The results of the present study define a novel mechanism of action of ACEI treatment in patients with stable CAD: the augmentation of circulating EPCs with enhanced functional activity. Given the well-established role of EPCs of participating in repair after ischemic injury, stimulation of EPCs by ACEI may contribute to the clinical benefit of ACEI therapy in patients with CAD.
BackgroundThe occurrence of mandibular defects caused by tumors has been continuously increasing in China in recent years. Conversely, results of the repair of mandibular defects affect the recovery of oral function and patient appearance, and the requirements for accuracy and high surgical quality must be more stringent. Digital techniques — including model reconstruction based on medical images, computer-aided design, and additive manufacturing — have been widely used in modern medicine to improve the accuracy and quality of diagnosis and surgery. However, some special software platforms and services from international companies are not always available for most of researchers and surgeons because they are expensive and time-consuming.MethodsHere, a new technical solution for guided surgery for the repair of mandibular defects is proposed, based on general popular tools in medical image processing, 3D (3 dimension) model reconstruction, digital design, and fabrication via 3D printing. First, CT (computerized tomography) images are processed to reconstruct the 3D model of the mandible and fibular bone. The defect area is then replaced by healthy contralateral bone to create the repair model. With the repair model as reference, the graft shape and cutline are designed on fibular bone, as is the guide for cutting and shaping. The physical model, fabricated via 3D printing, including surgical guide, the original model, and the repair model, can be used to preform a titanium locking plate, as well as to design and verify the surgical plan and guide. In clinics, surgeons can operate with the help of the surgical guide and preformed plate to realize the predesigned surgical plan.ResultsWith sufficient communication between engineers and surgeons, an optimal surgical plan can be designed via some common software platforms but needs to be translated to the clinic. Based on customized models and tools, including three surgical guides, preformed titanium plate for fixation, and physical models of the mandible, grafts for defect repair can be cut from fibular bone, shaped with high accuracy during surgery, and fixed with a well-fitting preformed locking plate, so that the predesigned plan can be performed in the clinic and the oral function and appearance of the patient are recovered. This method requires 20% less operating time compared with conventional surgery, and the advantages in cost and convenience are significant compared with those of existing commercial services in China.ConclusionsThis comparison between two groups of cases illustrates that, with the proposed method, the accuracy of mandibular defect repair surgery is increased significantly and is less time-consuming, and patients are satisfied with both the recovery of oral function and their appearance. Until now, more than 15 cases have been treated with the proposed methods, so their feasibility and validity have been verified.
Background: High glucose could induce structure and function change in cardiomyocytes, PKC plays a core effect in the onset and progression of diabetic cardiomyopathy, but its underlying downstream signal transduction pathway is still not completely understood.
Our previous studies have shown that Ginkgo biloba extract increased endothelial progenitor-cell (EPC) numbers and functional activity. However, the mechanisms remain to be determined. Recent studies have demonstrated that increased EPC numbers and activity were associated with the inhibition of EPC senescence, which involved activation of telomerase. Therefore, we investigated whether Ginkgo biloba extract inhibited the onset of EPC senescence through telomerase activation, leading to potentiation of cellular activity. After ex vivo cultivation, EPCs became senescent as determined by acidic ss-galactosidase staining. Ginkgo biloba extract dose-dependently prevented the onset of EPC senescence in culture. Moreover, Ginkgo biloba extract increased proliferation of EPCs as assessed by MTT assay and colony-forming capacity. To get further insights into the underlying mechanisms of these effects, we measured telomerase activity and determined the phosphorylation of Akt by Western blotting. Ginkgo biloba extract significantly increased telomerase activity and phosphorylation of the serine/threonine protein kinase Akt, a downstream effector of phosphoinositide 3-kinase (PI3K). Moreover, pretreatment with PI3K inhibitor, LY294002, significantly attenuated the Ginkgo biloba extract-induced telomerase activity. Taken together, the results indicated that Ginkgo biloba extract delayed the onset of EPC senescence, which may be related to activation of telomerase through the PI3k/Akt signaling pathway. The inhibition of EPC senescence by Ginkgo biloba extract in vitro may improve the functional activity of EPCs in a way that is important for potential cell therapy.
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