Correlation between CPT Data and Dynamic Properties of In Situ Frozen Samples

Correlations between cone penetration resistance and liquefaction resistance of sandy soils are examined, based on high quality undisturbed samples obtained by the in situ freezing method. For this purpose, the CPT tests are conducted at six sites where in situ frozen sands with fines contents up to 30 % were sampled and their dynamic properties were determined in the laboratory. The comparison of the CPT data with the soil properties of the in situ frozen samples has shown that: (1) Robertson\u27s soil classification chart performs well for sandy soils in Japan; (2) the CPT qt-value shows a good correlation with elastic shear modulus of the in situ frozen samples; and (3) the liquefaction resistance of the in situ frozen samples is uniquely expressed if the cone penetration resistance is normalized in terms of confining pressure and minimum void ratio

Scaling 5ules for a 6lab: aveguide 6tructure &omprising 1onlinear and 1egative, ndex 0aterials

We consider a Kerr-type nonlinear guiding layer surrounded by at least one medium made of a negative index material (NIM). Three different structures are investigated in this work. The first structure has a NIM cladding, the second has a NIM substrate, and the third has a NIM substrate and cladding. Three normalized parameters are used to study the dispersion characteristics of these waveguide structures. The dispersion curves are obtained and the effect of the NIM parameters on the guidance properties is presented. It is found that the dispersion characteristic of nonlinear waveguide structure with NIM cladding and dielectric substrate are similar to those for the same structure with NIM substrate and dielectric cladding. However, when both of them are NIMs new properties can be seen

Characteristics of electromagnetic waves in slab waveguide structures comprising chiral nihility film and left-handed material claddings

We analytically present the dispersion equation of an asymmetric three-layered chirowaveguides, in which the core and the claddings are different chiral materials. Then, we produce the dispersion equation for a symmetric three-layered chirowaveguides, in which the claddings chiral materials are the same, but different from the one in the core. After that, two modes of propagation through a chiral nihility core and left handed material (LHM) claddings waveguide are treated in details. The characteristic equations and the cut-off frequencies for both even and odd modes are derived. The electric field profiles are plotted and discussed. We show that each mode (odd and even) can be separated into right-handed and left-handed circularly polarized (RCP and LCP) modes. The results reveal that novel properties such as peculiar dispersion curves

Fibroblast migration and collagen deposition during dermal wound healing: mathematical modelling and clinical implications,

The extent to which collagen alignment occurs during dermal wound healing determines the severity of scar tissue formation. We have modelled this using a multiscale approach, in which extracellular materials, for example collagen and fibrin, are modelled as continua, while fibroblasts are considered as discrete units. Within this model framework, we have explored the effects that different parameters have on the alignment process, and we have used the model to investigate how manipulation of transforming growth factor-β levels can reduce scar tissue formation. We briefly review this body of work, then extend the modelling framework to investigate the role played by leucocyte signalling in wound repair. To this end, fibroblast migration and collagen deposition within both the wound region and healthy peripheral tissue are considered. Trajectories of individual fibroblasts are determined as they migrate towards the wound region under the combined influence of collagen/fibrin alignment and gradients in a paracrine chemoattractant produced by leucocytes. The effects of a number of different physiological and cellular parameters upon the collagen alignment and repair integrity are assessed. These parameters include fibroblast concentration, cellular speed, fibroblast sensitivity to chemoattractant concentration and chemoattractant diffusion coefficient. Our results show that chemoattractant gradients lead to increased collagen alignment at the interface between the wound and the healthy tissue. Results show that there is a trade-off between wound integrity and the degree of scarring. The former is found to be optimized under conditions of a large chemoattractant diffusion coefficient, while the latter can be minimized when repair takes place in the presence of a competitive inhibitor to chemoattractants

