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K E Lines, R P Vas Nunes, M Frost, C J Yates, M Stevenson and R V Thakker

in vivo studies several MEN1 mouse models have been generated and investigations of these have yielded important insights in NET cell proliferation and responses to treatments. For example, conventional heterozygous germline Men1 -knockout mouse

Open access

Ashley N Reeb, Andrea Ziegler and Reigh-Yi Lin

.e.m . of two independent experiments with three parallels. Tumorigenesis analysis using an orthotopic mouse model of thyroid cancer in immunodeficient mice To explore whether the FTC cell lines could initiate tumors in vivo , we used an

Open access

Tatiana V Novoselova, Peter J King, Leonardo Guasti, Louise A Metherell, Adrian J L Clark and Li F Chan

histopathology showing the absence of fasciculata or reticularis cells together with disorganisation of zona granulosa (ZG) cells ( 16 ). Recent data in mouse models show that PKA signalling overactivation drives the differentiation of a reticularis-like zone in

Open access

Neil R Chappell, Beth Zhou, Amy K Schutt, William E Gibbons and Chellakkan S Blesson

, 14 , 15 , 16 , 17 ). This group comprises 20–30% of the PCOS population and provides the opportunity to look at PCOS independent of obesity. Mouse models have long served as a useful platform to study PCOS, and several models have been described

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Yali Cheng, Qiaoying Lv, Bingying Xie, Bingyi Yang, Weiwei Shan, Chengcheng Ning, Bing Li, Liying Xie, Chao Gu, Xuezhen Luo, Xiaojun Chen and Qin Zhu

estrogen sensitivity are critical to endometrial tumorigenesis. To investigate the interaction between insulin resistance and estrogen in endometrial carcinogenesis, we established an ovariectomized C57BL/6 mouse model treated with subcutaneous

Open access

Emmanuelle Noirrit, Mélissa Buscato, Marion Dupuis, Bernard Payrastre, Coralie Fontaine, Jean-François Arnal and Marie-Cécile Valera

indicate that, after a chronic CE + BZA treatment, mouse models are protected from in vivo induced thrombosis without significant functional alterations to coagulation factor levels. Concerning the question of the thrombotic risk of TSEC, only

Open access

Yusaku Mori, Hiroyuki Shimizu, Hideki Kushima, Tomomi Saito, Munenori Hiromura, Michishige Terasaki, Masakazu Koshibu, Hirokazu Ohtaki and Tsutomu Hirano

the vasoprotective and vasopressor effects of nesfatin-1 at different doses in mouse models of peripheral arterial remodeling. Additionally, we sought to clarify the underlying mechanisms in cultured human vascular endothelial cells (VECs) and vascular

Open access

Sylvia Thiele, Anke Hannemann, Maria Winzer, Ulrike Baschant, Heike Weidner, Matthias Nauck, Rajesh V Thakker, Martin Bornhäuser, Lorenz C Hofbauer and Martina Rauner

treatment period, mice were killed to examine the effects on the skeleton. In addition, a mouse model for Cushing’s syndrome due to an N-ethyl-N-nitrosourea (ENU) induced mutation at −120 bp of the promoter region of the corticotropin releasing hormone

Open access

Sheila Leone, Lucia Recinella, Annalisa Chiavaroli, Claudio Ferrante, Giustino Orlando, Michele Vacca, Roberto Salvatori and Luigi Brunetti

beneficial effects on longevity, with anti-aging and life-extending actions ( 6 ). Several mouse models of GH deficiency or GH resistance, including Ames dwarf, GHRKO and GHRHKO (the strain we used in this work) mice have increased lifespan ( 7 , 8 , 29

Open access

Kate E Lines, Mahsa Javid, Anita A C Reed, Gerard V Walls, Mark Stevenson, Michelle Simon, Kreepa G Kooblall, Sian E Piret, Paul T Christie, Paul J Newey, Ann-Marie Mallon and Rajesh V Thakker

). In addition, studies of mutant mouse models for human disorders have also identified roles for genetic modifiers, in affecting the penetrance, dominance, expressivity and pleiotrophy of disease manifestations ( 12 , 13 ). For example, studies of