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The theory modal of dynamic AFM probe under vibration surface and also the corresponding normalized form are set up, while the frequency range of the out-of-plain vibration of the sample (i.e. the frequency ratio of the sample vibration frequency and the probe's working frequency in the normalized form) that dynamic AFM can measure is the most important to analyzed. Runge-Kutta numerical method is used to analyze the feasibility and the bandwidth of AFM vibration measuring technique. Taking fixed-fixed nanobeam resonator under electrostatic actuation as the measured sample, its out-of-plane amplitude frequency response characteristics are measured using micro-laser Doppler vibrometer (microLD), scanning tapping mode (TM) AFM and force-curve tapping mode (F-TM) AFM respectively. The accordant resonant frequency of 1.73 MHz are gained and the vibration-amplitude test results have small deviations. The frequency speciality of vibration measurement errors of dynamic AFM related with the quality and strength of the vibration sample is strongly put up.

Epigenetic silencing of E-cadherin via aberrant methylation has been investigated in various human tumors, whereas evidence for elucidating mechanism underlying reduction of E-cadherin mRNA remains unclear in non-small cell lung cancer (NSCLC). The authors previously found that reduction of E-cadherin mRNA or protein expression has been frequently observed in NSCLC. In this study, the authors explore the contribution of E-cadherin methylation to the development and progression of NSCLC. The authors directly performed the bisulfite DNA sequencing to examine CpG methylation within the 5' CpG island of E-cadherin in 35 tumor and paired normal tissue specimens from patients with primary NSCLC. Then, the authors measured the level of E-cadherin mRNA by real-time quantitative polymerase chain reaction (PCR) analysis. Despite of reduction in E-cadherin mRNA by 65.7% (23/35) and presence of methylation by 28.6% (10/35) in tumors, the authors found no association of reduction of E-cadherin mRNA level with methylation of 19 sites from -181 to -9 bp located upstream from the translation start of E-cadherin in NSCLC. In conclusion, the authors provide no evidence for the presence of aberrant methylation sites of E-cadherin in tumors from patients with NSCLC, which can explain decrease of E-cadherin mRNA. Decrease in E-cadherin mRNA may be regulated by methylation-independent pathways in NSCLC.