The validity of self-reported SARS-CoV-2 results among postpartum respondents.

Background: Rapid and reliable health data on SARS-CoV-2 infection among pregnant individuals are needed to understand the influence of the virus on maternal health and child development, yet the validity of self-reported COVID-19 testing and diagnosis remains unknown.

Objectives: We assessed the validity of self-reported COVID-19 polymerase chain reaction (PCR) testing and diagnosis during delivery among postpartum respondents as well as how diagnostic accuracy varied by respondent characteristics.

Methods: We validated receipt of a COVID-19 PCR test and test results by comparing self-reported results obtained through an electronic survey to electronic medical record data (gold standard) among a cross-sectional sample of postpartum respondents who delivered at four New York City hospitals between March 2020 and January 2021.

Outcomes in Critically Ill Patients With Traumatic Brain Injury: Ethnicity, Documentation, and Insurance Status.

Objectives: Disparities in traumatic brain injury outcomes for ethnic minorities and the uninsured have previously been demonstrated; however, outcomes in undocumented immigrants have not been examined. We wanted to determine whether ethnicity, insurance, and documentation status served as risk factors for disparities in traumatic brain injury outcomes between undocumented immigrants and documented residents.

Design: Retrospective study.

Aryl hydrocarbon receptor activation by dioxin targets phosphoenolpyruvate carboxykinase (PEPCK) for ADP-ribosylation via 2,3,7,8-tetrachlorodibenzo-p-dioxin (TCDD)-inducible poly(ADP-ribose) polymerase (TiPARP).

Effects of the environmental toxin and carcinogen 2,3,7,8-tetrachlorodibenzo-p-dioxin (TCDD, dioxin) include a wasting syndrome associated with decreased gluconeogenesis. TCDD is a potent activator of the aryl hydrocarbon receptor (AHR), a ligand activated transcription factor. The relationship between gene activation by the AHR and TCDD toxicities is not well understood.

Identification of the aryl hydrocarbon receptor target gene TiPARP as a mediator of suppression of hepatic gluconeogenesis by 2,3,7,8-tetrachlorodibenzo-p-dioxin and of nicotinamide as a corrective agent for this effect.

The environmental toxin TCDD (2,3,7,8-tetrachlorodibenzo-p-dioxin, dioxin) produces diverse toxic effects including a lethal wasting syndrome whose hallmark is suppressed hepatic gluconeogenesis. All TCDD toxicities require activation of the aryl hydrocarbon receptor (AHR), a ligand-activated transcription factor. Whereas the mechanism for AHR induction of target genes is well understood, it is not known how AHR activation produces any TCDD toxicity.