[The effects of different occluder selection on cardiac remodeling post transcatheter closure in patients with secundum atrial septal defect].

OBJECTIVE: To evaluate the effects on cardiac remodeling post transcatheter closure by Amplatzer septal occluder selected by oval circumference formula in patients with atrial septal defect (ASD). METHODS: A total of 146 patients with ASD (68 males,mean 33.5 years) treated by transcatheter closure with the Amplatzer occluder were enrolled in this study. The diameter of defects was corrected with the oval circumference formula (group A, 73 cases) or by echocardiography (group B, 73 cases). Cardiac remodeling was assessed by transthoracic echocardiography (TTE) before the procedure, 3 days, 3 months and 6 months after ASD closure. RESULTS: The mean ASD diameter was similar between the two groups [(20.16 +/- 4.98) mm vs. (21.36 +/- 5.69) mm, P > 0.05] and the mean diameter of the selected occluder of group A was significantly smaller than that in group B [(21.95 +/- 6.78) mm vs. (25.85 +/- 6.75) mm, P < 0.05]. Procedural success rate was identical between the two groups (97.3%) and the defects were completely occluded and there was no residual shunt during the 6 months follow up period, there were also no complications during and after the procedure. The lateral diameter of right atrial (RALD), the diastolic diameter of right ventricle (RVDD), RALD/LALD, RVDD/LVDD and pulmonary diameter (PD) were significantly decreased while the lateral diameter of left atrial (LALD) and left ventricle (LVDD) were significantly increased post ASD closure in both groups. At 6 months follow up, RALD decreased by (18.63 +/- 10.59)% in group A versus (10.14 +/- 6.59)% in group B, LALD increased by (13.42 +/- 8.38)% in group A versus (9.28 +/- 4.95)% in group B and RALD/LALD ratio decreased by (26.35 +/- 11.24)% in group A versus (13.98 +/- 8.96)% in groups B (all P < 0.05). CONCLUSION: ASD occluder selection based on the oval circumferen ce formula is superior to that made by echocardiography in terms of more favorable cardiac remodeling post ASD closure.

Preliminary study of feasibility of whole body diffusion weighted imaging in diagnosis of metastasis of tumor.

OBJECTIVE: To evaluate the feasibility of whole body diffusion weighted imaging (DWI) in the diagnosis of metastatic tumor. METHODS: Fifty-six patients (40 males and 16 females, age ranging from 29 to 84 years with a mean age of 57 years) with a variety of primary tumors were investigated by whole body DWI combined with computed tomography (CT) and/or conventional magnetic resonance imaging (MRI) scans. Twelve patients underwent positron emission tomography. The final diagnosis was made on the basis of CT or high resolution CT result for lung lesion and MRI or CT result for skull, abdomen and other parts. All tumors were classified into four groups by their diameter: below 1.0 cm, 1.0-1.9 cm, 2.0-2.9 cm, and above 3.0 cm. The sensitivity and specificity of whole body DWI in the detection of metastatic tumor were analyzed. RESULTS: The sensitivities of whole body DWI for screening metastasis of the four groups were 38%, 75%, 97%, and 100%, respectively. Whole body DWI showed the highest sensitivity and specificity for detecting metastasis of the skeletal system. It was difficult to find metastatic tumor whose diameter was below 1.0 cm, or lymph nodes located in the pelvis with diameter below 2.0 cm. CONCLUSIONS: Whole body DWI is a promising method in the diagnosis of metastastic tumors. With the perfection of scanning parameter, whole body DWI should be a new effective whole body technique for tumor detection.

Schlafen 1 inhibits the proliferation and tube formation of endothelial progenitor cells.

Endothelial progenitor cells (EPCs) are the major source of cells that restore the endothelium during reendothelialization. This study was designed to investigate whether Schlafen 1 (Slfn1) has an effect on the proliferation and tube formation of EPCs in vivo. Slfn1 was expressed in rat EPCs. The overexpression of Slfn1 suppressed the proliferation and tube formation of EPCs; conversely, the knockdown of Slfn1 by shRNA promoted the proliferation and tube formation of EPCs. Furthermore, when Slfn1 was overexpressed, the EPCs were arrested in the G1 phase of the cell cycle. In contrast, when Slfn1 was knocked down, the EPCs progressed into the S phase of the cell cycle. Additionally, the overexpression of Slfn1 decreased the expression of Cyclin D1, whereas the knockdown of Slfn1 increased the expression of Cyclin D1; these findings suggest that Cyclin D1 is downstream of Slfn1 in Slfn1-mediated EPC proliferation. Taken together, these results indicate a key role for Slfn1 in the regulation of EPC biological behavior, which may provide a new target for the use of EPCs during reendothelialization.