Influence of Body Mass Index on the Evaluation and Management of Pediatric Abdominal Pain in the Emergency Department.

Introduction: Childhood obesity is a serious concern in the United States, with over one third of the pediatric population classified as obese. Abdominal pain is one of the most common chief complaints among pediatric emergency department (ED) visits. We hypothesized that overweight and obese children being evaluated in the ED for abdominal pain would have higher resource utilization than their normal and underweight peers. Methods: This was a retrospective review of pediatric patients <18 years who presented with abdominal pain to the ED of a tertiary care center from January 1, 2014-September 3, 2020. Patients were excluded if they did not have both a height and weight recorded. We categorized patients as underweight (body mass index [BMI] <5th percentile); normal weight (BMI 5th to <85th percentile), overweight (BMI 85th to <95th percentile); or obese (BMI ≥95th percentile). Descriptive statistics were used to examine the study population. We used chi-square tests to examine the differences in patient characteristics between normal/underweight patients and overweight/obese patients. The Kruskal-Wallis test was completed for examining differences in the medians. We used multivariable logistic regression to examine visit characteristics associated with overweight/obese patients, including ED interventions, testing, and length of stay (LOS). Results: Of the 184 subjects included in the analysis, nine (4.9%) were underweight, 108 (58.7%) were normal weight, 21 (11.4%) were overweight, and 46 (25.0%) were obese. Patients with a BMI of ≥85th percentile were older (median 15 vs 13 years, P = 0.01). They were otherwise similar in demographics. There was no significant difference between normal/underweight and overweight/obese subjects in disposition (37% vs 43% discharge, P = 0.38), 72-hour return (7% vs 6%, P = 0.82), ED LOS (median 4.42 vs 3.95 hours, P = 0.195), or inpatient LOS (median 42.0 vs 34.2 hours, P = 0.06). There were no statistically significant differences in total number of ED tests or interventions received by overweight/obese patients compared to normal/underweight patients, and each subject received a median of six tests (interquartile range [IQR] 4-7) and two interventions (IQR 1-3). Conclusion: Among pediatric patients presenting to the ED with abdominal pain, we found that patient characteristics and ED resource utilization (including testing, intervention, disposition, and LOS) did not differ significantly across BMI categories.

Hypersensitivity of Zebrafish htr2b Mutant Embryos to Sertraline Indicates a Role for Serotonin Signaling in Cardiac Development.

ABSTRACT: Selective serotonin reuptake inhibitors (SSRIs) are antidepressants prescribed in 10% of pregnancies in the United States. Maternal use of SSRIs has been linked to an elevated rate of congenital heart defects, but the exact mechanism of pathogenesis is unknown. Previously, we have shown a decrease in cardiomyocyte proliferation, left ventricle size, and reduced cardiac expression of the serotonin receptor 5-HT 2B in offspring of mice exposed to the SSRI sertraline during pregnancy, relative to offspring of untreated mice. These results suggest that disruption of serotonin signaling leads to heart defects. Supporting this conclusion, we show here that zebrafish embryos exposed to sertraline develop with a smaller ventricle, reduced cardiomyocyte number, and lower cardiac expression of htr2b relative to untreated embryos. Moreover, zebrafish embryos homozygous for a nonsense mutation of htr2b ( htr2bsa16649 ) were sensitized to sertraline treatment relative to wild-type embryos. Specifically, the ventricle area was reduced in the homozygous htr2b mutants treated with sertraline compared with wild-type embryos treated with sertraline and homozygous htr2b mutants treated with vehicle control. Whereas long-term effects on left ventricle shortening fraction and stroke volume were observed by echocardiography in adult mice exposed to sertraline in utero, echocardiograms of adult zebrafish exposed to sertraline as embryos were normal. These results implicate the 5-HT 2B receptor functions in heart development and suggest zebrafish are a relevant animal model that can be used to investigate the connection between maternal SSRI use and elevated risk of congenital heart defects.

