Estimation of Energy Consumption In Thermal Sterilization of Canned Liquid Foods in Still Retorts

Abstract

BACKGROUND: Maternal inflammation during pregnancy increases the risk for offspring psychiatric disorders and other adverse long-term health outcomes. The influence of inflammation on the developing fetal brain is hypothesized as one potential mechanism but has not been examined in humans. METHODS: Participants were adult women (N = 86) who were recruited during early pregnancy and whose offspring were born after 34 weeks' gestation. A biological indicator of maternal inflammation (interleukin-6) that has been shown to influence fetal brain development in animal models was quantified serially in early, mid-, and late pregnancy. Structural and functional brain magnetic resonance imaging scans were acquired in neonates shortly after birth. Infants' amygdalae were individually segmented for measures of volume and as seeds for resting state functional connectivity. At 24 months of age, children completed a snack delay task to assess impulse control. RESULTS: Higher average maternal interleukin-6 concentration during pregnancy was prospectively associated with larger right amygdala volume and stronger bilateral amygdala connectivity to brain regions involved in sensory processing and integration (fusiform, somatosensory cortex, and thalamus), salience detection (anterior insula), and learning and memory (caudate and parahippocampal gyrus). Larger newborn right amygdala volume and stronger left amygdala connectivity were in turn associated with lower impulse control at 24 months of age, and mediated the association between higher maternal interleukin-6 concentrations and lower impulse control. CONCLUSIONS: These findings provide new evidence in humans linking maternal inflammation during pregnancy with newborn brain and emerging behavioral phenotypes relevant for psychiatric disorders. A better understanding of intrauterine conditions that influence offspring disease susceptibility is warranted to inform targeted early intervention and prevention efforts. Maternal inflammation during pregnancy appears to increase the risk for neuropsychiatric disorders and adverse physical health outcomes in offspring (1–3). Strong epidemiological evidence identifies connections between common conditions associated with heightened inflammation during pregnancy, including infection (4–15), high maternal body mass index (16–18), maternal psychopathology (19), increased psychoso-cial stress (20), and elevated risk for offspring developing schizophrenia, autism, attention-deficit/hyperactivity disorder (21), and other neurological and psychiatric disorders (12). Thus, maternal inflammation during pregnancy is a strong candidate for mediating effects of diverse conditions on offspring neurodevelopment with implications for long-term health. However, to our knowledge, the influence of maternal inflammation during pregnancy on developing brain systems implicated in psychiatric disorders has not yet been examined in humans. Animal models support a key role for cytokines, inflamma-tory signaling proteins, as sensors, transducers, and effectors of environmental conditions on the developing embryonic and fetal brain. Maternal proinflammatory cytokine levels are elevated across a range of diverse high-risk conditions (sen-sors) (20,22,23), with accompanying increases in proin-flammatory cytokines in placental tissue, amniotic fluid, and the fetal brain (transducers) (24–27). Cytokines are also expressed in the fetal brain as part of typical neuro-developmental processes (28) and facilitate cellular survival, proliferation, and differentiation, axonal growth, and synapto-genesis (29–32). Elevated cytokine levels in the fetal brain, such as in response to maternal inflammation, trigger