55 research outputs found
Dust density waves in a dc flowing complex plasma with discharge polarity reversal
We report on the observation of the self-excited dust density waves in the dc
discharge complex plasma. The experiments were performed under microgravity
conditions in the Plasmakristall-4 facility on board the International Space
Station. In the experiment, the microparticle cloud was first trapped in an
inductively coupled plasma, then released to drift for some seconds in a dc
discharge with constant current. After that the discharge polarity was
reversed. DC plasma containing a drifting microparticle cloud was found to be
strongly non-uniform in terms of microparticle drift velocity and plasma
emission in accord with [Zobnin et.al., Phys. Plasmas 25, 033702 (2018)]. In
addition to that, non-uniformity in the self-excited wave pattern was observed:
In the front edge of the microparticle cloud (defined as head), the waves had
larger phase velocity than in the rear edge (defined as tail). Also, after the
polarity reversal, the wave pattern exhibited several bifurcations: Between
each of the two old wave crests, a new wave crest has formed. These
bifurcations, however, occurred only in the head of the microparticle cloud. We
show that spatial variations of electric field inside the drifting cloud play
an important role in the formation of the wave pattern. Comparison of the
theoretical estimations and measurements demonstrate the significant impact of
the electric field on the phase velocity of the wave. The same theoretical
approach applied to the instability growth rate, showed agreement between
estimated and measured values.Comment: 7 pages, 4 figure
ΠΠ»ΠΈΡΠ½ΠΈΠ΅ Π°Π²ΡΠΎΠΎΠ±Π»ΡΡΠ΅Π½ΠΈΡ Π½Π° ΡΠΎΡΠΌΠΈΡΠΎΠ²Π°Π½ΠΈΠ΅ Π½Π°Π½ΠΎΡΠ°Π·ΠΌΠ΅ΡΠ½ΡΡ ΡΠ»ΠΎΠ΅Π² Π·ΠΎΠ»ΠΎΡΠ° ΠΏΡΠΈ ΠΈΠΎΠ½Π½ΠΎ-Π»ΡΡΠ΅Π²ΠΎΠΌ Π½Π°ΠΏΡΠ»Π΅Π½ΠΈΠΈ
