AirMLP: A Multilayer Perceptron Neural Network for Temporal Correction of PM2.5 Values in Turin.

In recent times, pollution has emerged as a significant global concern, with European regulations stipulating limits on PM 2.5 particle levels. Addressing this challenge necessitates innovative approaches. Smart low-cost sensors suffer from imprecision, and can not replace legal stations in terms of accuracy, however, their potential to amplify the capillarity of air quality evaluation on the territory is not under discussion. In this paper, we propose an AI system to correct PM 2.5 levels in low-cost sensor data. Our research focuses on data from Turin, Italy, emphasizing the impact of humidity on low-cost sensor accuracy. In this study, different Neural Network architectures that vary the number of neurons per layer, consecutive records and batch sizes were used and compared to gain a deeper understanding of the network's performance under various conditions. The AirMLP7-1500 model, with an impressive R-squared score of 0.932, stands out for its ability to correct PM 2.5 measurements. While our approach is tailored to the city of Turin, it offers a systematic methodology for the definition of those models and holds the promise to significantly improve the accuracy of air quality data collected from low-cost sensors, increasing the awareness of citizens and municipalities about this critical environmental information.

Macrophages and platelets in liver fibrosis and hepatocellular carcinoma.

During fibrosis, (myo)fibroblasts deposit large amounts of extracellular matrix proteins, thereby replacing healthy functional tissue. In liver fibrosis, this leads to the loss of hepatocyte function, portal hypertension, variceal bleeding, and increased susceptibility to infection. At an early stage, liver fibrosis is a dynamic and reversible process, however, from the cirrhotic stage, there is significant progression to hepatocellular carcinoma. Both liver-resident macrophages (Kupffer cells) and monocyte-derived macrophages are important drivers of fibrosis progression, but can also induce its regression once triggers of chronic inflammation are eliminated. In liver cancer, they are attracted to the tumor site to become tumor-associated macrophages (TAMs) polarized towards a M2- anti-inflammatory/tumor-promoting phenotype. Besides their role in thrombosis and hemostasis, platelets can also stimulate fibrosis and tumor development by secreting profibrogenic factors and regulating the innate immune response, e.g., by interacting with monocytes and macrophages. Here, we review recent literature on the role of macrophages and platelets and their interplay in liver fibrosis and hepatocellular carcinoma.

Intravital Imaging of Thrombosis Models in Mice.

Intravital microscopy is a powerful tool to study thrombosis in real time. The kinetics of thrombus formation and progression in vivo is studied after inflicting damage to the endothelium through mechanical, chemical, or laser injury. Mouse models of atherosclerosis are also used to induce thrombus formation. Vessels of different sizes and from different vascular beds such as carotid artery or vena cava, mesenteric or cremaster arterioles, can be targeted. Using fluorescent dyes, antibodies, or reporter mouse strains allows to visualize key cells and factors mediating the thrombotic processes. Here, we review the latest literature on using intravital microscopy to study thrombosis as well as thromboinflammation following transient middle cerebral artery occlusion, infection-induced immunothrombosis, and liver ischemia reperfusion.

Beyond Hemostasis: Platelet Innate Immune Interactions and Thromboinflammation.

There is accumulating evidence that platelets play roles beyond their traditional functions in thrombosis and hemostasis, e.g., in inflammatory processes, infection and cancer, and that they interact, stimulate and regulate cells of the innate immune system such as neutrophils, monocytes and macrophages. In this review, we will focus on platelet activation in hemostatic and inflammatory processes, as well as platelet interactions with neutrophils and monocytes/macrophages. We take a closer look at the contributions of major platelet receptors GPIb, αIIbß3, TLT-1, CLEC-2 and Toll-like receptors (TLRs) as well as secretions from platelet granules on platelet-neutrophil aggregate and neutrophil extracellular trap (NET) formation in atherosclerosis, transfusion-related acute lung injury (TRALI) and COVID-19. Further, we will address platelet-monocyte and macrophage interactions during cancer metastasis, infection, sepsis and platelet clearance.