Microscopy Image Dataset for Deep Learning-Based Quantitative Assessment of Pulmonary Vascular Changes.

Pulmonary hypertension (PH) is a syndrome complex that accompanies a number of diseases of different etiologies, associated with basic mechanisms of structural and functional changes of the pulmonary circulation vessels and revealed pressure increasing in the pulmonary artery. The structural changes in the pulmonary circulation vessels are the main limiting factor determining the prognosis of patients with PH. Thickening and irreversible deposition of collagen in the pulmonary artery branches walls leads to rapid disease progression and a therapy effectiveness decreasing. In this regard, histological examination of the pulmonary circulation vessels is critical both in preclinical studies and clinical practice. However, measurements of quantitative parameters such as the average vessel outer diameter, the vessel walls area, and the hypertrophy index claimed significant time investment and the requirement for specialist training to analyze micrographs. A dataset of pulmonary circulation vessels for pathology assessment using semantic segmentation techniques based on deep-learning is presented in this work. 609 original microphotographs of vessels, numerical data from experts' measurements, and microphotographs with outlines of these measurements for each of the vessels are presented. Furthermore, here we cite an example of a deep learning pipeline using the U-Net semantic segmentation model to extract vascular regions. The presented database will be useful for the development of new software solutions for the analysis of histological micrograph.

Inhibition of JAK1,2 Prevents Fibrotic Remodeling of Pulmonary Vascular Bed and Improves Outcomes in the Rat Model of Chronic Thromboembolic Pulmonary Hypertension.

Chronic thromboembolic pulmonary hypertension (CTEPH) is a rare complication of acute pulmonary embolism with poor clinical outcomes. Therapeutic approaches to prevention of fibrotic remodeling of the pulmonary vascular bed in CTEPH are limited. In this work, we tested the hypothesis that Janus kinase 1/2 (JAK1/2) inhibition with ruxolitinib might prevent and attenuate CTEPH in a rat model. CTEPH was induced by repeated embolization of the pulmonary artery with partially biodegradable 180 ± 30 µm alginate microspheres. Two weeks after the last injection of microspheres, ruxolitinib was administered orally at doses of 0.86, 2.58, and 4.28 mg/kg per day for 4 weeks. Prednisolone (1.475 mg/kg, i.m.) was used as a reference drug. Ruxolitinib in all doses as well as prednisolone reduced pulmonary vascular wall hypertrophy. Ruxolitinib at a dose of 2.58 mg/kg and prednisolone reduced vascular wall fibrosis. Prednisolone treatment resulted in decreased right ventricular systolic pressure. Pulmonary vascular resistance was lower in the prednisolone and ruxolitinib (4.28 mg/kg) groups in comparison with the placebo group. The plasma level of brain natriuretic peptide was lower in groups receiving ruxolitinib at doses of 2.58 and 4.28 mg/kg versus placebo. This study demonstrated that JAK1/2 inhibitor ruxolitinib dose-dependently reduced pulmonary vascular remodeling, thereby preventing CTEPH formation in rats.