Simulation of Movement of the Device with Passive Vibration Isolation

Modern electronic systems, computer hardware and navigation equipment on board moving objects can be subjected to significant mechanical impulse and vibrational impacts. These impacts can introduce additional errors in readings of devices, and sometimes lead to their mechanical failure. One of the effective ways to solve the problem is to apply the method of passive vibration protection, which makes it possible to reduce vibrations due to the use of damping elements. This paper examines the vibration response of a device mounted on a moving platform. The device is protected against vibration by 4 dampers. The platform is subjected to translational motions in three mutually orthogonal directions. This leads to the appearance of coupled translational and rotational vibrations of the protected unit. The problem is solved within the framework of the general theory of the dynamic of a rigid body. The paper presents the results of numerical experiments, in which the intensity of rotational vibrations of the protected unit is investigated depending on various mechanical characteristics of the system. Admissible variation of these characteristics, at which the angular acceleration of the protected unit remains below a limit value, has been determined

Estimation of the nonlinear dependence of the indications of a fiber Bragg grating on temperature and strain from experimental data

The readings of the Bragg grating are determined based on the optical radiation reflected from it. A quantitative characteristic of this radiation is the wavelength at which the maximum power of the optical signal is achieved. This characteristic is called the central wavelength of the grating. The central wavelength shift depends on temperature and strain. As a rule, a linear approximation of this dependence is used. However, from the available literature it is known that, the grating wavelength shift demonstrates a strong nonlinear dependence on temperature at 5<T<200K and a weak quadratic dependence close to room temperature. Thus far, the authors have not found studies that consider all terms in the quadratic expansion of the central wavelength of the Bragg grating as a function of temperature and strain at near-room temperatures. Our work is intended to fill this gap. The article describes an experiment in which an optical fiber with Bragg grating was subjected to loading using three different weights. A step-wise temperature change from 5 to 100 0С was realized for each weight. Based on these data, all terms of the quadratic expansion of the desired function are determined. The contribution of each term is estimated

Investigation of the effect of cracks on the vibration processes in reinforced concrete structures

The validity of the mathematical model describing the propagation of vibrations in the reinforced concrete structures (RC structures) was verified by comparing the experimental and numerical data. The proposed model allowed us to perform numerical experiments aimed at comparing vibrorecords obtained for the structure without defects and the structure with typical fracture caused by crack formation. Based on the results of comparison, an informative diagnostic parameter was proposed. This parameter makes it possible to control the nucleation and growth of cracks in a RC structure

Амилоид-бета 40 как биомаркер когнитивных нарушений в остром периоде ишемического инсульта

