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The reactions of 1-amino-2-nitroguanidine with 3-nitro- acrylates afford aza-Michael adducts. The latter when refluxed in an aqueous alkaline medium undergo elimination of nitrous ...acid followed by shift of the resulting C=C bond into C=N position giving finally N-substituted alkylpyruvate hydrazones. These compounds can also be prepared in a one-pot procedure; NMR spectroscopy and X-ray diffraction analysis confirmed the existence of the obtained hydrazones as E-isomers.
A convenient diastereoselective method for the preparation of methyl (2
R*
,3
R*
)-3-aryl(pyridyl)-5-oxopyrrolidine-2-carboxylates was developed on the basis of the neutralization reaction of ...diastereohomogeneous dimethyl (2
R*
,3
R*
)-3-aryl(pyridyl)glutamate hydrochlorides.
Single diastereomers of 4-hetaryl-2-pyrrolidone-3(5)-carbo- and 2-4-hetaryl-2-pyrrolidon-1-ylacetohydrazides were used in reactions with 2,4-pentanedione, providing (3
R*
,4
S*
)-3-, (4
R*
,5
R*
...)-5-(3,5-dimethyl-1
H
-pyrazole-1-carbonyl)- and 1-2-(3,5-dimethyl-1
H
-pyrazol-1-yl)-2-oxoethyl-4-hetaryl-2-pyrrolidones. The structures of the synthesized compounds were confirmed by spectral methods and X-ray structural analysis. Some of the obtained compounds were shown to possess nootropic and anxiolytic activity.
To obtain new polyfunctional inhibitors of radical-chain oxidative processes, C- and N-benzylation of a number of phosphorylacetic acid hydrazide derivatives is realized in their reactions with ...3,5-di-tert-butyl-4-hydroxybenzyl acetate. N-benzylation of mixtures of Z and E isomers of hydrazones of phosphorylacetic acid derivatives proceeds stereoselectively with the formation of only E
C=N
isomers.
Conformal multilayer micro-nanocrystalline diamond coatings were grown on substrates of a hard alloy with 9% Co with a high aspect number in microwave plasma from gas mixtures CH4/H2 and CH4/H2/N2. ...The substrates were of a cylindrical axial tool model with a size ratio: d = 12 mm to l = 75 mm. An original tool holder made of molybdenum, in the form of a sector of the excessive ring with the axis of the hole parallel to the central conductive platform, protects part of the substrate from heating due to the edge effect of plasma. The uniformity of heating of the growth part, which is located inside the excessive ring, is calculated using mathematical modeling and is provided by rotation at a speed of at least 12 rpm, which ensures the uniformity of the coating. The average grain size of the nanocrystalline film measured along the cylinder forming was 41 nm.
Various adhesion molecules play an important role in defining cell fate and maintaining tissue integrity. Therefore, cross-signaling between adhesion receptors should be a common phenomenon to ...support the orchestrated changes of cells’ connections to the substrate and to the neighboring cells during tissue remodeling. Recently, we have demonstrated that the epithelial cell adhesion molecule Ep-CAM negatively modulates cadherin-mediated adhesions in direct relation to its expression levels. Here, we used E-cadherin/α-catenin chimera constructs to define the site of Ep-CAM’s negative effect on cadherin-mediated adhesions. Murine L-cells transfected with either E-cadherin/α-catenin fusion protein, or E-cadherin fused to the carboxy-terminal half of α-catenin, were subsequently supertransfected with an inducible Ep-CAM construct. Introduction of Ep-CAM altered the cell’s morphology, weakened the strength of cell-cell interactions, and decreased the cytoskeleton-bound fraction of the cadherin/catenin chimeras in both cell models. Furthermore, expression of Ep-CAM induced restructuring of F-actin, with changes in thickness and orientation of the actin filaments. The results showed that Ep-CAM affects E-cadherin-mediated adhesions without involvement of β-catenin by disrupting the link between α-catenin and F-actin. The latter is likely achieved through remodeling of the actin cytoskeleton by Ep-CAM, possibly through pp120.
