ZNF217 is overexpressed and enhances cell migration and invasion in colorectal carcinoma.

BACKGROUND: To investigate the expression and clinical significance of zinc finger protein 217 (ZNF217) in human colorectal carcinoma (CRC). MATERIALS AND METHODS: The expression of ZNF217 in 60 CRC tissues and matched tumor adjacent tissues, collected between January 2013 and June 2014, was assessed immunohistochemically. The relationship between the expression of ZNF217 and clinicopathlogical features was analyzed by Pearson chi-square test. In addition, siRNA was used to down-regulate the expression of ZNF217 in CRC cells. The effects of ZNF217 for cell migration and invasion were measured by wound healing assay and transwell assay, respectively. RESULTS: The expression level of ZNF217 was significantly higher in CRC tissues than in tumor adjacent tissues (p<0.05), positively correlating with tumor size, lymphatic metastasis and advanced TNM stage (p<0.05). Down-regulation of ZNF217 in CRC cells could significantly suppress cell migration and invasion. CONCLUSIONS: ZNF217 is overexpressed in colorectal carcinoma tissues and is associated with tumor malignant clinicopathological features. ZNF217 may promote CRC progression by inducing cell migration and invasion.

[A aquaporin 4 expression and effects in rat hippocampus after microwave radiation].

OBJECTIVE: To investigate the expression of aquaporin 4 (AQP4) after microwave exposure and the correlation with the brain injury by radiation. METHODS: 70 male rats were exposed to microwave whose average power density was 0, 10, 30 and 100 mW/cm(2) respectively. Rats were sacrificed at 6 h, 1 d, 3 d and 7 d after exposure. Immunohistochemistry and Western blot were used to detect the expression of AQP4 in protein level in rat hippocampus, and the expression of AQP4 in gene level was measured by in situ hybridization and RT-PCR. RESULTS: The expression of AQP4 in rat hippocampus was abnormal after 10, 30, 100 mW/cm(2) microwave exposure. The protein level showed increased at first and then recovered at 10 and 30 mW/cm(2) groups, while increased progressively in 100 mW/cm(2) group within 14 d (P < 0.01). The gene expression of AQP4 was increased (0.51 +/- 0.02) at the beginning (6 h) and then regained after 10 mW/cm(2) microwave exposure, while in 30 and 100 mW/cm(2) groups, it rose to the peak at 7 d (0.46 +/- 0.02 and 0.43 +/- 0.08) and didn't get back (P = 0.004; P = 0.012). CONCLUSION: Microwave radiation can increase the expression of AQP4 in rat hippocampus. The change might participate in the process of increasing permeability of blood-brain barrier and lead to the brain edema after microwave radiation.

Theophylline attenuates microwave-induced impairment of memory acquisition.

Numerous studies have shown that acute microwave exposure causes cognitive deficits in animals, possibly via hyperthermia, but the biological effect of microwave exposure on memory processing is still unknown. The release of adenosine is demonstrated to be a general way for the cells to respond to metabolically stressful conditions such as hypoxia and ischemia. The present study aimed to examine whether adenosine mediates biological effects of microwave exposure on memory processing using a continuous multiple-trial inhibitory avoidance task. Results demonstrated that microwave exposure for 20 min before training impaired memory acquisition and retention performance in mice, assessed by the number of training trials and by latency to enter the dark compartment. The mice exposed to microwave radiation showed a dose-dependent hyperthermia. Moreover, the cell numbers of hippocampus were decreased in the mice receiving microwave exposure at an average power density of 50 mW/cm(2), indicating the anatomical correlation to hippocampal-amygdaloid structures corresponding with the memory disrupt of the mice. Administration of theophylline, a nonspecific adenosine receptor antagonist, 30 min before microwave exposure, completely antagonized the impairment of inhibitory avoidance acquisition but not retention. These results suggest that the adenosine regulation pathway was partially involved in microwave-induced impairment of inhibitory avoidance memory.

[Changes of the expression of beta1-adrenergic receptor and M2-muscarinic acetylcholine receptor in rat hearts after high power microwave radiation].

OBJECTIVE: To investigate the effect of high power microwave (HPM) radiation on the expression of beta(1)-adrenergic receptor (beta(1)-AR) and M(2)-muscarinic acetylcholine receptor (M(2)-AchR) in cardiomyocytes. METHODS: S-band HPM device of mean power density 2 approximately 90 mW/cm(2) was used to irradiate 150 healthy Wistar male rats. Immunohistochemistry and image analysis were used to study the pathological characteristics of heart tissue and the expression of beta(1)-AR and M(2)-AchR. RESULTS: Radiation of over 10 mW/cm(2) made myocardial fibers disordered in arrangement, degeneration even sarcoplasm condensation, Pace cells necrosis, and Purkinje cells lysis in a dose-dependent manner (r = 0.968, P < 0.05). beta(1)-AR expression in endocardium, membrane and cytoplasm of myocardium of left ventricle was increased on d1 after radiation, peaked on d3 (P < 0.05) and recovered on d14. M(2)-AchR expression was peaked on d1 (P < 0.01) and recovered on d14. CONCLUSION: Certain degree intensity of HPM radiation may cause heart injury, and increased expressions of beta(1)-AR and M(2)-AchR, which may play an important role in the pathophysiology of heart injury induced by HPM.

[Studies on the injury effects of hippocampus induced by high power microwave radiation in rat].

OBJECTIVE: To study the changes of morphology and function in rat hippocampus induced by high power microwave (HPM) radiation. METHODS: Fifty male Wistar rats were radiated by HPM. Then their learning and memory abilities were tested with Y maze and were sacrificed 6 h, 1 d, 3 d and 7 d after radiation. The hippocampus was taken out to study the basic pathologic changes, apoptosis and the expressions of neuron-specific enolase (NSE) and glial fibrillary acidic protein (GFAP) by means of HE staining, Nissel body staining, in situ terminal end labeling and immunohistochemistry. RESULTS: The learning and memory abilities of rats reduced significantly after HPM radiation. HPM also resulted in rarefaction, edema and hemangiectasia of hippocampus, nervous cells degeneration and necrosis, decrease or disappearance of Nissel bodies. The injuries were more serious in field CA4 and dentate gyrus, which showed dose-effect relationship, and were progressively aggravated within 7 days. The apoptosis cells were significantly increased. NSE was increased in neurons. The NSE positive areas were also seen in the interstitial matrix and blood vessels. GFAP was increased in astrocytes, which became shorter and thicker. CONCLUSION: HPM can damage the abilities of learning and memory and results in morphologic changes in hippocampus. The major pathologic changes are degeneration, apoptosis and necrosis of neurons and edema in interstitium. NSE and GFAP play an important role in the pathologic process.