The biomechanical effects of different membrane layer structures and material constitutive modeling on patient-specific cerebral aneurysms.

The prevention, control and treatment of cerebral aneurysm (CA) has become a common concern of human society, and by simulating the biomechanical environment of CA using finite element analysis (FEA), the risk of aneurysm rupture can be predicted and evaluated. The target models of the current study are mainly idealized single-layer linear elastic cerebral aneurysm models, which do not take into account the effects of the vessel wall structure, material constitution, and structure of the real CA model on the mechanical parameters. This study proposes a reconstruction method for patient-specific trilaminar CA structural modeling. Using two-way fluid-structure interaction (FSI), we comparatively analyzed the effects of the differences between linear and hyperelastic materials and three-layer and single-layer membrane structures on various hemodynamic parameters of the CA model. It was found that the numerical effects of the different CA membrane structures and material constitution on the stresses and wall deformations were obvious, but does not affect the change in its distribution pattern and had little effect on the blood flow patterns. For the same material constitution, the stress of the three-layer membrane structure were more than 10.1% larger than that of the single-layer membrane structure. For the same membrane structure, the stress of the hyperelastic material were more than 5.4% larger than that of the linear elastic material, and the displacement of the hyperelastic material is smaller than that of the linear elastic material by about 20%. And the maximum value of stress occurred in the media, and the maximum displacement occurred in the intima. In addition, the upper region of the tumor is the maximum rupture risk region for CA, and the neck of the tumor and the bifurcation of the artery are also the sub-rupture risk regions to focus on. This study can provide data support for the selection of model materials for CA simulation and analysis, as well as a theoretical basis for clinical studies and subsequent research methods.

Serum Homocysteine Level Predictive Capability for Severity of Restenosis Post Percutaneous Coronary Intervention.

Background: In stent restenosis (ISR) is one of the major complications after stent implantation. Thus, there is a growing interest in identifying a biomarker for the onset of ISR. High levels of serum homocysteine (Hcy) have been associated with the progression of cardiovascular disease. Therefore, the study was carried out to quantify the correlation between serum Hcy and ISR severity. Compared with coronary angiography (CAG), Hcy levels provided a significantly better clinical detection of ISR severity after PCI. Methods: A total of 155 patients were recruited from Shanxi Bethune hospital, from 6 months to 2 years post PCI. Serum Hcy levels and postoperative angiography results were used to differentiate the patients into two experimental groups: ISR (>50% diametrical stenosis), and non-ISR. The non-ISR included two subgroups: intimal hyperplasia (10-50% diametrical stenosis), and recovery (<10% diametrical stenosis). In addition, a group of 80 healthy individuals was used as a negative control. The correlation between homocysteine level and ISR severity t was analyzed for all groups. In addition, the correlation between serum Hcy level and the severity of ISR in the experimental group was analyzed by the Pearson correlation test. Results: The serum Hcy level in the experimental group and control group was determined to be (20.21 ± 11.42) µmol/L and (15.11 ± 10.25) µmol/L respectively. The level of serum Hcy in the experimental group was significantly higher than in the control group (t-value of 2.385; p-value of 0.019). The serum Hcy level in the restenosis and the intimal hyperplasia group was (25.72 ± 13.71) µmol/L and (17.35 ± 7.70) µmol/L respectively. The serum Hcy level in the restenosis group was significantly higher than in the intimal hyperplasia group (t-value of 2.215; p-value of 0.033). The level of serum Hcy in the group without a plaque in the stent was (16.30 ± 6.08) µmol/L, whereas in the control group was (15.11 ± 10.25) µmol/L. The no plaque group had a slightly higher serum Hcy level than the control group (t-value of 0.634; p-value of 0.528). All included patients were divided into four quartiles based on the serum Hcy concentration: quartile 1 (8.90-13.20 µmol/L), quartile 2 (13.30-16.45 µmol/L), quartile 3 (16.60-24.25 µmol/L) and quartile 4 (24.30-65.30 µ mol/L). The incidence of ISR was 5, 6.25, 7.5 and 15%, in the 1,2,3 and four quartiles respectively. The serum Hcy level in the experimental group was (20.21 ± 11.42) µmol/L, the severity of in-stent restenosis was (0.25 ± 0.31), (R-value was 0.234; p-value was 0.037), indicating a correlation between serum Hcy and the severity of restenosis (p < 0.05). Taking coronary angiography as the gold standard, a ROC curve analysis was performed on the serum Hcy levels for the experimental group. The area under the curve (AUC) was 0.718 (95% CI 0.585-0.854, p < 0.001), indicating that the serum Hcy concentration could predict ISR. On the ROC curve, the best critical value of serum Hcy concentration for predicting ISR was 20.05 µmol/L, with a sensitivity of 45% and specificity of 88.1%. Conclusion: A positive correlation was observed between homocysteine and the severity of restenosis after PCI, The level of Hcy could serve as a predictive biomarker for the severity of ISR.

