MPO77 is a protein involved in the activation of neutrophils, a process that occurs during the formation of atherosclerotic plaques. The function of this protein is regulated by the interaction with its receptor, PON-1. When PON-1 is active, it binds to HDL particles, thereby inhibiting MPO activity through oxidation of the amino acid tyrosine 71 in MPO. The balance between PON-1 and MPO is crucial for the antioxidant and anti-inflammatory properties of HDL. Inhibition of the MPO pathway reduces the inflammatory activity of atherosclerotic lesions.

Atherosclerosis is a chronic disease with multiple etiologies. The development of atherosclerotic plaques occurs in the inner wall of arteries, mainly due to the accumulation of lipids, cellular debris and other substances that form a thrombotic plaque. This plaque is surrounded by an intimal media that consists of a thin layer of smooth muscle cells and macrophages.

The intimal media is a source of proteases and enzymes that cause vascular damage, such as MPO, which cleaves the protein ApoA1, which is required for the formation of the atherosclerotic plaque. The accumulation of atherosclerotic plaques results in an increased risk for cardiovascular events and death. The progression of atherosclerosis is accompanied by the onset and progression of ECOPD, which is associated with impaired quality of life and increased healthcare costs. Looking More

Pulmonary biomarkers, such as FeNO, sputum eosinophilia and BAL IL-8, are promising markers of the occurrence of an imminent ECOPD exacerbation. In multivariate analyses, sputum eosinophilia has shown to be a strong predictor of frequent ECOPD exacerbations. However, the specificity of sputum eosinophilia for predicting ECOPD exacerbations and for identifying patients who might benefit from the introduction or cessation of ICS remains to be established.

The performance of our large-scale implementation of DMRG on multicore TPU configurations is based on three main points: (i) individual MPS tensors and other auxiliaries are distributed through the available TPU cores; (ii) an out-of-core approach is adopted in order to more efficiently utilize the 16 GB of high-bandwidth memory per TPU core; (iii) tensor contractions are accelerated through parallelization. These methods can be straightforwardly extended to TPU v4.