Publications by authors named "Carrie Quinn"

7 Publications

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Evaluating the Keystones of Development - An Online Curriculum for Residents to Promote Positive Parenting in Primary Care.

Acad Pediatr 2021 Jun 12. Epub 2021 Jun 12.

Mount Sinai Parenting Center, 207 East 94th Street, 2nd Floor New York, NY 10128. USA; Department of Pediatrics, Icahn School of Medicine at Mount Sinai, 1 Gustave Levy Place, Box 1198, New York, NY 10029. USA. Electronic address:

Objective: This pilot outcome evaluation assesses the effectiveness of an online curriculum, the Keystones of Development, aimed at improving residents' knowledge, attitudes, and reported behaviors around promoting positive parenting and childhood development in well-child visits.

Methods: We used an explanatory mixed-methods approach, including a single-arm pre-posttest of intervention effects on self-reported behavioral outcomes (discussing, modeling, and praising) and secondary outcomes (knowledge, perceived barriers, attitudes, and self-efficacy). Following this, a subset of residents participated in in-depth interviews to describe participant responses to the intervention.

Results: The study was conducted at 8 pediatric residency programs across the United States with 67 pediatric residents (mean age=29; 79% female; 57% PGY1). Within one month post-intervention, there was a statistically significant increase in the behaviors that promote positive parenting: discussing (p<0.01;d=0.73) and modeling (p<0.01;d=0.61) but not praising (p=0.05; d=0.3). Significant changes in the secondary outcomes: knowledge (p<0.01), perceived barriers, (p<0.01), and retrospective self-efficacy (p<0.01) were seen. Interviews revealed that integration of curriculum content into clinical practice was due to the relevance of the material to primary care and the modeling of how to apply in the clinical setting. Curriculum format, content, and clinical application helped participants weave recommendations into the well-child visit.

Conclusion: In this study, we demonstrated that the online curriculum, Keystones of Development, increased resident behaviors, knowledge, and self-efficacy, and decreased perceived barriers to promote parenting behaviors associated with improved child development outcomes in well-child visits. These findings were observed across participants demonstrating equal success regardless of demographic characteristics or study site.
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http://dx.doi.org/10.1016/j.acap.2021.06.005DOI Listing
June 2021

Educating Pediatric Residents About Parenting: A Survey of Residency Program Leaders.

Clin Pediatr (Phila) 2020 06 28;59(7):699-705. Epub 2020 Feb 28.

Mount Sinai Medical Center, New York, NY, USA.

The American Academic of Pediatrics guides pediatricians to counsel parents about how to promote their children's cognitive, emotional, and self-regulatory development, but the extent to which pediatricians receive the training needed to do so is unknown. An online survey was distributed to members of the Association of Pediatric Program Directors. Although most respondents agreed that it was "very important" to educate residents about parenting skills, only 11% rated their program as doing so "very well." The most frequently reported reason for not doing very well was lack of a curriculum. Residents currently learn about parenting most commonly in continuity clinic talks, are educated via lectures, and are taught most frequently by clinic preceptors. Nearly half of the respondents reported that their residents relied on self-learning about parenting behaviors. When asked which topics respondents would like covered by an evidence-based parenting curriculum, the most commonly endorsed topic was positive discipline.
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http://dx.doi.org/10.1177/0009922820908584DOI Listing
June 2020

Altered hypothalamic inflammatory gene expression correlates with heat stroke severity in a conscious rodent model.

Brain Res 2016 Apr 12;1637:81-90. Epub 2016 Feb 12.

US Army Research Institute of Environmental Medicine, Thermal and Mountain Medicine Division, Natick, MA 01760-5007, United States.

