Decision on economical rail grinding interval for controlling rolling contact fatigue

Rail players around the world have been increasing axle loads to improve the productivity of freight and heavy haul operations. This has increased the risk of surface cracks at curves because of rolling contact fatigue. Rail grinding has been considered an effective process for controlling these cracks and reducing risks of rail breaks. The complexity of deciding the optimal rail grinding intervals for improving the reliability and safety of rails is because of insufficient understanding of the various factors involved in the crack initiation and propagation process. This paper focuses on identifying the factors influencing rail degradation, developing models for rail failures and analyzing the costs of various grinding intervals for economic decision making. Various costs involved in rail maintenance, such as rail grinding, downtime, inspection, rail failures and derailment, and replacement of worn‐out rails, are incorporated into the total cost model developed in this paper. Field data from the rail industry have been used for illustration.     

Multielement analysis in cereals and pulses by k0 instrumental neutron activation analysis

The concentrations of some elements in a few varieties of cereals and pulses are determined by Instrumental Neutron Activation Analysis using a single comparator method (k0-standardised NAA method). A total of 15 elements are measured. The method was validated by analysing the Standard Reference Material (SRM-1571) of NIST; the results are within +/-10% of the reported values for the majority of the elements. The measured concentrations of major and minor elements are analysed in terms of the average intake of mineral content and the role of these elements in terms of the nutritional value.     

High-frequency dielectric behaviour of polycrystalline zinc substituted cobalt ferrites

The dielectric constant () and complex dielectric constant () of zinc substituted cobalt ferrites have been measured at room temperature in the high frequency range 100 kHz to 1 MHz. The values of dielectric loss tangent (tan ) have been computed from and . Plots of dielectric constant () versus frequency show a normal dielectric behaviour of the spinel ferrites. The frequency dependence of dielectric loss tangent (tan ) is found to be abnormal, giving a peak at certain frequency for all the ferrites under investigation. A qualitative explanation is given for the composition and frequency dependence of the dielectric constant and dielectric loss tangent. The dielectric constant for these mixed ferrites is approximately inversely proportional to the square root of the resistivity. A plot of dielectric constant versus temperature shows a transition near the Curie temperature. An attempt is made to explain the possible mechanism for this observation.     

Induction of apoptosis and apoptotic mediators in balb/C splenic lymphocytes by dietary n−3 and n−6 fatty acids

The present study was designed to investigate the effect of diatery n−6 and n−3 polyunsaturated fatty acids (PUFA) on anti-CD3 and anti-Fas antibody-induced apoptosis and its mediators in mouse spleen cells. Nutritionally adequate semipurified diets containing either 5% w/w corn oil (n−6 PUFA) or fish oil (n−3 PUFA) were fed to weanling female Balb/C mice, and 24 wk later mice were sacrificed. In n−3 PUFA-fed mice, serum and splenocyte lipid peroxides were increased by 20 and 28.3% respectively, compared to n−6 PUFA-fed mice. Further, serum vitamin F levels were decreased by 50% in the n−3 PUFA-fed group, whereas higher anti0Fas- and anti-CD3-induced apoptosis (65 and 66%) and necrosis (17 and 25%), compared to the n−6 PUFA-fed group, were found when measured with Annexin V and propidium iodide staining, respectively. In addition, decreased Bcl-2 and increased Fas-ligand (Fas-L) also were observed in the n−3 PUFA-fed group compared to the n−6 PUFA-fed group. No difference in the ratio of splenocyte subsets nor their Fas expression was observed between the n−3 PUFA-fed and n−6 PUFA-fed groups, whereas decreased proliferation of splenocytes was found in n−3 PUFA-fed mice compared to n−6 PUFA-fed mice. In conclusion, our results indicate that dietary n−3 PUFA induces higher apoptosis by increasing the generation of lipid peroxides and elevating Fas-L expression along with decreasing Bcl-2 expression. A reduced proliferative response of immune cells also was observed in n−3 PUFA-fed mice.     

