Matsumura, M., Kimura, M., Yoshimura, M., Ishikawa, I., Kishi, S., Kondo, Y., Uchida, Y., Harada, H., Mandai, M., Kikuchi, T., Mishima, K., Yamagata, Y., Suyama, T., Kawagoe, K., Inagawa, T., Kishimoto, S., Sugiya, T., Kai, T., Miyoshi, A., Fukumoto, S., Watanabe, K., Kojo, H., Turuhara, I., Miyoshi, Y., Okamoto, K., Inata, H., Okamoto, H., Sakurai, S., Sugiyama, M., Sasaki, H., Miura, K., Kurihara, T., Sakumoto, K., Okita, E., Tanaka, H., Ishihara, K., Okawa, M., Okumura, Y., Watanabe, Y., Nishizaki, N., Murakami, T., Saito, K., Aoyagi, K., Hamaguchi, E., Kitamura, T., Matsuo, Y., Seki, A., Mori, H., Ishikawa, T., Nakajima, T., Shimomura, T., Sengoku, K., Aoyagi, K., Hamaguchi, E., Uchiya, Y., Yabana, T., Konta, M., Kamijo, K., Yachi, A., Okuse, S., Ohara, H., Sato, K., Wada, T., Kurata, M., Furuta, K., Nishii, M., Yamawaki, T., Nishii, K., Umeda, K., Yoshida, H., Ito, H., Okabayashi, T., Kato, Y., Yatsuji, Y., Suzuki, Y., Nomura, K., Matsumoto, K., Kamisaka, K., Motoki, T., Kamii, K., Kameda, H., Imamura, H., Uchiya, T., Ishizawa, M., Nishizaki, H., Murakami, T., Orimo, H., Yoshida, A., Yoshida, A., Orimo, H., Fujita, T., Oda, T., Itoh, Z., Honda, R., Takeuchi, S., Fukushima, T., Suda, T., Shinonaga, M., Ishiguro, N., Fujisawa, S., Nishiyama, K., and Ohkubo, T.

Published
1973
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42. External Genitalia Development

Author

Suzuki, K., Nishida, H., Ohta, S., Satoh, Y., Xu, Y., Zhang, Y., Wada, Y., Ogino, Y., Naomi Nakagata, Ohba, T., and Yamada, G.

Published
2005

43. 5α-Dihydrotestosterone negatively regulates cell proliferation of the periurethral ventral mesenchyme during urethral tube formation in the murine male genital tubercle.

Author

Suzuki, H., Matsushita, S., Suzuki, K., and Yamada, G.

Subjects
STANOLONE, CELL proliferation, FINASTERIDE, HYPOSPADIAS, URETHRA
Abstract

Androgen is an essential factor involved in masculinization of external genitalia. Failure of the exposure to 5α-dihydrotestosterone ( DHT) causes a hypoplastic penile size and urethral abnormality. The main pathology of hypospadias is defective urethral closure on the ventral side of the penis. Hormone-dependent genes are suggested as the causative factors. However, the detailed mechanisms of DHT functions on urethral tube formation remain unknown. Androgen is both a positive and negative regulator of cell proliferation. The roles of locally converted DHT in cell proliferation at the periurethral mesenchyme have not been elucidated. We revealed the expression pattern of 5α-reductase type 2 mRNA ( Srd5a2) and local DHT distribution by direct measurement in this study. We also analyzed periurethral mesenchymal cell proliferation status using systematic three-dimensional (3D) reconstruction analyses. A prominent Srd5a2 expression and localized DHT distribution on the ventral side of the genital tubercle were detected. Cell proliferation was reduced in this mesenchymal region during urethral formation. The current results suggest the presence of the possible negative regulation of cell proliferation by DHT. Moreover, cell proliferation related to urethral tube formation was revealed to be DHT dose dependent. These data are expected to contribute to the understanding of the mode of regulation of cell proliferation related to urethral tube formation by DHT. These findings may also offer insight into the understanding of human hypospadias and related hormone-dependent factors. [ABSTRACT FROM AUTHOR]

