ABSTRACT
<p><b>OBJECTIVE</b>To investigate whether mammalian target of rapamycin (mTOR) kinase was abnormally activated in maldeveloped balloon cells and dysmorphic neurons of focal cortical dysplasia (FCD) with refractory epilepsy.</p><p><b>METHODS</b>A total of 12 archival cases of FCD typeIIwith medically intractable epilepsy treated between 2008 and 2010 were retrieved. Perilesional brain tissue was used as control specimens (n = 8). The expression of phosphorylated p-AKT (Ser473), p-mTOR (Ser2448) and p-P70S6K (Thr389) was investigated by imunocytochemistry.</p><p><b>RESULTS</b>The expression of p-AKT (Ser473), p-mTOR (Ser2448) and p-P70S6K (Thr389) was found in meldeveloped balloon cells and dysmorphic neurons of FCD. A weak stain in a small amount of pyramid neurons was also found in the control group.</p><p><b>CONCLUSION</b>Abnormal activation of mTOR in maldeveloped balloon cells and dysmorphic neurons of FCD may be a key molecular mechanism underlying the histological changes and repeated seizures.</p>
Subject(s)
Adolescent , Adult , Child, Preschool , Female , Humans , Male , Young Adult , Brain Diseases , Metabolism , Pathology , Epilepsy , Metabolism , Pathology , Glial Fibrillary Acidic Protein , Metabolism , Immunohistochemistry , Malformations of Cortical Development , Metabolism , Pathology , Malformations of Cortical Development, Group I , Nestin , Metabolism , Neurons , Metabolism , Phosphorylation , Proto-Oncogene Proteins c-akt , Metabolism , Ribosomal Protein S6 Kinases, 70-kDa , Metabolism , TOR Serine-Threonine Kinases , MetabolismABSTRACT
<p><b>OBJECTIVE</b>To study the clinicopathologic features of delayed radiation-induced brain injury after radiotherapy for brain tumor.</p><p><b>METHODS</b>The clinical, histopathologic and immunohistochemical features of 9 cases with delayed radiation-induced injury were evaluated.</p><p><b>RESULTS</b>The disease occurred from 6 months to 12 years after radiotherapy and often presented with headache and muscle weakness. Magnetic resonance imaging showed peripheral enhancing lesions with slight mass effect and surrounding edema. Microscopically, the major changes included coagulative necrosis, fibrinoid necrosis of vessels, vascular hyalinization with luminal stenosis and peripheral reactive gliosis. Immunostaining for hypoxia-inducible factors 1α was positive in reactive astrocytes.</p><p><b>CONCLUSIONS</b>Delayed radiation-induced brain injury is a relatively common complication of radiation therapy. The lesion was frequently misdiagnosed as brain tumor. Correct diagnosis relies on clinical, radiologic and pathologic correlation.</p>
Subject(s)
Aged , Female , Humans , Male , Middle Aged , Brain Neoplasms , Radiotherapy , Glioma , Radiotherapy , Hypoxia-Inducible Factor 1, alpha Subunit , Metabolism , Magnetic Resonance Imaging , Radiation Injuries , Diagnosis , Diagnostic Imaging , Metabolism , Pathology , General Surgery , Radiotherapy , Tomography, X-Ray ComputedABSTRACT
Objective To investigate the effects of exercise training(ET)on the expression of glucogen synthase kinase 3 bate(GSK 3?)in the adipose tissues of insulin resistant(IR)rats on a high fat diet(HFD). Methods Thirty male Wistar rats were randomly divided into a control group(n=10)and a model group(M group,n=20).Insulin resistance was established by feeding a HFD to the M group for 4 w,while rats in the control group were fed a normal diet.The IR rats were then randomly divided into two subgroups:an IR group and an ET group.All rats in the IR and ET groups were fed a HFD,but ET was administrated to the ET group for 6w.The expres- sion of GSK 3?protein in the rats'epididymis adipose tissue was detected using Western blotting,and body weight (BW),the concentrations of serum triglyceride and cholesterol(TG and TC),fasting plasma glucose(FPG)and serum insulin(FINS),as well as insulin sensitivity index(ISI)were regularly detected.Results Compared with the con- trol group,BW and the concentrations of serum TG and TC,FPG and FINS in the model group were significantly in- creased(P＜0.05),while ISI was decreased(P＜0.01).Compared with the control group,there was no difference in GSK 3 protein expression in the ET group,but the expression of GSK 3?protein in the ET group was obviously de- creased in comparison with that in the IR group(P＜0.05).Conclusion ET can ameliorate IR by decreasing GSK 3?protein expression in adipose tissues and enhancing the ingestion of glucose and the synthesis of glycogen.