CFD/CSD Coupling for an Isolated Rotor Using preCICE

Modeling a rotor blade flow field involves computing the blade motion, elastic deformation, and the three-dimensional forces and moments for specific trim conditions. Such a complex multiphysics problem, which includes a strong fluid-structure interaction, should be modeled by coupling separate solvers which are specialized on solving single-physics problems. In this work, we present a modular and extensible TAU-CAMRAD II coupling environment using the preCICE coupling library [1]. In this coupling, the aerodynamic forces and moments were computed with the CFD solver TAU. The blade control angle for the CFD simulation were determined by the CSD solver CAMRAD II. We validated the implementation using a modified model of the HART-II rotor at an advancing ratio of µ=0.3. Besides the potential that this work unlocks for future simulations of an active rotor, it also serves as an example of using preCICE for geometric multi-scale (1D-3D) coupling of closed-source solvers for periodic phenomena

MicroRNA-30a regulates cell proliferation and tumor growth of colorectal cancer by targeting CD73

Abstract Background MicroRNAs are non-coding RNAs which regulate a variety of cellular functions in the development of tumors. Among the numerous microRNAs, microRNA-30a (miR-30a) is thought to play an important role in the processes of various human tumors. In this study, we aimed to explore the role of miR-30a in the process of colorectal cancer (CRC). Methods The quantitative real-time PCR and western blot analysis were used to detect the expressions of miR-30a and CD73 in CRC cell lines and clinical tissues. The luciferase reporter assay was conducted to validate the association between miR-30a and CD73. The CCK-8, terminal deoxynucleotidyl transferase dUTP -biotin nick end labeling (TUNEL) assays and cell cycle flow cytometry were carried out to verify the biological functions of miR-30a in vitro. The nude mouse tumorigenicity experiment was used to clarify the biological role of miR-30a in vivo. Results The expression of miR-30a was significantly reduced in tumor cells and tissues of CRC. The proliferation ability of CRC cells was suppressed and the apoptosis of cells was promoted when miR-30a is over-regulated, however, the biological effects would be inverse since the miR-30a is down-regulated. CD73 is thought to be a target binding gene of miR-30a because miR-30a can bind directly to the 3′-UTR of CD73 mRNA, subsequently reducing its expression. The proliferation suppression of the CRC cells mediated by miR-30a could be rescued after up-regulating the expression of CD73. Conclusions MiR-30a plays an important role on regulating the cell proliferation and apoptosis, thus affecting the growth of the tumor in CRC. And it may participate in the disease process of CRC by regulating the expression of CD73

Additional file 1: Figure S1. of MicroRNA-30a regulates cell proliferation and tumor growth of colorectal cancer by targeting CD73

A. miR-30a expression assessed by Real-time PCR in eight CRC cell lines. B. CD73 expression assessed by western blot in eight CRC cell lines. (TIFF 1311 kb

Additional file 5: Figure S5. of MicroRNA-30a regulates cell proliferation and tumor growth of colorectal cancer by targeting CD73

A. Wild-type (WT) and mutant (Mut) of putative miR-30a targeting sequences in CD73 mRNA. Mutant sequences were shown in underline. B. The miR-30a target sequence from CD73 was cloned into the 3′-UTR of a luciferase reporter gene. Seed site mutagenesis was used to control for binding specificity. Luciferase activity was determined by Dual-Luciferase Reporter Assay System. Error bars represent mean ± SD from three independent experiments. *P < 0.05, **P < 0.01 compared with the NC group. (TIFF 568 kb

Additional file 4: Figure S4. of MicroRNA-30a regulates cell proliferation and tumor growth of colorectal cancer by targeting CD73

The results of western blot for the new collected colorectal cancer tissues. (TIFF 2972 kb

Challenges in HPCQC Integration

Quantum computing's potential as an adjunct to high-performance computing (HPC) infrastructure is clear, but the integration of the two (HPCQC) faces numerous challenges. These issues primarily lie in the complex infrastructure needed for integration. Key to the HPCQC integration is the creation of a unified hybrid quantum-classical toolchain that reduces latency and supports various quantum technologies. Other obstacles include hardware-related requirements like maintaining uptime and networking. This poster focuses on the challenges