Разработка методов тепловой дефектоскопии и дефектометрии авиационных композитов

Диссертация посвящена разработке методов дефектометрии в рамках импульсного теплового контроля авиационных композитов. Проведён сравнительный анализ существующих термографических методов количественной оценки глубины дефектов. Выявлены их преимущества и недостатки и обозначены существующие проблемы в этой сфере. Представлен термографический метод количественной оценки глубины дефектов в материалах, обладающих свойством оптической полупрозрачности. Разработан метод количественной оценки глубины дефектов, характеризующихся малым отношением поперечных размеров к глубине. Разработан метод оценки толщины тонких покрытий основанный на пороговой отсечке кажущейся тепловой инерции.This study is focused on quantitative estimation of defect depth by applying pulsed thermal nondestructive testing. A novel method for estimating defect depth is proposed by taking into account the phenomenon of 3D heat diffusion finite lateral size of defects and thermal reflection coefficient at the boundary between a host material and defects. The method is based on the combination of a known analytical model and non-linear fitting (NLF) procedure. The apparent effusivity method for the quantitative evaluation of coating thickness in a one-sided thermal NDT procedure is presented. And the depth prediction method based on neural networks is presented

Development, Function, and Clinical Significance of Plasmacytoid Dendritic Cells in Chronic Myeloid Leukemia.

Plasmacytoid dendritic cells (pDC) are the main producers of a key T-cell-stimulatory cytokine, IFNα, and critical regulators of antiviral immunity. Chronic myeloid leukemia (CML) is caused by BCR-ABL, which is an oncogenic tyrosine kinase that can be effectively inhibited with ABL-selective tyrosine kinase inhibitors (TKI). BCR-ABL-induced suppression of the transcription factor interferon regulatory factor 8 was previously proposed to block pDC development and compromise immune surveillance in CML. Here, we demonstrate that pDCs in newly diagnosed CML (CML-pDC) develop quantitatively normal and are frequently positive for the costimulatory antigen CD86. They originate from low-level BCR-ABL-expressing precursors. CML-pDCs also retain their competence to maturate and to secrete IFN. RNA sequencing reveals a strong inflammatory gene expression signature in CML-pDCs. Patients with high CML-pDC counts at diagnosis achieve inferior rates of deep molecular remission (MR) under nilotinib, unless nilotinib therapy is combined with IFN, which strongly suppresses circulating pDC counts. Although most pDCs are BCR-ABL-negative in MR, a substantial proportion of BCR-ABL + CML-pDCs persists under TKI treatment. This could be of relevance, because CML-pDCs elicit CD8+ T cells, which protect wild-type mice from CML. Together, pDCs are identified as novel functional DC population in CML, regulating antileukemic immunity and treatment outcome in CML.Significance: CML-pDC originates from low-level BCR-ABL expressing stem cells into a functional immunogenic DC-population regulating antileukemic immunity and treatment outcome in CM