Objective To investigate the efficacy and safety of nebulized inhalation of budesonide combined with intravenous injection of dexamethasone in the treatment of preterm infants with bronchopulmonary dysplasia (BPD). Methods A total of 130 preterm infants with BPD were randomly divided into control group (n=65) and experimental group (n=65). The control group received dexamethasone acetate injection on the basis of conventional treatment, while the experimental group was treated with nebulized inhalation of budesonide suspension on the basis of the control group, and both groups were treated continuously for 10 days. The oxygen inhalation time, mechanical ventilation time, hospitalization time, clinical efficacy, and adverse reactions were compared between the two groups, and the BPD grading was also compared between the two groups at 36 weeks of corrected gestational age or at discharge. Results After treatment, the oxygen inhalation time, mechanical ventilation time, and hospitalization time in theexperimental group were shorter than those in the control group; the BPD grading in the experimental group was better than that in the control group; the clinical total effective rate in the experimental group was 89.23%, which was higher than 69.23% in the control group; all the between-group differences mentioned above were statistically significant (P < 0.05). There was no significant difference in the incidence of adverse reactions between the two groups (P>0.05). Conclusion Nebulized inhalation of budesonide combined with intravenous injection of dexamethasone is safe and effective in treating preterm infants with BPD, which can significantly shorten oxygen inhalation time, mechanical ventilation time and hospitalization time, and improve disease grading.

Humans ; RNA, Long Noncoding/genetics* ; MicroRNAs/genetics* ; Cell Line, Tumor ; Inflammation/genetics* ; Apolipoproteins E ; Apoptosis

Although the mTOR-4E-BP1 signaling pathway is implicated in aging and aging-related disorders, the role of 4E-BP1 in regulating human stem cell homeostasis remains largely unknown. Here, we report that the expression of 4E-BP1 decreases along with the senescence of human mesenchymal stem cells (hMSCs). Genetic inactivation of 4E-BP1 in hMSCs compromises mitochondrial respiration, increases mitochondrial reactive oxygen species (ROS) production, and accelerates cellular senescence. Mechanistically, the absence of 4E-BP1 destabilizes proteins in mitochondrial respiration complexes, especially several key subunits of complex III including UQCRC2. Ectopic expression of 4E-BP1 attenuates mitochondrial abnormalities and alleviates cellular senescence in 4E-BP1-deficient hMSCs as well as in physiologically aged hMSCs. These f indings together demonstrate that 4E-BP1 functions as a geroprotector to mitigate human stem cell senescence and maintain mitochondrial homeostasis, particularly for the mitochondrial respiration complex III, thus providing a new potential target to counteract human stem cell senescence.
Mesenchymal Stem Cells/physiology* ; Cellular Senescence ; Homeostasis ; Cell Cycle Proteins/metabolism* ; Adaptor Proteins, Signal Transducing/metabolism* ; Mitochondria/metabolism* ; Electron Transport Complex III/metabolism* ; Humans ; Cells, Cultured

Progressive functional deterioration in the cochlea is associated with age-related hearing loss (ARHL). However, the cellular and molecular basis underlying cochlear aging remains largely unknown. Here, we established a dynamic single-cell transcriptomic landscape of mouse cochlear aging, in which we characterized aging-associated transcriptomic changes in 27 different cochlear cell types across five different time points. Overall, our analysis pinpoints loss of proteostasis and elevated apoptosis as the hallmark features of cochlear aging, highlights unexpected age-related transcriptional fluctuations in intermediate cells localized in the stria vascularis (SV) and demonstrates that upregulation of endoplasmic reticulum (ER) chaperon protein HSP90AA1 mitigates ER stress-induced damages associated with aging. Our work suggests that targeting unfolded protein response pathways may help alleviate aging-related SV atrophy and hence delay the progression of ARHL.
Mice ; Animals ; Transcriptome ; Aging/metabolism* ; Cochlea ; Stria Vascularis ; Presbycusis

Animals ; Antlers ; Exosomes ; Mesenchymal Stem Cells ; Osteoarthritis/therapy*

Gallic Acid/pharmacology* ; Humans ; Senotherapeutics ; Stem Cells

Animals ; Chloroquine/pharmacology* ; Longevity ; Rats

Cell Differentiation ; Humans ; Hyperthermia, Induced ; Stem Cells

Cell Cycle Proteins ; Microtubule-Associated Proteins