Aldimine derivatives as photosensitizers for dye-sensitized solar cells

Five aldimine derivatives were prepared by condensation of the appropriate amine with salicylaldehyde (m1-m4) and 4-aminobenzoic acid with 2-thiophene carboxaldehyde (m5). A molar ratio of 1: 1 was used and the mixture was refluxed in ethanol for 2 h to obtain the corresponding aldimine derivative. These derivatives were used as photosensitizers for dye-sensitized solar cells (DSSCs). The best performance was obtained for the DSSC sensitized with 2-(2-hydroxybenzylideneamino) benzoic acid, for which a short-circuit current of 2.86 mA/cm^ 2, an open-circuit voltage of 0.562 V, and an efficiency of 0.575% were obtained.Five aldimine derivatives were prepared by condensation of the appropriate amine with salicylaldehyde (m1-m4) and 4-aminobenzoic acid with 2-thiophene carboxaldehyde (m5). A molar ratio of 1: 1 was used and the mixture was refluxed in ethanol for 2 h to obtain the corresponding aldimine derivative. These derivatives were used as photosensitizers for dye-sensitized solar cells (DSSCs). The best performance was obtained for the DSSC sensitized with 2-(2-hydroxybenzylideneamino) benzoic acid, for which a short-circuit current of 2.86 mA/cm^ 2, an open-circuit voltage of 0.562 V, and an efficiency of 0.575% were obtained

ATM protein and p53-serine 15 phosphorylation in ataxia-telangiectasia (AT) patients and at heterozygotes

ATM (ataxia-telangiectasia mutated) gene plays a central role in the DNA-damage response pathway. We characterized the ATM protein expression in immortalized cells from AT and AT-variant patients, and heterozygotes and correlated it with two ATM-dependent radiation responses, G1 checkpoint arrest and p53-Ser 15 phosphorylation. On Western blots, the full-length ATM protein was detected in eight of 18 AT cases, albeit at 1–32% of the normal levels, whereas a truncated ATM protein was detected in a single case, despite the prevalence among cases of truncation mutations. Of two ataxia without telangiectasia [A-(T)] cases, one expressed 20% and the other ~70% of the normal ATM levels. Noteworthy, among ten asymptomatic heterozygous carriers for AT, normal amounts of ATM protein were found in one and reduced by 40–50% in the remaining cases. The radiation-induced phosphorylation of p53 protein at serine 15, largely mediated by ATM kinase, was defective in AT, A(-T) and in 2/4 heterozygous carriers, while the G1 cell cycle checkpoint was disrupted in all AT and A(-T) cases, and in 3/10 AT heterozygotes. Altogether, our study shows that AT and A(-T) cases bearing truncation mutations of the ATM gene can produce modest amounts of full-length (and only rarely truncated) ATM protein. However, this limited expression of ATM protein provides no benefit regarding the ATM-dependent responses related to G1 arrest and p53-ser15 phosphorylation. Our study additionally shows that the majority of AT heterozygotes express almost halved levels of ATM protein, sufficient in most cases to normally regulate the ATM-dependent DNA damage-response pathway. © 2000 Cancer Research Campaig

CXCL12 promotes CCR7 ligand-mediated breast cancer cell invasion and migration toward lymphatic vessels

Chemokines are a family of cytokines that mediate leukocyte trafficking and are involved in tumor cell migration, growth, and progression. Although there is emerging evidence that multiple chemokines are expressed in tumor tissues and that each chemokine induces receptor-mediated signaling, their collaboration to regulate tumor invasion and lymph node metastasis has not been fully elucidated. In this study, we examined the effect of CXCL12 on the CCR7-dependent signaling in MDA-MB-231 human breast cancer cells to determine the role of CXCL12 and CCR7 ligand chemokines in breast cancer metastasis to lymph nodes. CXCL12 enhanced the CCR7-dependent in vitro chemotaxis and cell invasion into collagen gels at suboptimal concentrations of CCL21. CXCL12 promoted CCR7 homodimer formation, ligand binding, CCR7 accumulation into membrane ruffles, and cell response at lower concentrations of CCL19. Immunohistochemistry of MDA-MB-231-derived xenograft tumors revealed that CXCL12 is primarily located in the pericellular matrix surrounding tumor cells, whereas the CCR7 ligand, CCL21, mainly associates with LYVE-1(+) intratumoral and peritumoral lymphatic vessels. In the three-dimensional tumor invasion model with lymph networks, CXCL12 stimulation facilitates breast cancer cell migration to CCL21-reconstituted lymphatic networks. These results indicate that CXCL12/CXCR4 signaling promotes breast cancer cell migration and invasion toward CCR7 ligand-expressing intratumoral lymphatic vessels and supports CCR7 signaling associated with lymph node metastasis

