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Chordotonal neurons are responsible for sound sensation in Drosophila. However, little is known about how they respond to sound with high sensitivity. Using genetic labeling, we found one of the Drosophila axonemal dynein heavy chains, CG9492 (DNAH5), was specifically expressed in larval chordotonal neurons and showed a distribution restricted to proximal cilia. While DNAH5 mutation did not affect the cilium morphology or the trafficking of Inactive, a candidate auditory transduction channel, larvae with DNAH5 mutation had reduced startle responses to sound at low and medium intensities. Calcium imaging confirmed that DNAH5 functioned autonomously in chordotonal neurons for larval sound sensation. Furthermore, disrupting DNAH5 resulted in a decrease of spike firing responses to low-level sound in chordotonal neurons. Intriguingly, DNAH5 mutant larvae displayed an altered frequency tuning curve of the auditory organs. All together, our findings support a critical role of DNAH5 in tuning the frequency selectivity and the sound sensitivity of larval auditory neurons.
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Objective:To observe the effects of aging performance on the property of dental zirconia sintered by microwave furnace and conventional furnace.Methods:48 zirconia wafer specimens were fabricated and randomly divided equally into 2 groups.The samples were sintered in a microwave furnace(Mgroup)and a conventional furnace(C group)respectively.The samples from the 2 groups were divided into 2 sub-groups and treated by room temperature and dry condition(A group)and 1 34 ℃ with 0.2 MPa pres-sure(B group,accelerated aging)respectively.The m phase fraction of the samples was determined by X-ray diffraction analysis.The biaxial flexural strength was examined by universal testing machine.The fracture cross section was observed by SEM.Results:CB and MB groups showed higher m phase fraction than CA and MA groups(P 0.05).Conclusion:The aging perform-ance of zircinia sintered by microwave method were similar to that sintered by conventional method.
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Objective To investigate the dynamic expression of SOCS-3, TNF-α in live and spleen of mice induced by AOPP, and to discuss the mechanism of MODS induced by AOPP, so that to give some intervention method over MODS in the future. Method Thirty-six adult BALB/c mice were divided into 3 groups randomly: AOPP group (n=12). Water normal group (n=12) and normal group (n=12). After post poison 2 hours, 6 hours, 12 hours and 24 hours,the fiver and the spleen tissue were taken out. The expression of SOCS-3 and TNF-α were detected by RT-PCR. And data were analyzed with ANOVA. Results After AOPP of 2,6,12,24 hours, the mRNA expression of SOCS-3 increased obviously in the liver and spleen compared with the normal group (P<0.05), it reached peak at the 24th hour in liver,and reached peak at the 12th hour in spleen, then descended at 24th hour (P<0.05). The mRNA expression of TNF-α increased obviously in the liver and spleen than normal group (P<0.05), and reached peak at the 12th hour,then descended at 24th hour (P<0.05), the electro-phoresis image of RNA was 5 s 15 s and 30 s,RT-PCR amplification of β-actin showed,the expression of SOCS-3, reached peak at the 24th hour in liver and it reached peak at the 12th hour in spleen, then descended at 24th hour (P<0.05), TNF-α reached peak at 12th hour in the liver and spleen, then descended at 24th hour. By statistic analysis, positive correlation was indicated among SOCS-3 and TNF-α mRNA expression in liver (y=0.089+0.758x, r=0.939, F=252. 168, P<0.01) positive correlation was indicated among socs-3 and TNF-α mRNA expression in spleen (y=0.057+0.361x,r=0.953,F=336.122, P<0.01). Conclusions At different point of time after Aopp,the mRNA expression of socs-3 and TNF-α showe the same trend in liver and spleen,the levels of SOCS-3, TNF-α all increase significenfly.
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Objective To investigate the incidence and clinicopathologic significance of MSI in breast caner.Methods 40 paired sporadic invasive breast cancer were collected.Genomic DNA was extracted from live sample.Twelve microsatellites on chromosomes 2p,3p,5q,6q,16q,17q were amplified for MSI,respectively,by polymerase chain reaction(PCR)with designed primers and detecting after polyacrylamide gel electrophoresis.Results MSI in 15 out of 40(35%)of the carcinomas were observed.There was no MSI in benign hyperplasia.MSI was mainly located at D3S1766,D2S2739 and TP53 in the breast cancer.The incidence rate of MSI in breast cancer is associated with the degree of carcinoma differentiation.Conclusions Microsatellite instability might play a role in the early stage during multistep breast carcinogenesis.MSI indicated poor histologic differentiation in breast carcinoma.D3S1766,D2S2739 and TP53 might be the sensitive sites to detect MSI in breast carcinoma transformation.