2β13 nm gold films were obtained by the method of ion-beam sputtering on silicon and quartz substrates. It is shown that the use of an additional operation of deposition followed by the sputtering of a gold layer of 2β3 nm thickness makes it possible to reduce the electrical resistance and surface roughness of the metal films, in comparison with similar films obtained without its use. The results of measuring the temperature coefficient of resistance of nanosized gold films on silicon substrates allowed us to conclude that the films deposited become continuous at a thickness of 6-8 nm. The results of optical measurements of 10 nm gold films, obtained on quartz substrates, showed that the reflection coefficient of electromagnetic radiation at a wavelength of 850 nm is 2.8 % higher than the corresponding coefficient for the same films obtained without using this operation, and is 83 %. An important role in the formation of nanoscale gold layers is played by the processes of self-irradiation of the growing layer of the high-energy component of the gold atoms flux. When using an additional operation of deposition/sputtering, high-energy gold atoms are implanted into the substrate to a depth of about 2 nm. On the one hand, these atoms are point defects in the surface damaged layer of the substrate; on the other hand, they serve as additional centers of cluster formation. This ensures strong adhesion of the metal layer to the substrate and, therefore, the gold films become continuous and more homogeneous in microstructure. The method of ion-beam deposition can be successfully applied to obtain high-quality conductive optically transparent nanosized gold films.ΠΠ΅ΡΠΎΠ΄ΠΎΠΌ ΠΈΠΎΠ½Π½ΠΎ-Π»ΡΡΠ΅Π²ΠΎΠ³ΠΎ Π½Π°ΠΏΡΠ»Π΅Π½ΠΈΡ ΠΏΠΎΠ»ΡΡΠ΅Π½Ρ ΠΏΠ»Π΅Π½ΠΊΠΈ Π·ΠΎΠ»ΠΎΡΠ° ΡΠΎΠ»ΡΠΈΠ½ΠΎΠΉ 2β13 Π½ΠΌ Π½Π° ΠΊΡΠ΅ΠΌΠ½ΠΈΠ΅Π²ΡΡ
ΠΈ ΠΊΠ²Π°ΡΡΠ΅Π²ΡΡ
ΠΏΠΎΠ΄Π»ΠΎΠΆΠΊΠ°Ρ
. ΠΠΎΠΊΠ°Π·Π°Π½ΠΎ, ΡΡΠΎ ΠΏΡΠΈΠΌΠ΅Π½Π΅Π½ΠΈΠ΅ Π΄ΠΎΠΏΠΎΠ»Π½ΠΈΡΠ΅Π»ΡΠ½ΠΎΠΉ ΠΎΠΏΠ΅ΡΠ°ΡΠΈΠΈ Π½Π°ΠΏΡΠ»Π΅Π½ΠΈΡ Ρ ΠΏΠΎΡΠ»Π΅Π΄ΡΡΡΠΈΠΌ ΡΠ°ΡΠΏΡΠ»Π΅Π½ΠΈΠ΅ΠΌ ΡΠ»ΠΎΡ Π·ΠΎΠ»ΠΎΡΠ° ΡΠΎΠ»ΡΠΈΠ½ΠΎΠΉ 2β3 Π½ΠΌ ΠΏΠΎΠ·Π²ΠΎΠ»ΡΠ΅Ρ ΡΠ½ΠΈΠ·ΠΈΡΡ ΡΠ»Π΅ΠΊΡΡΠΈΡΠ΅ΡΠΊΠΎΠ΅ ΡΠΎΠΏΡΠΎΡΠΈΠ²Π»Π΅Π½ΠΈΠ΅ ΠΈ ΠΏΠΎΠ²Π΅ΡΡ
Π½ΠΎΡΡΠ½ΡΡ ΡΠ΅ΡΠΎΡ
ΠΎΠ²Π°ΡΠΎΡΡΡ ΠΏΠΎΠ»ΡΡΠ°Π΅ΠΌΡΡ
ΠΌΠ΅ΡΠ°Π»Π»ΠΈΡΠ΅ΡΠΊΠΈΡ
ΠΏΠ»Π΅Π½ΠΎΠΊ ΠΏΠΎ ΡΡΠ°Π²Π½Π΅Π½ΠΈΡ Ρ Π°Π½Π°Π»ΠΎΠ³ΠΈΡΠ½ΡΠΌΠΈ ΠΏΠ»Π΅Π½ΠΊΠ°ΠΌΠΈ, ΠΏΠΎΠ»ΡΡΠ΅Π½Π½ΡΠΌΠΈ Π±Π΅Π· Π΅Π΅ ΠΈΡΠΏΠΎΠ»ΡΠ·ΠΎΠ²Π°Π½ΠΈΡ. Π Π΅Π·ΡΠ»ΡΡΠ°ΡΡ ΠΈΠ·ΠΌΠ΅ΡΠ΅Π½ΠΈΡ ΡΠ΅ΠΌΠΏΠ΅ΡΠ°ΡΡΡΠ½ΠΎΠ³ΠΎ ΠΊΠΎΡΡΡΠΈΡΠΈΠ΅Π½ΡΠ° ΡΠΎΠΏΡΠΎΡΠΈΠ²Π»Π΅Π½ΠΈΡ ΠΎΠ±ΡΠ°Π·ΡΠΎΠ² Π½Π°Π½ΠΎΡΠ°Π·ΠΌΠ΅ΡΠ½ΡΡ
