Introduction
The use of animal models in research is most often justified based on the idea that humans and animals are related to a certain degree and hence data obtained from animal experimentation can be extrapolated and applied to humans. Evidently, this does not apply to all species even those who share anatomical similarities or are closely related from an evolutionary standpoint as physiological responses may vary. However, animal models are required simply because experimentation on humans is tightly regulated while being surrounded by controversial ethical issues. As such, animal testing can be inaccurate but it possesses predictive value and the inaccuracy in relation to humans does not necessarily invalidate animal models but rather …show more content…
Prenatal gene-environment is an important determinant of postnatal phenotype as it can predispose the fetus to development of the metabolic syndrome (Gluckman & Hanson 2004). The growth and maturation of each system and organ consist of a critical period when it is sensitive to the environment. As such, the production of phenotypes in a prenatal environment, termed predicted adaptive responses (PARs) has a significant role in preparing the fetus in anticipation of the expected postnatal environment. However, a possible risk related to inappropriate PARs arises when the pre- and postnatal environments are inconsistent and thus these adaptations may later prove to be disadvantageous (Vickers & Sloboda 2012). In the event that the baby is exposed to a substantially different postnatal environment, it adopts a compensatory growth mechanism for survival. In animals it has been shown that this compensatory mechanism comes with physiological and metabolic costs (Barker & Thornburg 2013) and may contribute to the current epidemic of type 2 diabetes and …show more content…
2008). Spontaneous labour and the premature rupture of membrane (PROM) are promoted by these cytokines, which in turn stimulate the production of prostaglandins, matrix metalloproteases (MMPs) and other inflammatory mediators (Wadhwa et al. 2001). Uterine contractility is stimulated as a result of prostaglandin synthesis while the release of MMPs consequently breaks down the extracellular matrix in fetal membranes leading to preterm PROM (Goldenberg et al.
The use of animal models in research is most often justified based on the idea that humans and animals are related to a certain degree and hence data obtained from animal experimentation can be extrapolated and applied to humans. Evidently, this does not apply to all species even those who share anatomical similarities or are closely related from an evolutionary standpoint as physiological responses may vary. However, animal models are required simply because experimentation on humans is tightly regulated while being surrounded by controversial ethical issues. As such, animal testing can be inaccurate but it possesses predictive value and the inaccuracy in relation to humans does not necessarily invalidate animal models but rather …show more content…
Prenatal gene-environment is an important determinant of postnatal phenotype as it can predispose the fetus to development of the metabolic syndrome (Gluckman & Hanson 2004). The growth and maturation of each system and organ consist of a critical period when it is sensitive to the environment. As such, the production of phenotypes in a prenatal environment, termed predicted adaptive responses (PARs) has a significant role in preparing the fetus in anticipation of the expected postnatal environment. However, a possible risk related to inappropriate PARs arises when the pre- and postnatal environments are inconsistent and thus these adaptations may later prove to be disadvantageous (Vickers & Sloboda 2012). In the event that the baby is exposed to a substantially different postnatal environment, it adopts a compensatory growth mechanism for survival. In animals it has been shown that this compensatory mechanism comes with physiological and metabolic costs (Barker & Thornburg 2013) and may contribute to the current epidemic of type 2 diabetes and …show more content…
2008). Spontaneous labour and the premature rupture of membrane (PROM) are promoted by these cytokines, which in turn stimulate the production of prostaglandins, matrix metalloproteases (MMPs) and other inflammatory mediators (Wadhwa et al. 2001). Uterine contractility is stimulated as a result of prostaglandin synthesis while the release of MMPs consequently breaks down the extracellular matrix in fetal membranes leading to preterm PROM (Goldenberg et al.