Stabilization of a human recombinant factor VIII by poloxamer 188 in relation to polysorbate 80.

Detection of enhanced surface tension depression by surfactant in the presence of protein was recently suggested as a basis for determining whether protein stabilization by that surfactant is owing to surfactant forming a steric barrier at interfaces or surfactant association with the protein. In particular, protein interaction with surfactant aggregates may lead to an increased concentration of monomers thus enhancing surfactant adsorption, or to formation of surfactant-protein complexes having little or no effect on adsorption. We compared the initial rates of surface tension depression by poloxamer 188 and polysorbate 80 (PS 80) in the presence and absence of a human recombinant factor VIII (rFVIII). Indirect evidence had suggested poloxamer 188 enters into stable associations with rFVIII in solution but does not form a steric barrier at the interface, while PS 80 behaves in contrary fashion. In this study, we show the presence of rFVIII caused an increase in the rate (reduction in the activation energy) of PS 80 adsorption, while no such change was recorded in the case of poloxamer 188. Thus, we provide substantiation for detection of protein-mediated acceleration of surfactant adsorption as a means to compare different surfactants in relation to their favored mechanism for protein stabilization.

Col11a1 Regulates Bone Microarchitecture during Embryonic Development.

Collagen XI alpha 1 (Col11a1) is an extracellular matrix molecule required for embryonic development with a role in both nucleating the formation of fibrils and regulating the diameter of heterotypic fibrils during collagen fibrillar assembly. Although found in many different tissues throughout the vertebrate body, Col11a1 plays an essential role in endochondral ossification. To further understand the function of Col11a1 in the process of bone formation, we compared skeletal mineralization in wild-type (WT) mice and Col11a1-deficient mice using X-ray microtomography (micro-CT) and histology. Changes in trabecular bone microstructure were observed and are presented here. Additionally, changes to the periosteal bone collar of developing long bones were observed and resulted in an increase in thickness in the case of Col11a1-deficient mice compared to WT littermates. Vertebral bodies were incompletely formed in the absence of Col11a1. The data demonstrate that Col11a1 depletion results in alteration to newly-formed bone and is consistent with a role for Col11a1 in mineralization. These findings indicate that expression of Col11a1 in the growth plate and perichondrium is essential for trabecular bone and bone collar formation during endochondral ossification. The observed changes to mineralized tissues further define the function of Col11a1.

Structural variations in articular cartilage matrix are associated with early-onset osteoarthritis in the spondyloepiphyseal dysplasia congenita (sedc) mouse.

Heterozgyous spondyloepiphyseal dysplasia congenita (sedc/+) mice expressing a missense mutation in col2a1 exhibit a normal skeletal morphology but early-onset osteoarthritis (OA). We have recently examined knee articular cartilage obtained from homozygous (sedc/sedc) mice, which express a Stickler-like phenotype including dwarfism. We examined sedc/sedc mice at various levels to better understand the mechanistic process resulting in OA. Mutant sedc/sedc, and control (+/+) cartilages were compared at two, six and nine months of age. Tissues were fixed, decalcified, processed to paraffin sections, and stained with hematoxylin/eosin and safranin O/fast green. Samples were analyzed under the light microscope and the modified Mankin and OARSI scoring system was used to quantify the OA-like changes. Knees were stained with 1C10 antibody to detect the presence and distribution of type II collagen. Electron microscopy was used to study chondrocyte morphology and collagen fibril diameter. Compared with controls, mutant articular cartilage displayed decreased fibril diameter concomitant with increases in size of the pericellular space, Mankin and OARSI scores, cartilage thickness, chondrocyte clustering, proteoglycan staining and horizontal fissuring. In conclusion, homozygous sedc mice are subject to early-onset knee OA. We conclude that collagen in the mutant's articular cartilage (both heterozygote and homozygote) fails to provide the normal meshwork required for matrix integrity and overall cartilage stability.