Aim: to study the role of amyloid-beta 40 (Aβ 40) in the development of cognitive impairment in acute ischemic stroke.Materials and methods. The study included 70 patients aged 33–86 years, 46 men and 24 women. In patients with acute ischemic stroke cognitive status was assessed with Mini-Mental State Examination (MMSE), Montreal Cognitive Assessment Test (MoCA), Frontal Assessment Battery (FAB), Schulte tables, Clock Drawing Test, Test for Semantic Verbal Fluency and Five Words Test. The concentration of Aβ 40 in the cerebrospinal fluid was determined. Morphometric (size of the infarct and leukoaraiosis area, volume of the brain ventricles and hippocampus) and diffusion-tensor parameters of MRI (fractional anisotropy of putamen, thalamus, hippocampus, corpus callosum, limbs of the internal capsule, the cingulate, the superior longitudinal and inferior fronto-occipital tracts) were studied.Results. The concentration of Aβ 40 in the cerebrospinal fluid was 436,4 (226,0–514,0) pg/ml. The protein level was associated with the result of subtests «Orientation» (MMSE) and «Attention» (MoCA), as well as indirect recall with cues in MoCA. Patients with MMSE score of 24–27 points were characterized by a lower concentration of Aβ 40 as compared to patients with a score less than 24 points. Aβ 40 concentration more than 436,4 pg/mL was associated with a more severe somatic co-morbidity of stroke (hypertension, lower hemoglobin and albumin level, higher erythrocyte sedimentation rate), a smaller volume of the brain ventricles, lower fractional anisotropy of the thalamus, cingulate tracts and contralateral hippocampus. Aβ 40 concentration more than 436,4 pg/mL was also associated with a lower global cognitive status (according to the MMSE and MoCA), as well as the reduction in certain cognitive functions, namely, attention, visual-spatial functions and memory.Conclusions. The concentration of Aβ 40 in the cerebrospinal fluid is a biological marker of severity type of post-stroke cognitive impairment. This interaction is probably due to the damage to the hippocampus, thalamus and cingulate tracts. In our opinion, the biomarker reflects both ischemic and neurodegenerative components of the pathogenesis of cognitive impairment in acute ischemic stroke.Цель исследования. Изучение роли амилоида-бета 40 (Aβ 40) в развитии когнитивных нарушений в остром периоде ишемического инсульта.Материал и методы. Обследованы 70 пациентов в возрасте 33–86 лет, из которых 46 мужчин и 24 женщины.У пациентов в остром периоде ишемического инсульта проводилась оценка когнитивного статуса (краткая шкала оценки психического статуса (MMSE), Монреальская шкала оценки когнитивных функций (MoCA), батарея лобных тестов (FAB), таблицы Шульте, тест рисования часов, тест на семантическую вербальную беглость и тест пяти слов). Также исследовалась концентрации Аβ 40 в ликворе, изучались морфометрические (размер очага инфаркта и площадь лейкоареоза, объем желудочков мозга и гиппокампов) и диффузионно-тензорные показатели (фракционная анизотропия скорлупы, таламуса, гиппокампа, мозолистого тела, ножек внутренней капсулы, цингулярного, верхнего продольного и нижнего фронто-окципитального пучков) магнитно-резонансной томографии.Результаты. Концентрация Аβ 40 в ликворе составила 436,4 (226,0–514,0) пг/мл и была ассоциирована с результатом субтестов «ориентация» (MMSE) и «внимание» (MoCA), а также опосредованным воспроизведением в MoCA. Пациенты с результатом MMSE 24–27 баллов характеризовались более низкой концентрацией Аβ 40 по сравнению с пациентами с результатом шкалы менее 24 баллов. Концентрация Аβ 40 более 436,4 пг/мл была связана с более выраженной соматической коморбидностью инсульта (артериальная гипертензия, более низкое содержание гемоглобина и альбумина крови, более высокая скорость оседания эритороцитов), меньшим объемом желудочков мозга, более низкой фракционной анизотропией таламусов, цингулярных пучков и контралатерального гиппокапма и ассоциирована с более низким глобальным когнитивным статусом (по результатам MMSE и MoCA), а также снижением отдельных когнитивных функций, а именно внимания, зрительно-пространственного гнозиса и памяти.Выводы. Концентрация Аβ 40 в спинномозговой жидкости является биологическим маркером как выраженности, так и характера постинсультных когнитивных нарушений, что, вероятно, опосредовано повреждением гиппокампов, таламуса и цингулярных трактов. При этом, на наш взгляд, биомаркер отражает как сосудистый, или ишемический, компонент патогенеза когнитивных нарушений в остром периоде ишемического инсульта, так и влияние амилоид-опосредованной нейродегенерации

Amyloid-beta 40 as a biomarker of cognitive impairment in acute ischemic stroke

Aim: to study the role of amyloid-beta 40 (Aβ 40) in the development of cognitive impairment in acute ischemic stroke.Materials and methods. The study included 70 patients aged 33–86 years, 46 men and 24 women. In patients with acute ischemic stroke cognitive status was assessed with Mini-Mental State Examination (MMSE), Montreal Cognitive Assessment Test (MoCA), Frontal Assessment Battery (FAB), Schulte tables, Clock Drawing Test, Test for Semantic Verbal Fluency and Five Words Test. The concentration of Aβ 40 in the cerebrospinal fluid was determined. Morphometric (size of the infarct and leukoaraiosis area, volume of the brain ventricles and hippocampus) and diffusion-tensor parameters of MRI (fractional anisotropy of putamen, thalamus, hippocampus, corpus callosum, limbs of the internal capsule, the cingulate, the superior longitudinal and inferior fronto-occipital tracts) were studied.Results. The concentration of Aβ 40 in the cerebrospinal fluid was 436,4 (226,0–514,0) pg/ml. The protein level was associated with the result of subtests «Orientation» (MMSE) and «Attention» (MoCA), as well as indirect recall with cues in MoCA. Patients with MMSE score of 24–27 points were characterized by a lower concentration of Aβ 40 as compared to patients with a score less than 24 points. Aβ 40 concentration more than 436,4 pg/mL was associated with a more severe somatic co-morbidity of stroke (hypertension, lower hemoglobin and albumin level, higher erythrocyte sedimentation rate), a smaller volume of the brain ventricles, lower fractional anisotropy of the thalamus, cingulate tracts and contralateral hippocampus. Aβ 40 concentration more than 436,4 pg/mL was also associated with a lower global cognitive status (according to the MMSE and MoCA), as well as the reduction in certain cognitive functions, namely, attention, visual-spatial functions and memory.Conclusions. The concentration of Aβ 40 in the cerebrospinal fluid is a biological marker of severity type of post-stroke cognitive impairment. This interaction is probably due to the damage to the hippocampus, thalamus and cingulate tracts. In our opinion, the biomarker reflects both ischemic and neurodegenerative components of the pathogenesis of cognitive impairment in acute ischemic stroke

