Clinical Monitoring of Serum Levels of Vitamins A, D and E in Children with Recurrent Respiratory Tract Infections of Different Ages: A Clinical Controlled Trial.

Objective: To study serum levels of vitamins A, D and E in children with recurrent respiratory tract infections of different ages and the correlation. Methods: The clinical data of two groups of children of different ages were collected. The serum levels and deficiencies of vitamins A, D and E in children were statistically analyzed. Results: The proportions of premature infants, low body weight infants, special physique, hospitalization history, hypocalcemia, living in a bungalow, and daily outdoor activities in less than 30 minutes in the case group were higher than those in the control group (χ 2=4.507, 5.165, 7.040, 14.907, 4.267, 33.800, 4.507, 8.571, P < 0.05). The serum levels of vitamins A, D and E of children aged 0-1, 2-5, and 6-12 in the case group were lower than those in the control group (P < 0.05). Compared with the control group, the serum vitamin A level of children in the case group was lower (t = 2.631, P < 0.05), and the deficiency rate was higher (χ 2=24.200, P < 0.05). Conclusion: Serum levels of vitamins A, D and E, which are related to birth mode, physical fitness, hospitalization history, hypocalcemia, vitamin deficiency, living environment, and daily outdoor activity time, vary in children with recurrent respiratory tract infections of different ages, and are lower in children with recurrent respiratory tract infections than in healthy children.

Dynamic monitoring and a clinical correlation analysis of the serum vitamin A, D, and E levels in children with recurrent respiratory tract infections.

OBJECTIVE: To investigate the correlation of the serum vitamin A, D, and E (VA, VD, and VE) levels with the occurrence and development of recurrent respiratory tract infections (RRTIs). METHODS: A total of 129 children with respiratory tract infections (RTIs) treated in our hospital from January 2018 to February 2020 (the RTIs group) and 50 healthy children undergoing physical examinations (the control group) in our hospital were recruited as the study cohort. The serum VA, VD, and VE levels were measured upon admission (the active phase) and at two weeks after discharge (the stable phase). The serum VA, VD, and VE levels in the children with RRTIs were compared with the levels in the control group, and the correlation between these three vitamins and the occurrence and development of RRTIs was analyzed. RESULTS: The RRTIs group and the RTIs group witnessed markedly lower serum VA, VD, VE, and humoral immunity index levels, including IgG, IgA, and IgM, compared to the control group, with an apparent lower outcome in the RRTIs group than in the RTIs group. The serum levels of the above indexes in the RRTIs children were reduced in the active phase compared with the stable phase. A Pearson correlation analysis showed a positive correlation between VA and IgA. A multivariate logistic regression analysis revealed that a low BMI (Body mass index), prematurity, VA deficiency, VD deficiency, and VE deficiency were the risk factors for RRTIs in children, and outdoor activity was the protective factor. CONCLUSION: The VA, VD, and VE levels are closely related to RRTIs in children. It is important to determine and supplement the VA, VD, and VE levels to prevent RTIs in children.

Cell cycle kinase CHEK2 in macrophages alleviates the inflammatory response to Staphylococcus aureus-induced pneumonia.

BACKGROUND: Excessive macrophage-mediated inflammation participates in the development of Staphylococcus aureus (S. aureus)-induced pneumonia. Checkpoint kinase 2 (Chek2) was screened out as macrophage-related infantile pneumonia gene after the differentially expressed analysis of RNAseq data derived from pam3CSK4 stimulated bone marrow-derived macrophages (BMDMs). METHODS: RAW264.7 macrophage cells were transfected with Chek2-specific gRNA, which were further overexpressed with wide-type Chek2 or Chek2 kinase activity mutant (Chek2 KD, D368N). At the same time, the relative protein and mRNA expression of inflammatory cytokines were determined. C57BL/6J WT mice were intranasally infected with S. aureus to induce S. aureus-induced pneumonia, which was treated with BML-277, an inhibitor of Chek2. The symptoms of pneumonia mice and inflammatory cytokines associated with the nuclear factor kappa B (NF-κB) signaling pathways were further examined. RESULTS: In vivo, BML-277 significantly promoted pneumonia symptoms, including mortality, lung infiltration of immune cells, and the abundance of lung pro-inflammatory cytokines. Mechanically, BML-277 did not affect BMDMs survival but up-regulated the mRNA expression of tumor necrosis factor (Tnf), nitric oxide synthase 2 (Nos2), interleukin (Il)23a, and the secretion of Tnf-α and Il-23a. At the same time, genetic complementation experiment testified that Chek2 KD did not inhibit NF-κB and relevant inflammatory cytokines expression. CONCLUSION: Chek2 functions through the kinase mechanism to down-regulate the NF-κB pathway in macrophages to alleviate S. aureus-induced pneumonia in mice.

The correlation between the vitamin A, D, and E levels and recurrent respiratory tract infections in children of different ages.

