Lee–Yang theory clearly demonstrates where the phase transition of many-body systems occurs and the asymptotic behavior near the phase transition using the partition function under complex parameters. The complex par...Lee–Yang theory clearly demonstrates where the phase transition of many-body systems occurs and the asymptotic behavior near the phase transition using the partition function under complex parameters. The complex parameters make the direct investigation of Lee–Yang theory in practical systems challenging. Here we construct a non-Hermitian quantum system that can correspond to the one-dimensional Ising model with imaginary parameters through the equality of partition functions. By adjusting the non-Hermitian parameter,we successfully obtain the partition function under different imaginary magnetic fields and observe the Lee–Yang zeros. We also observe the critical behavior of free energy in vicinity of Lee–Yang zero that is consistent with theoretical prediction. Our work provides a protocol to study Lee–Yang zeros of the one-dimensional Ising model using a single-qubit non-Hermitian system.展开更多
Studies have shown that C1q/tumor necrosis factor-related protein-6 (CTRP6) can alleviate renal ischemia/reperfusion injury in mice. However, its role in the brain remains poorly understood. To investigate the role of...Studies have shown that C1q/tumor necrosis factor-related protein-6 (CTRP6) can alleviate renal ischemia/reperfusion injury in mice. However, its role in the brain remains poorly understood. To investigate the role of CTRP6 in cerebral ischemia/reperfusion injury associated with diabetes mellitus, a diabetes mellitus mouse model of cerebral ischemia/reperfusion injury was established by occlusion of the middle cerebral artery. To overexpress CTRP6 in the brain, an adeno-associated virus carrying CTRP6 was injected into the lateral ventricle. The result was that oxygen injury and inflammation in brain tissue were clearly attenuated, and the number of neurons was greatly reduced. In vitro experiments showed that CTRP6 knockout exacerbated oxidative damage, inflammatory reaction, and apoptosis in cerebral cortical neurons in high glucose hypoxia-simulated diabetic cerebral ischemia/reperfusion injury. CTRP6 overexpression enhanced the sirtuin-1 signaling pathway in diabetic brains after ischemia/reperfusion injury. To investigate the mechanism underlying these effects, we examined mice with depletion of brain tissue-specific sirtuin-1. CTRP6-like protection was achieved by activating the sirtuin-1 signaling pathway. Taken together, these results indicate that CTRP6 likely attenuates cerebral ischemia/reperfusion injury through activation of the sirtuin-1 signaling pathway.展开更多
基金supported by the National Key R&D Program of China (Grant No. 2021YFB3202800)the National Natural Science Foundation of China (Grant No. 12174373)+2 种基金the Chinese Academy of Sciences (Grant No. GJJSTD20200001)the Innovation Program for Quantum Science and Technology (Grant No. 2021ZD0302200)Anhui Initiative in Quantum Information Technologies (Grant No. AHY050000)。
文摘Lee–Yang theory clearly demonstrates where the phase transition of many-body systems occurs and the asymptotic behavior near the phase transition using the partition function under complex parameters. The complex parameters make the direct investigation of Lee–Yang theory in practical systems challenging. Here we construct a non-Hermitian quantum system that can correspond to the one-dimensional Ising model with imaginary parameters through the equality of partition functions. By adjusting the non-Hermitian parameter,we successfully obtain the partition function under different imaginary magnetic fields and observe the Lee–Yang zeros. We also observe the critical behavior of free energy in vicinity of Lee–Yang zero that is consistent with theoretical prediction. Our work provides a protocol to study Lee–Yang zeros of the one-dimensional Ising model using a single-qubit non-Hermitian system.
基金supported by the National Natural Science Foundation of China,Nos.82102295(to WG),82071339(to LG),82001119(to JH),and 81901994(to BZ).
文摘Studies have shown that C1q/tumor necrosis factor-related protein-6 (CTRP6) can alleviate renal ischemia/reperfusion injury in mice. However, its role in the brain remains poorly understood. To investigate the role of CTRP6 in cerebral ischemia/reperfusion injury associated with diabetes mellitus, a diabetes mellitus mouse model of cerebral ischemia/reperfusion injury was established by occlusion of the middle cerebral artery. To overexpress CTRP6 in the brain, an adeno-associated virus carrying CTRP6 was injected into the lateral ventricle. The result was that oxygen injury and inflammation in brain tissue were clearly attenuated, and the number of neurons was greatly reduced. In vitro experiments showed that CTRP6 knockout exacerbated oxidative damage, inflammatory reaction, and apoptosis in cerebral cortical neurons in high glucose hypoxia-simulated diabetic cerebral ischemia/reperfusion injury. CTRP6 overexpression enhanced the sirtuin-1 signaling pathway in diabetic brains after ischemia/reperfusion injury. To investigate the mechanism underlying these effects, we examined mice with depletion of brain tissue-specific sirtuin-1. CTRP6-like protection was achieved by activating the sirtuin-1 signaling pathway. Taken together, these results indicate that CTRP6 likely attenuates cerebral ischemia/reperfusion injury through activation of the sirtuin-1 signaling pathway.