ΠΏΠ»Π΅Π½ΠΎΠΊ Π·ΠΎΠ»ΠΎΡΠ° Π½Π° ΠΊΡΠ΅ΠΌΠ½ΠΈΠ΅Π²ΡΡ
ΠΏΠΎΠ΄Π»ΠΎΠΆΠΊΠ°Ρ
ΠΏΠΎΠ·Π²ΠΎΠ»ΠΈΠ»ΠΈ Π·Π°ΠΊΠ»ΡΡΠΈΡΡ, ΡΡΠΎ Π½Π°ΠΏΡΠ»ΡΠ΅ΠΌΡΠ΅ ΠΏΠ»Π΅Π½ΠΊΠΈ ΡΡΠ°Π½ΠΎΠ²ΡΡΡΡ ΡΠΏΠ»ΠΎΡΠ½ΡΠΌΠΈ ΠΏΡΠΈ ΡΠΎΠ»ΡΠΈΠ½Π΅ 6β8 Π½ΠΌ. Π Π΅Π·ΡΠ»ΡΡΠ°ΡΡ ΠΎΠΏΡΠΈΡΠ΅ΡΠΊΠΈΡ
ΠΈΠ·ΠΌΠ΅ΡΠ΅Π½ΠΈΠΉ ΠΏΠ»Π΅Π½ΠΎΠΊ Π·ΠΎΠ»ΠΎΡΠ° ΡΠΎΠ»ΡΠΈΠ½ΠΎΠΉ 10 Π½ΠΌ, ΠΏΠΎΠ»ΡΡΠ΅Π½Π½ΡΡ
Π½Π° ΠΊΠ²Π°ΡΡΠ΅Π²ΡΡ
ΠΏΠΎΠ΄Π»ΠΎΠΆΠΊΠ°Ρ
, ΠΏΠΎΠΊΠ°Π·Π°Π»ΠΈ, ΡΡΠΎ ΠΊΠΎΡΡΡΠΈΡΠΈΠ΅Π½Ρ ΠΎΡΡΠ°ΠΆΠ΅Π½ΠΈΡ ΡΠ»Π΅ΠΊΡΡΠΎΠΌΠ°Π³Π½ΠΈΡΠ½ΠΎΠ³ΠΎ ΠΈΠ·Π»ΡΡΠ΅Π½ΠΈΡ Π½Π° Π΄Π»ΠΈΠ½Π΅ Π²ΠΎΠ»Π½Ρ 850 Π½ΠΌ Π½Π° 2,8 % Π²ΡΡΠ΅ ΡΠΎΠΎΡΠ²Π΅ΡΡΡΠ²ΡΡΡΠ΅Π³ΠΎ ΠΊΠΎΡΡΡΠΈΡΠΈΠ΅Π½ΡΠ° Π΄Π»Ρ ΡΠ°ΠΊΠΈΡ
ΠΆΠ΅ ΠΏΠ»Π΅Π½ΠΎΠΊ, ΠΏΠΎΠ»ΡΡΠ΅Π½Π½ΡΡ
Π±Π΅Π· ΠΈΡΠΏΠΎΠ»ΡΠ·ΠΎΠ²Π°Π½ΠΈΡ Π΄Π°Π½Π½ΠΎΠΉ ΠΎΠΏΠ΅ΡΠ°ΡΠΈΠΈ, ΠΈ ΡΠΎΡΡΠ°Π²Π»ΡΠ΅Ρ 83 %. ΠΠ°ΠΆΠ½ΡΡ ΡΠΎΠ»Ρ Π² ΡΠΎΡΠΌΠΈΡΠΎΠ²Π°Π½ΠΈΠΈ Π½Π°Π½ΠΎΡΠ°Π·ΠΌΠ΅ΡΠ½ΡΡ
ΡΠ»ΠΎΠ΅Π² Π·ΠΎΠ»ΠΎΡΠ° ΠΈΠ³ΡΠ°ΡΡ ΠΏΡΠΎΡΠ΅ΡΡΡ Π°Π²ΡΠΎΠΎΠ±Π»ΡΡΠ΅Π½ΠΈΡ ΡΠ°ΡΡΡΡΠ΅Π³ΠΎ ΡΠ»ΠΎΡ Π²ΡΡΠΎΠΊΠΎΡΠ½Π΅ΡΠ³Π΅ΡΠΈΡΠ΅ΡΠΊΠΎΠΉ ΡΠΎΡΡΠ°Π²Π»ΡΡΡΠ΅ΠΉ ΠΏΠΎΡΠΎΠΊΠ° Π°ΡΠΎΠΌΠΎΠ² Π·ΠΎΠ»ΠΎΡΠ°. ΠΡΠΈ ΠΈΡΠΏΠΎΠ»ΡΠ·ΠΎΠ²Π°Π½ΠΈΠΈ Π΄ΠΎΠΏΠΎΠ»Π½ΠΈΡΠ΅Π»ΡΠ½ΠΎΠΉ ΠΎΠΏΠ΅ΡΠ°ΡΠΈΠΈ Π½Π°ΠΏΡΠ»Π΅Π½ΠΈΡ/ΡΠ°ΡΠΏΡΠ»Π΅Π½ΠΈΡ ΠΏΡΠΎΠΈΡΡ
ΠΎΠ΄ΠΈΡ Π²Π½Π΅Π΄ΡΠ΅Π½ΠΈΠ΅ Π² ΠΏΠΎΠ΄Π»ΠΎΠΆΠΊΡ Π²ΡΡΠΎΠΊΠΎΡΠ½Π΅ΡΠ³Π΅ΡΠΈΡΠ΅ΡΠΊΠΈΡ
Π°ΡΠΎΠΌΠΎΠ² Π·ΠΎΠ»ΠΎΡΠ° Π½Π° Π³Π»ΡΠ±ΠΈΠ½Ρ Π΄ΠΎ 2 Π½ΠΌ. Π‘ ΠΎΠ΄Π½ΠΎΠΉ ΡΡΠΎΡΠΎΠ½Ρ, ΡΡΠΈ Π°ΡΠΎΠΌΡ ΡΠ²Π»ΡΡΡΡΡ ΠΈΡΡΠΎΡΠ½ΠΈΠΊΠ°ΠΌΠΈ ΡΠΎΡΠ΅ΡΠ½ΡΡ
Π΄Π΅ΡΠ΅ΠΊΡΠΎΠ² Π² ΠΏΡΠΈΠΏΠΎΠ²Π΅ΡΡ
Π½ΠΎΡΡΠ½ΠΎΠΌ Π½Π°ΡΡΡΠ΅Π½Π½ΠΎΠΌ ΡΠ»ΠΎΠ΅ ΠΏΠΎΠ΄Π»ΠΎΠΆΠΊΠΈ; Π° Ρ Π΄ΡΡΠ³ΠΎΠΉ β ΠΎΠ½ΠΈ ΡΠ»ΡΠΆΠ°Ρ Π΄ΠΎΠΏΠΎΠ»Π½ΠΈΡΠ΅Π»ΡΠ½ΡΠΌΠΈ ΡΠ΅Π½ΡΡΠ°ΠΌΠΈ ΠΊΠ»Π°ΡΡΠ΅ΡΠΎΠΎΠ±ΡΠ°Π·ΠΎΠ²Π°Π½ΠΈΡ. ΠΠ° ΡΡΠ΅Ρ ΡΡΠΎΠ³ΠΎ ΠΎΠ±Π΅ΡΠΏΠ΅ΡΠΈΠ²Π°Π΅ΡΡΡ Π²ΡΡΠΎΠΊΠ°Ρ Π°Π΄Π³Π΅Π·ΠΈΡ ΡΠ»ΠΎΡ ΠΌΠ΅ΡΠ°Π»Π»Π° ΠΊ ΠΏΠΎΠ΄Π»ΠΎΠΆΠΊΠ΅, ΠΈ, ΠΊΠ°ΠΊ ΡΠ»Π΅Π΄ΡΡΠ²ΠΈΠ΅, ΠΏΠ»Π΅Π½ΠΊΠΈ Π·ΠΎΠ»ΠΎΡΠ° ΡΡΠ°Π½ΠΎΠ²ΡΡΡΡ ΡΠΏΠ»ΠΎΡΠ½ΡΠΌΠΈ ΠΈ Π±ΠΎΠ»Π΅Π΅ ΠΎΠ΄Π½ΠΎΡΠΎΠ΄Π½ΡΠΌΠΈ ΠΏΠΎ ΠΌΠΈΠΊΡΠΎΡΡΡΡΠΊΡΡΡΠ΅. ΠΠ΅ΡΠΎΠ΄ ΠΈΠΎΠ½Π½ΠΎ-Π»ΡΡΠ΅Π²ΠΎΠ³ΠΎ Π½Π°ΠΏΡΠ»Π΅Π½ΠΈΡ ΠΌΠΎΠΆΠ΅Ρ Π±ΡΡΡ ΡΡΠΏΠ΅ΡΠ½ΠΎ ΠΏΡΠΈΠΌΠ΅Π½Π΅Π½ Π΄Π»Ρ ΠΏΠΎΠ»ΡΡΠ΅Π½ΠΈΡ ΠΊΠ°ΡΠ΅ΡΡΠ²Π΅Π½Π½ΡΡ
ΠΏΡΠΎΠ²ΠΎΠ΄ΡΡΠΈΡ
ΠΎΠΏΡΠΈΡΠ΅ΡΠΊΠΈ ΠΏΡΠΎΠ·ΡΠ°ΡΠ½ΡΡ
Π½Π°Π½ΠΎΡΠ°Π·ΠΌΠ΅ΡΠ½ΡΡ
ΠΏΠ»Π΅Π½ΠΎΠΊ Π·ΠΎΠ»ΠΎΡΠ°
ΠΠ°ΠΊΡΠΎΡΠ°Π³ΠΈ ΠΏΡΠΈ Π±Π°ΠΊΡΠ΅ΡΠΈΠ°Π»ΡΠ½ΡΡ Π±ΠΎΠ»Π΅Π·Π½ΡΡ Π»Π΅Π³ΠΊΠΈΡ : ΡΠ΅Π½ΠΎΡΠΈΠΏ ΠΈ ΡΡΠ½ΠΊΡΠΈΠΈ (ΠΎΠ±Π·ΠΎΡ)
