Application of lung ultrasound in monitoring bronchopulmonary dysplasia and pulmonary arterial pressure in preterm infants.

OBJECTIVE: The aim of this study was to evaluate the application value of lung ultrasound in monitoring bronchopulmonary dysplasia (BPD) and pulmonary artery pressure in premature infants. PATIENTS AND METHODS: A total of 98 preterm infants diagnosed with BPD in the Fourth Hospital in Shijiazhuang were recruited, and their disease severity was classified as mild (n=32), moderate (n=33), or severe BPD (n=33) based on gestational age and oxygen concentration. Lung ultrasonography of the children was performed. The correlation between lung ventilation scores and disease severity was statistically analyzed, and the discrete optimization results were documented. The pulmonary hypertension indexes of the three groups of children were compared. RESULTS: Aberrant alterations of the pleural line were observed in all included children, and the B-line rose as the disease progressed. The duration of invasive ventilation, medication, and hospital stay increased with disease exacerbation (p<0.05). The three groups significantly differed in terms of ultrasound pulmonary ventilation scores and clinical severity (p<0.05). Only mild BDP was identified by lung ultrasound on the first day of birth (T1), and severe BDP was detectable during the first and second week (T2-T3) as well as the third and fourth week (T4-T5). Severe BPD was associated with significantly higher levels of pulmonary hypertension indices vs. mild and moderate BPD (p<0.05). CONCLUSIONS: Pulmonary ultrasonography demonstrates great potential to predict pulmonary hypertension in children and assesses the disease severity. Pulmonary ultrasound allows for dynamical real-time observation of the pulmonary lesions in children with pulmonary hypertension, thereby revealing the severity of pulmonary hypertension in premature children.

Research on mechanism of sevoflurane in alleviating cerebral ischemia-reperfusion injury in rats through JNK signaling pathway.

OBJECTIVE: To explore the specific mechanism of sevoflurane in alleviating cerebral ischemia-reperfusion injury (CIRI) in rats through the c-Jun N-terminal kinase (JNK) signaling pathway. MATERIALS AND METHODS: A total of 60 male specific pathogen-free Sprague-Dawley rats were randomly divided into sham group (n=20), model group (n=20), and sevoflurane group (n=20). In the sevoflurane group, sevoflurane (2.5%) was inhaled for 60 min at 24 h before the blockage of cerebral blood supply. The CIRI model was established using the suture method in the model group and sevoflurane group, while the right common carotid artery and external carotid artery were separated and ligated only, without suture placement, in the sham group. At 24 h after reperfusion, the neurological deficit score in each group was calculated, the water content in brain tissues in each group was detected based on dry-wet weight ratio, the infarction volume of brain tissues in each group was detected via 2,3,5-triphenyltetrazolium chloride (TTC) staining, and the apoptosis rate of brain cells in each group was detected using terminal deoxynucleotidyl transferase-mediated dUTP nick end labeling (TUNEL) assay. Moreover, the protein levels of JNK, p-JNK, B-cell lymphoma-2 (Bcl-2), and the Bcl-2 associated X protein (Bax) in brain tissues were determined using Western blotting, and the gene expressions of Bax and Bcl-2 in brain tissues were determined through fluorescence quantitative Polymerase Chain Reaction (qPCR). RESULTS: It was found that the water content in brain tissues and the cerebral infarction volume were significantly increased in the model group compared with those in the sham group (p<0.01, p<0.01), while they were notably decreased in the sevoflurane group compared with those in the model group (p<0.05, p<0.01). The neurological deficit score was significantly higher in the model group than that in the sham group (p<0.01), while it was remarkably lower in the sevoflurane group than that in the model group (p<0.01). According to the results of the TUNEL assay, the model group had an evidently higher apoptosis rate of brain cells than the sham group (p<0.01), while the sevoflurane group had a lower apoptosis rate of brain cells than the model group (p<0.05). Besides, the results of Western blotting revealed that the model group exhibited remarkably increased protein levels of JNK, p-JNK, and Bax (p<0.05, p<0.01, p<0.01) and a remarkably decreased protein level of Bcl-2 (p<0.01) compared with the sham group. Sevoflurane group had decreased protein levels of JNK, p-JNK, and Bax (p<0.05, p<0.01, p<0.01) and an increased protein level of Bcl-2 (p<0.05) in comparison with the model group. In addition, the gene expression of Bcl-2 significantly declined (p<0.01), and that of Bax remarkably rose (p<0.01) in the model group compared with those in the sham group, while the contrary is the case in the sevoflurane group compared with those in the model group (p<0.05, p<0.01). CONCLUSIONS: Sevoflurane can regulate the protein and gene expressions of Bax and Bcl-2 and reduce apoptosis in CIRI by regulating the JNK signaling pathway, thereby exerting a protective effect on brain tissues and improving the symptoms of neurological deficit.

