Chen, Huo | Search NASA

DOE OSTI2024

Adaptive variational simulation for open quantum systems

Emerging quantum hardware provides new possibilities for quantum simulation. While much of the research has focused on simulating closed quantum systems, the real-world quantum systems are mostly open. Therefore, it is essential to develop quantum algorithms that can effectively simulate open quantum systems. Here we present an adaptive variational quantum algorithm for simulating open quantum system dynamics described by the Lindblad equation. The algorithm is designed to build resource-efficient ansatze through the dynamical addition of operators by maintaining the simulation accuracy. We validate the effectiveness of our algorithm on both noiseless simulators and IBM quantum processors and observe good quantitative and qualitative agreement with the exact solution. We also investigate the scaling of the required resources with system size and accuracy and find polynomial behavior. Our results demonstrate that near-future quantum processors are capable of simulating open quantum systems.

97 MATHEMATICS AND COMPUTING↗

DOE OSTI2016

miR-203a is involved in HBx-induced inflammation by targeting Rap1a

Hepatitis B virus (HBV) causes acute and chronic hepatitis, and is one of the major causes of cirrhosis and hepatocellular carcinoma. Accumulating evidence suggests that inflammation is the key factor for liver cirrhosis and hepatocellular carcinoma. MicroRNAs play important roles in many biological processes. Here, we aim to explore the function of microRNAs in the HBX-induced inflammation. First, microarray experiment showed that HBV{sup +} liver samples expressed higher level of miR-203a compared to HBV{sup -} liver samples. To verify these alterations, HBx-coding plasmid was transfected into HepG2 cells to overexpress HBx protein. The real-time PCR results suggested that over-expression of HBx could induce up-regulation of miR-203a. To define how up-regulation of miR-203a can induce liver cells inflammation, we over-expressed miR-203a in HepG2 cells. Annexin V staining and BrdU staining suggested that overexpression of miR-203a significantly increased the cell apoptosis and proliferation, meanwhile, over-expression of miR-203a could lead to a decrease in G0/G1 phase cells and an increase in G2/M phase cells. Some cytokines production including IL-6 and IL-8 were significantly increased, but TGFβ and IFNγ were decreased in miR-203a over-expressed HepG2 cells. Luciferase reporter assay experiments, protein mass-spectrum assay and real-time PCR all together demonstrated that Rap1a was the target gene of miR-203a. Further experiments showed that these alterations were modulated through PI3K/ERK/p38/NFκB pathways. These data suggested that HBV-infection could up-regulate the expression of miR-203a, thus down regulated the expression of Rap1a and affected the PI3K/ERK/p38/NFκB pathways, finally induced the hepatitis inflammation. - Highlights: • HBX induces the over-expression of miR-203a in HepG2 cells. • miR-203a targets Rap1a to induce the inflammation in HepG2 cells. • miR-203a regulates the apoptosis and cell cycles of HepG2 cells. • miR-203a alters the MAPK signaling pathway by down-regulating the Rap1a.

60 APPLIED LIFE SCIENCES↗