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Perinatal Research Laboratories, Department of Pediatrics, Department of Animal Sciences, Department of Obstetrics and Gynecology, School Medicine and Public Health, University of Wisconsin–Madison, 7E Meriter Hospital/Park, 202 South Park Street, Madison, Wisconsin 53715, USA
Perinatal Research Laboratories, Department of Pediatrics, Department of Animal Sciences, Department of Obstetrics and Gynecology, School Medicine and Public Health, University of Wisconsin–Madison, 7E Meriter Hospital/Park, 202 South Park Street, Madison, Wisconsin 53715, USA
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Perinatal Research Laboratories, Department of Pediatrics, Department of Animal Sciences, Department of Obstetrics and Gynecology, School Medicine and Public Health, University of Wisconsin–Madison, 7E Meriter Hospital/Park, 202 South Park Street, Madison, Wisconsin 53715, USA
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Introduction Pregnancy is a time of dramatic vascular adaptation. Through initial angiogenesis and then sustained vasodilation, the pregnant uterus achieves the biggest drop in vascular resistance of any organ system. This in turn promotes a
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Severance Biomedical Research Institute, Department of Internal Medicine, Yonsei University College of Medicine, 50 Yonsei‐ro, Seodaemun‐gu, Seoul 120-752, Korea
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Introduction All known organisms have the capability to maintain homeostasis in response to environmental challenges. The ability to modify gene expression is a fundamental organismal mechanism of adaptation to environmental stimuli. In particular
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. Physiologic and anatomic adaptation of vasculature to pregnancy Implantation and early vascular remodeling Although it could certainly be argued that hormonal changes associated with the menstrual cycle prepare the uterus for any impending pregnancy
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confer to the latter, a relatively stronger adaptation profile that appears to be related to the ability to regulate NO production ( Rodríguez et al. 2015 ). Considering that thyroid status alterations are one of the major endocrine diseases in
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Introduction Maternal physiological adaptations are central to pregnancy success, balancing fetal and placental demands with the maintenance of maternal homeostasis. Among these maternal adaptations, enhanced activity of the hypothalamic
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). To understand the underlying mechanisms of stress adaptation and related disorders is of high clinical interest. Stress in humans mainly occurs as a consequence of personal interactions or due to a fear of social state loss, for example because of
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of β-cell adaptations in rodent pregnancy ( Rieck & Kaestner 2010 ). Similarly, in human pregnancy, levels of CRH in the peripheral circulation increase as gestation progresses ( Campbell et al . 1987 , Sasaki et al . 1987 ) and CRH
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adaptive growth induced by refeeding ( Shin et al . 2005 , Bahrami et al . 2010 ) or by resection in rodents ( Dahly et al . 2003 ). Exogenous GLP2 enhances intestinal adaptation after major small bowel resection in the rat ( Scott et al . 1998 ) and
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adaptation syndrome (GAS) ‘the symptoms of which are independent of the nature of the damaging agent or the pharmacological type of the drug employed and represent rather a response to damage as such.’ The main features of the syndrome were a fall of body
School of Animal and Comparative Biomedical Sciences, University of Arizona, Tucson, Arizona, USA
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these two distinct models of chronic hypercatecholaminemia, PI-IUGR and NE infusion indicate that sustained adrenergic stimulation produces a compensatory augmentation in β-cell responsiveness. Therefore, we propose that NE-induced adaptations in fetal