OBJECTIVE: To investigate the correlation between the vitamin A, D, and E levels and recurrent respiratory tract infections (RRTIs) in children of different ages. METHODS: A total of 150 RRTI patients were divided into three groups: the 0 to 2 year-old group, the 3-5 year-old group, and the 6-14 year-old group. Collectively, we refer to the three groups as the RRTI group. The serum vitamin A, D and E levels were measured in the three groups. Healthy children without RRTIs were recruited as a control group. The correlations between the changes in the vitamin A, D, and E levels and the RRTIs were analyzed. RESULTS: The vitamin A, D, and E levels decreased significantly in the children with RRTIs, but only the vitamin A and D levels were negatively correlated with the incidence of RRTIs, while the vitamin E levels were not significantly correlated with the incidence of RRTIs. The follow-up results showed that the serum vitamin A, D, and E levels in the RRTI group were significantly increased after the treatment, and the WBC and CRP levels were remarkably reduced. CONCLUSION: Monitoring the serum vitamin A and D levels helps determine the disease severity, and the supplementation of adequate vitamin A and D through diet or drugs is of great help in treating RRTIs.

Carbon monoxide offers neuroprotection from hippocampal cell damage induced by recurrent febrile seizures through the PERK-activated ER stress pathway.

Carbon monoxide (CO) is neuroprotective in various models of brain injury, but the precise mechanisms for this are yet to be established. In the present study, using a rat model of recurrent febrile seizures (FSs), we found an increase in plasma CO, evidence of neuronal damage and apoptosis, an increase in the expression of the endoplasmic reticulum stress (ERS) marker glucose-regulated protein 78 (GRP78) and C/EBP homologous binding protein (CHOP), and an increase in phosphorylated protein kinase RNA-like endoplasmic reticulum kinase (p-PERK)/eukaryotic translation initiation factor 2 alpha (p-eIF2α) in the hippocampus after 10 FSs. Administration of Hemin (a CO donor) in FS rats alleviated the neuronal damage, reduced neuronal apoptosis, upregulated GRP78 expression, decreased CHOP, and increased p-PERK and p-eIF2α expression in the hippocampus, compared to FS control rats. In contrast, treating FS rats with ZnPP-IX (a CO synthase inhibitor) aggravated the neuronal damage, enhanced neuronal apoptosis, downregulated GRP78 expression, increased CHOP, and decreased p-PERK and p-eIF2α expression, compared to FS control rats. These results suggest that endogenous CO limits the neuronal damage induced by recurrent FSs, through the PERK-activated ERS pathway.

[Long-term outcome and related factors of epileptic seizures in children].

OBJECTIVE: To analyze the Long-term outcome of seizures, and to explore the effects of related factors, including the age at onset, types of epileptic syndromes, and etiological factors, etc. METHODS: The clinical data were retrospectively surveyed from 265 children with regular follow-ups for over 1 year at Peking University First Hospital (Jan. 2003 to Dec. 2006). The seizure-free rate was calculated as an at least one-year non-occurrence of seizures. The Long-term outcome of seizures was analyzed in association with factors including the age at onset, types of epileptic syndromes, and etiology. RESULTS: (1) Seizure types were clarified in all the cases, with combined types of seizures in 17. Epileptic syndromes were identified in 163/265 cases (61.5%). With regular antiepileptic drug therapy, 57.9% children with epilepsy could be seizure-free. (2) Seizure-free was demonstrated in 142/265 cases with a seizure-free rate of 53.6% in this group. (3) The age at onset was youngest in the non-efficacy group. (4) The seizure-free rate was different by syndrome types of epilepsies, with a higher seizure-free rate in idiopathic generalized epilepsy (72.4%) and benign epilepsy in children with centro-temporal spikes (65.5%), whereas a lowest rate (21.7%) in infantile spasms. (5) A significant difference of seizure-free rates was revealed in different etiological groups. Children with idiopathic epilepsy achieved higher seizure-free rate (69.2%) than those with symptomatic and cryptogenic epilepsy (45.4%). CONCLUSION: The epilepsy children with regular antiepileptic drug therapy had generally satisfactory outcome of seizures, with over half cases of seizure-free. The prognosis was demonstrated to be closely related with the etiological factors, syndrome types and age at onset.

Dose-dependent effect of sulfur dioxide on brain damage induced by recurrent febrile seizures in rats.

Sulfur dioxide (SO2) regulates many physiological processes. Little is known about its roles in neurological disorders. In this study, we investigated the role of endogenous SO2 in the development of febrile seizures (FS) and related brain damages. In the rat model of recurrent FS, we found that endogenous SO2 in the plasma and hippocampus was increased, accompanied by upregulation of aspartate amino-transferase 1 (AAT1) and AAT2, and neuronal apoptosis and mossy fiber sprouting (MFS) in the hippocampus. Preconditioning with low concentration of SO2 (1-10 µmol/kg) alleviated the neuronal damage, and attenuated neuronal apoptosis and MFS, whereas preconditioning with high concentration of SO2 (100 µmol/kg) or inhibition of AAT aggravated the neuronal damage, and promoted neuronal apoptosis and MFS in hippocampus of rats with recurrent FS. These data indicate that endogenous SO2 is involved in the development of FS and related brain damage. Preconditioning with low concentration of SO2 may protect neurons from toxicity caused by FS.