Published
2017
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47. Disruption of the temporally regulated cloaca endodermal β-catenin signaling causes anorectal malformations

Author

Miyagawa, S, primary, Harada, M, additional, Matsumaru, D, additional, Tanaka, K, additional, Inoue, C, additional, Nakahara, C, additional, Haraguchi, R, additional, Matsushita, S, additional, Suzuki, K, additional, Nakagata, N, additional, Ng, R C-L, additional, Akita, K, additional, Lui, V C-H, additional, and Yamada, G, additional

Published
2014
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48. Genetic analysis of Hedgehog signaling in ventral body wall development and the onset of omphalocele formation

Author

Matsumaru, D., Haraguchi, R., Miyagawa, S., Motoyama, J., Nakagata, N., Meijlink, F., Yamada, G., Matsumaru, D., Haraguchi, R., Miyagawa, S., Motoyama, J., Nakagata, N., Meijlink, F., and Yamada, G.

Abstract

BACKGROUND: An omphalocele is one of the major ventral body wall malformations and is characterized by abnormally herniated viscera from the body trunk. It has been frequently found to be associated with other structural malformations, such as genitourinary malformations and digit abnormalities. In spite of its clinical importance, the etiology of omphalocele formation is still controversial. Hedgehog (Hh) signaling is one of the essential growth factor signaling pathways involved in the formation of the limbs and urogenital system. However, the relationship between Hh signaling and ventral body wall formation remains unclear. METHODOLOGY/PRINCIPAL FINDINGS: To gain insight into the roles of Hh signaling in ventral body wall formation and its malformation, we analyzed phenotypes of mouse mutants of Sonic hedgehog (Shh), GLI-Kruppel family member 3 (Gli3) and Aristaless-like homeobox 4 (Alx4). Introduction of additional Alx4(Lst) mutations into the Gli3(Xt/Xt) background resulted in various degrees of severe omphalocele and pubic diastasis. In addition, loss of a single Shh allele restored the omphalocele and pubic symphysis of Gli3(Xt/+); Alx4(Lst/Lst) embryos. We also observed ectopic Hh activity in the ventral body wall region of Gli3(Xt/Xt) embryos. Moreover, tamoxifen-inducible gain-of-function experiments to induce ectopic Hh signaling revealed Hh signal dose-dependent formation of omphaloceles. CONCLUSIONS/SIGNIFICANCE: We suggest that one of the possible causes of omphalocele and pubic diastasis is ectopically-induced Hh signaling. To our knowledge, this would be the first demonstration of the involvement of Hh signaling in ventral body wall malformation and the genetic rescue of omphalocele phenotypes. [KEYWORDS: Animals, Dose-Response Relationship, Drug, Embryo, Mammalian, Embryonic Development, Gene Therapy/methods, Hedgehog Proteins/genetics/pharmacology/physiology, Hernia, Umbilical/ etiology/pathology/ therapy, Kruppel-Like Transcription Factors/genetic, BACKGROUND: An omphalocele is one of the major ventral body wall malformations and is characterized by abnormally herniated viscera from the body trunk. It has been frequently found to be associated with other structural malformations, such as genitourinary malformations and digit abnormalities. In spite of its clinical importance, the etiology of omphalocele formation is still controversial. Hedgehog (Hh) signaling is one of the essential growth factor signaling pathways involved in the formation of the limbs and urogenital system. However, the relationship between Hh signaling and ventral body wall formation remains unclear. METHODOLOGY/PRINCIPAL FINDINGS: To gain insight into the roles of Hh signaling in ventral body wall formation and its malformation, we analyzed phenotypes of mouse mutants of Sonic hedgehog (Shh), GLI-Kruppel family member 3 (Gli3) and Aristaless-like homeobox 4 (Alx4). Introduction of additional Alx4(Lst) mutations into the Gli3(Xt/Xt) background resulted in various degrees of severe omphalocele and pubic diastasis. In addition, loss of a single Shh allele restored the omphalocele and pubic symphysis of Gli3(Xt/+); Alx4(Lst/Lst) embryos. We also observed ectopic Hh activity in the ventral body wall region of Gli3(Xt/Xt) embryos. Moreover, tamoxifen-inducible gain-of-function experiments to induce ectopic Hh signaling revealed Hh signal dose-dependent formation of omphaloceles. CONCLUSIONS/SIGNIFICANCE: We suggest that one of the possible causes of omphalocele and pubic diastasis is ectopically-induced Hh signaling. To our knowledge, this would be the first demonstration of the involvement of Hh signaling in ventral body wall malformation and the genetic rescue of omphalocele phenotypes. [KEYWORDS: Animals, Dose-Response Relationship, Drug, Embryo, Mammalian, Embryonic Development, Gene Therapy/methods, Hedgehog Proteins/genetics/pharmacology/physiology, Hernia, Umbilical/ etiology/pathology/ therapy, Kruppel-Like Transcription Factors/genetic