Solid State Structure, and Optical and Magnetic Properties, of Free Base Tetra(4-pyridyl)porphyrin {H₂T(4-Py)P}^•– Radical Anions

A crystalline {cryptand[2.2.2.]­(K⁺)}­{H₂T­(4-Py)­P^•–}·C₆H₄Cl₂ (<b>1</b>) salt with tetra­(4-pyridyl)­porphyrin radical anions was obtained, enabling the effect of reduction on a metal-free porphyrin macrocycle to be studied. In contrast to pristine H₂T­(4-Py)­P, the H₂T­(4-Py)­P^•– radical anions have altered C–C­(meso) bonds due to partial loss of aromaticity from the porphyrin macrocycle. Short and long bonds have average lengths of 1.396(3) and 1.426(3) Å, which thus differ by 0.03 Å. Reduction affects the positions of the Soret and Q-bands of porphyrin observed in the spectrum of <b>1</b> at 439 and 512, 583, and 614 nm, and new bands of the radical anion appear at 684, 755, and 900 nm. The H₂T­(4-Py)­P^•– radical anions have a spin state of <i>S</i> = 1/2 and a magnetic moment of 1.64 μ_B at 300 K. Salt <b>1</b> shows a narrow asymmetric EPR signal fitted with two Lorentzian lines, with <i>g</i>_⊥ = 2.0031 and a line width (Δ<i>H</i>) of 0.186 mT, and <i>g</i>_∥ = 2.0019 (Δ<i>H</i> = 0.284 mT) at 295 K, and this signal splits into three components below 39 K. Salt <b>1</b> shows antiferromagnetic spin coupling with a Weiss temperature of −2 K

Large-scale assessment of pros and cons of autopsy-derived or tumor-matched tissues as the norms for gene expression analysis in cancers.

Normal tissues are essential for studying disease-specific differential gene expression. However, healthy human controls are typically available only in postmortal/autopsy settings. In cancer research, fragments of pathologically normal tissue adjacent to tumor site are frequently used as the controls. However, it is largely underexplored how cancers can systematically influence gene expression of the neighboring tissues. Here we performed a comprehensive pan-cancer comparison of molecular profiles of solid tumor-adjacent and autopsy-derived healthy normal tissues. We found a number of systemic molecular differences related to activation of the immune cells, intracellular transport and autophagy, cellular respiration, telomerase activation, p38 signaling, cytoskeleton remodeling, and reorganization of the extracellular matrix. The tumor-adjacent tissues were deficient in apoptotic signaling and negative regulation of cell growth including G2/M cell cycle transition checkpoint. We also detected an extensive rearrangement of the chemical perception network. Molecular targets of 32 and 37 cancer drugs were over- or underexpressed, respectively, in the tumor-adjacent norms. These processes may be driven by molecular events that are correlated between the paired cancer and adjacent normal tissues, that mostly relate to inflammation and regulation of intracellular molecular pathways such as the p38, MAPK, Notch, and IGF1 signaling. However, using a model of macaque postmortal tissues we showed that for the 30&nbsp;min - 24-hour time frame at 4ºC, an RNA degradation pattern in lung biosamples resulted in an artifact differential expression profile for 1140 genes, although no differences could be detected in liver. Thus, such concerns should be addressed in practice

Large-scale assessment of pros and cons of autopsy-derived or tumor-matched tissues as the norms for gene expression analysis in cancers

Normal tissues are essential for studying disease-specific differential gene expression. However, healthy human controls are typically available only in postmortal/autopsy settings. In cancer research, fragments of pathologically normal tissue adjacent to tumor site are frequently used as the controls. However, it is largely underexplored how cancers can systematically influence gene expression of the neighboring tissues. Here we performed a comprehensive pan-cancer comparison of molecular profiles of solid tumor-adjacent and autopsy-derived “healthy” normal tissues. We found a number of systemic molecular differences related to activation of the immune cells, intracellular transport and autophagy, cellular respiration, telomerase activation, p38 signaling, cytoskeleton remodeling, and reorganization of the extracellular matrix. The tumor-adjacent tissues were deficient in apoptotic signaling and negative regulation of cell growth including G2/M cell cycle transition checkpoint. We also detected an extensive rearrangement of the chemical perception network. Molecular targets of 32 and 37 cancer drugs were over- or underexpressed, respectively, in the tumor-adjacent norms. These processes may be driven by molecular events that are correlated between the paired cancer and adjacent normal tissues, that mostly relate to inflammation and regulation of intracellular molecular pathways such as the p38, MAPK, Notch, and IGF1 signaling. However, using a model of macaque postmortal tissues we showed that for the 30 min – 24-hour time frame at 4ºC, an RNA degradation pattern in lung biosamples resulted in an artifact “differential” expression profile for 1140 genes, although no differences could be detected in liver. Thus, such concerns should be addressed in practice