The coronavirus disease 2019 (COVID-19) is a substantial threat to people’s lives and health due to its high infectivity and rapid spread. Computed tomography (CT) scan is one of the important auxiliary methods for the clinical diagnosis of COVID-19. However, CT image lesion edge is normally affected by pixels with uneven grayscale and isolated noise, which makes weak edge detection of the COVID-19 lesion more complicated. In order to solve this problem, an edge detection method is proposed, which combines the histogram equalization and the improved Canny algorithm. Specifically, the histogram equalization is applied to enhance image contrast. In the improved Canny algorithm, the median filter, instead of the Gaussian filter, is used to remove the isolated noise points. The K -means algorithm is applied to separate the image background and edge. And the Canny algorithm is improved continuously by combining the mathematical morphology and the maximum between class variance method (OTSU). On selecting four types of lesion images from COVID-CT date set, MSE, MAE, SNR, and the running time are applied to evaluate the performance of the proposed method. The average values of these evaluation indicators are 1.7322, 7.9010, 57.1241, and 5.4887, respectively. Compared with other three methods, these values indicate that the proposed method achieves better result. The experimental results prove that the proposed algorithm can effectively detect the weak edge of the lesion, which is helpful for the diagnosis of COVID-19.

No abstract

Ferroptosis is a new form of nonapoptotic cell death closely associated with glutathione (GSH) peroxidase 4 inhibition and/or GSH depletion, resulting in the accumulation of cellular iron and lipid peroxides. The exact mechanism by which GSH depletion causes the accumulation of reactive oxygen species (ROS) and lipid-ROS and subsequent ferroptotic cell death in neuronal cells remains unclear. In the present study, using immortalized HT22 mouse hippocampal neuronal cells as a model, we show that nitric oxide (NO) accumulation via protein disulfide isomerase (PDI)-mediated neuronal nitric oxide synthase (nNOS) activation plays a critical role in chemically-induced ferroptosis. Mechanistically, we find that erastin-induced GSH depletion leads to activation of PDI, which then mediates ferroptosis by catalyzing nNOS dimerization, followed by accumulation of cellular NO, ROS and lipid ROS and ultimately ferroptotic cell death. Pharmacological inhibition of PDI enzymatic activity or selective PDI knockdown can effectively abrogate erastin-induced ferroptosis in HT22 cells. The results of this study reveal an important role of PDI in mediating chemically induced ferroptosis in a neuronal cell model, and PDI may serve as a potential drug target for protection against GSH depletion-associated ferroptotic neuronal cell death.

Alzheimer's disease (AD) is a common form of neurodegenerative disease in the elderly. Amyloid‐β (Aβ)‐associated neurotoxicity is an important component of the neurodegenerative change in AD. Recent studies have revealed a beneficial effect of anthocyanins in improving learning and memory in AD animal models. Using cultured HT22 mouse hippocampal neuronal cells as an in vitro model, we examined in this study the protective effect of ten pure components of anthocyanins against Aβ42‐induced cytotoxicity and also investigated the mechanism of their protective effects. We found that treatment of HT22 cells with the pure components of anthocyanins dose‐dependently rescued Aβ42‐induced cytotoxicity, with slightly different potencies. Using petunidin as a representative compound, we found that it enhanced mitochondrial homeostasis and function in Aβ42‐treated HT22 cells. Mechanistically, petunidin facilitated β‐catenin nuclear translocation and enhanced the interaction between β‐catenin and TCF7, which subsequently upregulated mitochondrial homeostasis‐related protein Mfn2, thereby promoting restoration of mitochondrial homeostasis and function in Aβ42‐treated HT22 cells. Together, these results reveal that the pure components of anthocyanins have a strong protective effect in HT22 cells against Aβ42‐induced cytotoxicity by ameliorating mitochondrial homeostasis and function in a β‐catenin/TCF‐dependent manner.