The efficacy of reducing agents or antioxidants in blocking the formation of dense cells and irreversibly sickled cells in vitro

We show that N-acetylcysteine (NAC) has the ability to cause statistically significant diminishment in the in vitro formation of irreversibly sickled cells (ISCs) at concentrations greater than 250 micromol/L. Other antioxidants, approved for human use (cysteamine, succimer, dimercaprol), were not efficacious. NAC had the ability to cause statistically significant conversion of ISCs formed in vivo back to the biconcave shape. NAC was also shown to reduce the formation of dense cells and increase the available thiols in beta-actin. We showed that diminishing reduced glutathione (GSH), by treatment with 1-chloro-2,4-dinitrobenzene, resulted in increased dense cells. We conclude the NAC blocks dense cell formation and ISC formation by targeting channels involved in cellular dehydration and beta-actin, respectively. The efficacy of NAC is probably due to its combined antioxidant activity and ability to increase intracellular GSH.     

On the lattice deformation in martensite transformation of steel

Simple mathematical expressions for the lattice deformation process of martensite transformation of steel are developed to generally treat so far proposed deformation mechanisms, such as the uniform 19 deg 28 min shear, half dislocation motion, and shuffling of (111)f planes in direction, and the concerned lattice structures,i.e. fee, hep, bcc, and their modifications. All possible transformation paths are examined by this method, and four paths including a new proposal by the author are considered the reasonable ones as far as the theory is concerned. Four important experimental facts,i.e. the lattice parameter anomalies at low temperatures, octahedral and tetrahedral interstitial carbon occupancy, intermediate bcc modification structure with six layers, and premartensitic phenomena in steel, are introduced and compared with the above transformation mechanisms, and the best interpretations of them are given by the newly proposed lattice deformation mechanism through the intermediate six layer structure.     

Irreversible deformation and the superplasticity of a TN-1 alloy during thermal cycling through the martensitic transformations ranges under loading

The influence of the thermal cycling conditions on the thermal-cycling creep of a TN-1 alloy and the related irreversible deformations is studied. The conditions under which an anomalous increase in the irreversible deformations begins are determined. The structural mechanism of the irreversible deformations of an equiatomic alloy is shown to be analogous to the structural mechanism of metal creep at high temperatures: it predominantly has a dislocation character. It is proposed to use the effect of anomalous increase in the deformation of materials with reversible martensitic transformations for forming parts made of these materials at low temperatures.     

Assessing the life of boiler steel on the basis of anomalous thermal deformation of its crystal lattice

In vacuum thermocyclic tests, high-temperature X-ray diffraction patterns reveal anomalous thermal lattice deformation (λ-anomalies) of St10 (Ct10), 08H18N10T (08X18H10T), 12H1MF (12X1MФ), and Di-59 (ДИ-59) 10H13G12BS2N2TS2 (10X13Г12БC2H2Ц2) boiler steel within a narrow temperature range. That lattice deformation cannot be explained in terms of familiar phase transitions of types I and II and, according to analysis of the relative integral diffraction-line intensities, is associated with grain-boundary transformations and reorientation of the grains, with consequent modification of the physical and mechanical characteristics and the life of the heat-transfer surfaces.     

Special traits of structure formation in powdered iron-manganese alloys in deformation and recrystallization. II. Formation of the recrystallization structure after cold deformation in dependence on the type of crystal lattice and the energy of stacking faults

Translated from Poroshkovaya Metallurgiya, No. 6(354), pp. 1–7, June, 1992.     

Adducin is an in vivo substrate for protein kinase C: phosphorylation in the MARCKS-related domain inhibits activity in promoting spectrin-actin complexes and occurs in many cells, including dendritic spines of neurons

Adducin is a heteromeric protein with subunits containing a COOH-terminal myristoylated alanine-rich C kinase substrate (MARCKS)-related domain that caps and preferentially recruits spectrin to the fast-growing ends of actin filaments. The basic MARCKS-related domain, present in alpha, beta, and gamma adducin subunits, binds calmodulin and contains the major phosphorylation site for protein kinase C (PKC). This report presents the first evidence that phosphorylation of the MARCKS-related domain modifies in vitro and in vivo activities of adducin involving actin and spectrin, and we demonstrate that adducin is a prominent in vivo substrate for PKC or other phorbol 12-myristate 13-acetate (PMA)-activated kinases in multiple cell types, including neurons. PKC phosphorylation of native and recombinant adducin inhibited actin capping measured using pyrene-actin polymerization and abolished activity of adducin in recruiting spectrin to ends and sides of actin filaments. A polyclonal antibody specific to the phosphorylated state of the RTPS-serine, which is the major PKC phosphorylation site in the MARCKS-related domain, was used to evaluate phosphorylation of adducin in cells. Reactivity with phosphoadducin antibody in immunoblots increased twofold in rat hippocampal slices, eight- to ninefold in human embryonal kidney (HEK 293) cells, threefold in MDCK cells, and greater than 10-fold in human erythrocytes after treatments with PMA, but not with forskolin. Thus, the RTPS-serine of adducin is an in vivo phosphorylation site for PKC or other PMA-activated kinases but not for cAMP-dependent protein kinase in a variety of cell types. Physiological consequences of the two PKC phosphorylation sites in the MARCKS-related domain were investigated by stably transfecting MDCK cells with either wild-type or PKC-unphosphorylatable S716A/S726A mutant alpha adducin. The mutant alpha adducin was no longer concentrated at the cell membrane at sites of cell-cell contact, and instead it was distributed as a cytoplasmic punctate pattern. Moreover, the cells expressing the mutant alpha adducin exhibited increased levels of cytoplasmic spectrin, which was colocalized with the mutant alpha adducin in a punctate pattern. Immunofluorescence with the phosphoadducin-specific antibody revealed the RTPS-serine phosphorylation of adducin in postsynaptic areas in the developing rat hippocampus. High levels of the phosphoadducin were detected in the dendritic spines of cultured hippocampal neurons. Spectrin also was a component of dendritic spines, although at distinct sites from the ones containing phosphoadducin. These data demonstrate that adducin is a significant in vivo substrate for PKC or other PMA-activated kinases in a variety of cells, and that phosphorylation of adducin occurs in dendritic spines that are believed to respond to external signals by changes in morphology and reorganization of cytoskeletal structures.     

Estimation of plastic deformation in the technologies of bulk cold deformation

A technique for determining the degree of reduction upon forming by cold bulk shaping has been proposed. The technique is based on a comparison of the measurement data on the hardness of a cold-worked metal with that of the same metal subjected to a compression test at a certain strain intensity. The technique has been tested in technological operations of reduction and thread rolling.