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Kevin M Sargent, Renee M McFee, Renata Spuri Gomes and Andrea S Cupp

's expression as well as VEGFA upregulating upstream factors in the arachidonic pathway to further enhance COX2 activity. COX1 is thought to be constitutively expressed while most of the effects of hypoxia and VEGFA may be through stimulation of the inducible

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Harman S Mattu and Harpal S Randeva

. Leptin delays mitochondrial permeability transition pore (MPTP) opening (possibly determining protection against I/R injury) ( Halestrap et al . 2004 ). Leptin also protects cardiomyocytes from hypoxia-induced damage ( Erkasap et al . 2006 ). JAK

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Odelia Katz, Matthew Stuible, Nathalia Golishevski, Lilach Lifshitz, Michel L Tremblay, Max Gassmann, Moshe Mittelman and Drorit Neumann

Introduction The hematopoietic growth factor erythropoietin (EPO) is produced in the kidney in response to hypoxia, and stimulates erythropoiesis in the bone marrow ( Krantz 1991 , Spivak et al . 1991 ). Recombinant human EPO (rHuEPO) is an

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Kenichiro Watanabe, Takahiro Nemoto, Shigeo Akira, Toshiyuki Takeshita and Tamotsu Shibasaki

, adrenal, uterus, ovary, and testis ( Hsu & Hsueh 2001 , Yamauchi et al . 2005 , Lee et al . 2011 ). It has been reported that expression of Ucn2 mRNA in various tissues is controlled by stress, inflammation, and hypoxia ( Tanaka et al . 2003 , Tao

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Motoi Sohmiya and Yuzuru Kato

with a molecular mass of 34 000 Da. EPO secretion was strongly stimulated by hypoxia ( Goldberg et al. 1989 ). EPO secretion is regulated endocrinologically. Thyroid hormones and adrenocortical hormone enhance EPO secretion ( Peschle et al. 1978

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Elena Maneschi, Annamaria Morelli, Sandra Filippi, Ilaria Cellai, Paolo Comeglio, Benedetta Mazzanti, Tommaso Mello, Alessandra Calcagno, Erica Sarchielli, Linda Vignozzi, Farid Saad, Roberto Vettor, Gabriella B Vannelli and Mario Maggi

. Negative staining controls were used in order to evaluate and subtract background. The diameter of adipocytes was measured using the Nikon Microphot-FXA microscope, considering the adipocytes more regularly spherical and using the program ImageJ. Hypoxia

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Hélène Buteau-Lozano, Guillaume Velasco, Monique Cristofari, Patrick Balaguer and Martine Perrot-Applanat

factors such SP1/3 sites ( Stoner et al . 2004 ) and the hypoxia-responsive element ( Kazi et al . 2005 ), or through activation of kinase cascade pathways ( Yen et al . 2005 ), depending on the nature of cells and the microenvironment including

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A M Carter, M J Kingston, K K Han, D M Mazzuca, K Nygard and V K M Han

action, whereas levels of the nonphosphorylated isoform of IGFBP-1 are similar in small and average for gestational age infants ( Iwashita et al. 1998 ). Circulating IGFBP-1 levels also rise in response to fetal hypoxia, and the Igfbp-1 gene has a

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P D Taylor, S G Hillier and H M Fraser

hypoxia, as seen in solid tumours ( Shweiki et al. 1992 ) and the endometrium ( Sharkey et al. 2000 ), occurring in granulosa cells in tertiary follicles deprived of gonadotrophic support requires to be investigated. However, this phenomenon does not

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Kok Lim Kua, Shanming Hu, Chunlin Wang, Jianrong Yao, Diana Dang, Alexander B Sawatzke, Jeffrey L Segar, Kai Wang and Andrew W Norris

hyperglycemic exposure, uteroplacental insufficiency and fetal hyperinsulinemia. Isolated uteroplacental insufficiency was examined because fetal hypoxia results from maternal diabetes, owing to a relative uteroplacental insufficiency via mechanisms that may