Superhelasticity in aged single crystals of FeMnAlNi alloy

На [112]-монокристаллах Fe[43,5]Mnx[34]Al[15]Ni[7,5] показано, что при старении при T=437 K, 3 h наблюдается высокотемпературная сверхэластичность при деформации растяжением в температурном интервале от 298 K до 473 K. Экспериментально установлено, что механические и функциональные свойства зависят от ориентации кристалла, которая определяет вклад деформации раздвойникованием [epsilon][detw] в теоретическую величину деформации решетки

Metformin accelerates myelin recovery and ameliorates behavioral deficits in the animal model of multiple sclerosis via adjustment of AMPK/Nrf2/mTOR signaling and maintenance of endogenous oligodendrogenesis during brain self-repairing period

BACKGROUND: Multiple sclerosis (MS) is a devastating autoimmune disorder characterized by oligodendrocytes (OLGs) loss and demyelination. In this study, we have examined the effects of metformin (MET) on the oligodendrogenesis, redox signaling, apoptosis, and glial responses during a self-repairing period (1-week) in the animal model of MS. METHODS: For induction of demyelination, C57BL/6 J mice were fed a 0.2% cuprizone (CPZ) for 5 weeks. Thereafter, CPZ was removed for 1-week and molecular and behavioral changes were monitored in the presence or absence of MET (50 mg/kg body weight/day). RESULTS: MET remarkably increased the localization of precursor OLGs (NG2+/O4+ cells) and subsequently the renewal of mature OLGs (MOG+ cells) in the corpus callosum via AMPK/mammalian target of rapamycin (mTOR) pathway. Moreover, we observed a significant elevation in the antioxidant responses, especially in mature OLGs (MOG+/nuclear factor erythroid 2-related factor 2 (Nrf2+) cells) after MET intervention. MET also reduced brain apoptosis markers and lessened motor dysfunction in the open-field test. While MET was unable to decrease active astrogliosis (GFAP mRNA), it reduced microgliosis by down-regulation of Mac-3 mRNA a marker of pro-inflammatory microglia/macrophages. Molecular modeling studies, likewise, confirmed that MET exerts its effects via direct interaction with AMPK. CONCLUSIONS: Altogether, our study reveals that MET effectively induces lesion reduction and elevated molecular processes that support myelin recovery via direct activation of AMPK and indirect regulation of AMPK/Nrf2/mTOR pathway in OLGs. These findings facilitate the development of new therapeutic strategies based on AMPK activation for MS in the near future. KEYWORDS: AMPK; Cuprizone; Multiple sclerosis; Nrf2; mTO

Comparative assessment of subsipopulations of tumor-associated macrophages in breast cancer depending on the response to chemotherapy

The key cells of the immune system that determine the relationship between tumor cells and the microenvironment, beginning with early stages of tumor growth, including regulation of neoangiogenesis and the terminal stage of malignant process, are tumor-associated macrophages (TAM). In the present study, identification of TAM markers in breast tumors in patients with neoadjuvant chemotherapy and a comparative assessment of the differences in the macrophages subpopulation in tumors with different response to chemotherapy were carried out. The data we obtained indicate the functional differences between TAM subpopulations that have various phenotypes, that are confirmed at the level of associative links with the effectiveness of chemotherapy

Разработка системы управления сепаратора факельной системы установки комплексной подготовки газа

Объектом исследования является блок подготовки газа (сепаратор факельной системы) установки комплексной подготовки газа. Цель работы – разработка системы управления сепаратора факельной системы установки комплексной подготовки газа с использованием ПЛК, на основе выбранной SCADA-системы.The object of the study is the gas treatment unit (flare system separator) of the complex gas treatment unit. The aim of the work is the development of a control system for the flare system separator of the complex gas treatment unit using PLCs, based on the selected SCADA system

Анализ напряженно-деформированного состояния компенсаторов при проектировании нефтепроводов с использованием программного комплекса ANSYS

В работе рассмотрены характеристики исследуемого объекта – термокомпенсационные блоки на участке нефтепровода "Заполярье-Пурпе". Приведен расчет толщины стенки трубопровода, проверка его прочности и устойчивости, расчет компенсатора и его компенсирующей способности. Выполнено моделирование компенсаторов различного типа в программном комплексе Autodesk Inventor. Проведен анализ напряженно-деформированного состояния конструкций в программной среде ANSYS.The paper describes the characteristics of the studied object - thermal compensation blocks on the section of the Zapolyarye-Purpe oil pipeline. The calculation of the wall thickness of the pipeline, the verification of its strength and stability, the calculation of the compensator and its compensating ability. Compensators of various types have been simulated in the Autodesk Inventor software package. The analysis of the stress-strain state of structures in the ANSYS program is carried out

Region specific characterization of the cuprizone model for Multiple Sclerosis and impairment of remyelination by corticosteroids

Multiple sclerosis is a widespread demyelinating disease where primary oligodendrocyte dysfunction represents a possible underlying mechanism of myelin loss. Cuprizone intoxication which causes primary oligodendrocyte apoptosis, mimics some aspects of this disease. In the first part of my thesis, the extent and pattern of demyelination in this MS animal model was analyzed. Additionally, the innate immune responses to the cuprizone challenge were investigated. Our results regarding the cerebellum were included in this thesis, and the different pattern of demyelination in the basal ganglia, hippocampus, and cerebellum was highlighted. Striking differences were found in the magnitude of demyelination between different white and grey matter areas. Distinct cerebellar white matter regions, the cerebellar cortical grey matter, the medial basal ganglia, and the hippocampal fimbria were resistant to the cuprizone challenge. In contrast, other regions displayed severe myelin loss and activation of microglia and astroglia. We discuss the advantages and limitations of this model with regard to regional differences and “protection”. In the second part of this work, we used the cuprizone model to investigate the impact of corticosteroid (CS) treatment on spontaneously remyelinating lesions and addressed the underlying mechanisms by several in vitro and in vivo approaches. We are able to demonstrate that while CS-treatment accelerates the differentiation of oligodendrocyte progenitors in vitro, it impairs endogenous remyelination in vivo. We additionally identified CS-induced changes in the growth factor expression profile of cultured astrocytes that might explain the impairment of repair processes in the brain. The importance of astrocytes for early and late repair processes was further highlighted by our finding that astrocytosis but not microgliosis persists after an acute demyelinating event. Our data clearly show that promotion of the intrinsic oligodendroyte differentiation program might negatively affect myelin repair in vivo. We speculate that CS treatment induces a preterm oligodendrocytes differentiation and, thus, might impair endogenous remyelination cascades. Furthermore, beneficial steroidal effects during inflammation have to be balaced against possible remyelination-inhibiting effects. In the third part of the presented thesis, we focused on astrocyte’s response during an acute demyelinating event. The amyloid precursor protein (APP) which is well known to be expressed in activated astroglia, microglia and stressed neurons in several disease models, was in the focus of the study. We found that the expression of APP is strongly induced during acute cuprizone-induced demyelination. Exclusively astrocytes express APP during cuprizone-induced demyelination. Our in vitro experiments using primary astrocyte cultures indicate that this is a highly specific response to toxic demyelination. The cuprizone model, therefore, is a suitable tool to study the role of astrocyte derived APP in a MS animal model. The results of my thesis significantly broaden the knowledge regarding the potential of the cuprizone model as a tool for studying underlying mechanisms of de- and remyelination