The apoptotic cell death caused by such stress is of particular interest. Apoptosis during development is generally thought to be triggered by growth factors and other environmental cues, and the role of mechanical stress in this process has only recently been considered. Our results suggest that inhomogeneities in the mechanical properties of the confining tissue can guide morphological changes in tumor growth, independent of cell migration, by inducing apoptosis in regions of high compressive stress and allowing proliferation in regions of low stress. Furthermore, the compression-induced apoptosis occurs via the mitochondrial pathway, a regulatory control mechanism that cancer cells with elevated Bcl-2 activity might escape to produce more malignant tumors. Prenatal events can affect development of certain adult diseases, but the mechanisms are not clear. For example, maternal atopy/allergy can predispose offspring to the development of asthma, more so than paternal disease. Moreover, there is evidence in mice and humans that allergic sensitization may occur in the prenatal period. Our laboratory has developed a mouse model that recapitulates this ‘maternal effect’ Tubercidin. In this model, offspring of mother mice with ovalbumin -induced asthma develop an asthma-like phenotype following an ‘intentionally suboptimal’ asthma induction protocol, whereas offspring of non-asthmatic mother mice do not. Importantly, this maternal effect is allergen-independent, since offspring show increased susceptibility to other allergens besides OVA. This suggests a role for mediators with broad effects, e.g., cytokines, rather then specific antibodies. These data taken together with prenatal sensitization observations, imply that the in utero environment may be causing increased asthma risk in offspring. One possible mechanism by which maternal asthma could cause increased asthma susceptibility in the developing immune system is the transplacental passage of ‘proallergic’ cytokines. In addition to providing the fetus with oxygen and nutrients, the placenta synthesizes and secretes hormones, growth factors, and cytokines. Moreover, many maternally-derived molecules cross the placental via a variety of mechanisms. Based on findings in our mouse model of maternal transmission, we postulated that passage of pro-asthmatic maternal cytokines could mediate increased susceptibility of offspring to asthma. The aim of this study was to characterize a novel assay to assess for the transplacental passage of functional cytokines, and to use this technique to assess for passage of the pro-asthmatic/proinflammatory cytokines interleukin 4 and 13 previously implicated in maternal transmission of asthma risk. The mothers were injected with supraphysiologic doses of IL-4 or IL-13, and the nuclear extracts of the embryonic lungs were analyzed using Western Blot for presence of GJ103 sodium salt phosphorylated STAT-6. Both IL4 and IL13 act via binding to a receptor heterodimer complex that includes an IL4Ra subunit. Following binding, Janus family of protein kinases that are constitutively associated with IL-4Ra are activated. Because the mothers lacked IL4Ra, and are unable to phosporylate STAT-6 in response to either IL-4 or 13, then any phosphorylation of STAT-6 in the heterozygote embryos would be a result of transplacental passage of functional cytokines. The maternal-fetal interface is an immunologically active site rich in cytokines. However, few studies have looked specifically at the transplacental passage of cytokines.