Biological activity differences between TGF-β1 and TGF-β3 correlate with differences in the rigidity and arrangement of their component monomers

[Image: see text] TGF-β1, -β2, and -β3 are small, secreted signaling proteins. They share 71–80% sequence identity and signal through the same receptors, yet the isoform-specific null mice have distinctive phenotypes and are inviable. The replacement of the coding sequence of TGF-β1 with TGF-β3 and TGF-β3 with TGF-β1 led to only partial rescue of the mutant phenotypes, suggesting that intrinsic differences between them contribute to the requirement of each in vivo. Here, we investigated whether the previously reported differences in the flexibility of the interfacial helix and arrangement of monomers was responsible for the differences in activity by generating two chimeric proteins in which residues 54–75 in the homodimer interface were swapped. Structural analysis of these using NMR and functional analysis using a dermal fibroblast migration assay showed that swapping the interfacial region swapped both the conformational preferences and activity. Conformational and activity differences were also observed between TGF-β3 and a variant with four helix-stabilizing residues from TGF-β1, suggesting that the observed changes were due to increased helical stability and the altered conformation, as proposed. Surface plasmon resonance analysis showed that TGF-β1, TGF-β3, and variants bound the type II signaling receptor, TβRII, nearly identically, but had small differences in the dissociation rate constant for recruitment of the type I signaling receptor, TβRI. However, the latter did not correlate with conformational preference or activity. Hence, the difference in activity arises from differences in their conformations, not their manner of receptor binding, suggesting that a matrix protein that differentially binds them might determine their distinct activities

Complex Regulation of p73 Isoforms after Alteration of Amyloid Precursor Polypeptide (APP) Function and DNA Damage in Neurons

Background: Alterations of the APP pathway or DNA damage induce neuronal cell death. Results: Alterations of the APP pathway or DNA damage increase TAp73 expression and reduce Delta Np73 protein levels. Conclusion: A tight control of the expression of p73 isoforms participates in neuronal cell death. Significance: p73 isoforms may play a role in neurodegenerative diseases such as Alzheimer and in the neurotoxicity of anticancer drug therapies

Amelioration of endotoxemia by a synthetic analog of Omega-3 epoxyeicosanoids

Sepsis, a systemic inflammatory response to pathogenic factors, is a difficult to treat life-threatening condition associated with cytokine and eicosanoid storms and multi-organ damage. Omega-3 polyunsaturated fatty acids, such as eicosapentaenoic (EPA) and docosahexaenoic acid, are the precursors of potent anti-inflammatory lipid mediators, including 17,18-epoxyeicosatetraenoic acid (17,18-EEQ), the main metabolite of EPA generated by cytochrome P450 epoxygenases. Searching for novel therapeutic or preventative agents in sepsis, we tested a metabolically robust synthetic analog of 17,18-EEQ (EEQ-A) for its ability to reduce mortality, organ damage, and pro-inflammatory cytokine transcript level in a mouse model of lipopolysaccharide (LPS)-induced endotoxemia, which is closely related to sepsis. Overall survival significantly improved following preventative EEQ-A administration along with decreased transcript level of pro-inflammatory cytokines. On the other hand, the therapeutic protocol was effective in improving survival at 48 hours but insignificant at 72 hours. Histopathological analyses showed significant reductions in hemorrhagic and necrotic damage and infiltration in the liver. In vitro studies with THP-1 and U937 cells showed EEQ-A mediated repression of LPS-induced M1 polarization and enhancement of IL-4-induced M2 polarization of macrophages. Moreover, EEQ-A attenuated the LPS-induced decline of mitochondrial function in THP-1 cells, as indicated by increased basal respiration and ATP production as well as reduction of the metabolic shift to glycolysis. Taken together, these data demonstrate that EEQ-A has potent anti-inflammatory and immunomodulatory properties that may support therapeutic strategies for ameliorating the endotoxemia