Numerical simulation and fast method for the 0D-1D multi-scale coupled model and its application in ischemic brain tissue blood flow problems.

As living standards rise, more and more people are paying attention to their own health, especially issues such as cerebral thrombosis, cerebral infarction, and other cerebral blood flow problems. An accurate simulation of blood flow within cerebral vessels has emerged as a crucial area of research. In this study, we focus on microcirculatory blood flow in ischemic brain tissue and employ a 0D-1D geometric multi-scale coupled model to characterize this process. Given the intricate nature of human cerebral vessels, we apply a numerical method combining the finite element method and the third-order Runge-Kutta method to resolve the coupled model. To enhance computational efficiency, we introduce a fast method based on the reduced-order extrapolation algorithm. Our numerical example underscores the stability of the method and convergence accuracy to O h 3 + τ 3 , while significantly improving the accuracy and efficiency of blood flow simulation, making the mechanism analysis more accurate. Additionally, we present examples detailing variations and distribution of intracranial pressure and blood flow in ischemic brain tissue throughout a cardiac cycle. Both reduced vascular compliance and vascular stenosis can have adverse effects on intracranial cerebral pressure and blood flow, leading to insufficient local oxygen supply and negative effects on brain function. Meanwhile, there will also be corresponding changes in volume flow and pulsatile blood pressure.

Overexpression of miR-532-5p restrains oxidative stress response of chondrocytes in nontraumatic osteonecrosis of the femoral head by inhibiting ABL1.

This study is to probe into the meaning of serum miR-532-5p in nontraumatic osteonecrosis of the femoral head (ONFH), and a molecular mechanism of miR-532-5p in the development of nontraumatic ONFH. This study enrolled 96 patients diagnosed with nontraumatic ONFH and 96 patients with femoral neck fracture. The levels of miR-532-5p, ABL1, MMP-3, MMP-13, and cleaved-caspase3 were determined. Radiographic progression was assessed by ARCO staging system. Visual analog scale (VAS) and Harris hip score (HHS) were employed for evaluation of the symptomatic severity of nontraumatic ONFH. Cell viability and apoptosis in chondrocytes isolated from clinical samples were investigated with CCK-8 and flow cytometry. The levels of lactic dehydrogenase (LDH), superoxide dismutase (SOD), and malondialdehyde (MDA), mitochondrial membrane potential (ΔΨm), and reactive oxygen species (ROS) were determined. miR-532-5p was downregulated in tissues and serum of patients with nontraumatic ONFH, negatively related with ARCO staging and VAS, and positively correlated with HHS. Cell apoptosis, LDH, MDA, and ROS strengthened, while cell viability, ΔΨm, and SOD reduced in chondrocytes of nontraumatic ONFH patients. ABL1 was upregulated in cartilage tissues from nontraumatic ONFH patients. miR-532-5p targeted ABL1, and overexpressed miR-532-5p alleviated nontraumatic ONFH-induced oxidative stress damage of chondrocytes by restraining ABL1. miR-532-5p ameliorated oxidative stress injury in nontraumatic ONFH by inhibiting ABL1.