Objective To observe the influence of inactive FRMD4A gene′s expression on the biological behavior of tongue cancer CAL-27cell. Methods FRMD4A-siRNA was transfered into CAL-27 cell by lipidosome, to the expression of FRMD4A-siRNA in CAL-27 cell after transfection was detect by qRT-PCR cell proliferation , was checked by CCK-8,the influence of inactive FRMD4A gene on cell cycle distribution of CAL-27 cell was assayed by flow cytometry. Results Compared with the control group, FRMD4A mRNA expression significantly reduced in FRMD4A-siRNA interfering group (94%) and the cell proliferation index decreased(P<0.05). The cell cycle arrested in G1 period (P<0.05). Conclusion FRMD4A-siRNA could effectively inhibit FRMD4A mRNA expression in tongue cancer CAL-27cell, impact the distribution of cell cycle, and reduce cell proliferation.

Objective: To assess the impact of viable myocardium in left ventricular aneurysm (LVA) and ventricular arrhythmia on prognosis of LVA patients.
Methods: A total of one hundred and sixty LVA patients who received99Tcm-MIBI SPECT and18F-FDG PET were enrolled, including 139 male and 21 female with the mean age of (58 ± 10) years.There were 42 (26.3%) patients combining ventricular arrhythmia. LVEDV, LVESV and LVEF were detected. Semi-quantitative analysis of myocardium perfusion imaging was conducted, viable myocardium in aneurysm was deifned as the perfusion-metabolism mismatch score (MMS) ≥ 2.0. According to myocardium viability, the patients were divided into 2 groups: No viability group,n=97 and With viability group,n=63;based on ventricular arrhythmia, the patients were divided into another 4 groups: Group①, viability-, ventricular arrhythmia-, n=68, Group②, viability-, ventricular arrhythmias+,n=29, Group③, viability+, ventricular arrhythmias-,n=50 and Group④, viability+,ventricular arrhythmias+,n=13. The average follow-up time was (50 ± 7) months, the end point was cardiac death. The survival curve was obtained by Kaplan-Meier method and survival rates were compared by Log-rank analysis.
Results: The mean LVEF in 160 patients was (34 ± 11) %, cardiac death occurred in 19 (11.9%) patients. Long-term survival rates in Groups①,② and③ were 94.1%, 89.7% and 86.0%, respectively,P>0.05; while in Group④, the survival rate was 61.5%, which was lower than the other 3 groups,P=0.004. Multivariate Cox regression analysis showed that female (HR=5.101, 95% CI 1.853-14.044, P=0.002), GPET-ESV (HR=1.009, 95% CI 1.002-1.015,P=0.013), interaction between MMS and ventricular arrhythmia (HR=1.368, 95%CI 1.113-1.681,P=0.003) were independent risk factors for cardiac death;while surgical treatment (HR=0.199, 95% CI 0.054-0.742,P=0.016) could decrease the risk of cardiac death.
Conclusion: Patients with viable aneurysm and ventricular arrhythmia had poor long-term prognosis; while early and active treatment is needed for them (surgery with anti-arrhythmic therapy).

Objective: To study the effect of continuous static pressure on the endoplasmic reticulum of human periodontal ligament cells (hPDLCs) and the mechanism of osteogenic differentiation. Methods: hPDLCs cultured in vitro were subjected to 1 g/cm 2 of continuous compressive pressure (CCP) by custom-made, round, glass panes for 0, 2, 4, and 6 h, respectively. Alkaline phosphatase staining was used to detect osteogenic differentiation, and real-time quantitative PCR was used to detect the expression of protein kinase receptor-like ER kinase (PERK), eukaryotic translation initiation factor 2α (eIF2α), and transcription activation factor 4 (ATF-4). The 0 h loading group was the control group. Results: After CCP treatment, the alkaline phosphatase staining of hPDLCs was blue-violet and significantly stronger than that of cells in the control group. The expression levels of PERK and ATF4 in the hPDLCs after CCP treatment were higher than those of cells in the control group (P < 0.05) and increased over time (P < 0.05). The expression of eIF2α was lower in the experimental groups than in the control group (P < 0.05) and decreased over time (P < 0.05). Conclusion Mechanical stimulation can activate ERS in hPDLCs, leading to enhanced PERK-eIF2α-ATF4 signaling and inducing osteogenic differentiation.