The current study was a case-control, focused on the presence of environmental exposures during pregnancy in mothers of children diagnosed with autism spectrum disorder (ASD) and children who were not. Exposures investigated included: acetaminophen/paracetamol use, air pollution, fever, smoking, parental age, maternal diabetes, prenatal vitamin use, workplace exposures, recreational drug use, seafood consumption, obesity, and maternal thyroid issues. Two-hundred and fifteen mothers of children (107 with ASD and 108 without ASD) aged 0-10 years participated in a telephone survey regarding prenatal exposures followed by a chart review. Data were analyzed with a series of univariate tests and a multivariate logistic regression. Univariate analyses showed correlation for the presence of siblings with ASD, presence of family members with ASD, maternal use of medications and maternal smoking during pregnancy; and child's gestational age at the start of prenatal vitamins with a diagnosis of ASD. Multivariate logistic regression analysis demonstrated an association with the use of medications (although specific medications could not be delineated due to small sample size), smoking, and gestational age at the start of prenatal vitamins. These preliminary results suggest that certain prenatal exposures (medication use, smoking, and gestational age at the start of prenatal vitamins) may be associated with a later diagnosis of ASD. Future research should be conducted with larger sample sizes and control for potentially confounding factors. Working towards an understanding of factors that come together to create or prevent a diagnosis of autism will be helpful for families, physicians, and allocating government resources.

Results suggest a way to operationalise mind wandering using the symptoms of ADHD.

While preliminary, findings suggest that paternal smoking at conception may be a risk factor for ADHD in the offspring.

No abstract

A 78-year-old woman presented twice with high sensitivity troponin I (hs-TnI) elevation. Two cardiac catheterizations showed nonocclusive coronary artery disease, and 2 cardiac magnetic resonance imaging scans were normal. With these investigations unable to explain the troponin I (hs-TnI) elevation, alternate troponin samples were sent to check for assay interference. Results from these troponin assays were low. With the patient having elevated rheumatoid factor as a potential contributor to assay interference, the lab reanalyzed the samples using heterophile antibody blocking tubes, revealing lower hs-TnI levels. This case serves as a reminder to consider assay interference when the clinical picture is inconsistent with ischemia.