Hypericin enhances β-lactam antibiotics activity by inhibiting sarA expression in methicillin-resistant Staphylococcus aureus.

Bacteremia is a life-threating syndrome often caused by methicillin-resistant Staphylococcus aureus (MRSA). Thus, there is an urgent need to develop novel approaches to successfully treat this infection. Staphylococcal accessory regulator A (SarA), a global virulence regulator, plays a critical role in pathogenesis and β-lactam antibiotic resistance in Staphylococcus aureus. Hypericin is believed to act as an antibiotic, antidepressant, antiviral and non-specific kinase inhibitor. In the current study, we investigated the impact of hypericin on β-lactam antibiotics susceptibility and mechanism(s) of its activity. We demonstrated that hypericin significantly decreased the minimum inhibitory concentrations of β-lactam antibiotics (e.g., oxacillin, cefazolin and nafcillin), biofilm formation and fibronectin binding in MRSA strain JE2. In addition, hypericin significantly reduced sarA expression, and subsequently decreased mecA, and virulence-related regulators (e.g., agr RNAⅢ) and genes (e.g., fnbA and hla) expression in the studied MRSA strain. Importantly, the in vitro synergistic effect of hypericin with β-lactam antibiotic (e.g., oxacillin) translated into in vivo therapeutic outcome in a murine MRSA bacteremia model. These findings suggest that hypericin plays an important role in abrogation of β-lactam resistance against MRSA through sarA inhibition, and may allow us to repurpose the use of β-lactam antibiotics, which are normally ineffective in the treatment of MRSA infections (e.g., oxacillin)

Realization of the unidirectional amplification in a cavity magnonic system

We experimentally demonstrate the nonreciprocal microwave amplification using a cavity magnonic system, consisting of a passive cavity (i.e., the split-ring resonator), an active feedback circuit integrated with an amplifier, and a ferromagnetic spin ensemble (i.e., a yttrium-iron-garnet sphere). Combining the amplification provided by the active circuit and the nonreciprocity supported by the cavity magnonics, we implement a nonreciprocal amplifier with the functions of both unidirectional amplification and reverse isolation. The microwave signal is amplified by 11.5 dB in the forward propagating direction and attenuated in the reverse direction by -34.7 dB, giving an isolation ratio of 46.2 dB. Such a unidirectional amplifier can be readily employed in quantum technologies, where the device can simultaneously amplify the weak signal output by the quantum system and isolate the sensitive quantum system from the backscattered external noise. Also, it is promising to explore more functions and applications using a cavity magnonic system with real gain.Comment: 7 pages, 4 figure

Enhanced Strong Coupling between Spin Ensemble and non-Hermitian Topological Edge States

Light-matter interaction is crucial to both understanding fundamental phenomena and developing versatile applications. Strong coupling, robustness, and controllability are the three most important aspects in realizing light-matter interactions. Topological and non-Hermitian photonics, have provided frameworks for robustness and extensive control freedom, respectively. How to engineer the properties of the edge state such as photonic density of state, scattering parameters by using non-Hermitian engineering while ensuring topological protection has not been fully studied. Here we construct a parity-time-symmetric dimerized photonic lattice and generate complex-valued edge states via spontaneous PT-symmetry breaking. The enhanced strong coupling between the topological photonic edge mode and magnon mode in a ferromagnetic spin ensemble is demonstrated. Our research reveals the subtle non-Hermitian topological edge states and provides strategies for realizing and engineering topological light-matter interactions.Comment: 6 pages, 4 figure

Effect of PPARγ agonist (rosiglitazone) on the secretion of Th2 cytokine in asthma mice

AbstractObjectiveTo explore the effect of PPARγ agonist (rosiglitazone) on the secretion of Th2 cytokines and the proportion of immune cell subsets in asthma mice.MethodsOvalbumin (OVA)-sensitized mice were used to build asthma models. Those mice were divided into the normal control group, model group and rosiglitazone group. Differences of the changes in lung histopathology of mice in the three groups were observed through hematoxylin and eosin (HE) strain, and the numbers of the total cells, eosinophils and neutrophils in BALF of mice in the three groups were compared. ELISA and real-time PCR were employed to detect the protein levels of interleukin (IL)-5, IL-13, IL-4 and IL-10 and mRNA level, respectively. Flow cytometry number was implied to analyze the proportion of immune cell subsets in peripheral blood of mice.ResultsCompared with the mice in the control group, and mice of the model group, the infiltration of inflammatory cells in BALF increased, bronchial smooth muscle became thickened, a large amount of collagen deposited, the secretion of Th2 cytokine increased significantly, the ratio of regulatory T cells (Treg) decreased, the ratio of T17 cells rose distinctly; while in mice of the rosiglitazone group, the changes of their lung histopathology were improved obviously, the number of infiltration of inflammatory cells declined, the thickened smooth muscle relieved, the deposition of collagen decreased, the secretion of Th2 cytokine was inhibited, the ratio of Treg went up, and the increased of the ratio of T17 cells was inhibited but still not return to normal level.ConclusionsRosiglitazone can regulate the proportion of Treg and Th17 cells and inhibit the secretion of Th2 cytokines, which inhibit the airway inflammatory response for asthma mice effectively