COVID-19 lesion detection and segmentation-A deep learning method.

PURPOSE: In this paper, we utilized deep learning methods to screen the positive COVID-19 cases in chest CT. Our primary goal is to supply rapid and precise assistance for disease surveillance on the medical imaging aspect. MATERIALS AND METHODS: Basing on deep learning, we combined semantic segmentation and object detection methods to study the lesion performance of COVID-19. We put forward a novel end-to-end model which takes advantage of the Spatio-temporal features. Furthermore, a segmentation model attached with a fully connected CRF was designed for a more effective ROI input. RESULTS: Our method showed a better performance across different metrics against the comparison models. Moreover, our strategy highlighted strong robustness for the processed augmented testing samples. CONCLUSION: The comprehensive fusion of Spatio-temporal correlations can exploit more valuable features for locating target regions, and this mechanism is friendly to detect tiny lesions. Although it remains in discrete form, the feature extracting in temporal dimension improves the precision of final prediction.

Nicotine promotes Staphylococcus aureus-induced osteomyelitis by activating the Nrf2/Slc7a11 signaling axis.

Although smoking is a significant risk factor for osteomyelitis, there is limited experimental evidence that nicotine, a key tobacco constituent, is associated with this condition, leaving its mechanistic implications uncharacterized. This study revealed that nicotine promotes Staphylococcus aureus-induced osteomyelitis by increasing Nrf2 and Slc7a11 expression in vivo and in vitro. Inhibition of Slc7a11 using Erastin augmented bacterial phagocytosis/killing capabilities and fortified antimicrobial responses in an osteomyelitis model. Moreover, untargeted metabolomic analysis demonstrated that Erastin mitigated the effects of nicotine on S. aureus-induced osteomyelitis by altering glutamate/glutathione metabolism. These findings suggest that nicotine aggravates S. aureus-induced osteomyelitis by activating the Nrf2/Slc7a11 signaling pathway and that Slc7a11 inhibition can counteract the detrimental health effects of nicotine.

Gelsolin-like actin-capping protein has prognostic value and promotes tumorigenesis and epithelial-mesenchymal transition via the Hippo signaling pathway in human bladder cancer.

BACKGROUND: Transitional cell carcinoma (TCC) of the bladder, the major histologic subtype of bladder cancer, is increasing in incidence and mortality, which requires the identification of effective biomarkers. Actin-regulating proteins have recently been proposed as important antitumor druggable targets. As a gelsolin-family actin-modulating protein, CAPG (gelsolin-like actin-capping protein) generated great interest due to its crucial effects in various biological and physiological processes; however, the role and mechanism of CAPG in TCCs remain unknown. MATERIALS AND METHODS: Bioinformatic analysis and immunohistochemistry of clinical specimens were performed to detect the expression level of CAPG. Both in vitro and in vivo assays were used to determine the oncogenic effect of CAPG in TCCs. Male 4-5-week-old BALB/c nude mice were used for in vivo tumorigenesis assays, while SCID mice were used for in vivo metastatic assays. Affymetrix microarray was used to identify the underlying molecular mechanism. Western blot and immunofluorescence were used to validate the expression and localization of proteins. RESULTS: CAPG was frequently upregulated in TCCs and associated with clinical aggressiveness and worse prognosis. Functional assays demonstrated that CAPG could contribute to the tumorigenesis, metastasis and epithelial-mesenchymal transition (EMT) of TCCs both in vitro and in vivo. A novel mechanism that CAPG promoted TCC development via inactivating the Hippo pathway, leading to a nucleus translocation of Yes-associated protein was suggested. CONCLUSIONS: The current study identified CAPG as a novel and critical oncogene in TCCs, supporting the pursuit of CAPG as a potential target for TCC intervention.