OBJECTIVE:To observe the efficacy and safety of azithromycin sequential therapy combined with terbutaline in the treatment of mycoplasma pneumonia. METHODS:130 children with mycoplasma pneumonia were randomly divided into control group and observation group. Control group was given azithromycin sequential therapy by using 10 mg/kg Azithromycin dispersible tablet by intravenous infusion,once a day,for continuous 3-5 d,then rested for 4 d,and then given 10 mg/kg Azithromycin dis-persible tablet at a draught,once a day,for continuous 3 d,then rested for 4 d;observation group was additionally given 2.5 mg Terbutaline injection adding into 5 ml sodium chloride injection by inhalation via oxygen atomization,twice a day,10-15 min ev-ery times,and then the children were fed with warm boiled waterafter atomization. The treatment course for both groups was 4 weeks. Clinical efficacy,and changes of cytokines levels [tumor necrosis factor-α(TNF-α),interleukin-6 (IL-6),IL-8],disap-peared time of related symptoms and signs (wheezing,rales,coughing,fever),hospitalization time before and after treatment, and incidence of adverse reactions in 2 groups were observed. RESULTS:After treatment,the effective rate in observation group was significantly higher than control group,levels of TNF-α,IL-6 and IL-8 were significantly lower than control group,disap-peared time of related symptoms and signs and hospitalization time were significantly shorter than control group,the differences were statistically significant(P<0.05). There was no significant difference in the incidence of adverse reactions between 2 groups (P>0.05). CONCLUSIONS:Azithromycin sequential therapy combined with terbutalineaerosol therapycan effectively improve the cytokines levels and clinical efficacy,with good safety.

Sleep deprivation (SD) has a profound impact on the central nervous system, resulting in an array of mood disorders, including depression and anxiety. Despite this, the dynamic alterations in neuronal activity during sleep deprivation have not been extensively investigated. While some researchers propose that sleep deprivation diminishes neuronal activity, thereby leading to depression. Others argue that short-term sleep deprivation enhances neuronal activity and dendritic spine density, potentially yielding antidepressant effects. In this study, a two-photon microscope was utilized to examine the calcium transients of anterior cingulate cortex (ACC) neurons in awake SD mice in vivo at 24-hour intervals. It was observed that SD reduced the frequency and amplitude of Ca2+ transients while increasing the proportions of inactive neurons. Following the cessation of sleep deprivation, neuronal calcium transients demonstrated a gradual recovery. Moreover, whole-cell patch-clamp recordings revealed a significant decrease in the frequency of spontaneous excitatory post-synaptic current (sEPSC) after SD. The investigation also assessed several oxidative stress parameters, finding that sleep deprivation substantially elevated the level of malondialdehyde (MDA), while simultaneously decreasing the expression of Nuclear Factor erythroid 2-Related Factor 2 (Nrf2) and activities of Superoxide dismutase (SOD) in the ACC. Importantly, the administration of gallic acid (GA) notably mitigated the decline of calcium transients in ACC neurons. GA was also shown to alleviate oxidative stress in the brain and improve cognitive impairment caused by sleep deprivation. These findings indicate that the calcium transients of ACC neurons experience a continuous decline during sleep deprivation, a process that is reversible. GA may serve as a potential candidate agent for the prevention and treatment of cognitive impairment induced by sleep deprivation.