Thermodynamics of spin-orbit-coupled Bose-Einstein condensates

In this paper we develop a quantum field approach to reveal the thermodynamic properties of the trapped BEC with the equal Rashba and Dresselhaus spin-orbit couplings. In the experimentally-feasible regime, the phase transition from the separate phase to the single minimum phase can be well driven by the tunable temperature. Moreover, the critical temperature, which is independent of the trapped potential, can be derived exactly. At the critical point, the specific heat has a large jump and can be thus regarded as a promising candidate to detect this temperature-driven phase transition. In addition, we obtain the analytical expressions for the specific heat and the entropy in the different phases. In the single minimum phase, the specific heat as well as the entropy are governed only by the Rabi frequency. However, in the separate phase with lower temperature, we find that they are determined only by the strength of spin-orbit coupling. Finally, the effect of the effective atom interaction is also addressed. In the separate phase, this effective atom interaction affects dramatically on the critical temperature and the corresponding thermodynamic properties.Comment: 8 pages, 6 figure

Finite temperature Dicke phase transition of a Bose-Einstein condensate in an optical cavity

Dicke model predicts a quantum phase transition from normal to superradiant phases for a two-level atomic ensemble coupled with an optical cavity at zero temperature. In a recent pioneer experiment [Nature 464, 1301 (2010)], such a phase transition has been observed using a Bose-Einstein condensate (BEC) in an optical cavity. Compared with the original Dicke model, the experimental system features finite temperature and strong atom-photon nonlinear interaction in BEC. In this Letter, we develop a finite temperature theory for the Dicke phase transition of a BEC in an optical cavity, taking into account the atom-photon nonlinear interaction. In addition to explaining the experimentally observed transition from normal to superradiant phases at finite-temperature, we point it out that a new phase, the coexistence of normal and superradient phases, was also observed in the experiment. We show rich finite temperature phase diagrams existing in the experimental system by tuning various experimental parameters. We find that the specific heat of the BEC can serve as a powerful tool for probing various phases.Comment: 5 pages, 5 figure

Low-intensity pulsed ultrasound of different intensities differently affects myocardial ischemia/reperfusion injury by modulating cardiac oxidative stress and inflammatory reaction

IntroductionThe prevalence of ischemic heart disease has reached pandemic levels worldwide. Early revascularization is currently the most effective therapy for ischemic heart diseases but paradoxically induces myocardial ischemia/reperfusion (MI/R) injury. Cardiac inflammatory reaction and oxidative stress are primarily involved in the pathology of MI/R injury. Low-intensity pulsed ultrasound (LIPUS) has been demonstrated to reduce cell injury by protecting against inflammatory reaction and oxidative stress in many diseases, including cardiovascular diseases, but rarely on MI/R injury.MethodsThis study was designed to clarify whether LIPUS alleviates MI/R injury by alleviating inflammatory reaction and oxidative stress. Simultaneously, we have also tried to confirm which intensity of the LIPUS might be more suitable to ameliorate the MI/R injury, as well as to clarify the signaling mechanisms. MI/R and simulated ischemia/reperfusion (SI/R) were respectively induced in Sprague Dawley rats and human pluripotent stem cell-derived cardiomyocytes (hPSC-CMs). LIPUS treatment, biochemical measurements, cell death assay, estimation of cardiac oxidative stress and inflammatory reaction, and protein detections by western blotting were performed according to the protocol.ResultsIn our study, both in vivo and in vitro, LIPUS of 0.1 W/cm2 (LIPUS0.1) and 0.5 W/cm2 (LIPUS0.5) make no significant difference in the cardiomyocytes under normoxic condition. Under the hypoxic condition, MI/R injury, inflammatory reaction, and oxidative stress were partially ameliorated by LIPUS0.5 but were significantly aggravated by LIPUS of 2.5 W/cm2 (LIPUS2.5) both in vivo and in vitro. The activation of the apoptosis signal-regulating kinase 1 (ASK1)/c-Jun N-terminal kinase (JNK) pathway in cardiomyocytes with MI/R injury was partly rectified LIPUS0.5 both in vivo and in vitro.ConclusionOur study firstly demonstrated that LIPUS of different intensities differently affects MI/R injury by regulating cardiac inflammatory reaction and oxidative stress. Modulations on the ASK1/JNK pathway are the signaling mechanism by which LIPUS0.5 exerts cardioprotective effects. LIPUS0.5 is promising for clinical translation in protecting against MI/R injury. This will be great welfare for patients suffering from MI/R injury

EEG-Based Target Detection Using an RSVP Paradigm under Five Levels of Weak Hidden Conditions

