Updates in Diagnosis and Management of Croup

Sheikh, Mohammed Hussen; Albalawi, Haya Jamal M.; Albalawi, Yazeed Ali S.; Alotaibi, Mohammed; Alsharef, Sultan Makki M.; Alshehri, Ali; Albalawi, Ahmed Saad A.; Albalawi, Abdulaziz Saed A.; Alamri, Mohammed Abdulwahed H.; Mohammed, AlTurki Abdulrahman; Al-Ruwaili, Sultan Suliman Q.; Alqrafi, Mohammad; Alenzi, Sarah Awad Muhammad; Alharbi, Rahaf Saad D.; Alomrani, Heba Homoud H.

doi:10.9734/jpri/2021/v33i49b33366

Cited by 2 publications

(2 citation statements)

References 26 publications

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“…Its main role is to promote the absorption of calcium and phosphorus from the gastrointestinal tract and to reduce the excretion of calcium and phosphorus from the gastrointestinal tract, which leads to an increase in the concentration of calcium and phosphorus in the blood [2][3][4] In addition to this, it is also involved in immune regulation, neurotransmission and cell differentiation, and has a role in promoting cartilage synthesis, chondrocyte development, and bone maturation. In recent years, the effect of vitamin D on neonatal lung disease has received widespread attention.…”

Section: Introductionmentioning

confidence: 99%

A Cohort Study of Serum 25-Hydroxyvitamin D Levels and Lung Disease in Preterm Infants

Gao,

Hong

2024

Asian J. Pediatr. Res.

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Objectives: To analyze the relationship between serum 25-hydroxyvitamin D [25(OH)D] levels and lung diseases (wet lung, RDS, BPD, pneumothorax) in preterm infants. Methods: Preterm infants (corrected gestational age <37 weeks) hospitalized in the neonatology department of Yan'an University Hospital from January 2023 to December 2023 were selected as the study subjects, and their clinical data and 25-hydroxyvitamin D [25(OH)D] levels in the first 24 h of life were collected (by the random number table method to avoid selection bias) in a retrospective cohort study with the basis of the Serum 25(OH)D level was used to categorize preterm infants into high vitamin D and low vitamin D groups, and to compare the incidence of lung diseases in preterm infants in the 2 groups. Results: A total of 414 preterm infants were selected, and 237 preterm infants were finally included for analysis. The mean serum 25(OH)D level in preterm infants within 24 hours of birth was 16.97 ng/mL. 140 cases in the low-vitamin D group had a serum 25(OH)D level of (11.88± 2.74) ng/mL. 97 cases in the high-vitamin D group had a serum 25(OH)D level of (24.31± 7.52) ng/mL; the rate of births in the fall in the low-vitamin D group was was significantly higher than that of the high-vitamin D group (P<0.05), the utilization rate of lung surface active substance was higher than that of the high-vitamin D group (P<0.05), and the incidence of RDS and BPD was significantly higher than that of the high-vitamin D group (P<0.05). Univariate logistic regression analysis suggested that season of birth, serum 25(OH)D level, 5 min Apgar score and prenatal hormone use were associated with pulmonary complications in preterm infants (P<0.05). Multifactorial logistic regression analysis showed that higher serum 25(OH)D levels reduced the risk of pulmonary complications in preterm infants, which was statistically significant (B=-0.056, RR= 0.946, 95% CI: 0.910-0.984, P=0.006); higher 5-min Apgar scores had a lower incidence of pulmonary complications in preterm infants, which was statistical significance (B=-0.722, RR= 0.486, 95% CI: 0.281~0.840, P=0.010); prenatal use of hormones will reduce the risk of pulmonary complications in preterm infants (B=-0.763, RR= 0.466, 95% CI: 0.261~0.833, P=0.010). Conclusion: Low vitamin D levels at birth in preterm infants may increase the incidence of RDS and BPD.

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Section: Introductionmentioning

confidence: 99%

A Cohort Study of Serum 25-Hydroxyvitamin D Levels and Lung Disease in Preterm Infants

Gao,

Hong

2024

Asian J. Pediatr. Res.

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“…Human studies of adolescents and adults have linked metabolic syndrome and insulin resistance to decreased executive function and declarative memory, while animal studies have linked obesity and high-fat diet to increased amyloid β (Aβ) levels, indicating a mediating role for diet-induced peripheral inflammation in AD (Yates et al, 2012;Radler et al, 2015;Wakabayashi et al, 2019). Peripheral inflammation, including that associated with a high-fat diet, increases blood-brain barrier (BBB) leakiness and microglia activation (Sheikh et al, 2022). Changes in the regulation of peripheral immune cell traffic due to a leaky BBB may be a contributor to diet-induced neuroinflammation and acceleration of AD-like pathology.…”

Section: Introductionmentioning

confidence: 99%

Soluble TNF mediates amyloid-independent, diet-induced alterations to immune and neuronal functions in an Alzheimer’s disease mouse model

MacPherson

Eidson

Houser

et al. 2023

Front. Cell. Neurosci.

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Introduction: Increasing evidence indicates that neurodegenerative diseases, including Alzheimer’s disease (AD), are a product of gene-by-environment interplay. The immune system is a major contributor mediating these interactions. Signaling between peripheral immune cells and those within the microvasculature and meninges of the central nervous system (CNS), at the blood-brain barrier, and in the gut likely plays an important role in AD. The cytokine tumor necrosis factor (TNF) is elevated in AD patients, regulates brain and gut barrier permeability, and is produced by central and peripheral immune cells. Our group previously reported that soluble TNF (sTNF) modulates cytokine and chemokine cascades that regulate peripheral immune cell traffic to the brain in young 5xFAD female mice, and in separate studies that a diet high in fat and sugar (HFHS) dysregulates signaling pathways that trigger sTNF-dependent immune and metabolic responses that can result in metabolic syndrome, which is a risk factor for AD. We hypothesized that sTNF is a key mediator of peripheral immune cell contributions to gene-by-environment interactions to AD-like pathology, metabolic dysfunction, and diet-induced gut dysbiosis.Methods: Female 5xFAD mice were subjected to HFHS diet for 2 months and then given XPro1595 to inhibit sTNF for the last month or saline vehicle. We quantified immune cell profiles by multi-color flow cytometry on cells isolated from brain and blood; metabolic, immune, and inflammatory mRNA and protein marker biochemical and immunhistological analyses, gut microbiome, and electrophysiology in brain slices were also performed.Results: Here, we show that selective inhibition of sTNF signaling via the biologic XPro1595 modulates the effects of an HFHS diet in 5xFAD mice on peripheral and central immune profiles including CNS-associated CD8+ T cells, the composition of gut microbiota, and long-term potentiation deficits.Discussion: Obesogenic diet induces immune and neuronal dysfunction in 5xFAD mice and sTNF inhibition mitigates its effects. A clinical trial in subjects at risk for AD due to genetic predisposition and underlying inflammation associated with peripheral inflammatory co-morbidities will be needed to investigate the extent to which these findings translate to the clinic.

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Updates in Diagnosis and Management of Croup

Cited by 2 publications

References 26 publications

A Cohort Study of Serum 25-Hydroxyvitamin D Levels and Lung Disease in Preterm Infants

A Cohort Study of Serum 25-Hydroxyvitamin D Levels and Lung Disease in Preterm Infants

Soluble TNF mediates amyloid-independent, diet-induced alterations to immune and neuronal functions in an Alzheimer’s disease mouse model

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