Published
2011

49. Aberrant regulation of bone trace elements in motheaten and osteopetrosis mutant mice

Author

Yamada G, Nakamura S, Haraguchi R, Sakai M, Suzuki K, Kenji Miyado, Hasuwa H, Ogino Y, Minami T, Tohno Y, Blum M, and Ld, Shultz

Subjects
Mice, Knockout, Mice, Inbred C3H, Macrophage Colony-Stimulating Factor, Protein Tyrosine Phosphatase, Non-Receptor Type 6, Immunologic Deficiency Syndromes, Intracellular Signaling Peptides and Proteins, Osteoclasts, Receptor, Macrophage Colony-Stimulating Factor, Bone and Bones, Mice, Mutant Strains, Trace Elements, Mice, Inbred C57BL, Mice, Zinc, Osteopetrosis, Animals, Protein Tyrosine Phosphatases
Abstract

Increasing numbers of genetic diseases involving bone development and models for these diseases have been identified recently. Analysis of these bone diseases have revealed that regulated action of multiple growth factors and subsequent signal transduction are essential for normal bone formation. In this paper, two murine mutant mice viable motheaten and osteopetrosis are analyzed. Mice with the recessive 'viable motheaten' mutation express a severe immunodeficiency syndrome and bone defects. Mutations at the motheaten locus were shown to be the result of aberrant splicing of the gene encoding hematopoietic cell phosphatase (Hcph). Mice homozygous for the osteopetrosis mutation develop congenital osteopetrosis due to a severe deficiency of osteoclasts. It has been recognized that bone trace element composition analysis helps to define bone-related physiological conditions. We have analyzed bone trace element composition in viable motheaten and osteopetrosis mutant animal models in this study. In order to gain insights into the effects of particular genetic defects on bone trace element composition, inductively coupled plasma atomic emissions spectrometry (ICP-AES) analysis was performed. Marked changes in bone trace element levels were found in limb bones of viable motheaten and osteopetrosis mutant mice. An assessment of these trace element spectrum in the two mutant models with respect to each genetic defects are discussed in this paper.

Published
1998

50. The prechordal midline of the chondrocranium is defective in Goosecoid-1 mouse mutants

Author

Belo, J. A., Luc Leyns, Yamada, G., Robertis, E. M., Cell Genetics, and Vrije Universiteit Brussel

Subjects
endocrine system, animal structures, fungi, embryonic structures
Abstract

Gsc-1 expression marks cells with Spemann organizer, or axis-inducing, activity in the vertebrate gastrula. Gsc-1 knockouts, however, did not display phenotypes related to the early phase of expression. In this paper, additional phenotypes for the Gsc-1 mouse mutant are presented. Examination of the base of the cranium in the dorsal view revealed fusions and deletions in the midline of the prechordal chondrocranium. These defects were correlated with the sites of expression of Gsc-1 in the prechordal plate/foregut endoderm in the day 7.5/8.5 embryo. Gsc-1 expression in proximal limb buds was correlated with malformations of the shoulder and hip articulations. In addition, ribs in the seventh cervical vertebra were observed with low penetrance. The role of Gsc-1 during gastrulation and axial development is discussed in relation to possible compensatory interactions with other genes such as HNF-3beta and the recently identified Gsc-2 and Gsc-3 genes.

Published
1998

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