A tandem queue with general bulk service and servers' “vacation”

This paper analyses two queueing models consisting of two units I and II connected in series, separated by a finite buffer of size N. In both models, unit I has only one exponential server capable of serving customers one at a time and unit II consist of c parallel exponential servers, each of them serving customers in groups according to general bulk service rules. When the queue length in front of unit II is less than the minimum of batch size, the free servers take a vacation. On return from vacation, if the queue length is less than the minimum, they leave for another vacation in the first model, whereas in the second model they wait in the system until they get the minimum number of customers and then start servicing. The steady-state probability vector of the number of customers waiting and receiving service in unit I and waiting in the buffer is obtained for both the models, using the modified matrix geometric method. Numerical results are also presented.     

Effect of high fat corn oil, olive oil and fish oil on phospholipid fatty acid composition in male F344 rats

Venous stasis associated with prolonged bed rest can enhance the risk of deep venous thrombosis (DVT). Pneumatic compression of the lower extremities can reduce this risk by preventing venous stasis. When selecting a method of leg compression for their patients, physicians must chose between two distinctly different types of compression devices. One device applies pressure with a single-chambered sleeve to the below knee region while the other applies pressure in a sequential gradient fashion from the ankle to the thigh. The current prospective study was designed to evaluated the ability of two such devices to increase blood flow in the profunda femoral vein. Venous blood flow velocity, compression time, and vein diameter were measured in nine normal experimental subjects using an Accuson duplex-Doppler before, during and after leg compression. Compression with the single-chambered device produced a significant rise in venous blood flow velocity; however, this could not be maintained and our results indicate a higher average velocity was achieved with the sequential gradient device. The sequential gradient device also moved a greater volume of blood and achieved a higher average blood flow rate. The time between deflation of the sleeve and return of a phasic respiratory signal was greater after compression with the sequential gradient device. These results suggest that sequential gradient compression produces the type of hemodynamic alterations needed to reduce the risk of DVT by achieving a sustained increase in venous blood flow and more completely emptying of the veins in the leg.     

Three-dimensional structure of meso-diaminopimelic acid dehydrogenase from Corynebacterium glutamicum

Diaminopimelate dehydrogenase catalyzes the NADPH-dependent reduction of ammonia and L-2-amino-6-ketopimelate to form meso-diaminopimelate, the direct precursor of L-lysine in the bacterial lysine biosynthetic pathway. Since mammals lack this metabolic pathway inhibitors of enzymes in this pathway may be useful as antibiotics or herbicides. Diaminopimelate dehydrogenase catalyzes the only oxidative deamination of an amino acid of D configuration and must additionally distinguish between two chiral amino acid centers on the same symmetric substrate. The Corynebacterium glutamicum enzyme has been cloned, expressed in Escherichia coli, and purified to homogeneity using standard biochemical procedures [Reddy, S. G., Scapin, G., & Blanchard, J. S. (1996) Proteins: Structure, Funct. Genet. 25, 514-516]. The three-dimensional structure of the binary complex of diaminopimelate dehydrogenase with NADP+ has been solved using multiple isomorphous replacement procedures and noncrystallographic symmetry averaging. The resulting model has been refined against 2.2 A diffraction data to a conventional crystallographic R-factor of 17.0%. Diaminopimelate dehydrogenase is a homodimer of structurally not identical subunits. Each subunit is composed of three domains. The N-terminal domain contains a modified dinucleotide binding domain, or Rossman fold (six central beta-strands in a 213456 topology surrounded by five alpha-helices). The second domain contains two alpha-helices and three beta-strands. This domain is referred to as the dimerization domain, since it is involved in forming the monomer--monomer interface of the dimer. The third or C-terminal domain is composed of six beta-strands and five alpha-helices. The relative position of the N- and C-terminal domain in the two monomers is different, defining an open and a closed conformation that may represent the enzyme's binding and active state, respectively. In both monomers the nucleotide is bound in an extended conformation across the C-terminal portion of the beta-sheet of the Rossman fold, with its C4 facing the C-terminal domain. In the closed conformer two molecules of acetate have been refined in this region, and we postulate that they define the DAP binding site. The structure of diaminopimelate dehydrogenase shows interesting similarities to the structure of glutamate dehydrogenase [Baker, P. J., Britton, K. L., Rice, D. W., Rob, A., & Stillmann, T.J. (1992a) J. Mol. Biol. 228, 662-671] and leucine dehydrogenase [Baker, P.J., Turnbull, A.P., Sedelnikova, S.E., Stillman, T. J., & Rice, D. W. (1995) Structure 3, 693-705] and also resembles the structure of dihydrodipicolinate reductase [Scapin, G., Blanchard, J. S., & Sacchettini, J. C. (1995) Biochemistry 34, 3502-3512], the enzyme immediately preceding it in the diaminopimelic acid/lysine biosynthetic pathway.     

