Observation on Application Effect of Arterial Puncture and Catheterization under Guidance of Intelligent Medical Care Ultrasound in Clinical Anesthesia.

In clinical anesthesia and the rescue of critically ill patients, arterial puncture and catheterization are the most commonly chosen ways to establish central arterial access for patients. Invasive arterial puncture and catheterization facilitate the grasp of real-time vital sign information of patients during surgery, which strengthens patient monitoring during surgery and improves safety. However, the traditional method of arterial puncture and cannulation through palpation of the radial artery is often prone to complications related to mechanical injury, such as hemorrhage, hematoma, and accidental perforation of the artery. Studies have shown that ultrasound-guided radial artery puncture and cannulation can shorten the puncture cannulation time, reduce the incidence of complications related to puncture cannulation, and improve the success rate of puncture cannulation. In order to verify it, this paper uses the experimental group and the control group to conduct comparative experiments and uses the neural network method to evaluate the effects of the two methods. As a more mature method of artificial intelligence, BP neural network is widely used in a wide range of applications and has the characteristics of strong generalization ability and fast convergence, so we choose it as the base model. The specific work of this paper is as follows: (1) in-depth study of the relevant theory of BP neural network (BPNN), focusing on the structure of BPNN and the working principle of algorithm; the problems to be solved in the clinical anesthesia effect evaluation have laid a theoretical foundation for the establishment of an improved BPNN evaluation model in the following chapters. (2) introduce the basic principle of genetic neural network, analyze the benefits of combining genetic neural network and BPNN; introduce in detail the process of genetic algorithm to optimize the weights and thresholds of BPNN, and establish a GA-BP evaluation model. The test proves the feasibility and superiority of the model.

GSK-3ß inhibition protects human nucleus pulposus cell against oxidative stress-inducing apoptosis through mitochondrial pathway.

BACKGROUND: Oxidative stress in the intervertebral disc leads to nucleus pulposus (NP) degeneration by inducing cell apoptosis. However, the molecular mechanisms underlying this process remain unclear. Increasing evidence indicates that GSK-3ß is related to cell apoptosis induced by oxidative stress. In this study, we explored whether GSK-3ß inhibition protects human NP cell against apoptosis under oxidative stress. METHODS AND RESULTS: Immunofluorescence staining was used to show the expression of GSK-3ß in human NP cells (NPCs). Flow cytometry, mitochondrial staining and western blot (WB) were used to detect apoptosis of treated NPCs, changes of mitochondrial membrane potential and the expression of mitochondrial apoptosis-related proteins using GSK-3ß specific inhibitor SB216763. Co-Immunoprecipitation (Co-IP) was used to demonstrate the interaction between GSK-3ß and Bcl-2. We delineated the protective effect of GSK-3ß specific inhibitor SB216763 on human NPCs apoptosis induced by oxidative stress in vitro. Further, we showed SB216763 exert the protective effect by preservation of the mitochondrial membrane potential and inhibition of caspase 3/7 activity during oxidative injury. The detailed mechanism underlying the antiapoptotic effect of GSK-3ß inhibition was also studied by analyzing mitochondrial apoptosis pathway in vitro. CONCLUSIONS: We concluded that the GSK-3ß inhibitor SB216763 protected mitochondrial membrane potential to delay nucleus pulposus cell apoptosis by inhibiting the interaction between GSK-3ß and Bcl-2 and subsequently reducing cytochrome c(Cyto-C) release and caspase-3 activation. Together, inhibition of GSK-3ß using SB216763 in NPCs may be a favorable therapeutic strategy to slow intervertebral disc degeneration.