miR-15a and miR-16 modulate drug resistance by targeting bcl-2 in human colon cancer cells / 中华肿瘤杂志

<p><b>OBJECTIVE</b>To investigate the reversal effect of targeted modulation of bcl-2 expression by miR-15a and miR-16 on drug resistance of human colon cancer cells.</p><p><b>METHODS</b>Mimics or inhibitors of miR-15a and miR-16 were transfected into HCT8 or HCT8/VCR cells with the help of Lipofectamine 2000. The expressions of miR-15a and miR-16 mRNA were detected by RT-qPCR. The levels of bcl-2 and P-gp proteins were measured by Western blot. The inhibitory effects of VCR on growth of HCT8 and HCT8/VCR cells were detected by CCK8.</p><p><b>RESULTS</b>After transfection of the mimics, the expression of miR-15a in the blank control group, negative control group and miR-15a mimic group was 1.00, 0.87 ± 0.24, and 223.44 ± 59.07, respectively, and miR-15a was increased significantly (P < 0.001). The expression of miR-16 in the blank control group, negative control group and miR-16 mimic group was 1.00, 0.66 ± 0.19, and 107.32 ± 22.58, respectively, and miR-16 expression was increased significantly (P < 0.001). The Western blot assay showed that the relative expressions of bcl-2 protein in the blank control group, negative control group, miR-15a mimic group and miR-16 mimic group were 1.00, 0.97 ± 0.02, 0.51 ± 0.06, and 0.65 ± 0.03, respectively, and the expression of bcl-2 protein was decreased significantly (P < 0.05), however, the expressions of P-gp protein showed no significant difference. The CCK8 test showed that at 1, 5, 25 and 125 µg/ml concentration of VCR, the survival rates of HCT8/VCR cells were basically the same in the blank control group, negative control group, miR-15a mimic group and miR-16 mimic group, but the survival rate of HCT8/VCR cells was significantly decreased after transfection of mimics (P < 0.05). After transfection of the inhibitors, the expressions of both miR-15a and miR-16 were decreased significantly (P < 0.001). The Western blot showed that the expression of bcl-2 protein was increased (P < 0.05), while the expression of P-gp protein showed no significant difference. The CCK8 test showed that the survival rate of HCT8 cells which were transfected with inhibitors was significantly higher than that of the blank control group (P < 0.05).</p><p><b>CONCLUSIONS</b>miR-15a and miR-16 may reverse the drug resistance in human colon cancer cells. A possible mechanism is regulating the expression of bcl-2.</p>

Advances in research on automatic exposure control of mammography system / 生物医学工程学杂志

Mammography imaging is one of the most demanding imaging modalities from the point of view of the bal- ance between image quality (the visibility of small size and/or low contrast structures) and dose (screening of many asymptomatic people). Therefore, since the introduction of the first dedicated mammographic units, many efforts have been directed to seek the best possible image quality while minimizing patient dose. The performance of auto- matic exposure control (AEC) is the manifestation of this demand. The theory of AEC includes exposure detection and optimization and also involves some accomplished methodology. This review presents the development and present situa- tion of spectrum optimization, detector evolution, and the way how to accomplish and evaluate AEC methods.

Effect of Midazolam on caspase-3 activation of cerebral neurons in 7-day-old rats / 第三军医大学学报

Objective To observe the effect of Midazolam on caspase-3 activation of cortical neurons in rat brain Methods The experiment consisted of part A and part B,including 64 7-day-old Sprague Dawley rats of either sex In part A 24 rats were randomly divided into 4 groups according to the time point when the arterial blood was collected after intraperitoneal injection of 180 mg/kg Midazolam(n=6 in each group),group A1 without Midazolam treatment as control,group A2 (15 min),group A3 (30 min),group A4 (60 min) In part B,40 rats were randomly divided into groups B2-B5 (n=8 in each group) according to the dose of Midazolam (45,90,145,180 mg/kg) and group B1 as control receiving 180 mg/kg normal saline Both control and experimental rats were perfused transcardially with paraformaldehyde 6 h after Midazolam treatment,then their brains takenout were used for caspase-3 examination by immunohistochemistry Results Single injection of Midazolam did not induce hypoxia/ischemia in 7-day-old SD rats,but led to the activation of caspase-3 in cerebral neurons Furthermore,higher single dose of Midazolam enhanced the activation of caspase-3 more Conclusion Midazolam triggers the activation of caspase-3 in cortical neurons and may lead to neuronal apoptosis