ABSTRACT
<p><b>OBJECTIVE</b>To investigate the clinical efficiency of electrocoagulation for the treatment of noninvoluting congenital hemangioma.</p><p><b>METHODS</b>Sixteen infants with noninvoluting congenital hemangioma who were admitted to our hospital from January 2011 to June 2013 were included in this study. Color Doppler ultrasound was used to determine the hemangioma location, as well as its size and depth. High frequency electrocoagulation was adopted for the treatment. The output power was set at 10-20 W. The probes were inserted around the tumor or at the surface of the tumor. After switching on for 1-2 seconds, the direction and position of the probe was modulated until covering the whole tumor. After the treatment, the absorption of tumor was about 3-6 months. The efficiency was evaluated during the follow-up.</p><p><b>RESULTS</b>Tumor atrophy was obvious after treatment in all patients. The temperature around the tumor mass was decreased, and the aberrant blood signals were decreased under the ultrasonic examination. Complete or partial atrophy were observed. The efficiency was graded as level I, II, III, IV in 0, 2, 9 and 5 patients, respectively. One patient showed local infection due to improper nursing, which was completely relieved after corresponding treatment. No severe adverse events were observed.</p><p><b>CONCLUSIONS</b>High-frequency electrocoagulation is effective for treating noninvoluting congenital hemangioma through coagulating the aberrant blood vessels in the tumor, interrupting the vascular endothelial cell, blocking the aberrant blood flow, as well as leading to atrophy and absorption of tumor mass. Besides, no obvious scar is observed after the surgery.</p>
Subject(s)
Humans , Infant , Electrocoagulation , Methods , Hemangioma , Diagnostic Imaging , General Surgery , Hemangioma, Capillary , Diagnostic Imaging , General Surgery , Skin Neoplasms , Diagnostic Imaging , General Surgery , Temperature , UltrasonographyABSTRACT
Researches have shown that melatonin is neuroprotectant in ischemia/reperfusion-mediated injury.Although melatonin is known as an effective antioxidant,the mechanism of the protection cannot be explained merely by antioxidation.This study was devoted to explore other existing mechanisms by investigating whether melatonin protects ischemia/reperfusion-injured neurons through elevating autophagy,since autophagy has been frequently suggested to play a crucial role in neuron survival.To find it out,an ischemia/reperfusion model in N2a cells was established for examinations.The results showed that autophagy was significantly enhanced in N2a cells treated with melatonin at reper-fusion onset following ischemia and greatly promoted cell survival,while autophagy blockage by 3-MA led to the shortened N2a cell survival as assessed by MTT,transmission electron microscopy,and laser confocal scanning microscopy.Besides,the protein levels of LC311 and Beclinl were remarkably increased in ischemia/reperfusion-injured N2a in the presence of melatonin,whereas the expression of p-PKB,key kinase in PI3K/PKB signaling pathway,showed a decrease when compared with untreated subjects as accessed by immunoblotting.Taken together these data suggest that autophagy is possibly one of the mechanisms underlying neuroprotection of melatonin.