Cancer is a malignant tumor that threatens the health of human beings, and has become the leading cause of death in urban and rural residents in China. The glycocalyx is a layer of multifunctional glycans that covers the surfaces of a variety of cells, including vascular endothelial cells, smooth muscle cells, stem cells, epithelial, osteocytes, as well as cancer cells. The glycosylation and syndecan of cancer cell glycocalyx are unique. However, heparan sulfate (HS), hyaluronic acid (HA), and syndecan are all closely associated with the processes of cancer progression, including cell migration and metastasis, tumor cell adhesion, tumorigenesis, and tumor growth. The possible underlying mechanisms may be the interruption of its barrier function, its radical role in growth factor storage, signaling, and mechanotransduction. In the later sections, we discuss glycocalyx targeting therapeutic approaches reported in animal and clinical experiments. The study concludes that cancer cells’ glycocalyx and its role in cancer progression are beginning to be known by more groups, and future studies should pay more attention to its mechanotransduction of interstitial flow-induced shear stress, seeking promising therapeutic targets with less toxicity but more specificity.

In accordance with the response to injury theory, the entry of monocytes into the intima guided by inflammation signals, taking up cholesterol and transforming into foam cells, and egress from plaques determines the progression of atherosclerosis. Multiple cytokines and receptors have been reported to be involved in monocyte recruitment such as CCL2/CCR2, CCL5/CCR5, and CX3CL1/CX3CR1, and the egress of macrophages from the plaque like CCR7/CCL19/CCL21. Interestingly, some neural guidance molecules such as Netrin-1 and Semaphorin 3E have been demonstrated to show an inhibitory effect on monocyte migration. During the processes of monocytes recruitment and migration, factors affecting the biomechanical properties (e.g., the membrane fluidity, the deformability, and stiffness) of the monocytes, like cholesterol, amyloid-β peptide (Aβ), and lipopolysaccharides (LPS), as well as the biomechanical environment that the monocytes are exposed, like the extracellular matrix stiffness, mechanical stretch, blood flow, and hypertension, were discussed in the latter section. Till now, several small interfering RNAs (siRNAs), monoclonal antibodies, and antagonists for CCR2 have been designed and shown promising efficiency on atherosclerosis therapy. Seeking more possible biochemical factors that are chemotactic or can affect the biomechanical properties of monocytes, and uncovering the underlying mechanism, will be helpful in future studies.

(1) Background: Thrombosis is the main complication in patients supported with ventricular assist devices (VAD). Models that accurately predict the risk of thrombus formation in VADs are still lacking. When VADs are clinically assisted, their complex geometric configuration and high rotating speed inevitably generate complex flow fields and high shear stress. These non-physiological factors can damage blood cells and proteins, release coagulant factors and trigger thrombosis. In this study, a more accurate model for thrombus assessment was constructed by integrating parameters such as shear stress, residence time and coagulant factors, so as to accurately assess the probability of thrombosis in three clinical VADs. (2) Methods: A mathematical model was constructed to assess platelet activation and thrombosis within VADs. By solving the transport equation, the influence of various factors such as shear stress, residence time and coagulation factors on platelet activation was considered. The diffusion equation was applied to determine the role of activated platelets and substance deposition on thrombus formation. The momentum equation was introduced to describe the obstruction to blood flow when thrombus is formed, and finally a more comprehensive and accurate model for thrombus assessment in patients with VAD was obtained. Numerical simulations of three clinically VADs (CH-VAD, HVAD and HMII) were performed using this model. The simulation results were compared with experimental data on platelet activation caused by the three VADs. The simulated thrombogenic potential in different regions of MHII was compared with the frequency of thrombosis occurring in the regions in clinic. The regions of high thrombotic risk for HVAD and HMII observed in experiments were compared with the regions predicted by simulation. (3) Results: It was found that the percentage of activated platelets within the VAD obtained by solving the thrombosis model developed in this study was in high agreement with the experimental data (r² = 0.984), the likelihood of thrombosis in the regions of the simulation showed excellent correlation with the clinical statistics (r² = 0.994), and the regions of high thrombotic risk predicted by the simulation were consistent with the experimental results. Further study revealed that the three clinical VADs (CH-VAD, HVAD and HMII) were prone to thrombus formation in the inner side of the secondary flow passage, the clearance between cone and impeller, and the corner region of the inlet pipe, respectively. The risk of platelet activation and thrombus formation for the three VADs was low to high for CH-VAD, HVAD, and HM II, respectively. (4) Conclusions: In this study, a more comprehensive and accurate thrombosis model was constructed by combining parameters such as shear stress, residence time, and coagulation factors. Simulation results of thrombotic risk received with this model showed excellent correlation with experimental and clinical data. It is important for determining the degree of platelet activation in VAD and identifying regions prone to thrombus formation, as well as guiding the optimal design of VAD and clinical treatment.

Background: Gender difference in cardiovascular diseases (CVDs) is an important topic in the field of cardiovascular medicine. In this study, we focused on the mortality difference of abdominal aortic aneurysms (AAA), which is higher for female than that of male. The aim of this study was to verify whether morphological and hemodynamic factors play their roles in this phenomenon. Methods: Patient-specific AAA models of 11 females and 23 males with similar age and body mass index (BMI) have been reconstructed based on clinical computed tomography (CT) data. Firstly, the morphological parameters (diameters, curvature, intraluminal thrombus volume, etc.) of AAA models and lumbar vertebrae models were collected and analyzed. Then, based on statistical results of morphological parameters, uniformed male and female AAA models were reconstructed, and hemodynamic simulations were conducted respectively. In post-processing, the hemodynamic performances induced by gender-different morphological geometries were analyzed and compared. Results: The comparison of morphological parameters revealed that the average curvature of lumbar vertebrae and AAA centerline of female AAA models were obviously higher than that of the male. The amount of intraluminal thrombus in female AAA models was relatively lower than that of the male. According to the hemodynamic simulation, the uniform female AAA model has higher peak pressure, lower oscillatory shear stress index (OSI), and lower relative residence time (RRT) than that of the male model, all of which put female AAA to a relatively higher risk hemodynamic situation. Conclusions: The morphological and hemodynamic features of AAA have very obvious gender differences that would induce higher risk of rupture for female AAA biomechanically. These findings would help to explore the mechanism of gender differences in AAA and draw attention to gender-specific consideration for AAA treatment. More morphological and hemodynamic indictors are suggested to be involved in the future guidelines.