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SUMMARY OBJECTIVE: This study aimed to explore the risk factors of bronchopulmonary dysplasia in premature infants and the clinical application value of lung ultrasound in the diagnosis of bronchopulmonary dysplasia. METHODS: A total of 80 premature infants with a gestational age of <32 weeks or a birth weight of <1,500 g who were treated in our hospital from January to August 2021 were randomly divided into a bronchopulmonary dysplasia group (n=12) and a non-bronchopulmonary dysplasia group (n=62). The clinical data, lung ultrasound, and X-ray image characteristics of the two groups were compared. RESULTS: Among the 74 preterm infants, 12 preterm infants were diagnosed with bronchopulmonary dysplasia, and 62 preterm infants were determined not to have bronchopulmonary dysplasia. There were significant differences in sex, severe asphyxia, invasive mechanical ventilation, premature membrane ruptures, and intrauterine infection between the two groups (p<0.05). Lung ultrasound showed abnormal pleural lines and alveolar-interstitial syndrome in all 12 patients with bronchopulmonary dysplasia and vesicle inflatable signs in 3 patients. Before clinical diagnosis, the accuracy, sensitivity, specificity, positive predictive value, and negative predictive value of lung ultrasound in the diagnosis of bronchopulmonary dysplasia were 98.65, 100, 98.39, 92.31, and 100%, respectively. The accuracy, sensitivity, specificity, positive predictive value, and negative predictive value of X-rays in the diagnosis of bronchopulmonary dysplasia were 85.14, 75.00, 87.10, 52.94, and 94.74%, respectively. CONCLUSION: The diagnostic efficiency of lung ultrasound for premature bronchopulmonary dysplasia is better than that of X-rays. The application of lung ultrasound can screen patients with bronchopulmonary dysplasia early for timely intervention.
ABSTRACT
Aberrant regulation of DNA methylation plays a crucial causative role in haematological malignancies (HMs). Targeted therapy, aiming for DNA methylation, is an effective mainstay of modern medicine; however, many issues remain to be addressed. The progress of epigenetic studies and the proposed theory of "state-target medicine" have provided conditions to form a new treatment paradigm that combines the "body state adjustment" of CM with targeted therapy. We discussed the correlation between Chinese medicine (CM) syndromes/states and DNA methylation in this paper. Additionally, the latest research findings on the intervention and regulation of DNA methylation in HMs, including the core targets, therapy status, CM compounds and active components of the Chinese materia medica were concisely summarized to establish a theoretical foundation of "state-target synchronous conditioning" pattern of integrative medicine for HMs, simultaneously leading a new perspective in clinical diagnosis and therapy.
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Humans , DNA Methylation/genetics , Drugs, Chinese Herbal , Hematologic Neoplasms/genetics , Materia Medica , Medicine, Chinese TraditionalABSTRACT
Objective To explore the effect of dexmedetomidine preconditioning on antioxidant ability in Rats Brain with focal cerebral ischemia/reperfusion.Methods Forty-two healthy male SD rats,weighted 250-280 g,were randomly divided into three groups (n = 14):sham-operation group (group Sham):in which carotid artery was exposed but MCAO was not performed;ischemia/reper-fusion group(group IR):NS were injected intraperitoneally at 30 minutes before the MCAO;dexme-detomidine group (group Dex):dexmedetomidine 100 μg/kg were injected intraperitioneally injected at 30 minutes before the MCAO.Focal cerebral ischemia-reperfusion (IR)model in rats was made by transient occlusion of the middle cerebral artery occlusion (MCAO)using a nylon thread with rounded tip inserted into internal carotid artery and advanced cranially until resistance was met.MCAO was maintained for 2 hours followed by 24 hours reperfusion.Neurologic deficit scores(NDS),the infarc-tion volume as well as the activities of endogenous antioxidants (such as superoxide dismutase(SOD), glutathione peroxidase(GSH-PX),glutathione reductase (GR),catalase (CAT))in ischemic brain were evaluated 24 h after reperfusion.Results Compared to group Sham,the neurologic deficit scores and the infarction volume in group Dex and IR were significantly higher,but the concentration of SOD,GSH-PX,GR,CAT were significantly lower(P <0.05).Compared to group IR,however,the neurologic deficit scores and the infarction volume in group Dex were significantly lower,but the concentra-tion of SOD,GSH-PX,GR,CAT were significantly higher (P <0.05).Conclusion Dexmedetomidine can protect the brain from focal cerebral ischemia-reperfusion injury,and its mechanism maybe relate to preserving the activities of endogenous antioxidants.
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Objective To investigate the effect of emulsified isoflurane preconditioning on focal cerebral ischemia-reperfusion (I/R) injury in rats and the mechanism. Methods Fifty-six healthy male adult SD rats weighing 250-280 g were randomly divided into 4 groups (n = 14): group Ⅰ sham operation (group S); group Ⅱfocal cerebral I/R; group Ⅲ emulsified isoflurane preconditioning and group Ⅳ fat emulsion preconditioning. Focal cerebral ischemia was induced by middle cerebral artery occlusion (MCAO) using a nylon thread with rounded tip inserted into internal carotid artery and advanced cranially until resistance was met. MCAO was maintained for 2 h followed by 24 h reperfusion. In group Ⅲ and Ⅳ 8% emulsified isoflurane 7.5 ml/kg and 3% fat emulsion 7.5 ml/kg were injected intraperitoneally at 24 h before MCAO respectively. Neurologic outcome was evaluated at 24 h of reperfusion and scored (0 = no deficit, 4 = unable to crawl, loss of consciousness). The animals were then killed and brains removed. The infarct size was assessed. The apoptotic cells were detected by TUNEL and calculated. The expression of Bax, Bcl-2, cytochrome C and caspase-3 protein was detected by immunohistochemical staining. Results The neurologic deficit scores were significantly lower in emulsified isoflurane preconditioning group than in I/R group. Preconditioning with emulsified isoflurane significantly decreased the infarct size and the number of apoptotic cells and increased the expression of Bcl-2 protein and inhibited the expression of Bax, cytochrome C and caspace-3 protein. Conclusion Emulsified iscflurane preconditioning can protect the brain from focal cerebral I/R by increasing Bcl-2 protein expression and decreasing Bax protein expression, and reducing cytochrome C release from mitochondria, caspase-3 activation and neuronal apoptosis.