Pediatric obesity in the United States: Age-period-cohort analysis.

The rates of obesity among American children aged 2-5 years has reached a historic high. It is crucial to identify the putative sources of population-level increases in obesity prevalence among preschool-aged children because early childhood is a critical window for obesity prevention and thus reduction of future incidence. We used the National Health and Nutrition Examination Survey data and hierarchical age-period-cohort analysis to examine lifecycle (i.

Neighborhood disadvantage and pediatric inpatient opioid prescription patterns.

Background: To explore the role of children's residential environment on opioid prescribing patterns in a predominantly Latinx sample.

Methods: We connected geocoded data from electronic medical records in a diverse sample of pediatric patients to neighborhood environments constructed using latent profile modeling techniques. We then estimated a series of multilevel models to determine whether opioid prescribing patterns vary by residential context.

Explaining adult obesity, severe obesity, and BMI: Five decades of change.

Obesity rates have increased across all segments of society since the late 1970s, but the reason behind population-level increases in body weight remains unclear. We used the 1971-2020 NHANES data to examine whether the observed trend in obesity prevalence is attributable to changing public health behaviors (i.e.

Obesity Heterogeneity by Neighborhood Context in a Largely Latinx Sample.

Neighborhood socioeconomic context where Latinx children live may influence body weight status. Los Angeles County and Orange County of Southern California both are on the list of the top ten counties with the largest Latinx population in the USA. This heterogeneity allowed us to estimate differential impacts of neighborhood environment on children's body mass index z-scores by race/ethnicity using novel methods and a rich data source.

Deconstructing sex differences in C-reactive protein trends over time.

Objectives: Heightened inflammatory state, as measured by circulating C-reactive protein (CRP) levels, can promote inflammation-mediated disease risk. It is important to account for population fluctuation and sex variation in serum CRP concentrations on overall time trends.

Methods: Using the National Health and Nutrition Examination Survey data, we specify linear and algebraic decomposition models separately by sex to identify the drivers of the changing trends in the distribution of CRP values in the population.

County-Level Factors That Influenced the Trajectory of COVID-19 Incidence in the New York City Area.

More than a century of research has shown that sociodemographic conditions affect infectious disease transmission. In the late spring and early summer of 2020, reports of the effects of sociodemographic variables on the spread of COVID-19 were used in the media with minimal scientific proof attached. With new cases of COVID-19 surging in the United States at that time, it became essential to better understand how the spread of COVID-19 was varying across all segments of the population.

Surgical Patients' Hospital Experience Scores: Neighborhood Context Conceptual Framework.

Objective: Through geocoding the physical residential address included in the electronic medical record to the census tract level, we present a novel model for concomitant examination of individual patient-related and residential context-related factors that are associated with patient-reported experience scores.

Summary Background Data: When assessing patient experience in the surgical setting, researchers need to examine the potential influence of neighborhood-level characteristics on patient experience-of-care ratings.

Methods: We geocoded the residential address included in the electronic medical record (EMR) from a tertiary care facility to the census tract level of Orange County, CA.

Decomposing Differences in Coronavirus disease 2019-related Case-Fatality Rates across Seventeen Nations.

As of 1 November 2020, estimated case-fatality rates associated with coronavirus disease 2019 are not uniformly patterned across the world and differ substantially in magnitude. Given the global spatial heterogeneity in case-fatality rates, we applied the Blinder-Oaxaca regression decomposition technique to identify how putative sociodemographic, structural, and environmental sources influence variation in case-fatality rates. We show that compositional and associational differences in country-level risk factors explain a substantial proportion of the coronavirus disease 2019-related case-fatality rate gap across nations.

Peripheral administration of poly I:C leads to increased hippocampal amyloid-beta and cognitive deficits in a non-transgenic mouse.

Alzheimer's disease (AD) is a progressive disorder characterized by neuronal and behavioral deterioration. Two hallmark pathologies of AD are amyloid-beta (Aβ) plaques and neurofibrillary tangles, and the presence of such pathology can limit cell-to-cell communication, leading to cognitive deficits, and neuronal cell death. Although Aβ plaques were originally thought to cause the cognitive deficits, more simple forms of Aβ, such as monomers, dimers, tetramers and oligomers, have also been shown to be neurotoxic.