The contribution of noncadherin-type, Ca2+-independent cell-cell adhesion molecules to the organization of epithelial tissues is, as yet, unclear. A homophilic, epithelial Ca2+-independent adhesion ...molecule (Ep-CAM) is expressed in most epithelia, benign or malignant proliferative lesions, or during embryogenesis. Here we demonstrate that ectopic Ep-CAM, when expressed in cells interconnected by classic cadherins (E- or N-cadherin), induces segregation of the transfectants from the parental cell type in coaggregation assays and in cultured mixed aggregates, respectively. In the latter assay, Ep-CAM-positive transfectants behave like cells with a decreased strength of cell-cell adhesion as compared to the parental cells. Using transfectants with an inducible Ep-CAM-cDNA construct, we demonstrate that increasing expression of Ep-CAM in cadherin-positive cells leads to the gradual abrogation of adherens junctions. Overexpression of Ep-CAM has no influence on the total amount of cellular cadherin, but affects the interaction of cadherins with the cytoskeleton since a substantial decrease in the detergent-insoluble fraction of cadherin molecules was observed. Similarly, the detergent-insoluble fractions of α- and β-catenins decreased in cells overexpressing Ep-CAM. While the total β-catenin content remains unchanged, a reduction in total cellular α-catenin is observed as Ep-CAM expression increases. As the cadherin-mediated cell-cell adhesions diminish, Ep-CAM-mediated intercellular connections become predominant. An adhesion-defective mutant of Ep-CAM lacking the cytoplasmic domain has no effect on the cadherin-mediated cell-cell adhesions. The ability of Ep-CAM to modulate the cadherin-mediated cell-cell interactions, as demonstrated in the present study, suggests a role for this molecule in development of the proliferative, and probably malignant, phenotype of epithelial cells, since an increase of Ep-CAM expression was observed in vivo in association with hyperplastic and malignant proliferation of epithelial cells.
Serum prevalence to six different non-viral pathogens was estimated for big Russian cats (Amur tiger (Panthera tigris altaica) and the Far Eastern leopard (Panthera pardus orientalis)) in Southern ...Primorye, Russia (n = 26) in 2008–2016. Serum samples from smaller cats (Eurasian lynx (Lynx lynx) and Far Eastern wildcat (Prionailurus bengalensis euptilurus)) were also tested for these pathogens (n = 28) during the same period. Felids of Russian Southern Primorye showed serum prevalence to five out of six tested pathogens. Antibodies to Candida sp. and Trichinella sp. were found to be much more widespread in cats (47% and 42%) than antibodies to other tested pathogens (20% and less). Large cats demonstrated a higher serum prevalence to these pathogens than smaller ones. We did not detect animals seropositive to Coxiella burnetii.
The reaction of 2-(1-phenylvinyloxy)benzo-1,3,2-dioxaphosphole with hexafluoroacetone, ethyltrifluoropyruvate and chloral leads to the formation of cage phosphoranes possessing the ...1-phospha-2,6,8-trioxabicyclo3.2.1octane framework whose structure was established by the XRD method and NMR spectroscopy. The process involves dihetero-Diels–Alder and Huisgen 1,3-dipolar cycloaddition reactions and is accompanied by the simultaneous formation of the P–C and C–C bonds. Despite the generation of three chiral carbon atoms, the stereoselectivity of the process exceeds 96%. Hydrolysis leads to the formation of functionalized aldols and phosphonates.
Human airways are frequently exposed to potentially harmful agents that cause tissue injury. Upon such injury, a repair process is initiated that comprises cell migration, proliferation, and ...differentiation. We have previously shown that human neutrophil defensins (human neutrophil peptides 1-3 HNP1-3) induce airway epithelial cell proliferation. Because of the role of cell proliferation in epithelial wound repair, we investigated the effect of HNP1-3 on airway epithelial wound closure and mucin gene expression in vitro. Using NCI-H292 airway epithelial cell cultures, we demonstrated that HNP1-3 cause a dose- and time-dependent increase of wound closure as well as increased cell migration. Furthermore, HNP1-3 caused a biphasic activation of the mitogen-activated protein kinase extracellular-regulated kinase 1 and 2 (ERK1/2). Both the effects of HNP1-3 on wound closure and ERK1/2 activation were blocked by specific inhibitors of the mitogen-activated protein kinase kinase MEK, whereas inhibitors of epidermal growth factor receptor tyrosine kinase, phosphatidylinositol 3-kinase, and Src did block defensin-enhanced wound closure but not ERK1/2 activation. Finally, HNP1-3 increased mRNA encoding the mucins MUC5B and MUC5AC, suggesting a role for defensins in mucous cell differentiation. These results indicate that neutrophil defensins increase epithelial wound repair in vitro, which involves migration and proliferation, and mucin production. Neutrophil defensin-enhanced wound repair appears to require epidermal growth factor receptor activation and downstream signaling pathways.
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