High-capacity data hiding for medical images based on the mask-RCNN model.

This study introduces a novel approach for integrating sensitive patient information within medical images with minimal impact on their diagnostic quality. Utilizing the mask region-based convolutional neural network for identifying regions of minimal medical significance, the method embeds information using discrete cosine transform-based steganography. The focus is on embedding within "insignificant areas", determined by deep learning models, to ensure image quality and confidentiality are maintained. The methodology comprises three main steps: neural network training for area identification, an embedding process for data concealment, and an extraction process for retrieving embedded information. Experimental evaluations on the CHAOS dataset demonstrate the method's effectiveness, with the model achieving an average intersection over union score of 0.9146, indicating accurate segmentation. Imperceptibility metrics, including peak signal-to-noise ratio, were employed to assess the quality of stego images, with results showing high capacity embedding with minimal distortion. Furthermore, the embedding capacity and payload analysis reveal the method's high capacity for data concealment. The proposed method outperforms existing techniques by offering superior image quality, as evidenced by higher peak signal-to-noise ratio values, and efficient concealment capacity, making it a promising solution for secure medical image handling.

Involvement of Alveolar Macrophages and Neutrophils in Acute Lung Injury After Scorpion Envenomation: New Pharmacological Targets.

Androctonus australis hector (Aah) scorpion venom is well known to induce a systemic inflammatory response associated with cell infiltration in lung and edema formation. The present study investigate (i) in vivo the evolution of lung and systemic inflammation triggered by Aah venom and (ii) analyze in vitro the signaling cascade, upstream of inflammatory cytokine expression after Aah venom-stimulated mouse alveolar macrophage (MH-S), the main resident immune cells in the lung. The inflammation induced by Aah venom was assessed in mice through inflammatory cell count, nitric oxide metabolite, and lactate dehydrogenase (LDH) activity in blood, concordantly with neutrophil sequestration in tissue and lung histology. In the in vitro study, MH-S cells are stimulated with Aah venom in the presence of signaling pathway inhibitors, NG25 an inhibitor of transforming growth factor ß-activated kinase (TAK1), PD184352 MAP kinase (MKK)1/2 inhibitor, BI605906 an inhibitor of IKκ-ß (inhibitor of nuclear factor kappa B), and BIRB0796 an inhibitor of p38 MAPK. Obtained results showed that leukocyte transmigration is important in some area of the lung and is closely associated with systemic increase of nitric oxide and LDH. The in vitro study showed that Aah venom induce significantly an increase of the expression of TNF-α, IL-1ß, and MIP-2 in MH-S cells. The pretreatment with inhibitors showed that cytokine increase involves TAK1, IKκ-ß, and ERK1/2 pathways, similarly to Toll-like receptor activation. These findings highlight the contribution of alveolar macrophage and their secretory products to tissue damage and made of TAK1 and ERK1/2, an interesting target in scorpion envenomation.

Effects of atropine and propranolol on lung inflammation in experimental envenomation: comparison of two buthidae venoms.

BACKGROUND: Previous works had shown that scorpion venom induced neurotransmitter elevation and an inflammatory response associated with various anatomo-pathological modifications. The most dangerous scorpions species in Algeria responsible for these effects are Androctonus australis hector (Aah) and Androctonus amoreuxi (Aam). RESULTS: Comparison of the physiopathological effects induced by the two venoms showed differences in the kinetic of cytokine release and in lung injury.The lung edema was only observed in response to Aah venom and it was correlated with cell infiltration. In order to better understand the involved mechanism in inflammatory response, we used two antagonists, atropine (non-selective muscarinic antagonist) and propranolol (ß adrenergic antagonist), which lead to a decrease of cell infiltration but has no effect on edema forming. CONCLUSION: These results suggest another pathway in the development of lung injury following envenomation with Aam or Aah venom.

Effects of atropine and propranolol on lung inflammation in experimental envenomation: comparison of two buthidae venoms

Previous works had shown that scorpion venom induced neurotransmitter elevation and an inflammatory response associated with various anatomo-pathological modifications. The most dangerous scorpions species in Algeria responsible for these effects are Androctonus australis hector(Aah) and Androctonus amoreuxi (Aam). Results Comparison of the physiopathological effects induced by the two venoms showed differences in the kinetic of cytokine release and in lung injury. The lung edema was only observed in response to Aah venom and it was correlated with cell infiltration. In order to better understand the involved mechanism in inflammatory response, we used two antagonists, atropine (non-selective muscarinic antagonist) and propranolol (β adrenergic antagonist), which lead to a decrease of cell infiltration but has no effect on edema forming.Conclusion These results suggest another pathway in the development of lung injury following envenomation with Aam or Aah venom.

Effects of atropine and propranolol on lung inflammation in experimental envenomation: comparison of two buthidae venoms

Background: Previous works had shown that scorpion venom induced neurotransmitter elevation and an inflammatory response associated with various anatomo-pathological modifications. The most dangerous scorpions species in Algeria responsible for these effects are Androctonus australis hector (Aah) and Androctonus amoreuxi (Aam). Results: Comparison of the physiopathological effects induced by the two venoms showed differences in the kinetic of cytokine release and in lung injury. The lung edema was only observed in response to Aah venom and it was correlated with cell infiltration. In order to better understand the involved mechanism in inflammatory response, we used two antagonists, atropine (non-selective muscarinic antagonist) and propranolol (ß adrenergic antagonist), which lead to a decrease of cell infiltration but has no effect on edema forming. Conclusion: These results suggest another pathway in the development of lung injury following envenomation with Aam or Aah venom.(AU)