This literature review is devoted to the analysis of the role of macrophages in the immunopathogenesis of infectious lung diseases of bacterial etiology. The article summarizes information about the origin of macrophages, their phenotypic and functional heterogeneity. The mechanisms of impaired protective function of innate immunity are associated with the polarization of the program of maturation and activation of macrophages in the direction to tolerogenic or immunoregulatory cells with phenotype of M2. Alveolar macrophages perform a variety of functions (from pro-inflammatory to regenerative) in the development of inflammation in the respiratory organs. Their inherent plasticity suggests that the same macrophages can change their phenotype and function depending on the microenvironment in the inflammatory focus at different stages of the disease. Understanding the mechanisms that regulate macrophage plasticity will be an important step towards realizing the potential of personalized immunomodulatory therapy.ΠΠ±Π·ΠΎΡ Π»ΠΈΡΠ΅ΡΠ°ΡΡΡΡ ΠΏΠΎΡΠ²ΡΡΠ΅Π½ Π°Π½Π°Π»ΠΈΠ·Ρ ΡΠΎΠ»ΠΈ ΠΌΠ°ΠΊΡΠΎΡΠ°Π³ΠΎΠ² Π² ΠΈΠΌΠΌΡΠ½ΠΎΠΏΠ°ΡΠΎΠ³Π΅Π½Π΅Π·Π΅ ΠΈΠ½ΡΠ΅ΠΊΡΠΈΠΎΠ½Π½ΡΡ
Π·Π°Π±ΠΎΠ»Π΅Π²Π°Π½ΠΈΠΉ Π»Π΅Π³ΠΊΠΈΡ
Π±Π°ΠΊΡΠ΅ΡΠΈΠ°Π»ΡΠ½ΠΎΠΉ ΡΡΠΈΠΎΠ»ΠΎΠ³ΠΈΠΈ. Π ΡΡΠ°ΡΡΠ΅ ΠΎΠ±ΠΎΠ±ΡΠ΅Π½Ρ ΡΠ²Π΅Π΄Π΅Π½ΠΈΡ ΠΎ ΠΏΡΠΎΠΈΡΡ
ΠΎΠΆΠ΄Π΅Π½ΠΈΠΈ ΠΌΠ°ΠΊΡΠΎΡΠ°Π³ΠΎΠ², ΠΈΡ
ΡΠ΅Π½ΠΎΡΠΈΠΏΠΈΡΠ΅ΡΠΊΠΎΠΉ ΠΈ ΡΡΠ½ΠΊΡΠΈΠΎΠ½Π°Π»ΡΠ½ΠΎΠΉ Π³Π΅ΡΠ΅ΡΠΎΠ³Π΅Π½Π½ΠΎΡΡΠΈ. ΠΠ΅Ρ
Π°Π½ΠΈΠ·ΠΌΡ Π½Π°ΡΡΡΠ΅Π½ΠΈΠΉ Π·Π°ΡΠΈΡΠ½ΠΎΠΉ ΡΡΠ½ΠΊΡΠΈΠΈ Π²ΡΠΎΠΆΠ΄Π΅Π½Π½ΠΎΠ³ΠΎ ΠΈΠΌΠΌΡΠ½ΠΈΡΠ΅ΡΠ° ΡΠ²ΡΠ·Π°Π½Ρ Ρ ΠΏΠΎΠ»ΡΡΠΈΠ·Π°ΡΠΈΠ΅ΠΉ ΠΏΡΠΎΠ³ΡΠ°ΠΌΠΌΡ ΡΠΎΠ·ΡΠ΅Π²Π°Π½ΠΈΡ ΠΈ Π°ΠΊΡΠΈΠ²Π°ΡΠΈΠΈ ΠΌΠ°ΠΊΡΠΎΡΠ°Π³ΠΎΠ² Π² Π½Π°ΠΏΡΠ°Π²Π»Π΅Π½ΠΈΠΈ ΡΠΎΠ»Π΅ΡΠΎΠ³Π΅Π½Π½ΡΡ
ΠΈΠ»ΠΈ ΠΈΠΌΠΌΡΠ½ΠΎΡΠ΅Π³ΡΠ»ΡΡΠΎΡΠ½ΡΡ
ΠΊΠ»Π΅ΡΠΎΠΊ Ρ ΡΠ΅Π½ΠΎΡΠΈΠΏΠΎΠΌ Π2. ΠΠ»ΡΠ²Π΅ΠΎΠ»ΡΡΠ½ΡΠ΅ ΠΌΠ°ΠΊΡΠΎΡΠ°Π³ΠΈ Π²ΡΠΏΠΎΠ»Π½ΡΡΡ ΡΠ°Π·Π½ΠΎΠΎΠ±ΡΠ°Π·Π½ΡΠ΅ ΡΡΠ½ΠΊΡΠΈΠΈ (ΠΎΡ ΠΏΡΠΎΠ²ΠΎΡΠΏΠ°Π»ΠΈΡΠ΅Π»ΡΠ½ΠΎΠΉ Π΄ΠΎ ΡΠ΅Π³Π΅Π½Π΅ΡΠ°ΡΠΎΡΠ½ΠΎΠΉ) ΠΏΡΠΈ ΡΠ°Π·Π²ΠΈΡΠΈΠΈ Π²ΠΎΡΠΏΠ°Π»Π΅Π½ΠΈΡ Π² ΠΎΡΠ³Π°Π½Π°Ρ
Π΄ΡΡ
Π°Π½ΠΈΡ. ΠΡΠΈΡΡΡΠ°Ρ ΠΈΠΌ ΠΏΠ»Π°ΡΡΠΈΡΠ½ΠΎΡΡΡ ΡΠ²ΠΈΠ΄Π΅ΡΠ΅Π»ΡΡΡΠ²ΡΠ΅Ρ, ΡΡΠΎ ΠΎΠ΄Π½ΠΈ ΠΈ ΡΠ΅ ΠΆΠ΅ ΠΌΠ°ΠΊΡΠΎΡΠ°Π³ΠΈ ΠΌΠΎΠ³ΡΡ ΠΈΠ·ΠΌΠ΅Π½ΡΡΡ ΡΠ²ΠΎΠΉ ΡΠ΅Π½ΠΎΡΠΈΠΏ ΠΈ ΡΡΠ½ΠΊΡΠΈΠΈ Π² Π·Π°Π²ΠΈΡΠΈΠΌΠΎΡΡΠΈ ΠΎΡ ΠΌΠΈΠΊΡΠΎΠΎΠΊΡΡΠΆΠ΅Π½ΠΈΡ Π² ΠΎΡΠ°Π³Π΅ Π²ΠΎΡΠΏΠ°Π»Π΅Π½ΠΈΡ Π½Π° ΡΠ°Π·Π½ΡΡ