Dexmedetomidine protects against lidocaine-induced neurotoxicity through SIRT1 downregulation-mediated activation of FOXO3a.

Lidocaine, a typical local anesthetic, has been shown to directly induce neurotoxicity in clinical settings. Dexmedetomidine (DEX) is an alpha-2-adrenoreceptor agonist that has been used as anxiolytic, sedative, and analgesic agent which has recently found to protect against lidocaine-induced neurotoxicity. Nicotinamide adenine dinucleotide-dependent deacetylase sirtuin-1 (SIRT1)/forkhead box O3 (FOXO3a) signaling is critical for maintaining neuronal function and regulation of the apoptotic pathway. In the present study, we designed in vitro and in vivo models to investigate the potential effects of lidocaine and DEX on SIRT1 and FOXO3a and to verify whether SIRT1/FOXO3a-mediated regulation of apoptosis is involved in DEX-induced neuroprotective effects against lidocaine. We found that in both PC12 cells and brains of mice, lidocaine decreased SIRT1 level through promoting the degradation of SIRT1 protein. Lidocaine also increased FOXO3a protein level and increased the acetylation of SIRT1 through inhibiting SIRT1. Upregulation of SIRT1 or downregulation of FOXO3a significantly inhibited lidocaine-induced changes in both cell viability and apoptosis. DEX significantly inhibited the lidocaine-induced decrease of SIRT1 protein level and increase of FOXO3a protein level and acetylation of FOXO3a. Downregulation of SIRT1 or upregulation of FOXO3a suppressed DEX-induced neuroprotective effects against lidocaine. The data suggest that SIRT1/FOXO3a is a potential novel target for alleviating lidocaine-induced neurotoxicity and provide more theoretical support for the use of DEX as an effective adjunct to alleviate chronic neurotoxicity induced by lidocaine.

Evaluation of the function status of the ulnar nerve in carpal tunnel syndrome.

Many carpal tunnel syndrome (CTS) patients have symptoms in both the median and ulnar digits more frequently than in the median digits alone. This is possibly because of close anatomical contiguity of the carpal tunnel and Guyon's canal, and the high pressure may also affect the latter, causing indirect compression of ulnar nerve fibers. Thus, we evaluated the functional status of the ulnar nerve in patients with CTS in order to investigate the relationship between ulnar nerve impairment and sensory symptoms of the ulnar territory. Electrophysiological studies were conducted in CTS patients and healthy controls. CTS patients were divided into the mild/moderate group and severe group; they were further divided into the symptomatic and asymptomatic subgroups according to the sensory symptom of the fifth digit region. The findings suggest that CTS patients could have coexisting ulnar nerve wrist entrapments that might exacerbate the severity of CTS. Sensory impairment in the ulnar territory was observed more frequently in the mild/moderate stage of CTS, which is associated with ulnar nerve involvement. These findings also suggest that damage to the ulnar nerve fibers caused by compression forces in Guyon's canal may underlie the ulnar spread of symptoms in CTS.