Establishment of an individualized three-dimensional finite element model of type A coronary artery lesions / 中国组织工程研究

BACKGROUND:A cardiac model can be established by finite element analysis based on patient's MRI imaging data.The established model can be used to evaluate the rheological changes of the coronary artery by liquid-solid coupling.OBJECTIVE:To establish finite element models of the heart and coronary artery in patients with type A coronary artery disease using finite element analysis software,followed by three-dimensional (3D) printing,thereby providing a scientific basis for further simulation of interventional surgery.METHODS:Three patients with type A coronary artery lesions underwent MRI scanning from the aortic arch to the apex.The MRI images were then imported into the Mimics 17.0 software in Dicom format,and a complete cardiac model involving the coronary arteries was established by modeling and geometry cleanup.The 3D model was imported into Geomagic Studio 11.0 software,and was further processed.Finally,the 3D model was imported into ANSYS14.0 finite element analysis software.The finite element model with biofunction was established by attaching the material properties,followed by 3D printing on a 3D printer.RESULTS AND CONCLUSION:The 3D finite element model of type A coronary artery lesion was established successfully in three cases.The established heart model in each case presented with grid-based hexahedral solid elements.The number of solid elements was 24 532,25 771,and 24 330,respectively.In the meanwhile,the model of each coronary branch was established:the number of element at the right coronary artery was 3 320,3 518,and 3 310;the number of elements at the circumflex branch was 1 148,1 176,and 1 164;and the number of elements at the anterior descending coronary artery was 1 025,1 049,and 1 068,respectively.Afterwards,the 3D printing was performed successfully.These results suggest that the established 3D finite element model of the heart with coronary arteries,after 3D printing,displays the right coronary artery,anterior descending artery,circumflex artery and coronary sinus clearly,which paves ways for interventional simulation.Most importantly,it lays a solid foundation for the study on the blood-vessel dual-directional coupling,which is expected to be a new scientific method for rheological research.

Mechanism of anti-apoptotic action of dipfluzine on neuronal damage of the rat hippocampal CA1 region subjected to transient forebrain ischemia / 药学学报

<p><b>AIM</b>To explore the relations between anti-apoptotic role of dipfluzine (DIP) and the death signaling transduction pathway initiated by CD95 molecules, and the transcription factor involved in the transcription regulation of CD95 molecules in the hippocampal CA1 region after transient forebrain ischemia.</p><p><b>METHODS</b>The rat forebrain transient ischemia model was established through 15 min ischemia followed by 3 days reperfusion by using the four-vessel method. The rats were divided randomly into five groups: sham control group, ischemia/reperfusion (I/R) group, DIP treated groups (20, 40 and 80 mg x kg(-1) body weight, ig, separately). Western blotting and RT-PCR were performed to detect the expression changes of Fas, FasL, caspase 10 p20, caspase 8, I-kappaB-alpha, and p-I-kappaB-alpha molecules in protein and mRNA levels, separately, and immunohistochemistry for molecular localization of Fas and FasL in rat hippocampus.</p><p><b>RESULTS</b>The expression of Fas, FasL, and caspase 10 p20 in protein and mRNA levels increased after I/R, which was inhibited significantly after treatment with 20 and 40 mg x kg(-1) of DIP (P < 0.01). In 80 mg x kg(-1) of DIP group, the expression of Fas and FasL protein was not significantly different from that of I/R group (P > 0.05). The expression of caspase 8 and I-kappaB-alpha showed no significant differences in all groups (P > 0.05), and no gene expression was observed for p-I-kappaB-alpha protein in the study. DIP significantly affected molecular distribution of Fas and FasL protein in CA1 subregion of hippocampus.</p><p><b>CONCLUSION</b>DIP inhibits the death signaling transduction pathway initiated by CD95 molecules in rat hippocampal CA1 subregion, and NF-kappaB transcription factor may not be involved in the transcription regulation of CD95 molecules after transient forebrain ischemia.</p>

Involvement of nuclear factor of activated T-cells (NFATc) in calcineurin-mediated ischemic brain damage in vivo / 药学学报

<p><b>AIM</b>To study the involvements of nuclear factor of activated T-cells (NFATc) and NF-kappaB in calcineurin-mediated ischemic brain damage in vivo.</p><p><b>METHODS</b>The rat transient forebrain ischemia conducted through 15 min ischemia followed by 8, 24, and 72 h reperfusion was induced using the four-vessel method. The rats were divided randomly into five groups; sham control group, ischemia/reperfusion (I/R) group, CsA treated groups (for 8, 24, and 72 h reperfusion). Western blotting was performed to detect changes of FasL, NFATc, I-kappaB-alpha, and phospho-I-kappaB-alpha protein expression, and gel shift assays for NFAT FasL-DNA binding activities.</p><p><b>RESULTS</b>Western blotting showed that the expressions of both FasL and NFATc protein were significantly increased in the hippocampus of rat subjected to transient forebrain ischemia in comparison with those of the sham control group, which were markedly reduced by CsA. The I-kappaB-alpha protein showed no changes in all groups, and phospho-I-kappaB-alpha protein was not observed in this study. Proximal and distal FasL promoter NFAT sites bind NFAT proteins from the hippocampal neurons subjected to transient forebrain ischemia, and DNA-binding activities increased significantly compared with those of the sham control group. CsA markedly inhibited these changes.</p><p><b>CONCLUSION</b>NFATc may be involved in calcineurin-mediated ischemic brain damage and transcription factor NF-kappaB may not be involved.</p>