A close interaction between the virus SARS-CoV-2 and the
immune system of an individual results in a diverse clinical
manifestation of the COVID-19 disease. While adaptive immune
responses are essential for SARS-CoV-2 virus clearance, the
innate immune cells, such as macrophages, may contribute, in
some cases, to the disease progression. Macrophages have
shown a significant production of IL-6, suggesting they may
contribute to the excessive inflammation in COVID-19 disease.
Macrophage Activation Syndrome may further explain the high
serum levels of CRP, which are normally lacking in viral
infections. In adaptive immune responses, it has been revealed
that cytotoxic CD8+ T cells exhibit functional exhaustion patterns,
such as the expression of NKG2A, PD-1, and TIM-3. Since SARSCoV-2 restrains antigen presentation by downregulating
MHC class I and II molecules and, therefore, inhibits the T cellmediated immune responses, humoral immune responses also
play a substantial role. Specific IgA response appears to be
stronger and more persistent than the IgM response. Moreover,
IgM and IgG antibodies show similar dynamics in COVID-19
disease.
The distribution of the carboxylating enzyme nbulose-l,5-bisphosphate carboxylase/oxygenase (RuBPCO) and an enzyme of the photorespiratory pathway (glycine decarboxylase) was determined within the leaf tissue by immunocytochemical techniques in C3, C4 and C3:C4 intermediate species. The specificity of the method for all the materiál was demonstrated by sodium dodecyl sulphate acrylamide gels and Western blotting of crude protein extracts. In the C3 species (wheat) the enzymes were located in chloroplasts (RuBPCO) and mitochondria (glycine decarboxylase) of mesophyll cells, while in the three "classical" C4 standards, i.e. Zea mays ("NADP-ME" type). Panicům maximum ("PCK" type) and P. turgidum ("NAD-ME" type), these were found exclusively in the respective organelles of the bundle sheath. In the intermediate species, RuBPCO was not compartmented as it was located in chloroplasts of mesophyll and bundle sheath cells. Yet glycine decarboxylase was found exclusively in bundle sheath mitochondria. InAristida funiculata, a C4 species with "non-classical" leaf structure, RuBPCO was found in chloroplasts of both the inner and outer bundle sheaths and glycine decarboxylase was located exclusively in mitochondria of the inner bundle sheath cells. It is suggested that A. funiculata may be a C4 species with C3:C4-like intermediate characteristics based on the observed distribution of glycine decarboxylase, although gas-exchange characteristics of this species are required before any reclassification can be considered.
The article deals with the numerical solution of transitional flows. The single-point k-kL-ω model of [7] based on the use of a laminar kinetic energy transport equation is considered. The model doesn‘t require to evaluate integral boundary layer parameters (e.g. boundary layer thickness) and is therefore suitable for implementation into codes working with general unstructured meshes. The performance of the model has been tested for the case of flows over a flat plate with zero and non-zero pressure gradients. The results obtained with our implementation of the model are compared to the experimental data of ERCOFTAC. and Obsahuje seznam literatury
Vascular calcification (VC) is an independent risk factor for cardiovascular events and all-cause mortality with the absence of current treatment. This study aimed to investigate whether eIF2α phosphorylation inhibition could ameliorate VC. VC in rats was induced by administration of vitamin D3 (3×105 IU/kg, intramuscularly) plus nicotine (25 mg/kg, intragastrically). ISRIB (0.25 mg/kg·week), an inhibitor of eIF2α phosphorylation, ameliorated the elevation of calcium deposition and ALP activity in calcified rat aortas, accompanied by amelioration of increased SBP, PP, and PWV. The decreased protein levels of calponin and SM22α, and the increased levels of RUNX2 and BMP2 in calcified aorta were all rescued by ISRIB, while the increased levels of the GRP78, GRP94, and C/EBP homologous proteins in rats with VC were also attenuated. Moreover, ISRIB could prevent the elevation of eIF2α phosphorylation and ATF4, and partially inhibit PERK phosphorylation in the calcified aorta. These results suggested that an eIF2α phosphorylation inhibitor could ameliorate VC pathogenesis by blocking eIF2α/ATF4 signaling, which may provide a new target for VC prevention and treatment.