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Isabel García-Tornadú, Marcelo Rubinstein, Bruce D Gaylinn, David Hill, Edith Arany, Malcolm J Low, Graciela Díaz-Torga, and Damasia Becu-Villalobos

types of dwarf mouse, Snell ( dw , dw j , or Pit1; Eicher & Beamer 1980 ) and Ames ( df or Prop-1), with absent GH and prolactin (PRL) were used to elucidate physiological roles of GH and PRL long before the nature of the spontaneous mutations was

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Caroline Manhès, Christine Kayser, Philippe Bertheau, Bruce Kelder, John J Kopchick, Paul A Kelly, Philippe Touraine, and Vincent Goffin

exerts mitogenic activity on normal mouse mammary epithelial cells (MECs; reviewed in Das & Vonderhaar 1997 ). PRL also seems to be involved in proliferative activity in vivo , although it is more difficult to distinguish the role of PRL from the

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Sofianos Andrikopoulos, Christine M Massa, Kathryn Aston-Mourney, Alexandra Funkat, Barbara C Fam, Rebecca L Hull, Steven E Kahn, and Joseph Proietto

diabetes, it is has become increasingly popular to under- or over-express candidate genes by generating genetically-modified mouse models ( Valet et al. 2002 , Kahn 2003 b ). However, there are now a number of reports that demonstrate that the same

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M Yamaguchi, K Tasaka, K Ogura, M Sakata, J Mizuki, and A Miyake


The regulation of mouse placental lactogen (mPL)-I and mPL-II secretion by activin and inhibin and the expression of activin and inhibin subunit mRNAs in the mouse decidua were examined. Activin-A at a concentration of 10 nm/l significantly inhibited mPL-II secretion by placental cells from days 9 and 12 of pregnancy. However, activin-A did not affect mPL-I secretion by cells from days 7 and 9 of pregnancy nor mPL-II secretion by cells from day 7 of pregnancy. By contrast, 10 nm/l inhibin activated mPL-II secretion by cells from day 12 of pregnancy. These effects of activin and inhibin on mPL-II secretion were dose-dependent. Follistatin, which binds to activin and blocks its bioactivity, completely eliminated the inhibitory effect of activin on mPL-II secretion. Incubation of placental cells from day 12 of pregnancy with activin-A resulted in a significant reduction of the mPL-II mRNA level assessed by Northern blot analysis. Northern blot analysis using poly(A)+ RNA extracted from the decidua indicated that mouse decidua, as well as the placenta, express all activin and inhibin subunits and that their gene expressions increased during gestation. The expression of these mRNAs in the decidua was much higher than those in the placenta. These findings suggest that activin and inhibin regulate mPL-II secretion and suggest the presence of an autocrine or paracrine regulation of mPL-II secretion in mouse placenta by activin and inhibin after mid-pregnancy in vivo.

Journal of Endocrinology (1995) 146, 469–474

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Nabanita S Datta, Tareq A Samra, Chandrika D Mahalingam, Tanuka Datta, and Abdul B Abou-Samra

mice is possibly protective compared to male pd mice on a low calcium diet. In addition, distinct molecular regulation in primary osteoblasts was observed in pdPTH1R KI mice. Materials and Methods Mice We generated a pdPTH1R KI mouse model using

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Jodi F Evans, Shahidul Islam, Yoshihiro Urade, Naomi Eguchi, and Louis Ragolia

. The lipocalin-type prostaglandin D 2 synthase (L-PGDS) knockout (KO) mouse has been used to examine the role of L-PGDS in obesity and type 2 diabetes. This mouse model demonstrates glucose intolerance, accelerated insulin resistance, aggravated

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Vitaly Ablamunits, Simon Klebanov, Sharon Y Giese, and Kevan C Herold

can be avoided. We have reported that mouse WAT grafts transplanted into leptin-deficient mice may be monitored by reversal of the obese phenotype ( Klebanov et al . 2005 ) and that WAT allografts are acutely rejected unless the host is

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Mauricio da Silva Krause, Aline Bittencourt, Paulo Ivo Homem de Bittencourt Jr, Neville H McClenaghan, Peter R Flatt, Colin Murphy, and Philip Newsholme

of between 0.5 and 1.5 h. Absorbance at 450 nm was measured at 0.5, 1.0, and 1.5 h using a kinetic plate reader (Spectramax Plus; Molecular Devices, Sunnyvalle, CA, USA). Mouse islet isolation, culture, viability, and insulin secretion Pancreatic

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Yun Wang, Patsy M Nishina, and Jürgen K Naggert

mice heterozygous for IR and IRS1 null alleles ( Bruning et al . 1997 ). Hirosumi et al . (2002) proposed that activation of c-Jun N-terminal kinase (JNK) leads to a reduction in IRS1 levels and thus to insulin resistance in the Lep ob mouse and a

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J. Krug, A. J. K. Williams, P. E. Beales, I. Doniach, E. A. M. Gale, and P. Pozzilli


Autoimmune reactions to parathyroid cells have been observed in human autoimmune polyendocrinopathy, but such findings have not been described in animal models of polyendocrine autoimmunity. We report here three cases of lymphocytic infiltrations in 12 parathyroid glands identified in a total of 18 thyroid glands studied in the non-obese diabetic (NOD) mouse.

The majority of parathyroid-infiltrating lymphocytes possessed the helper/inducer phenotype as defined by the L3T4 monoclonal antibody. Parathyroiditis was accompanied by lymphocytic thyroiditis only on one occasion, whereas in other cases of thyroiditis, lymphocytic infiltration of the parathyroid was undetectable. We conclude that parathyroiditis in the NOD mouse is part of the wide spectrum of autoimmunity observed in this animal model of diabetes.

Journal of Endocrinology (1991) 131, 193–196