Although target detection based on electroencephalogram (EEG) signals has been extensively investigated recently, EEG-based target detection under weak hidden conditions remains a problem. In this paper, we proposed a rapid serial visual presentation (RSVP) paradigm for target detection corresponding to five levels of weak hidden conditions quantitively based on the RGB color space. Eighteen subjects participated in the experiment, and the neural signatures, including P300 amplitude and latency, were investigated. Detection performance was evaluated under five levels of weak hidden conditions using the linear discrimination analysis and support vector machine classifiers on different channel sets. The experimental results showed that, compared with the benchmark condition, (1) the P300 amplitude significantly decreased (8.92 ± 1.24 μV versus 7.84 ± 1.40 μV, p = 0.021) and latency was significantly prolonged (582.39 ± 25.02 ms versus 643.83 ± 26.16 ms, p = 0.028) only under the weakest hidden condition, and (2) the detection accuracy decreased by less than 2% (75.04 ± 3.24% versus 73.35 ± 3.15%, p = 0.029) with a more than 90% reduction in channel number (62 channels versus 6 channels), determined using the proposed channel selection method under the weakest hidden condition. Our study can provide new insights into target detection under weak hidden conditions based on EEG signals with a rapid serial visual presentation paradigm. In addition, it may expand the application of brain–computer interfaces in EEG-based target detection areas

Exploring the potential use of Chinese herbs in regulating the inflammatory microenvironment of tumours based on the concept of ‘state-target identification and treatment’: a scooping review

Abstract Tumours do not exist in isolation from the organism; their growth, proliferation, motility, and immunosuppressive response are intricately connected to the tumour’s microenvironment. As tumour cells and the microenvironment coevolve, an inflammatory microenvironment ensues, propelling the phenomenon of inflammation-cancer transformation—an idea proposed by modern medicine. This review aims to encapsulate the array of representative factors within the tumour’s inflammatory microenvironment, such as interleukins (IL-6, IL-10, IL-17, IL-1β), transforming growth factor-beta (TGF-β), interferon-gamma (IFN-γ), tumour necrosis factor-alpha (TNF-α), vascular endothelial growth factor (VEGF), and matrix metalloproteinases (MMPs). Moreover, drawing upon research in traditional Chinese medicine (TCM) and pharmacology, we explore the delicate interplay between these factors and tumour-associated inflammatory cells: tumour-associated macrophages (TAMs), myeloid-derived suppressor cells (MDSCs), tumour-associated neutrophils (TANs) and dendritic cells (DCs). By analyzing the tumour-promoting effects of these entities, we delve into the connotations of Academician Tong Xiao-lin’s novel model of “state-target differentiation” and its application in the diagnosis and treatment of tumours. Our aim is to enhance the precision and targeting of tumour treatment in clinical practice. Delving deeper into our understanding of tumour pathogenesis through the lens of modern medicine, we discern the key etiology and pathogenesis throughout the entire developmental stage of tumours, unveiling the evolutionary patterns of Chinese Medicine (CM) states: heat state → phlegm state → stagnation state → deficiency state. Building upon this foundation, we devised a state-regulating formula. Simultaneously, drawing on pharmacological research in traditional Chinese medicine (TCM), we meticulously identified a range of targeted drugs that effectively modulate the aforementioned tumour-related mediators. This comprehensive strategy—a harmonious integration of state identification, target recognition, and simultaneous regulation—aims to elevate clinical efficacy. The fusion of TCM with Western medicine in tumour treatment introduces novel dimensions to the precise and refined application of TCM in clinical practice

Selenoprotein P inhibits cell proliferation and ROX production in HCC cells.

Selenoprotein P (SEPP1) is a kind of secretory glycoproteins with an antioxidant effect during the development of some diseases. In this study, we attempted to observe the expression of SEPP1 in livers from the patients with hepatocellular carcinoma (HCC) and explore its effect on HCC cells. All the tissues from patients with HCC were obtained from Affiliated Hospital of Nantong University. Western blot and immunohistochemical results showed that SEPP1 was reduced in HCC liver tissues. Its expression was negatively correlated with Ki67 expression in tissues. The expression of SEPP1 in normal liver cell line was significantly higher than those in the liver cancer cell lines. Serum starvation and release experiment demonstrated that SEPP1 expression was reduced and PCNA expression was increased, when the serum was re-added into cell culture system and the cells were on a proliferation state. After SEPP1 over-expression plasmid was transfected into HepG2 cells, cell proliferation of HepG2 cells and PCNA expression level were all inhibited by SEPP1. Results obtained via 8-isoprostane ELISA further indicated that inhibited ROS level was found in HepG2 cells transfected with SEPP1 over-expression plasmid. In addition, RT-qPCR results demonstrated that GPX1 expression levels increased in HepG2 cells transfected with SEPP1 over-expression plasmid. In conclusion, SEPP1 may inhibit the proliferation of HCC cells, accompanied by the reduction of ROS production and the increasing of GPX1 expression