The coupled lattice Boltzmann method (CLBM) is applied in investigating contamination transport in shallow water flows. Shallow water equations and advection-diffusion equation are both solved using lattice Boltzmann method (LBM) on a D2Q9 square lattice and Bhatnagar-Gross-Krook (BGK) term. For extending application of CLBM in shallow water flows, the well-balanced scheme is introduced to replace the source term. Three cases including dam break, 2D pure diffusion and complex tidal flow are calculated and analyzed. Dam break and 2D pure diffusion are prepared to validate the flow module and water quality module, respectively. Both the cases show satisfactory consistency between predicting results and analytical solutions. Since clear reproduction of the shock wave propagation and precise prediction of contamination transport are derived, LBM is proved to be the numerical method naturally conservative with acceptable computing error. Furthermore, complex tidal flow with irregular geometry and sinus-varied bathymetry is simulated by adopting the well-balanced treating on the source term. The velocity fields, water levels, and water quality are compared between the ebb tide and flood tide, the results of which are in excellent accordance with the physical laws during the process. Hence, it may demonstrate that improved by well-balanced scheme CLBM can be widely applicable in shallow water flow.
Rationale: PGC1α (peroxisome proliferator-activated receptor gamma coactivator 1α) represents an attractive target interfering bioenergetics and mitochondrial homeostasis, yet multiple attempts have failed to upregulate PGC1α expression as a therapy, for instance, causing cardiomyopathy. Objective: To determine whether a fine-tuning of PGC1α expression is essential for cardiac homeostasis in a context-dependent manner. Methods and Results: Moderate cardiac-specific PGC1α overexpression through a ROSA26 locus knock-in strategy was utilized in WT (wild type) mice and in G3Terc −/− (third generation of telomerase deficient; hereafter as G3) mouse model, respectively. Ultrastructure, mitochondrial stress, echocardiographic, and a variety of biological approaches were applied to assess mitochondrial physiology and cardiac function. While WT mice showed a relatively consistent PGC1α expression from 3 to 12 months old, age-matched G3 mice exhibited declined PGC1α expression and compromised mitochondrial function. Cardiac-specific overexpression of PGC1α (PGC1α OE ) promoted mitochondrial and cardiac function in 3-month-old WT mice but accelerated cardiac aging and significantly shortened life span in 12-month-old WT mice because of increased mitochondrial damage and reactive oxygen species insult. In contrast, cardiac-specific PGC1α knock in in G3 (G3 PGC1α OE ) mice restored mitochondrial homeostasis and attenuated senescence-associated secretory phenotypes, thereby preserving cardiac performance with age and extending health span. Mechanistically, age-dependent defect in mitophagy is associated with accumulation of damaged mitochondria that leads to cardiac impairment and premature death in 12-month-old WT PGC1α OE mice. In the context of telomere dysfunction, PGC1α induction replenished energy supply through restoring the compromised mitochondrial biogenesis and thus is beneficial to old G3 heart. Conclusions: Fine-tuning the expression of PGC1α is crucial for the cardiac homeostasis because the balance between mitochondrial biogenesis and clearance is vital for regulating mitochondrial function and homeostasis. These results reinforce the importance of carefully evaluating the PGC1α-boosting strategies in a context-dependent manner to facilitate clinical translation of novel cardioprotective therapies.
To establish a 3D finite element model of the complete human thoracic cage, and to perform a biomechanical analysis.The multislice computed tomography (MSCT) images of human thorax were obtained and used to develop a 3D reconstruction and a finite element model of the thoracic cage by finite element modeling software. The right hypochondrium area of the model was simulated to sustain the frontal impacts by a blunt impactor with velocities of 4, 6 and 8 m/s, and the distribution of stress and strain after the impact of the model was analyzed.A highly anatomically simulated finite element model of human thoracic cage was successfully developed with a fine element mean quality which was above 0.7. The biomechanical analysis showed that the thoracic cage revealed both local bending and overall deformation after the impact. Stress and strain arose from the initial impact area of the ribs, and then spread along the ribs to both sides, at last concentrated in the posterior side of the ribs and near the sternum. Impacts with velocities of 6 m/s and 8 m/s were predicted to cause rib fractures when the strain of the ribs were beyond the threshold values.The finite element modeling software is capable of establishing a highly simulated 3D finite element model of human thoracic cage. And the established model could be applicable to analyze stress and strain distribution of the thoracic cage under forces and to provide a new method for the forensic identification of chest injury.
This report presents a case of a 40-year-old woman who was found dead in her house. The examination of the body revealed no external injuries. The whole body was scanned by multi-detector-row computed tomography (CT) before autopsy, revealing massive hemorrhage in the right frontal extending into the ventricular system. At autopsy, the brain parenchyma was removed. Then CT angiography was carried on the isolated brain. Computed tomography angiography suggested a mass of irregular, tortuous vessels in areas of hemorrhage in the right frontal lobe of the brain. Finally, histological examination confirmed the result of CT angiography due to an arteriovenous malformation. Hence, postmortem CT angiography played an important role in diagnosis of the cerebral arteriovenous malformation that was responsible for a massive hemorrhage in the skull.
'/%3e%3cuse xlink:href='%23a' transform='rotate(23.036 .093 25.536)'/%3e%3cuse xlink:href='%23a' transform='rotate(45.87 1.273 16.18)'/%3e%3cuse xlink:href='%23a' transform='rotate(69.945 .996 12.078)'/%3e%3cuse xlink:href='%23a' transform='rotate(20.66 -19.689 31.932)'/%3e%3c/svg%3e)
'/%3e%3cpath fill='%23fff' d='m8.751-17.959 10.11 11.373L3.997-9.844l13.94-6.1-7.692 13.129z'/%3e%3c/svg%3e)