ΡΡΠ°Π΄ΠΈΡΡ
Π·Π°Π±ΠΎΠ»Π΅Π²Π°Π½ΠΈΡ. ΠΠΎΠ½ΠΈΠΌΠ°Π½ΠΈΠ΅ ΠΌΠ΅Ρ
Π°Π½ΠΈΠ·ΠΌΠΎΠ², ΠΊΠΎΡΠΎΡΡΠ΅ ΡΠ΅Π³ΡΠ»ΠΈΡΡΡΡ ΠΏΠ»Π°ΡΡΠΈΡΠ½ΠΎΡΡΡ ΠΌΠ°ΠΊΡΠΎΡΠ°Π³ΠΎΠ², ΡΡΠ°Π½Π΅Ρ Π²Π°ΠΆΠ½ΡΠΌ ΡΠ°Π³ΠΎΠΌ Π½Π° ΠΏΡΡΠΈ ΡΠ΅Π°Π»ΠΈΠ·Π°ΡΠΈΠΈ ΠΏΠΎΡΠ΅Π½ΡΠΈΠ°Π»Π° ΠΏΠ΅ΡΡΠΎΠ½ΠΈΡΠΈΡΠΈΡΠΎΠ²Π°Π½Π½ΠΎΠΉ ΠΈΠΌΠΌΡΠ½ΠΎΠΌΠΎΠ΄ΡΠ»ΠΈΡΡΡΡΠ΅ΠΉ ΡΠ΅ΡΠ°ΠΏΠΈΠΈ
Π‘ΡΠ±ΠΏΠΎΠΏΡΠ»ΡΡΠΈΠΈ ΠΌΠΎΠ½ΠΎΡΠΈΡΠΎΠ² ΠΊΡΠΎΠ²ΠΈ Ρ Π±ΠΎΠ»ΡΠ½ΡΡ Ρ Π³Π΅Π½Π΅ΡΠ°Π»ΠΈΠ·ΠΎΠ²Π°Π½Π½ΠΎΠΉ Π³ΠΈΠΏΠΎΠΊΡΠΈΠ΅ΠΉ
The aim of the work is to establish general regularities and features of differentiation of blood monocytes into 4 subpopulations in diseases associated with circulatory and respiratory hypoxia.Materials and methods. 18 patients with ischemic heart disease (IHD), 12 patients with ischemic cardiomyopathy (ICMP), 14 patients with chronic obstructive pulmonary disease (COPD), 15 patients with newly diagnosed infiltrative pulmonary tuberculosis (PTB) and 12 healthy donors were examined. In whole blood, we determined the relative number of different subpopulations of monocytes by flow cytometry. The results were analyzed by statistical methods.Results. It is shown that an increase in the number of classical (80.56 [77.60; 83.55]%) and the deficit of intermediate (10.38 [9.36; 11.26]%), non-classical (6.03 [5.24; 6.77]%) and transitional (2.14 [1.41; 3.92] %) monocytes in the blood is determined in patients with COPD when compared with the group of healthy donors (p < 0.05). In groups of patients with PTB and IHD, an increase in the number of intermediate monocytes (26.24 respectively [22.38; 42.88] % and 25.27 [15.78; 31.39]%) and the lack of transitional cells (1.77 [1.36; 3.74]% and 2.68 [2.63; 4.0]%) at the normal content of classical and non-classical forms of monocytes (p < 0.05) is detected. In patients with ICMP, a decrease in the number of non-classical monocytes (up to 5.05 [4.08; 6.58]%) is combined with the normal cell content of other subpopulations (p < 0.05). The interrelation between the number of classical and intermediate monocytes in patients with COPD (r = β0.63; p < 0.05), PTB (r = β0.72; p < 0.01), IHD (r = β0.59; p < 0.05), ICMP (r = β0.58; p < 0.05) was established.Conclusion. In COPD associated with generalized hypoxia, an increase in the number of classical monocytes is combined with a deficiency of their other subpopulations in the blood. In PTB and IHD, antigenic stimulation of the immune system mediates accelerated differentiation of monocytes from classical to intermediate forms with a decrease in the number of transitional cells regardless of the etiology of the disease (infectious or non-infectious) and the type of hypoxia (respiratory or circulatory).Π¦Π΅Π»Ρ ΡΠ°Π±ΠΎΡΡ β ΡΡΡΠ°Π½ΠΎΠ²ΠΈΡΡ ΠΎΠ±ΡΠΈΠ΅ Π·Π°ΠΊΠΎΠ½ΠΎΠΌΠ΅ΡΠ½ΠΎΡΡΠΈ ΠΈ ΠΎΡΠΎΠ±Π΅Π½Π½ΠΎΡΡΠΈ Π΄ΠΈΡΡΠ΅ΡΠ΅Π½ΡΠΈΡΠΎΠ²ΠΊΠΈ ΠΌΠΎΠ½ΠΎΡΠΈΡΠΎΠ² ΠΊΡΠΎΠ²ΠΈ Π½Π° ΡΠ΅ΡΡΡΠ΅ ΡΡΠ±ΠΏΠΎΠΏΡΠ»ΡΡΠΈΠΈ (ΠΊΠ»Π°ΡΡΠΈΡΠ΅ΡΠΊΠΈΠ΅ (CD14hiCD16-), ΠΏΡΠΎΠΌΠ΅ΠΆΡΡΠΎΡΠ½ΡΠ΅ (CD14hiCD16lo), Π½Π΅ΠΊΠ»Π°ΡΡΠΈΡΠ΅ΡΠΊΠΈΠ΅ (CD14loCD16lo) ΠΈ ΠΏΠ΅ΡΠ΅Ρ
ΠΎΠ΄Π½ΡΠ΅ (CD14loCD16-)) ΠΏΡΠΈ Π·Π°Π±ΠΎΠ»Π΅Π²Π°Π½ΠΈΡΡ
, Π°ΡΡΠΎΡΠΈΠΈΡΠΎΠ²Π°Π½Π½ΡΡ
Ρ ΡΠΈΡΠΊΡΠ»ΡΡΠΎΡΠ½ΠΎΠΉ ΠΈ Π΄ΡΡ
Π°ΡΠ΅Π»ΡΠ½ΠΎΠΉ Π³ΠΈΠΏΠΎΠΊΡΠΈΠ΅ΠΉ.ΠΠ°ΡΠ΅ΡΠΈΠ°Π»Ρ ΠΈ ΠΌΠ΅ΡΠΎΠ΄Ρ. ΠΠ±ΡΠ»Π΅Π΄ΠΎΠ²Π°Π½Ρ 18 Π±ΠΎΠ»ΡΠ½ΡΡ
ΠΈΡΠ΅ΠΌΠΈΡΠ΅ΡΠΊΠΎΠΉ Π±ΠΎΠ»Π΅Π·Π½ΡΡ ΡΠ΅ΡΠ΄ΡΠ° (ΠΠΠ‘), 12 Π±ΠΎΠ»ΡΠ½ΡΡ
ΠΈΡΠ΅ΠΌΠΈΡΠ΅ΡΠΊΠΎΠΉ ΠΊΠ°ΡΠ΄ΠΈΠΎΠΌΠΈΠΎΠΏΠ°ΡΠΈΠ΅ΠΉ (ΠΠΠΠ), 14 Π±ΠΎΠ»ΡΠ½ΡΡ
Ρ Ρ
ΡΠΎΠ½ΠΈΡΠ΅ΡΠΊΠΎΠΉ ΠΎΠ±ΡΡΡΡΠΊΡΠΈΠ²Π½ΠΎΠΉ Π±ΠΎΠ»Π΅Π·Π½ΡΡ Π»Π΅Π³ΠΊΠΈΡ
(Π₯ΠΠΠ), 15 Π±ΠΎΠ»ΡΠ½ΡΡ
Ρ Π²ΠΏΠ΅ΡΠ²ΡΠ΅ Π²ΡΡΠ²Π»Π΅Π½Π½ΡΠΌ ΠΈΠ½ΡΠΈΠ»ΡΡΡΠ°ΡΠΈΠ²Π½ΡΠΌ ΡΡΠ±Π΅ΡΠΊΡΠ»Π΅Π·ΠΎΠΌ Π»Π΅Π³ΠΊΠΈΡ
(Π’ΠΠ) ΠΈ 12 Π·Π΄ΠΎΡΠΎΠ²ΡΡ
Π΄ΠΎΠ½ΠΎΡΠΎΠ². Π ΡΠ΅Π»ΡΠ½ΠΎΠΉ ΠΊΡΠΎΠ²ΠΈ ΠΎΠΏΡΠ΅Π΄Π΅Π»ΡΠ»ΠΈ ΠΎΡΠ½ΠΎΡΠΈΡΠ΅Π»ΡΠ½ΠΎΠ΅ ΠΊΠΎΠ»ΠΈΡΠ΅ΡΡΠ²ΠΎ ΡΠ°Π·Π»ΠΈΡΠ½ΡΡ
ΡΡΠ±ΠΏΠΎΠΏΡΠ»ΡΡΠΈΠΉ ΠΌΠΎΠ½ΠΎΡΠΈΡΠΎΠ² ΠΌΠ΅ΡΠΎΠ΄ΠΎΠΌ ΠΏΡΠΎΡΠΎΡΠ½ΠΎΠΉ ΡΠΈΡΠΎΠΌΠ΅ΡΡΠΈΠΈ. ΠΠΎΠ»ΡΡΠ΅Π½Π½ΡΠ΅ ΡΠ΅Π·ΡΠ»ΡΡΠ°ΡΡ Π°Π½Π°Π»ΠΈΠ·ΠΈΡΠΎΠ²Π°Π»ΠΈ ΡΡΠ°ΡΠΈΡΡΠΈΡΠ΅ΡΠΊΠΈΠΌΠΈ ΠΌΠ΅ΡΠΎΠ΄Π°ΠΌΠΈ.Π Π΅Π·ΡΠ»ΡΡΠ°ΡΡ. ΠΠΎΠΊΠ°Π·Π°Π½ΠΎ, ΡΡΠΎ Ρ Π±ΠΎΠ»ΡΠ½ΡΡ
Π₯ΠΠΠ ΠΎΠΏΡΠ΅Π΄Π΅Π»ΡΠ΅ΡΡΡ ΡΠ²Π΅Π»ΠΈΡΠ΅Π½ΠΈΠ΅ Π΄ΠΎΠ»ΠΈ ΠΊΠ»Π°ΡΡΠΈΡΠ΅ΡΠΊΠΈΡ
(80,56 [77,60; 83,55]%) ΠΈ Π΄Π΅ΡΠΈΡΠΈΡ ΠΏΡΠΎΠΌΠ΅ΠΆΡΡΠΎΡΠ½ΡΡ
(10,38 [9,36; 11,26]%), Π½Π΅ΠΊΠ»Π°ΡΡΠΈΡΠ΅ΡΠΊΠΈΡ
(6,03 [5,24; 6,77]%) ΠΈ ΠΏΠ΅ΡΠ΅Ρ
ΠΎΠ΄Π½ΡΡ
(2,14 [1,41; 3,92]%) ΠΌΠΎΠ½ΠΎΡΠΈΡΠΎΠ² Π² ΠΊΡΠΎΠ²ΠΈ ΠΏΠΎ ΡΡΠ°Π²Π½Π΅Π½ΠΈΡ Ρ Π³ΡΡΠΏΠΏΠΎΠΉ Π·Π΄ΠΎΡΠΎΠ²ΡΡ
Π΄ΠΎΠ½ΠΎΡΠΎΠ² (Ρ < 0,05). Π Π³ΡΡΠΏΠΏΠ°Ρ
Π±ΠΎΠ»ΡΠ½ΡΡ
