ABSTRACT
The case involved a one-month-old male infant. Around two weeks after birth, cold-like symptoms were observed within the family. Over the course of approximately one month, the infant gradually developed coughing, apnea, and cyanosis, leading to a visit to a nearby medical facility. The episodes of apnea were initiated by a wet-sounding, choking cough. Respiratory pathogen multiplex screening revealed rhinovirus infection. The infant was managed in the intensive care unit and treated with a high-flow nasal cannula (HFNC), which resulted in an improvement of the recurrent episodes of apnea. We discontinued HFNC on the 7th day of hospitalization; however, the patient had recurrence of apnea. After relieving abdominal distension through rectal enema, the infant was successfully weaned off HFNC and discharged on the 14th day of hospitalization. In addition to the immaturity of the respiratory center in infants, laryngeal chemoreflex triggered by chemical receptors in the larynx is known to contribute to apnea. In the present case, we considered that the reduction of respiratory effort through HFNC, the expectorant effect of warmed and humidified air, and the decrease in gastroesophageal reflux due to alleviation of abdominal distension played roles in the successful outcome.
ABSTRACT
BACKGROUND/OBJECTIVES@#Oocyte lipid droplets play a crucial role in meiosis and embryo development. Biotin is associated with fatty acid synthesis and is the coenzyme for acetyl-CoA carboxylase (ACC). The effects of a biotin deficiency on the oocyte lipid metabolism remain unknown. This study examined the effects of a biotin deficiency and its replenishment on murine 1) oocyte lipid droplet levels, 2) ovary lipid metabolism, and 3) oocyte meiosis.MATERIALS/METHODS: Mice were divided into 3 groups: control, biotin deficient (BD), and recovery groups. The control and BD groups were fed a control diet or BD diet (0.004 or 0 g biotin/kg), respectively. The recovery group mice were fed a BD diet until day 21, and were then fed the control diet from days 22 to 64. This study then quantified the oocyte lipid droplet levels, assessed the oocyte mitochondrial function, and examined the ability of oocytes to undergo meiosis. Ovarian phosphorylated ACC (p-ACC), lipogenesis, β-oxidation, and ATP production-related genes were evaluated. @*RESULTS@#The BD group showed a decrease in lipid droplets and mitochondrial membrane potential and increased p-ACC levels. In the recovery group, the hepatic biotin concentration, ovarian p-ACC levels, and mitochondrial membrane potential were restored to the control group levels. On the other hand, the quantity of lipid droplets in the recovery group was not restored to the control levels. Furthermore, the percentage of oocytes with meiotic abnormalities was higher in the recovery group than in the control group. @*CONCLUSIONS@#A biotin deficiency reduced the oocyte lipid droplet levels by downregulating lipogenesis. The decreased lipid droplets and increased oocyte meiosis failure were not fully restored, even though the biotin nutrition status and gene expression of lipid metabolism was resumed. These results suggest that a biotin deficiency remains robust and can be longlasting. Biotin might play a crucial role in maintaining the oocyte quality.