【Abstract】ObjectiveTo discuss the molecular structures and functions of Alu repeats,and its relationships with malignant tumors. MethodsAdvances in molecular biology and oncology of Alu repeats in recent years had been reviewed. ResultsHomologous recombination between Alu repeats may result in various genetic exchanges,including duplications, deletions and translocations,cause a series of malignancy alteration by activating some oncogenes. ConclusionAlu repeats as a sort of multifunction regulatory sequences may play an important role during the carcinogenesis and progression of some tumors.
【Abstract】Objective To investigate the recent studies on the biocharacters of keratin family (e.g. genetic mutations and abnormal expressions) and their relationships with the malignant tumors. Methods The literatures of recent years on the biocharacters of keratin family (e.g. genetic mutations and abnormal expressions) and their relationships with the malignant tumors were reviewed. Results Keratin family is a kind of structural proteins in cell which plays an important role in cytomechanics and regulates cell-cycle. The mutations of keratin genes (mRNA) or the overexpression of keratin proteins would interfere with the order of cell-cycle or the integrity of cytomechanics, and lead to some diseases and malignant tumors finally. Conclusion The studies on biocharaters of keratin family (e.g. genetic mutations and abnormal expressions) are helpful in the diagnosis, staging and the evaluation of prognosis of some diseases and cancers, e.g. liver cirrhosis, breast cancer, rectum carcinoma, etc.
ObjectiveTo make the model of Wistar suckling rats Focal cortical dysplasia (FCD) by liquid nitrogen freezing brain cortex and verify it. Analysed the electroencephalogram (EEG) and magnetic resonance imaging (MRI) features of the FCD model, in order to provide theoretical and experimental basis for human FCD diagnosis and treatment. MethodsTake the first day of Wistar suckling rats as experimental object, liquid nitrogen freezing Wistar suckling rats brain cortex.Make examination of EEG and MRI for Wistar suckling rats. The Brain tissue slice of Wistar suckling rats model dyed by HE and check with light microscope examination. ResultsIn experiment group, the sample epileptic discharge rate of EEG was about 41.6% on average, and showed visible spike wave, spine slow wave frequency distribution. Experimental Wistar suckling rats MRI showed positive performance for long T1 and long T2 signal, brain tissue slices HE staining showed brain cortex layer structure and columnar structure disorder, exist abnormal neurons and the balloon sample cells. ConclusionThe method of liquid nitrogen freezing Wistar suckling rats cortex can established FCDⅢd animal models successfully, and showed specific EEG and MRI, which has important value for diagnosis and treatment of human FCD.
ObjectiveTo analyze the effect of mitochondrial ultrastructural changes caused by morphine toxicity on abnormal discharge of cat cerebral cortex, and to explore the possible mechanism of brain function damage caused by morphine dependence.MethodsTwelve domestic cats were divided into control group (3 cats) and morphine exposed group (9 cats) according to the method of random number table. After the model was successfully established by the method of dose increasing, the changes of mitochondrial ultrastructure of cortical neurons were observed under the electron microscope.ResultsElectroencephalogram (EEG) monitoring in morphine exposed group showed that the cortical EEG was widely abnormal, physiological waves were reduced, and abnormal discharges were frequent. And the electron microscopy showed that the number, morphology, internal membrane structure and the inclusion body in the matrix of neurons changed in various aspects. The EEG and electron microscopy of the control group were normal.ConclusionMorphine can damage neurons in the cerebral cortex and lead to abnormal discharge, which is closely related to the ultrastructural changes of neuron mitochondria. The toxicity of morphine mitochondria can be the initial mechanism of energy metabolism dysfunction of brain cells and eventually lead to the disorder of brain electrophysiological function.