Ρ Π’ΠΠ ΠΈ ΠΠΠ‘ ΠΎΠ±Π½Π°ΡΡΠΆΠΈΠ²Π°Π΅ΡΡΡ ΠΏΠΎΠ²ΡΡΠ΅Π½ΠΈΠ΅ ΠΊΠΎΠ»ΠΈΡΠ΅ΡΡΠ²Π° ΠΏΡΠΎΠΌΠ΅ΠΆΡΡΠΎΡΠ½ΡΡ
ΠΌΠΎΠ½ΠΎΡΠΈΡΠΎΠ² (ΡΠΎΠΎΡΠ²Π΅ΡΡΡΠ²Π΅Π½Π½ΠΎ 26,24 [22,38; 42,88]% ΠΈ 25,27 [15,78; 31,39]%) Π½Π° ΡΠΎΠ½Π΅ Π΄Π΅ΡΠΈΡΠΈΡΠ° ΠΏΠ΅ΡΠ΅Ρ
ΠΎΠ΄Π½ΡΡ
ΠΊΠ»Π΅ΡΠΎΠΊ (1,77 [1,36; 3,74]% ΠΈ 2,68 [2,63; 4,0]%) ΠΏΡΠΈ Π½ΠΎΡΠΌΠ°Π»ΡΠ½ΠΎΠΌ ΡΠΎΠ΄Π΅ΡΠΆΠ°Π½ΠΈΠΈ ΠΊΠ»Π°ΡΡΠΈΡΠ΅ΡΠΊΠΈΡ
ΠΈ Π½Π΅ΠΊΠ»Π°ΡΡΠΈΡΠ΅ΡΠΊΠΈΡ
ΡΠΎΡΠΌ ΠΌΠΎΠ½ΠΎΡΠΈΡΠΎΠ² (Ρ < 0,05). Π£ Π±ΠΎΠ»ΡΠ½ΡΡ
ΠΠΠΠ ΡΠ½ΠΈΠΆΠ΅Π½ΠΈΠ΅ ΡΠΈΡΠ»Π΅Π½Π½ΠΎΡΡΠΈ Π½Π΅ΠΊΠ»Π°ΡΡΠΈΡΠ΅ΡΠΊΠΈΡ
ΠΌΠΎΠ½ΠΎΡΠΈΡΠΎΠ² (Π΄ΠΎ 5,05 [4,08; 6,58]%) ΡΠΎΡΠ΅ΡΠ°Π΅ΡΡΡ Ρ Π½ΠΎΡΠΌΠ°Π»ΡΠ½ΡΠΌ ΡΠΎΠ΄Π΅ΡΠΆΠ°Π½ΠΈΠ΅ΠΌ ΠΊΠ»Π΅ΡΠΎΠΊ ΠΎΡΡΠ°Π»ΡΠ½ΡΡ
ΡΡΠ±ΠΏΠΎΠΏΡΠ»ΡΡΠΈΠΉ (Ρ < 0,05). Π£ΡΡΠ°Π½ΠΎΠ²Π»Π΅Π½Π° Π²Π·Π°ΠΈΠΌΠΎΡΠ²ΡΠ·Ρ ΠΌΠ΅ΠΆΠ΄Ρ ΡΠΈΡΠ»Π΅Π½Π½ΠΎΡΡΡΡ ΠΊΠ»Π°ΡΡΠΈΡΠ΅ΡΠΊΠΈΡ
ΠΈ ΠΏΡΠΎΠΌΠ΅ΠΆΡΡΠΎΡΠ½ΡΡ
ΠΌΠΎΠ½ΠΎΡΠΈΡΠΎΠ² Ρ Π±ΠΎΠ»ΡΠ½ΡΡ
Π₯ΠΠΠ (r = β0,63; p < 0,05), Π’ΠΠ (r = β0,72; p < 0,01), ΠΠΠ‘ (r = β0,59; p < 0,05), ΠΠΠΠ (r = β0,58; p < 0,05).ΠΠ°ΠΊΠ»ΡΡΠ΅Π½ΠΈΠ΅. ΠΡΠΈ Π₯ΠΠΠ, Π°ΡΡΠΎΡΠΈΠΈΡΠΎΠ²Π°Π½Π½ΠΎΠΉ Ρ Π³Π΅Π½Π΅ΡΠ°Π»ΠΈΠ·ΠΎΠ²Π°Π½Π½ΠΎΠΉ Π³ΠΈΠΏΠΎΠΊΡΠΈΠ΅ΠΉ, ΡΠ²Π΅Π»ΠΈΡΠ΅Π½ΠΈΠ΅ ΡΠΈΡΠ»Π° ΠΊΠ»Π°ΡΡΠΈΡΠ΅ΡΠΊΠΈΡ
ΠΌΠΎΠ½ΠΎΡΠΈΡΠΎΠ² ΡΠΎΡΠ΅ΡΠ°Π΅ΡΡΡ Ρ Π΄Π΅ΡΠΈΡΠΈΡΠΎΠΌ ΠΎΡΡΠ°Π»ΡΠ½ΡΡ
ΠΈΡ
ΡΡΠ±ΠΏΠΎΠΏΡΠ»ΡΡΠΈΠΉ Π² ΠΊΡΠΎΠ²ΠΈ. ΠΡΠΈ Π’ΠΠ ΠΈ ΠΠΠ‘ Π°Π½ΡΠΈΠ³Π΅Π½Π½Π°Ρ ΡΡΠΈΠΌΡΠ»ΡΡΠΈΡ ΠΈΠΌΠΌΡΠ½Π½ΠΎΠΉ ΡΠΈΡΡΠ΅ΠΌΡ ΠΎΠΏΠΎΡΡΠ΅Π΄ΡΠ΅Ρ ΡΡΠΊΠΎΡΠ΅Π½Π½ΡΡ Π΄ΠΈΡΡΠ΅ΡΠ΅Π½ΡΠΈΡΠΎΠ²ΠΊΡ ΠΌΠΎΠ½ΠΎΡΠΈΡΠΎΠ² ΠΈΠ· ΠΊΠ»Π°ΡΡΠΈΡΠ΅ΡΠΊΠΈΡ
Π² ΠΏΡΠΎΠΌΠ΅ΠΆΡΡΠΎΡΠ½ΡΠ΅ ΡΠΎΡΠΌΡ ΠΏΡΠΈ ΡΠ½ΠΈΠΆΠ΅Π½ΠΈΠΈ ΡΠΈΡΠ»Π° ΠΏΠ΅ΡΠ΅Ρ
ΠΎΠ΄Π½ΡΡ
ΠΊΠ»Π΅ΡΠΎΠΊ Π²Π½Π΅ Π·Π°Π²ΠΈΡΠΈΠΌΠΎΡΡΠΈ ΠΎΡ ΡΡΠΈΠΎΠ»ΠΎΠ³ΠΈΠΈ Π·Π°Π±ΠΎΠ»Π΅Π²Π°Π½ΠΈΡ (ΠΈΠ½ΡΠ΅ΠΊΡΠΈΠΎΠ½Π½Π°Ρ ΠΈΠ»ΠΈ Π½Π΅ΠΈΠ½ΡΠ΅ΠΊΡΠΈΠΎΠ½Π½Π°Ρ) ΠΈ Π²ΠΈΠ΄Π° Π³ΠΈΠΏΠΎΠΊΡΠΈΠΈ (Π΄ΡΡ
Π°ΡΠ΅Π»ΡΠ½Π°Ρ ΠΈΠ»ΠΈ ΡΠΈΡΠΊΡΠ»ΡΡΠΎΡΠ½Π°Ρ)
Heat capacity of tantalum in the normal and superconducting states: Identification of the contributions
Development of the hydraulic circuit theory for solving problems of controlling the operation of heat supply systems
Subpopulation structure of IFNΞ³-producing T lymphocytes in patients with pulmonary tuberculosis