Imatinib methanesulfonate reduces hippocampal amyloid-β and restores cognitive function following repeated endotoxin exposure.

Alzheimer's disease (AD) is characterized, in part, by atrophy of the adult brain and increased presence of extracellular amyloid-beta (Aβ) plaques. Previous studies in our lab have shown that peripheral inflammation can lead to increased central Aβ and deficits in learning and memory. In order to determine whether Aβ accumulation in the brain is responsible for the learning deficits, we attempted to decrease peripheral production of Aβ in order to reduce central Aβ accumulation.

Peripheral administration of D-cycloserine rescues memory consolidation following bacterial endotoxin exposure.

In the current study, the partial NMDA receptor agonist D-cycloserine (DCS) rescued memory consolidation following systemic bacterial endotoxin exposure. DCS failed, however, to restore hippocampal BDNF mRNA levels that were diminished following a systemic administration of LPS, and did not alter NR1 or NR2C NMDA receptor subunit expression. These results extend prior research into the role of DCS in neural-immune interactions, and indicate that the detrimental effects of peripheral LPS administration on consolidation of contextual fear memory may be ameliorated with DCS treatment, though the mechanisms underlying these effects are currently unclear.

Prolonged elevation in hippocampal Aβ and cognitive deficits following repeated endotoxin exposure in the mouse.

Alzheimer's disease (AD) is characterized by neuronal cell death and atrophy in regions of the adult brain, including the hippocampus and cortex, due to formation of amyloid beta (Aβ) plaques and neurofibrillary tangles. The presence of these pathologies can limit normal signaling properties and ultimately lead to learning and memory deficits. Chronic inflammation has been implicated in the onset and progression of these AD-related pathologies.

Peripheral administration of poly I:C disrupts contextual fear memory consolidation and BDNF expression in mice.

In the current study, administration of poly I:C induced a deficit in contextual, but not auditory-cue, fear memory consolidation. This memory deficit coincided with a decrease in hippocampal and cortical BDNF mRNA expression. These results extend prior work, and suggest that a single peripheral injection of poly I:C disrupts contextual fear memory consolidation processes in adult mice, and that these deficits may potentially be mediated by diminished BDNF expression.

Peripheral bacterial endotoxin administration triggers both memory consolidation and reconsolidation deficits in mice.

Peripherally administered inflammatory stimuli, such as lipopolysaccharide (LPS), induce the synthesis and release of proinflammatory cytokines and chemokines in the periphery and the central nervous system, and trigger a variety of neurobiological responses. Indeed, prior reports indicate that peripheral LPS administration in rats disrupts contextual fear memory consolidation processes, potentially due to elevated cytokine expression. We used a similar, but partially olfaction-based, contextual fear conditioning paradigm to examine the effects of LPS on memory consolidation and reconsolidation in mice.

Age exacerbates sickness behavior following exposure to a viral mimetic.

Poly I:C, a viral mimetic, is a synthetic double-stranded RNA that is known to cause activation of the innate immune system, resulting in the emergence of sickness behaviors in otherwise healthy adult mice. However, the way in which such effects of poly I:C manifest themselves in aged mice are not currently known. We hypothesized that poly I:C administration would lead to burrowing deficits, but that these deficits would be exaggerated in aged subjects (19-months old) compared to young subjects (4-months old) that received the same dose.

The effects of age on lipopolysaccharide-induced cognitive deficits and interleukin-1β expression.

An acute LPS challenge immediately following day 1 of shuttlebox training triggered exacerbated central IL-1β production and disrupted memory consolidation and/or further acquisition of the task in 18-month-old mice, compared to 4-month-old controls. These deficits cannot be attributed to alterations in sickness behavior. The findings suggest that age and immune activation combine to impair learning and memory consolidation processes, and that increased central IL-1β production may play a role.