It has been suggested that heat-induced hypothalamic damage mediates core temperature (Tc) disturbances during heat stroke (HS) recovery; this is significant as hypothermia and/or fever have been linked to severity and overall pathological insult. However, to date there has been a lack of histological evidence in support of these claims. We hypothesized that local hypothalamic cytokines and/or chemokines, known regulators of Tc, are mediating the elevation in Tc during HS recovery even in the absence of histological damage. In experiment 1, the hypothalamus of Fischer 344 rats was examined for 84 cytokine/chemokine genes (real-time PCR) at multiple time points (Tc,Max, 1, 3, and 10 days) during mild HS recovery. In experiment 2, the hypothalamus of three different HS severities (MILD, moderate [MOD], and severe [SEV]) in rats were examined for the same genes as experiment 1 as well as six oxidative damage markers, at a single intermediate time point (1 day). Systemic cytokines were also analyzed in experiment 2 across the three severities. There were significant alterations in 25 cytokines/chemokines expression at Tc,Max, but little or no changes in expression at longer time points in experiment 1. In experiment 2 there were significant changes in gene expression in SEV rats only, with MILD and MOD rats showing baseline expression at 1 day, despite an absence of systemic cytokine expression in any severity. There was also no change in any oxidative marker of damage at 1 day, regardless of severity. In conclusion, we show only limited changes during long term recovery from HS, but demonstrate differences in hypothalamic gene expression patterns that may be driving HS pathology and morbidity. These findings contribute to our overall understanding of HS pathology in the CNS, as well as providing avenues for future pharmacological intervention.
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http://dx.doi.org/10.1016/j.brainres.2016.01.048DOI Listing
April 2016

Point-of-care cardiac troponin test accurately predicts heat stroke severity in rats.

Am J Physiol Regul Integr Comp Physiol 2015 Nov 19;309(10):R1264-72. Epub 2015 Aug 19.

Thermal and Mountain Medicine Division, United States Army Research Institute of Environmental Medicine, Natick, Massachusetts.

Heat stroke (HS) remains a significant public health concern. Despite the substantial threat posed by HS, there is still no field or clinical test of HS severity. We suggested previously that circulating cardiac troponin (cTnI) could serve as a robust biomarker of HS severity after heating. In the present study, we hypothesized that (cTnI) point-of-care test (ctPOC) could be used to predict severity and organ damage at the onset of HS. Conscious male Fischer 344 rats (n = 16) continuously monitored for heart rate (HR), blood pressure (BP), and core temperature (Tc) (radiotelemetry) were heated to maximum Tc (Tc,Max) of 41.9 ± 0.1°C and recovered undisturbed for 24 h at an ambient temperature of 20°C. Blood samples were taken at Tc,Max and 24 h after heat via submandibular bleed and analyzed on ctPOC test. POC cTnI band intensity was ranked using a simple four-point scale via two blinded observers and compared with cTnI levels measured by a clinical blood analyzer. Blood was also analyzed for biomarkers of systemic organ damage. HS severity, as previously defined using HR, BP, and recovery Tc profile during heat exposure, correlated strongly with cTnI (R(2) = 0.69) at Tc,Max. POC cTnI band intensity ranking accurately predicted cTnI levels (R(2) = 0.64) and HS severity (R(2) = 0.83). Five markers of systemic organ damage also correlated with ctPOC score (albumin, alanine aminotransferase, blood urea nitrogen, cholesterol, and total bilirubin; R(2) > 0.4). This suggests that cTnI POC tests can accurately determine HS severity and could serve as simple, portable, cost-effective HS field tests.
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http://dx.doi.org/10.1152/ajpregu.00286.2015DOI Listing
November 2015

Cardiovascular and thermoregulatory dysregulation over 24 h following acute heat stress in rats.

Am J Physiol Heart Circ Physiol 2015 Aug 12;309(4):H557-64. Epub 2015 Jun 12.

US Army Research Institute of Environmental Medicine, Thermal and Mountain Medicine Division, Natick, Massachusetts.

