Objective To investigate the protective effects of the extract of ginkgo biloba(EGb)on the spiralganglion neuron(SGNs)in cochlea tissues on the hearing loss induced by noise in rats.Methods Thirty-six healthy animals were randomly divided into three groups:the normal control group(n=12).the noise exposured group(n =12)and the EGb treamment group(n=12).The control group received no noise and no medications.The other two groups were exposed to the noise of 110 dB SPL for consecutively 10 days,6 hours per day.The treatment group rats were injected with 10 ml/d EGb while the other two groups with 0.9%saline of the same amount.The experiment lasted for ten days.The rats were measured by auditory brainsterm response(ABR)before and after niose exposure.The ultrastructural changes of SGNs were detected by tranismision electron microscpoe(TEM) and the contents of malondiadehyde(MDA) and activities of superoxide dismutase(SOD)were also measured.Results Hearing were signifcantlly decreased in the experimental group.Nevertheless,EGb relatively reduced the contents of MDA while increased the activities of SOD.Conclusion EGb seems to be able to moderately pretect SGNs and to play a preventive and remedial role in noise-induced hearing loss.

OBJECTIVE To investigate the effect of ischemic postcondioning on cochlea following cochlear ischemia-reperfusion injury in rats. METHODSForty two healthy male SD rats were randomly divided into 3 groups, namely, the sham operation control group, the ischemia reperfusion group and ischemic postcondinging group. There were 14 rats in each group. The content of molondialdehyde(MDA) as well as the activity of catalase(CAT)in cochlea was measured by histochemistry. The ultrastructural changes of stria vascularis capillaries of the cochlea in experimental rats were examined by transmission electron microscopy(TEM). RESULTS In the ischemia reperfusion group, the CAT activities were decreased and MDA concentrations were increased significantly compared with those in the control group. However, in the ischemic postcondinging group, the activities of CAT were increased and MDA concentrations were decreased compared with those in the ischemia reperfusion group. Moreover, lesions were detected in the stria vascularis capillaries in all the three groups. The capillaries of stria vascularis were injured severely in ischemia reperfusion group. In the ischemic postcondinging group, the damage of capillary of stria vascularis were reduced significantly compared with that in ischemia reperfusion group, the structures were near normal, and no obvious destruction was observed. COCLUSION Ischemic postconditioning may markedly reduce the excessive generation of oxygen free radical during the process of ischemia-reperfusion injury and might be a potential strategy for its therapy.

OBJECTIVE: To detect the roles of Livin and its relationship with bFGF in laryngeal squamous cell carcinoma (LSCC) through observing the expression of Livin and bFGF in laryngeal squamous cell carcinoma. METHOD: Expression of Livin and bFGF in 41 cases of LSCC (11 cases with lymph node metastasis) and 20 cases of normal soft palate mucosa were detected by immunohistochemistry. RESULT: Livin were positively detected in 29 (70.73%) cases of LSCC and negatively detected in all normal soft palate tissue. The positive rate of Livin was higher in LSCC than that in normal soft palate tissue and the expressions were significantly associated with lymph node metastasis status (P < 0.05) but not with histological grade, clinical stage and age (P > 0.05). The expression of Livin was positively correlated with the expression of bFGF. CONCLUSION The elevated expression of Livin in LSCC might play an important role in the development of laryngeal squamous cell carcinoma and bFGF might be involved in the process.
Adaptor Proteins, Signal Transducing ; metabolism ; Adult ; Aged ; Carcinoma, Squamous Cell ; metabolism ; pathology ; Female ; Fibroblast Growth Factor 2 ; metabolism ; Humans ; Inhibitor of Apoptosis Proteins ; metabolism ; Laryngeal Neoplasms ; metabolism ; pathology ; Male ; Middle Aged ; Neoplasm Proteins ; metabolism

Objectives: . Nicotine is an ingredient of tobacco, and exposure to nicotine increases the risks of various cancers, including oral cancer. Previous studies have focused on the addictive properties of nicotine, but its carcinogenic mechanism has rarely been studied. We aimed to explore the key genes in the process through which nicotine promotes the occurrence and development of oral cancer via data mining and experimental verification. Methods: . This study involved three parts. First, key genes related to nicotine-related oral cancer were screened through data mining; second, the expression and clinical significance of a key gene in oral cancer tissues were verified by bioinformatics. Finally, the expression and clinical significance of the key gene in oral cancer were histologically investigated, and the effects of its expression on cell proliferation, invasion, and drug resistance were cytologically assessed. Results: . SERPINE1 was identified as the key gene, which was upregulated in nicotine-treated oral cells and may be an independent prognostic factor for oral cancer. SERPINE1 was enriched in various pathways, such as the tumor necrosis factor and apelin pathways, and was related to the infiltration of macrophages, CD4+T cells, and CD8+T cells. Overexpression of SERPINE1 was associated with N staging and may be involved in hypoxia, angiogenesis, and metastasis. Knockdown of SERPINE1 in oral cancer cells resulted in weakened cell proliferation and invasion ability and increased sensitivity to bleomycin and docetaxel. Conclusion . This study revealed SERPINE1 as a key gene for nicotine-related oral cancer, indicating that SERPINE1 may be a novel prognostic indicator and therapeutic target for oral carcinoma.