The study of subpopulation structure of IFNΞ³-producing T cells in patients with pulmonary tuberculosis revealed a decrease in the number of CD3+ IFNΞ³+ cells against the background of significantly increased IFNΞ³ secretion in vitro irrespective of the clinical form of the disease and drug sensitivity of M. tuberculosis, most strongly expressed in case of the disseminated tuberculosis. In patients with infiltrative drug-sensitive and drug-resistant pulmonary tuberculosis, increased number of Th1/Th17 lymphocytes (CD4+ IFNΞ³+IL-17A+) and, conversely, decreased number of blood Ξ³Ξ΄T cells was detected
Subpopulation structure of IFNΞ³-producing T lymphocytes in patients with pulmonary tuberculosis
The study of subpopulation structure of IFNΞ³-producing T cells in patients with pulmonary tuberculosis revealed a decrease in the number of CD3+ IFNΞ³+ cells against the background of significantly increased IFNΞ³ secretion in vitro irrespective of the clinical form of the disease and drug sensitivity of M. tuberculosis, most strongly expressed in case of the disseminated tuberculosis. In patients with infiltrative drug-sensitive and drug-resistant pulmonary tuberculosis, increased number of Th1/Th17 lymphocytes (CD4+ IFNΞ³+IL-17A+) and, conversely, decreased number of blood Ξ³Ξ΄T cells was detected
STATE OF JNK AND P38 MAP-KINASE SYSTEM IN BLOOD monon uclea r le ucocytes DUR ING INFLAMMATION
Abstract. Pogrammed cell death of peripheral blood mononuclear leucocytes from patients with acute inflammatory diseases (non-nosocomial pneumonia, acute appendicitis) was investigated under ex vivo conditions, upon cultivation of the cells with selective inhibitors of JNK (SP600125) and Ρ38 ΠΠΠ Π (ML3403). In vitro addition of SP600125 and ML3403 under oxidative stress conditions prevents increase of annexinpositive mononuclear cells numbers, thus suggesting JNK and Ρ38 ΠΠΠ -kinases to be involved into oxidative mechanisms of apoptosis deregulation. A role of JNK in IL-8 production by mononuclear leucocytes was revealed in cases of acute inflammation. Regulatory effect of JNK and p38 MAP-kinases can be mediated through activation of redox-sensitive apoptogenic signal transduction systems, as well as due to changes in cellular cytokine-producing function
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