NISQ (Noisy, Intermediate-Scale Quantum) computing requires error mitigation to achieve meaningful computation. Our compilation tool development focuses on the fact that the error rates of individual qubits are not equal, with a goal of maximizing the success probability of real-world subroutines such as an adder circuit. We begin by establishing a metric for choosing among possible paths and circuit alternatives for executing gates between variables placed far apart within the processor, and test our approach on two IBM 20-qubit systems named Tokyo and Poughkeepsie. We find that a single-number metric describing the fidelity of individual gates is a useful but imperfect guide. Our compiler uses this subsystem and maps complete circuits onto the machine using a beam search-based heuristic that will scale as processor and program sizes grow. To evaluate the whole compilation process, we compiled and executed adder circuits, then calculated the Kullback–Leibler divergence (KL-divergence, a measure of the distance between two probability distributions). For a circuit within the capabilities of the hardware, our compilation increases estimated success probability and reduces KL-divergence relative to an error-oblivious placement.

5-Aminolevulinic acid-mediated photodynamic therapy (ALA‑PDT) is an effective treatment option for cervical intraepithelial neoplasia, the precancerous lesion of cervical cancer, and early cervical cancer, particularly for young or nulliparous women who want to remain fertile. A previous report described the involvement of histone deacetylases (HDAC) during ALA‑PDT mediated apoptosis in the cerebral cortex of a mouse model. Retinoblastoma‑associated protein 48 (RbAp48), a highly abundant component of HDACs, is a critical mediator that controls the transforming activity of human papillomavirus 16 in cervical cancer cells. The aim of the present study was to investigate the involvement of RbAp48 in ALA‑PDT‑induced cell death in cervical cancer cells. RbAp48 was significantly upregulated in cervical cancer cell lines treated with ALA‑PDT, including SiHa and HeLa cells. To establish the relevance of RbAp48 and the efficacy of ALA‑PDT in cervical cancer cells, the effect of ALA‑PDT was investigated in SiHa or HeLa cells following the depletion of RbAp48 by small interfering RNA (siRNA). Reduction of RbAp48 led to the reduced suppression of proliferation and apoptosis induced by ALA‑PDT in cervical cancer cells, which was associated with a reduction in tumor suppressor protein 53 (p53), retinoblastoma (Rb), apoptosis‑related enzyme caspase‑3, and increased levels of the oncogenic genes, human papillomavirus E6 and E7. These results provide evidence that RbAp48 is an important contributor to the efficacy of ALA‑PDT in cervical cancer cells. RbAp48 may be a therapeutic target that may help to improve the treatment of cervical cancer.

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