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Jay H Lo, Pinwen Peter Chiou, C M Lin, and Thomas T Chen

et al. 2002 ). CCAAT/enhancer-binding proteins (C/EBPs) are a family of leucine zipper transcription factors that consists of six members (α,β,γ,δ,ε,ζ), and have been isolated from several animal species since they were first identified

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Rahman M Hafizur, Randa Babiker, Sakina Yagi, Sidra Chishti, Nurul Kabir, and M Iqbal Choudhary

methanolic extract of G. alata root in vivo in diabetic rats. Streptozotocin (STZ)-induced diabetic rats were treated over a 14-day period, revealing efficiency of the treatment. G. alata extract was found to control blood glucose level, enhance insulin

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Swagat Ray, Michael J Fry, and Philippa D Darbre

( Lippman & Dickson 1990 , Herman & Katzenellenbogen 1994 , Chan et al . 2002 ) and T-47-D and ZR-75-1 cells ( Daly & Darbre 1990 a , b ). Increased levels of the insulin-like growth factor receptor type 1 (IGF1R) and enhanced sensitivity to IGFs in

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Patrick Müller, Kenneth W Merrell, Justin D Crofts, Caroline Rönnlund, Chin-Yo Lin, Jan-Åke Gustafsson, and Anders Ström

Introduction Hairy and enhancer of split homolog-1 (HES-1) is a basic-helix-loop-helix transcriptional repressor and an effector of the Notch signaling pathway. Studies of the HES-1 −/− mouse show that the factor plays an important role during

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Ivonne Gisèle Makom Ndifossap, Francesca Frigerio, Marina Casimir, Florence Ngueguim Tsofack, Etienne Dongo, Pierre Kamtchouing, Théophile Dimo, and Pierre Maechler

increased by 49% ( P <0.05) compared with control cells. These data show enhanced glucose metabolism following chronic treatment with SBE. Discussion SBE is widely used as traditional remedy against diabetes in Africa ( Dieye et al . 2008 ). However, very

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Yun-Ju Chen, Pei-Wen Hsiao, Ming-Ting Lee, J Ian Mason, Ferng-Chun Ke, and Jiuan-Jiuan Hwang

functions ( Ingman & Robertson 2002 ). TGFβ mainly acts as a positive regulator of granulosa cell differentiation as it enhances FSH-stimulated expression of LH receptor, inhibin, gap junction protein connexin 43, and steroidogenesis in rat and murine

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Thin Xuan Vo, Andrew Revesz, Gurjeev Sohi, Noelle Ma, and Daniel B Hardy

implicated in regulating genes involved in the metabolism and transport of cholesterol ( Lehmann et al . 1997 , Venkateswaran et al . 2000 ) and in enhancing the expression of lipogenic enzymes ( Repa et al . 2000 ). Recent studies have also demonstrated

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Gregorio Pérez-Palacios, René Santillán, Rocío García-Becerra, Elizabeth Borja-Cacho, Fernando Larrea, Pablo Damián-Matsumura, Leticia González, and Ana E Lemus

distinctive androgen-metabolic pathway in MCF-7 cells, characterised by overexpression and enhanced activities of the androgen-metabolising enzymes, resulting in a large formation of 3α,5α-diol and 3β,5α-diol. In subsequent studies, the oestrogen-like activity

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H Yamamoto, C Maake, and LJ Murphy

We have recently identified in serum an acid protease which is capable of generating des(1-3)IGF-I from intact IGF-I. Here we have utilized a synthetic substrate with the sequence, biotin-G-P-E-T-L-C-BSA which contains the N-terminal sequence of IGF-I, to investigate the levels of this protease activity in streptozotocin-diabetic rats. Protease activity, quantified in terms of the amount of the biotin label lost, was determined in serum and hepatic extracts from normal control rats, diabetic rats and insulin-treated diabetic rats. Both the serum protease activity and protease activity in hepatic extracts were significantly increased in diabetic rats compared with control rats (P<0.02 and P<0.005). Following acute administration of insulin, a rapid and marked reduction in serum protease activity was observed; with an approximately 50% reduction apparent at 30 min (P<0.001). Chronic insulin treatment of diabetic rats also significantly reduced the serum and hepatic protease activity to the levels seen in control rats. A positive correlation between protease activity and serum glucose level was observed (r=0.58, P<0.005). The abundance of Spi 2.1 mRNA, a serine protease inhibitor, capable of inhibiting the IGF-I protease activity in vitro, was significantly decreased in the liver of diabetic rats and insulin treatment of diabetic rats did not normalize Spi 2.1 mRNA levels. These data suggest that the conversion of IGF-I to the more active des(1-3)IGF-I variant may be enhanced in diabetic animals. Since serum IGF-I levels are reduced in diabetic rats, increased des(1-3)IGF-I-generating protease activity would enhance the functional activity of the circulating IGF-I.

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PB Colligan, HM Brown-Borg, J Duan, BH Ren, and J Ren

Growth hormone (GH) plays a key role in cardiac growth and function. However, excessive levels of GH often result in cardiac dysfunction, which is the major cause of death in acromegalic patients. Transgenic mice with GH over-expression serve as useful models for acromegaly and exhibit impaired cardiac functions using echocardiography, similar to those of human acromegaly. However, the mechanism underscoring the impaired ventricular function has not been well defined. This study was designed to evaluate the cardiac excitation-contraction coupling in GH over-expressing transgenic mice at the single ventricular myocyte level. Myocytes were isolated from GH and age-matched wild-type mouse hearts. Mechanical properties were evaluated using an IonOptix MyoCam system. The contractile properties analyzed included peak shortening (PS), time-to-peak shortening (TPS) and time-to-90% relengthening (TR(90)), and maximal velocities of shortening/relengthening (+/-dL/dt). Intracellular Ca2+ properties were evaluated by fura-2. GH transgenic mice exhibited significantly increased body weights and enlarged heart and myocyte size. Myocytes from GH transgenic mice displayed significantly enhanced PS and+/-dL/dt associated with similar TPS and TR(90) compared with the wild-type littermates. Myocytes from GH transgenic mice displayed a similar resting intracellular Ca2+ level and Ca2+ removal rate but exhibited an elevated peak intracellular Ca2+ level compared with the wild-type group. Myocytes from both groups were equally responsive to increases in extracellular Ca2+ concentration and stimulating frequency. These results suggest that GH over-expression is associated with enhanced contractile function in isolated myocytes and that the impaired cardiac function observed in whole hearts may not be due to defects at the myocyte level.