Total IgE in both serum and nasal secretion of 26 cases with perennial allergic rhinitis(PAR),14 cases with nonallergic rhinitis and 14 cases of healthy control was quantitatively measured by using Phadezym PRIST which is a solid phase enzyme immunossay based on sandwich technique.The geometric mean with standard deviation of total IgE in serum was significantly greater (P

Objective:To define the expression levels of MDM2 gene in nasopharyngeal carcinoma (NPC)and its relationship with p53 protein expression and EB virus latent infection. Method :MDM2 gene expression atmRNA and protein levels,p53 protein and EB virus DNA were detected by nonradioactive in situ hybridization(ISH) ,immunohistochemistry(IHC) and polymerase chain reaction (PCR) separately in 46 cases of NPC tissuesand 12 cases of chronic inflammation of nasopharyngeal epithelium (CINE). Result: Fourteen cases of NPCshowed MDM2 mRNA and protein overexpression, 38 cases were p53 protein positive,and 43 cases were EBV-DNA positive. Neither MDM2 nor p53 protein was expressed in any case of CINE. MDM2 expression was signifi-cantly related to p53 protein expression ( P ＜0. 05), but not to EB virus latent infection in NPC. Conclusion:MDM2 gene may play an important role in the pathogenesis of NPC through interacting with p53 protein.

Mitochondrial DNA (mtDNA) common deletion (CD) plays a significant role in aging and age-related diseases. In this study, we used D-galactose (D-gal) to generate an animal model of aging and the involvement and causative mechanisms of mitochondrial damage in such a model were investigated. Twenty 5-week-old male Sprague-Dawley rats were randomly divided into two groups: D-gal group (n=10) and control group (n=10). The quantity of the mtDNA CD in the hippocampus was determined using a TaqMan real-time PCR assay. Transmission electron microscopy was used to observe the mitochondrial ultrastructure in the hippocampus. Western blot was used to detect the protein levels of NADPH oxidase (NOX) and uncoupling protein 2 (UCP2). We found that the level of mtDNA CD was significantly higher in the hippocampus of D-gal-induced aging rats than in control rats. In comparison with the control group, the mitochondrial ultrastructure in the hippocampus of D-gal-treated rats was damaged, and the protein levels of NOX and UCP2 were significantly increased in the hippocampus of D-gal-induced aging rats. This study demonstrated that the levels of mtDNA CD and NOX protein expression were significantly increased in the hippocampus of D-gal-induced aging rats. These findings indicate that NOX-dependent reactive oxygen species generation may contribute to D-gal-induced mitochondrial damage.

Objective To observe the effect of rehabilitation therapy on functional recovery in patients with hemorrhagic infarction. Methods A total of 35 patients with hemorrhagic infarction were chosen as the study group, while 35 pa-tients with pure large-area cerebral infarction were chosen as the control group. The training were began after both groups vital signs were stable and nervous system signs were not progressing. Fugl-Meyer Motor Assessment Scale (FMA) was used to assess the motor function and Modified Barthel Index (MBI) was used to assess the activity of daily living (ADL).The two groups were respectively assessed before the treatment and after one-month treatment, using the statistic software to analyze the differences. Results There was no significant difference between the control group and the study group pre-treatment, but the differences were significant after one-month treatment in two groups (P<0.01), and more significant in the hemorrhagic infarction group(P<0.05). Conclusion Rehabilitation therapy could significantly improve the motor function and the ADL of hemiplegic patients with hemorrhagic infarction, and it is more significant than the patients with pure large-area cerebral infarction.

Mitochondrial DNA (mtDNA) common deletion (CD) plays a significant role in aging and age-related diseases. In this study, we used D-galactose (D-gal) to generate an animal model of aging and the involvement and causative mechanisms of mitochondrial damage in such a model were investigated. Twenty 5-week-old male Sprague-Dawley rats were randomly divided into two groups: D-gal group (n=10) and control group (n=10). The quantity of the mtDNA CD in the hippocampus was determined using a TaqMan real-time PCR assay. Transmission electron microscopy was used to observe the mitochondrial ultrastructure in the hippocampus. Western blot was used to detect the protein levels of NADPH oxidase (NOX) and uncoupling protein 2 (UCP2). We found that the level of mtDNA CD was significantly higher in the hippocampus of D-gal-induced aging rats than in control rats. In comparison with the control group, the mitochondrial ultrastructure in the hippocampus of D-gal-treated rats was damaged, and the protein levels of NOX and UCP2 were significantly increased in the hippocampus of D-gal-induced aging rats. This study demonstrated that the levels of mtDNA CD and NOX protein expression were significantly increased in the hippocampus of D-gal-induced aging rats. These findings indicate that NOX-dependent reactive oxygen species generation may contribute to D-gal-induced mitochondrial damage.
Aging ; metabolism ; physiology ; Animals ; Galactose ; adverse effects ; metabolism ; Hippocampus ; metabolism ; physiology ; Male ; Mitochondria ; metabolism ; physiology ; NADPH Oxidases ; metabolism ; Oxidative Stress ; physiology ; Rats ; Rats, Sprague-Dawley