[Research progress on the pathogenic mechanisms and treatment strategies of heat stroke].

Heat stroke (HS), also known as severe sunstroke, is one of the most serious heat-related disorders, characterized by rapid onset, rapid progression, aggressive condition, and high morbidity and mortality. The occurrence and development of HS are closely related to pathophysiological processes such as inflammation, oxidative stress, cell death, and coagulation failure. With the gradual discovery of the pathogenic mechanisms of HS, some drugs or therapeutic approaches targeting its molecular regulatory pathways have shown clinical promise. This review intends to provide an overview of research advances in HS types, pathogenic mechanisms, preclinical and clinically relevant therapeutic strategies, as well as to highlight the potential clinical applications of HS-related biomarkers and therapeutic targets with a view to informing the clinical management of HS.

Event-triggered distributed secure state estimation for homologous sensor attacks.

Network security technology is capable of mitigating attack signals launched by malicious attackers, thereby safeguarding and bolstering system security. Secure state estimation is a type of network defense technology that involves reconstructing the system state by measuring potential attacks. The relevant research has also been expanded to distributed systems to enable collaborative secure state estimation among different agents facing homogeneous attacks; however, such research significantly enhance the communication load of the system. On the other hand, if the homogeneous attack is non-existent or consistent, excessive network communication is definitely inefficient. An event-triggered approach is a potent technique that can alleviate communication overhead while having minimal impact on system performance. This paper proposes a mechanism for event-triggered transmission in the context of distributed secure state estimation. While communication latency and data transmission disorder may be present within the communication network, the estimation error of the proposed observer is constrained and bounded. The simulation results indicate that for stable malicious attack signals, system communication can be divided into high-frequency and low-frequency communication periods. The simulation results also shows that the maximum estimation error is proportional to the trigger threshold, allowing the observer's performance to be finely tuned to the required precision.

Ambipolar Photoresponsivity in an Ultrasensitive Photodetector Based on a WSe2/InSe Heterostructure by a Photogating Effect.

Ambipolar photoresponsivity mainly originates from intrinsic or interfacial defects. However, these defects are difficult to control and will prolong the response speed of the photodetector. Here, we demonstrate tunable ambipolar photoresponsivity in a photodetector built from vertical p-WSe2/n-InSe heterostructures with photogating effect, exhibiting ultrahigh photoresponsivity from -1.76 × 104 to 5.48 × 104 A/W. Moreover, the photodetector possesses broadband photodetection (365-965 nm), an ultrahigh specific detectivity (D*) of 5.8 × 1013 Jones, an external quantum efficiency of 1.86 × 107%, and a rapid response time of 20.8 ms. The WSe2/InSe vertical architecture has promising potential in developing high-performance nano-optoelectronics.

Research of nanopore structure of Ga2O3 film in MOCVD for improving the performance of UV photoresponse.

Using the mechanism of self-reactive etching between Ga and Ga2O3, Ga2O3 nanopore films were fabricated. The self-reactive etching effects based on as-grown and annealed Ga2O3 films by metal organic chemical vapor deposition were compared. It was found that the nanopore film based on as-grown Ga2O3 film has a uniform size, high density and a small diameter. Ultraviolet-visible light reflection spectra and transmission spectra show that the nanopore film could effectively reduce the reflectivity of light and enhance the light absorption. Based on the as-grown Ga2O3 film and its nanopore film, metal-semiconductor-metal structure solar blind ultraviolet photodetectors (PD) were fabricated. Under 5 V bias, the light-dark current ratio of the nanopore film PD is about 2.5 × 102 times that of the film PD, the peak responsivity of the nanopore film PD is about 49 times that of the film PD. The rejection ratio is 4.6 × 103, about 1.15 × 102 times that of the film PD. The nanopore structure effectively increases the surface-volume ratio of film. The photoelectric detection performance and response performance of the nanopore film PD could be significantly enhanced.

Knockdown of miR-1275 protects against cardiomyocytes injury through promoting neuromedin U type 1 receptor.

The present study aimed to assess the role of miR-1275 in cardiac ischemia reperfusion injury. H9 human embryonic stem cell (hESC)-derived cardiomyocytes stimulated by oxygen-glucose deprivation/reoxygenation (OGD/R) were used to simulate myocardial injury in vitro. miR-1275 expression levels in cells were measured by RT-qPCR. The release of lactate dehydrogenase (LDH) and creatine kinase (CK) was examined through LDH and CK ELISA kits. Cell apoptosis was detected through flow cytometry. A Fura-2 Calcium Flux Assay Kit and a Fluo-4 assay kit were used to determine the Ca2+ concentration. Expression levels of proteins were tested by Western blotting. The binding effect of miR-1275 and neuromedin U type 1 receptor (NMUR1) was detected by dual-luciferase activity assay. The results showed that miR-1275 was upregulated in OGD/R-stimulated cardiomyocytes. Inhibition of miR-1275 suppressed the increased activity of LDH and CK, cell apoptosis, reactive oxygen species (ROS) production, intracellular Ca2+ concentration and sarcoplasmic reticulum (SR) Ca2+ leak induced by OGD/R treatment in cardiomyocytes. miR-1275 directly targets 3'UTR of NMUR1 and negatively regulates NMUR1 expression. Silence of NMUR1 abolished the protecting effect of the miR-1275 antagomir on myocardial OGD/R injury. Our study indicated that the miR-1275 antagomir protects cardiomyocytes from OGD/R injury through the promotion of NMUR1.

Matrine suppresses airway inflammation by downregulating SOCS3 expression via inhibition of NF-κB signaling in airway epithelial cells and asthmatic mice.

UNLABELLED: Matrine has been demonstrated to attenuate allergic airway inflammation. Elevated suppressor of cytokine signaling 3 (SOCS3) was correlated with the severity of asthma. The aim of this study was to investigate the effect of matrine on SOCS3 expression in airway inflammation. In this study, we found that matrine significantly inhibited OVA-induced AHR, inflammatory cell infiltration, goblet cell differentiation, and mucous production in a dose-dependent manner in mice. Matrine also abrogated the level of interleukin (IL)-4 and IL-13, but enhanced interferon (IFN)-γ expression, both in BALF and in lung homogenates. Furthermore, matrine impeded TNF-α-induced the expression of IL-6 and adhesion molecules in airway epithelial cells (BEAS-2B and MLE-12). Additionally, we found that matrine inhibited SOCS3 expression, both in asthmatic mice and TNF-α-stimulated epithelial cells via suppression of the NF-κB signaling pathway by using pcDNA3.1-SOCS3 plasmid, SOCS3 siRNA, or nuclear factor kappa-B (NF-κB) inhibitor PDTC. CONCLUSIONS: Matrine suppresses airway inflammation by downregulating SOCS3 expression via inhibition of NF-κB signaling in airway epithelial cells and asthmatic mice.