Objective:To describe and compare caffeinated energy drink adverse event (AE) report/exposure call data from the US Food and Drug Administration Center for Food Safety and Applied Nutrition’s Adverse Event Reporting System (CAERS) and the American Association of Poison Control Centers’ National Poison Data System (NPDS).Design:Cross-sectional.Setting:Data were evaluated from US-based CAERS reports and NPDS exposure calls, including report/exposure call year, age, sex, location, single v. multiple product consumption, outcome, symptom, intentionality (NPDS only), report type, product name (CAERS only).Participants:The analysis defined participants (cases) by the number of caffeinated energy drink products indicated in each AE report or exposure call. Single product cases included 357 from CAERS and 12 822 from NPDS; multiple product cases included 153 from CAERS and 931 from NPDS.Results:CAERS v. NPDS single product cases were older and more frequently indicated serious symptoms. Multiple v. single product consumers were older in both. In CAERS, unlike NPDS, most multiple product consumers were female. CAERS single v. multiple product reports cited higher proportions of life-threatening events, but less often indicated hospitalization and serious events. NPDS multiple v. single product cases involved fewer ≤5-year-olds and were more often intentional.Conclusions:Despite limitations, both data sources contribute to post-market surveillance and improve understanding of public health concerns.

Purpose Obesity prevalence has reached an all-time high in the US, affecting >40% of the population. This study’s objective was to evaluate associations between demographics and self-reported calorie knowledge and self-perceived confidence in calorie knowledge (“calorie confidence”). The relationships between body mass index (BMI) and calorie knowledge and confidence were also explored. Methods We analyzed data from participants (n = 2171) in the crosssectional, nationally representative 2019 FDA Food Safety and Nutrition Survey using logistic regression to estimate adjusted odds ratios (AORs) and confidence intervals (95% CIs) for associations between BMI and calorie knowledge (correct/incorrect), calorie confidence (confident/not confident), and demographic characteristics, and the Wald chi square test to evaluate relationships between BMI and both calorie knowledge and confidence. Results Many of the same subgroups were more likely than others to report lack of calorie knowledge and lack of confidence in knowing the typical daily calorie intake needed to maintain a healthy weight [respective AORs (95% CIs): age (years), >60 vs 51-60, 1.7 (1.1-2.5), and 1.4 (1.0-2.0); sex, male vs female, 1.7 (1.3-2.3), and 1.7 (1.3-2.1); race/ethnicity, non-Hispanic Black vs non-Hispanic white, 3.4 (2.1-5.5), and 2.4 (1.6-3.8); education, ≤high school vs college grad, 1.5 (1.0- 2.3), and 1.9 (1.3-2.7)]. BMI was significantly correlated with calorie confidence ( P = .047), such that those reporting less confidence were more likely overweight or obese [underweight/healthy (BMI < 25): 29%, overweight (25 ≤ BMI < 30): 34%, obese (BMI ≥ 30): 37%]. Conclusion In certain demographic subgroups associations between calorie knowledge and confidence differed. Tailored education and outreach for these groups may help to address these disparities.

NO can regulate specific cellular functions by altering transcriptional programs and protein reactivity. With respect to global cellular processes, NO has also been demonstrated to inhibit total protein synthesis and cell proliferation. The underlying mechanisms are unknown. In a system of ANA-1 murine macrophages, iNOS expression and NO production were induced by exposure to endotoxin (LPS). In selected instances, cells were exposed to an exogenous NO donor, S-nitroso-N-acetylpenicillamine or a substrate inhibitor of NO synthesis. Cellular exposure to NO, from both endogenous and exogenous sources, was associated with a significant time-dependent decrease in total protein synthesis and cell proliferation. Gene transcription was unaltered. In parallel with decreased protein synthesis, cells exhibited a distinctive cleavage pattern of 28S and 18S rRNA that were the result of two distinct cuts in both 28S and 18S rRNA. Total levels of intact 28S rRNA, 18S rRNA, and the composite 60S ribosome were significantly decreased in the setting of cell exposure to NO. Finally, 60S ribosome-associated peptidyl transferase activity, a key enzyme for peptide chain elongation, was also significantly decreased. Our data suggest that NO-mediated cleavage of 28S and 18S rRNA results in decreased 60S ribosome associated peptidyl transferase activity and inhibition of total protein synthesis.

Toxoplasma gondii (T. gondii) is an intracellular parasite infecting one third of the world’s population. Latent T. gondii infection has been associated with mental illness, including schizophrenia and suicidal behavior. T. gondii IgG antibody titers were measured via ELISA. The heritability of T. gondii IgG was estimated using a mixed model that included fixed effects for age and sex and random kinship effect. Of 2017 Old Order Amish participants, 1098 had positive titers (54.4%). The heritability for T. gondii serointensity was estimated to be 0.22 (p = 1.7 × 10−8 and for seropositivity, it was estimated to be 0.28 (p = 1.9 × 10−5). Shared household environmental effects (i.e., household effects) were also determined. Household effects, modeled as a random variable, were assessed as the phenotypic covariance between any two individuals who had the same current address (i.e., contemporaneous household), and nuclear household (i.e., the phenotypic covariance between parents and children only, not other siblings or spouses). Household effects did not account for a significant proportion of variance in either T. gondii serointensity or T. gondii seropositivity. Our results suggest a significant familial aggregation of T. gondii serointensity and seropositivity with significant heritability. The shared household does not contribute significantly to family aggregation with T. gondii, suggesting that there are possible unmeasured non-household shared and non-shared environmental factors that may play a significant role. Furthermore, the small but significant heritability effects justify the exploration of genetic vulnerability to T. gondii exposure, infection, virulence, and neurotropism.