Cadherin-6 mediates the heterotypic interactions between the hemopoietic osteoclast cell lineage and stromal cells in a murine model of osteoclast differentiation

Osteoclasts are multinucleated cells of hemopoietic origin that are responsible for bone resorption during physiological bone remodeling and in a variety of bone diseases. Osteoclast development requires direct heterotypic cell-cell interactions of the hemopoietic osteoclast precursors with the neighboring osteoblast/stromal cells. However, the molecular mechanisms underlying these heterotypic interactions are poorly understood. We isolated cadherin-6 isoform, denoted cadherin-6/2 from a cDNA library of human osteoclast-like cells. The isolated cadherin-6/2 is 3,423 bp in size consisting of an open reading frame of 2,115 bp, which encodes 705 amino acids. This isoform lacks 85 amino acids between positions 333 and 418 and contains 9 different amino acids in the extracellular domain compared with the previously described cadherin-6. The human osteoclast-like cells also expressed another isoform denoted cadherin-6/1 together with the cadherin-6. Introduction of cadherin-6/2 into L-cells that showed no cell-cell contact caused evident morphological changes accompanied with tight cell-cell association, indicating the cadherin-6/2 we isolated here is functional. Moreover, expression of dominant-negative or antisense cadherin-6/2 construct in bone marrow-derived mouse stromal ST2 cells, which express only cadherin-6/2, markedly impaired their ability to support osteoclast formation in a mouse coculture model of osteoclastogenesis. Our results suggest that cadherin-6 may be a contributory molecule to the heterotypic interactions between the hemopoietic osteoclast cell lineage and osteoblast/bone marrow stromal cells required for the osteoclast differentiation. Since both osteoclasts and osteoblasts/bone marrow stromal cells are the primary cells controlling physiological bone remodeling, expression of cadherin-6 isoforms in these two cell types of different origin suggests a critical role of these molecules in the relationship of osteoclast precursors and cells of osteoblastic lineage within the bone microenvironment.     

Codistribution of procathepsin B and mature cathepsin B forms in human prostate tumors detected by confocal and immunofluorescence microscopy

Ascorbic acid can recycle alpha-tocopherol from the tocopheroxyl free radical in lipid bilayers and in micelles, but such recycling has not been demonstrated to occur across cell membranes. In this work the ability of intracellular ascorbate to protect and to recycle alpha-tocopherol in intact human erythrocytes and erythrocyte ghosts was investigated. In erythrocytes that were 80% depleted of intracellular ascorbate by treatment with the nitroxide Tempol, both 2,2'-azobis(2-amidinopropane) dihydrochloride (AAPH) and ferricyanide oxidized alpha-tocopherol to a greater extent than in cells not depleted of ascorbate. In contrast, in erythrocytes in which the intracellular ascorbate concentration had been increased by loading with dehydroascorbate, loss of alpha-tocopherol was less with both oxidants than in control cells. Protection against AAPH-induced oxidation of alpha-tocopherol was not prevented by extracellular ascorbate oxidase, indicating that the protection was due to intracellular and not to extracellular ascorbate. Incubation of erythrocytes with lecithin liposomes also generated an oxidant stress, which caused lipid peroxidation in the liposomes and depleted erythrocyte alpha-tocopherol, leading to hemolysis. Ascorbate loading of the erythrocytes delayed liposome oxidation and decreased loss of alpha-tocopherol from both cells and from alpha-tocopherol-loaded liposomes. When erythrocyte ghosts were resealed to contain ascorbate and challenged with free radicals generated by AAPH outside the ghosts, intravesicular ascorbate was totally depleted over 1 h of incubation, whereas alpha-tocopherol decreased only after ascorbate was substantially oxidized. These results suggest that ascorbate within the erythrocyte protects alpha-tocopherol in the cell membrane by a direct recycling mechanism.