Analysis on synergistic cocontraction of extrinsic finger flexors and extensors during flexion movements: A finite element digital human hand model.

Fine hand movements require the synergistic contraction of intrinsic and extrinsic muscles to achieve them. In this paper, a Finite Element Digital Human Hand Model (FE-DHHM) containing solid tendons and ligaments and driven by the Muscle-Tendon Junction (MTJ) displacements of FDS, FDP and ED measured by ultrasound imaging was developed. The synergistic contraction of these muscles during the finger flexion movements was analyzed by simulating five sets of finger flexion movements. The results showed that the FDS and FDP contracted together to provide power during the flexion movements, while the ED acted as an antagonist. The peak stresses of the FDS, FDP and ED were all at the joints. In the flexion without resistance, the FDS provided the main driving force, and the FDS and FDP alternated in a "plateau" of muscle force. In the flexion with resistance, the muscle forces of FDS, FDP, and ED were all positively correlated with fingertip forces. The FDS still provided the main driving force, but the stress maxima occurred in the FDP at the DIP joint.

Braided composite stent for peripheral vascular applications.

Braided composite stent (BCS), woven with nitinol wires and polyethylene terephthalate (PET) strips, provides a hybrid design of stent. The mechanical performance of this novel stent has not been fully investigated yet. In this work, the influence of five main design factors (number of nitinol wires, braiding angle, diameter of nitinol wire, thickness and stiffness of the PET strip) on the surface coverage, radial strength, and flexibility of the BCS were systematically studied using computational models. The orthogonal experimental design was adopted to quantitatively analyze the sensitivity of multiple factors using the minimal number of study cases. Results have shown that the nitinol wire diameter and the braiding angle are two most important factors determining the mechanical performance of the BCS. A larger nitinol wire diameter led to a larger radial strength and less flexibility of the BCS. A larger braiding angle could provide a larger radial strength and better flexibility. In addition, the impact of the braiding angle decreased when the stent underwent a large deformation. At the same time, the impact of the PET strips increased due to the interaction with nitinol wires. Moreover, the number of PET strips played an important role in the surface coverage. This study could help understand the mechanical performance of BCS stent and provides guidance on the optimal design of the stent targeting less complications.

Mechanical characterizations of braided composite stents made of helical polyethylene terephthalate strips and NiTi wires.

The novel braided composite stent (BCS), woven with both nitinol wires and polyethylene terephthalate (PET) strips, were characterized and compared with the braided nitinol stent in the same weaving pattern. Finite element models simulating the stent compression and bending were developed to quantify its radial strength and longitudinal flexibility. The interaction between the nitinol wires and the PET strips were also delineated. Results showed that the PET strips enforced more constrains on the BCS and thus enhance its radial strength especially at a larger compression load. The longitudinal flexibility of the BCS was less sensitive to the presence of the PET strips. This work suggested that the novel design of the BCS could acquire the advantage of a covered stent without compromising its mechanical performance. The fundamental understanding of the braided composite stent will facilitate a better device design.

Endoplasmic Reticulum Stress Mediated MDRV p10.8 Protein-Induced Cell Cycle Arrest and Apoptosis Through the PERK/eIF2α Pathway.

In this study, the mechanism of Muscovy duck reovirus (MDRV) p10.8 protein-induced pathogenesis was investigated, with a focus on endoplasmic reticulum (ER) stress. In chicken embryo fibroblasts cell lines (DF1), pCI-neo-flg-p10.8 protein transfection increased the phosphorylation (p-) levels of PERK and eIF2α as shown by Western blotting analysis and led to the dissociation of BiP from PERK as shown by co-immunoprecipitation (Co-IP) analysis. Results of treatment with both ER stress activator and inhibitor further confirmed that p10.8 protein induced ER stress. Subsequently, using flow cytometry analysis, it was also found that p10.8 protein induced cell cycle arrest during the G0/G1 phase. Furthermore, p10.8 transfection increased the phosphorylation levels of PERK and eIF2α, and reduced the expression levels of CDK2, CDK4, and Cyclin E according to Western blotting analysis. Treatment with ER stress activator and ER stress inhibitor after p10.8 protein transfection in DF1 cells further indicated that p10.8 protein induced ER stress, which resulted in cell cycle arrest. The results of knockdown of either PERK or eIF2α genes further confirmed that p10.8 protein-induced ER stress led to cell cycle arrest through the PERK/eIF2α pathway. Further results showed that p10.8 protein induced ER stress and apoptosis in DF1 cells. The expression levels of p-PERK, p-eIF2α, CHOP, cleaved-Caspase12, and cleaved-Caspase3 were increased by p10.8 protein. Test results of treatment with each of Tunicamycin, TUDCA and knockdown of PERK, and eIF2α, confirmed that p10.8 protein induced ER stress involving apoptosis via the PERK/eIF2α pathway. In conclusion, MDRV p10.8 protein induced ER stress that caused cell cycle arrest and apoptosis through the PERK/eIF2α pathway.