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Exposure to airborne fine particles with diameters ≤2.5 μm (PM
) pollution is a well-established cause of respiratory diseases in children; whether wildfire-specific PM
causes more damage, however, remains uncertain. We examine the associations between wildfire-specific PM
and pediatric respiratory health during the period 2011-2017 in San Diego County, California, and compare these results with other sources of PM
.
Visits to emergency and urgent care facilities of Rady's Children Hospital network in San Diego County, California, by individuals (aged ≤19 years) with ≥1 of the following respiratory conditions difficulty breathing, respiratory distress, wheezing, asthma, or cough were regressed on daily, community-level exposure to wildfire-specific PM
and PM
from ambient sources (eg, traffic emissions).
A 10-unit increase in PM
(from nonsmoke sources) was estimated to increase the number of admissions by 3.7% (95% confidence interval 1.2% to 6.1%). In contrast, the effect of PM
attributable to wildfire was estimated to be a 30.0% (95% confidence interval 26.6% to 33.4%) increase in visits.
Wildfire-specific PM
was found to be ∼10 times more harmful on children's respiratory health than PM
from other sources, particularly for children aged 0 to 5 years. Even relatively modest wildfires and associated PM
resolved on our record produced major health impacts, particularly for younger children, in comparison with ambient PM
.
Wildfire-specific PM2.5 was found to be ∼10 times more harmful on children's respiratory health than PM2.5 from other sources, particularly for children aged 0 to 5 years. Even relatively modest wildfires and associated PM2.5 resolved on our record produced major health impacts, particularly for younger children, in comparison with ambient PM2.5.
The coronavirus disease 2019 (COVID-19) pandemic has led to changes in health care use, including decreased emergency department visits for children. In this study, we sought to describe the impact of the COVID-19 pandemic on inpatient use within children's hospitals.
We performed a retrospective study using the Pediatric Health Information System. We compared inpatient use and clinical outcomes for children 0 to 18 years of age during the COVID-19 period (March 15 to August 29, 2020) to the same time frame in the previous 3 years (pre-COVID-19 period). Adjusted generalized linear mixed models were used to examine the association of the pandemic period with inpatient use. We assessed trends overall and for a subgroup of 15 medical All Patient Refined Diagnosis Related Groups (APR-DRGs).
We identified 424 856 hospitalizations (mean 141 619 hospitalizations per year) in the pre-COVID-19 period and 91 532 in the COVID-19 period. Compared with the median number of hospitalizations in the pre-COVID-19 perioddmissions for respiratory conditions, including asthma, bronchiolitis, and pneumonia.Hepatic glucose uptake (HGU) is critical for maintaining normal postprandial glucose metabolism. Insulin is clearly a key regulator of HGU, but the physiologic mechanisms by which it acts have yet to be established. This study sought to determine the mechanisms by which insulin regulates liver glucose uptake under postprandial-like conditions (hyperinsulinemia, hyperglycemia, and a positive portal vein-to-arterial glucose gradient). Portal vein insulin infusion increased hepatic insulin levels fivefold in healthy dogs. In one group (n = 7), the physiologic response was allowed to fully occur, while in another (n = 7), insulin's indirect hepatic effects, occurring secondary to its actions on adipose tissue, pancreas, and brain, were blocked. This was accomplished by infusing triglyceride (intravenous), glucagon (portal vein), and inhibitors of brain insulin action (intracerebroventricular) to prevent decreases in plasma free fatty acids or glucagon, while blocking increased hypothalamic insulin signaling for 4 h. In contrast to the indirect hepatic effects of insulin, which were previously shown capable of independently generating a half-maximal stimulation of HGU, direct hepatic insulin action was by itself able to fully stimulate HGU. This suggests that under hyperinsulinemic/hyperglycemic conditions insulin's indirect effects are redundant to direct engagement of hepatocyte insulin receptors.The thyroid hormone T3 and its nuclear receptor TRα1 control gut development and homeostasis through the modulation of intestinal crypt cell proliferation. Despite increasing data, in-depth analysis on their specific action on intestinal stem cells is lacking. By using ex vivo 3D organoid cultures and molecular approaches, we observed early responses to T3 involving the T3-metabolizing enzyme Dio1 and the transporter Mct10, accompanied by a complex response of stem cell- and progenitor-enriched genes. Interestingly, specific TRα1 loss-of-function (inducible or constitutive) was responsible for low ex vivo organoid development and impaired stem cell activity. T3 treatment of animals in vivo not only confirmed the positive action of this hormone on crypt cell proliferation but also demonstrated its key action in modulating the number of stem cells, the expression of their specific markers and the commitment of progenitors into lineage-specific differentiation. selleck products In conclusion, T3 treatment or TRα1 modulation has a rapid and strong effect on intestinal stem cells, broadening our perspectives in the study of T3/TRα1-dependent signaling in these cells.In the face, symmetry is established when bilateral streams of neural crest cells leave the neural tube at the same time, follow identical migration routes and then give rise to the facial prominences. However, developmental instability exists, particularly surrounding the steps of lip fusion. The causes of instability are unknown but inability to cope with developmental fluctuations are a likely cause of congenital malformations, such as non-syndromic orofacial clefts. Here, we tracked cell movements over time in the frontonasal mass, which forms the facial midline and participates in lip fusion, using live-cell imaging of chick embryos. Our mathematical examination of cell velocity vectors uncovered temporal fluctuations in several parameters, including order/disorder, symmetry/asymmetry and divergence/convergence. We found that treatment with a Rho GTPase inhibitor completely disrupted the temporal fluctuations in all measures and blocked morphogenesis. Thus, we discovered that genetic control of symmetry extends to mesenchymal cell movements and that these movements are of the type that could be perturbed in asymmetrical malformations, such as non-syndromic cleft lip.
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