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Qiskit is one of the common quantum computing frameworks and and the qiskit-aer package can accelerating quantum circuit simulation using NVIDIA GPU with the help of THRUST. AMD ROCm framework similar to CUDA, a heterogeneous computing framework supporting both the NVIDIA and AMD GPUs provides the possibility to porting Qiskit/Qiskit-Aer from CUDA platform to its own. We present the porting progress of Qiskit/QiskitAer and preliminary performance test on both NVIDA and AMD GPUs. Our results show that Qiskit/Qiskit-Aer cand work well on AMD GPUs with the help of ROCm/HIP, and has comparable performance on AMD platform.

C22H10F4I2N4, monoclinic, P21/c (no. 14), a = 9.7940(3) Å, b = 5.34970(10) Å, c = 20.5119(5) Å, β = 101.673(3)°, V = 1052.49(5) Å3, Z = 2, R gt(F) = 0.0222, wR ref(F 2) = 0.0505, T = 293(2) K.

The rapid integration of social media into personal, professional, and educational settings has catalyzed the need to assess social media competence. This study provides the rationale for developing an instrument to conduct such an assessment, and the research illustrates evidence of validity and reliability in assessing social media competence in the field of higher education. The instrument includes 28 items and 4 dimensions: technical usability, content interpretation, content generation, and anticipatory reflection. Data were collected from a sample of 622 college students. Exploratory and confirmatory factor analyses were conducted, and this study finds that the instrument shows no signs of deficiency in its validity or reliability when measuring social media competence. Accordingly, the instrument could be used to evaluate and improve levels of social media competence in higher education.

Based on an extensive literature review, in this study we proposed a model of influencing factors that affect teachers' intention to adopt mobile devices in teaching. An online survey questionnaire was developed to investigate K-12 teachers' intention to adopt mobile devices in teaching and the influencing factors of that intention. Partial least squares (PLS) was employed to validate the proposed model and hypotheses using data collected from 132 primary and secondary school teachers. Results showed that teachers' attitude and technology beliefs, and their self-efficacy regarding mobile-based teaching had significant positive impacts on their intention to adopt mobile devices in teaching. Meanwhile, teachers' mobile device skills and mobile-based pedagogical knowledge strongly influenced their self-efficacy of mobile device-based teaching. Finally, the subject culture clash had a significant negative influence on teachers' attitudes, technology beliefs, and self-efficacy toward mobile-based teaching. Based on these findings, we put forward a number of suggestions to promote teaching using mobile devices.

Chronic kidney disease (CKD) is often accompanied by dyslipidemia, and abnormal lipid metabolism in proximal tubule cells is considered closely related to the dysfunction of proximal tubule cells and eventually leads to accelerated kidney damage. Nuclear factor E2-related factor 2 (Nrf2), known as a redox-sensitive transcription factor, is responsible for regulating cellular redox homeostasis. However, the exact role of Nrf2 in dyslipidemia-induced dysfunction of proximal tubule cells is still not fully elucidated. In the present study, we showed that palmitic acid (PA) induced mitochondrial damage, excessive mitochondrial reactive oxygen species (ROS) (mtROS) generation, and cell injury in HK-2 cells. We further found that mtROS generation was involved in PA-induced mitochondrial dysfunction, cytoskeletal damage, and cell apoptosis in HK-2 cells. In addition, we demonstrated that the Nrf2/ARE signaling pathway was activated in PA-induced HK-2 cells and that silencing Nrf2 dramatically aggravated PA-induced mtROS production, mitochondrial damage, cytoskeletal damage and cell apoptosis in HK-2 cells. However, the mitochondrial antioxidant MitoTEMPOL effectively eliminated these negative effects of Nrf2 silencing in HK-2 cells under PA stimulation. Moreover, activation of the Nrf2/ARE signaling pathway with tBHQ attenuated renal injury, significantly reduced mtROS generation, and improved mitochondrial function in rats with HFD-induced obesity. Taken together, these results suggest that the Nrf2/ARE-mediated antioxidant response plays a protective role in hyperlipidemia-induced renal injury by ameliorating mtROS-mediated mitochondrial dysfunction and that enhancing Nrf2 antioxidant signaling provides a potential therapeutic strategy for kidney injury in CKD with hyperlipidemia.

Aims: Oxidative stress plays a crucial role in podocyte injury in diabetic nephropathy (DN). tert-Butylhydroquinone (tBHQ) is an activator of Nrf2 that exerts protective effects in diabetic mice, but the underlying mechanism of tBHQ in the podocytes of DN is not fully understood. Materials and methods: A high glucose (HG)-induced HK2 cell model and streptozotocin-induced rat model of DN were established and treated with tBHQ or apocynin. The expression levels of Nrf2, HO-1, NOX2 and NOX4 were determined by Western blot or immunohistochemical staining. The level of oxidative stress in podocytes or kidney tissues was assessed using DCFH-DA or dihydroethidium (DHE) staining. Cell injury was assessed by F-actin staining and flow cytometry analysis. Key findings: We showed that HG treatment increased the expressions of NOX2 and NOX4 and enhanced ROS production in podocytes. Inhibition of NADPH oxidase activity by apocynin dramatically attenuated HG-induced ROS production and further alleviated cell injury and apoptosis in podocytes. Moreover, we found that HG inhibited the Nrf2/HO-1 signalling pathway in podocytes; however, tBHQ treatment significantly activated the Nrf2 signalling pathway, inhibited NADPH oxidase activity, and attenuated ROS production and cell injury in HG-treated podocytes. Furthermore, we observed that tBHQ treatment partially attenuated renal injury, activated the Nrf2 signalling pathway, inhibited NADPH oxidase activity and reduced ROS generation in the kidneys of STZ-induced diabetic rats. Significance: These results suggest that tBHQ exerts a protective role in hyperglycaemia-induced podocyte injury, and that the potential protective mechanism of tBHQ involves inhibiting NADPH oxidase-derived ROS generation by activating the Nrf2/HO-1 signalling pathway.