This paper reviews several converging lines of research that suggest that prenatal exposure to environmental stress may increase risk for Autistic Disorder (AD). We first discuss studies finding that prenatal exposure to stressful life events is associated with significantly increased risk of AD, as well as other disorders, such as schizophrenia and depression. We then review evidence from animal and human studies that prenatal stress can produce both (a) abnormal postnatal behaviors that resemble the defining symptoms of AD, and (b) other abnormalities that have elevated rates in AD, such as learning deficits, seizure disorders, perinatal complications, immunologic and neuroinflammatory anomalies, and low postnatal tolerance for stress. We explain why an etiologic role for prenatal stress is compatible with genetic factors in AD, and describe how stress can disrupt fetal brain development. Finally, we discuss implications for understanding underlying processes in AD, including potential gene-environment interactions, and developing new therapies and early prevention programs.

Hurricanes and tropical storms served as natural experiments for investigating whether autism is associated with exposure to stressful events during sensitive periods of gestation. Weather service data identified severe storms in Louisiana from 1980 to 1995 and parishes hit by storm centers during this period. Autism prevalences in different cohorts were calculated using anonymous data on birth dates and parishes of children diagnosed with autism in the state mental health system, together with corresponding census data on all live births in Louisiana. Prevalence increased in dose-response fashion with severity of prenatal storm exposure, especially for cohorts exposed near the middle or end of gestation (p < 0.001). Results complement other evidence that factors disrupting development during sensitive gestational periods may contribute to autism.

The study findings highlight the need to implement a comprehensive approach to increasing Australian nursing students' pressure injury prevention and management knowledge, as well as ensuring that these students have adequate experiences in clinical units, with a high focus on pressure injury prevention to raise their personal capability.

Previous surveys found a large (>10-fold) variation in schizophrenia prevalence at different geographic sites and a tendency for prevalence to increase with latitude. We conducted meta-analyses of prevalence studies to investigate whether these findings pointed to underlying etiologic factors in schizophrenia or were the result of methodological artifacts or the confounding of sites' latitude with level of healthcare at those sites. We found that these patterns were still present after controlling for an index of healthcare--infant mortality--and focusing on 49 studies that used similar diagnostic and ascertainment methods. The tendencies for schizophrenia prevalence to increase with both latitude and colder climate were still large and significant and present on several continents. The increase in prevalence with latitude was greater for groups with low fish consumption, darker skin, and higher infant mortality--consistent with a role of prenatal vitamin D deficiency in schizophrenia. Previous research indicates that poor prenatal healthcare and nutrition increase risk for schizophrenia within the same region. These adverse conditions are more prevalent in developing countries concentrated near the equator, but schizophrenia prevalence is lowest at sites near the equator. This suggests that schizophrenia-producing environmental factors associated with higher latitude may be so powerful they overwhelm protective effects of better healthcare in industrialized countries. The observed patterns of correlations of risk factors with prevalence are consistent with an etiologic role for prenatal vitamin D deficiency and exposure to certain infectious diseases. Research to elucidate environmental factors that underlie variations in schizophrenia prevalence deserves high priority.

This article presents two studies investigating how computer interface affordances influence basic cognition, including ideational fluency, problem solving, and inferential reasoning. In one study comparing interfaces with different input capabilities, students expressed 56% more nonlinguistic representations (diagrams, symbols, numbers) when using pen interfaces. A linear regression confirmed that nonlinguistic communication directly mediated a substantial increase (38.5%) in students' ability to produce appropriate science ideas. In contrast, students expressed 41% more linguistic content when using a keyboard-based interface, which mediated a drop in science ideation. A follow-up study pursued the question of how interfaces that prime nonlinguistic communication so effectively facilitate cognition. This study examined the relation between students' expression of nonlinguistic representations and their inference accuracy when using analogous digital and non-digital pen tools. Perhaps surprisingly, the digital pen interface stimulated construction of more diagrams, more correct Venn diagrams, and more accurate domain inferences. Students' construction of multiple diagrams to represent a problem also directly suppressed overgeneralization errors, which were the most common inference failure. These research results reveal that computer interfaces have communications affordances which elicit communication patterns that can substantially stimulate or impede basic cognition. Implications are discussed for designing new digital tools for thinking, with an emphasis on nonlinguistic and especially spatial representations that are most poorly supported by current keyboard-based interfaces.