The influences of severe heat stroke (HS) on cardiovascular function during recovery are incompletely understood. We hypothesized that HS would elicit a heart rate (HR) increase persisting through 24 h of recovery due to hemodynamic, thermoregulatory, and inflammatory events, necessitating tachycardia to support mean arterial pressure (MAP). Core temperature (Tc), HR, and MAP were measured via radiotelemetry in conscious male Fischer 344 rats (n = 22; 282.4 ± 3.5 g) during exposure to 37°C ambient temperature until a maximum Tc of 42.0°C, and during recovery at 20°C ambient temperature through 24 h. Rats were divided into Mild, Moderate, and Severe groups based on pathophysiology. HS rats exhibited hysteresis relative to Tc with HR higher for a given Tc during recovery compared with heating (P < 0.0001). "Reverse" hysteresis occurred in MAP with pressure during cooling lower than heating per degree Tc (P < 0.0001). Mild HS rats showed tachycardia [P < 0.01 vs. control (Con)] through 8 h of recovery, elevated MAP (P < 0.05 vs. Con) for the initial 5 h of recovery, with sustained hyperthermia (P < 0.05 vs. Con) through 24 h. Moderate HS rats showed significant tachycardia (P < 0.01 vs. Con), normal MAP (P > 0.05 vs. Con), and rebound hyperthermia from 4 to 24 h post-HS (P < 0.05 vs. Con). Severe HS rats showed tachycardia (P < 0.05 vs. Con), hypotension (P < 0.01 vs. Con), and hypothermia for 24 h (P < 0.05 vs. Con). Severe HS rats showed 14- and 12-fold increase in heart and liver inducible nitric oxide synthase expression, respectively. Hypotension and hypothermia in Severe HS rats was consistent with inducible nitric oxide synthase-mediated systemic vasodilation. These findings provide mechanistic insight into hemodynamic and thermoregulatory impairments during 24 h of HS recovery.
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http://dx.doi.org/10.1152/ajpheart.00918.2014DOI Listing
August 2015

Cardiovascular and thermoregulatory biomarkers of heat stroke severity in a conscious rat model.

J Appl Physiol (1985) 2014 Nov 14;117(9):971-8. Epub 2014 Aug 14.

U.S. Army Research Institute of Environmental Medicine, Thermal and Mountain Medicine Division, Natick, Massachusetts.

Multiorgan failure is a catastrophic consequence of heat stroke (HS) and considered the underlying etiology of mortality. Identifying novel biomarkers capable of predicting the extent of HS-induced organ damage will enhance point-of-care triage and treatment. Conscious male F344 rats (n = 32) were radiotelemetered for continuous core temperature (Tc), heart rate, and arterial pressure measurement. Twenty-two animals were exposed to ambient temperature of 37°C to a maximum Tc of 41.9 ± 0.1°C. Rats were euthanized at 24 h of recovery for analysis of plasma biomarkers [cardiac troponin I (cTnI), blood urea nitrogen (BUN), alanine aminotransferase (ALT), albumin, glucose] and histology. Tc profiles observed during recovery stratified HS severity into Mild, Moderate, and Severe. Eleven (50%) animals exhibited an acute compensatory hemodynamic response to heat exposure and a monophasic Tc profile consisting of sustained hyperthermia (∼1°C). Five (23%) rats displayed hemodynamic challenge and a biphasic Tc profile with rapid return to baseline followed by rebound hyperthermia. All biomarkers were significantly altered from control values (P < 0.05). Four (18%) animals exhibited significant hemodynamic compromise during heat and a triphasic profile characterized by rapid cooling to baseline Tc, rebound hyperthermia, and subsequent hypothermia (∼35°C) through 24 h. cTnI showed a 40-fold increase over CON (P < 0.001) and correlated with BUN (r = 0.912) consistent with cardiorenal failure. Hypoglycemia correlated with ALT (r = 0.824) suggestive of liver dysfunction. Histology demonstrated myocardial infarction, renal tubular necrosis, and acute liver necrosis. Two (9%) animals succumbed during HS recovery. This study identified novel biomarkers that predict HS severity and organ damage during acute recovery that could provide clinical significance for identifying key biomarkers of HS pathogenesis.
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http://dx.doi.org/10.1152/japplphysiol.00365.2014DOI Listing
November 2014