Model-independent study of the QCD sum rule for the pi NN coupling constant

We reinvestigate the QCD sum rule for the pi NN coupling constant, g, starting from the vacuum-to-pion matrix element of the correlation function of the interpolating fields of two nucleons. We study in detail the physical content of the correlation function without referring to the effective theory. We consider the invariant correlation functions by splitting the correlation function into different Dirac structures. We show that the coefficients of the double-pole terms are proportional to g but that the coefficients of the single-pole terms are not determined by g. In the chiral limit the single-pole terms as well as the continuum terms are ill defined in the dispersion integral. Therefore, the use of naive QCD sum rules obtained from the invariant correlation functions is not justified. A possible procedure to avoid this difficulty is discussed.Comment: 20 pages, 2 figure

Elastic properties of Zr-based bulk metallic glasses studied\ud by resonant ultrasound spectroscopy

We report measurements of the elastic properties of Zr-based bulk metallic glasses,\ud Zr52.5Cu17.9Ni14.6Al10Ti5, Zr50Cu30Ni10Al10, and Zr50Cu40Al10 between 5 K and\ud 300 K. Both the shear and longitudinal modulus have been measured as a function of\ud temperature, allowing accurate determination of the Poisson’s ratio and the related\ud ratio of bulk modulus to shear modulus, K/G. These data make it possible to assess the\ud influence of the alloy’s composition on the mechanical properties and enable an\ud evaluation of the correlation between the elastic moduli and the ductility of the alloys

Elastic properties of Zr-based bulk metallic glasses studied by resonant ultrasound spectroscopy

We report measurements of the elastic properties of Zr-based bulk metallic glasses, Zr52.5Cu17.9Ni14.6Al10Ti5, Zr50Cu30Ni10Al10, and Zr50Cu40Al10 between 5 K and 300 K. Both the shear and longitudinal modulus have been measured as a function of temperature, allowing accurate determination of the Poisson’s ratio and the related ratio of bulk modulus to shear modulus, K/G. These data make it possible to assess the influence of the alloy’s composition on the mechanical properties and enable an evaluation of the correlation between the elastic moduli and the ductility of the alloys

Structure-activity study of a laminin α1 chain active peptide segment Ile-Lys-Val-Ala-Val (IKVAV)

AbstractThe IKVAV sequence, one of the most potent active sites of laminin-1, has been shown to promote cell adhesion, neurite outgrowth, and tumor growth. Here we have determined the structural requirements of the IKVAV sequence for cell attachment and neurite outgrowth using various 12-mer synthetic peptide analogs. All-l- and all-d-IKVAV peptides showed cell attachment and neurite outgrowth activities. In contrast, all-l- and all-d-reverse-sequence peptides were not active. Some of the analogs, in which the lysine and isoleucine residues of the IKVAV peptide were substituted with different amino acids, promoted cell attachment, but none of the analog peptides showed neurite outgrowth activity comparable to that of the IKVAV peptide. These results suggest that the lysine and isoleucine residues are critical for the biological functions of the IKVAV peptide

Immunoelectron Microscopic Study of Podoplanin Localization in Mouse Salivary Gland Myoepithelium

We have recently reported that salivary gland cells express the lymphatic endothelial cell marker podoplanin. The present study was aimed to immunohistochemically investigate the expression of the myoepithelial cell marker α-smooth muscle actin (SMA) on podoplanin-positive cells in mouse parotid and sublingual glands, and to elucidate podoplanin localization in salivary gland myoepithelial cells by immunoelectron microscopic study. The distribution of myoepithelial cells expressing podoplanin and α-SMA was examined by immunofluorescent staining, and the localization of reaction products of anti-podoplanin antibody was investigated by pre-embedded immunoelectron microscopic method. In immunohistochemistry, the surfaces of both the mucous acini terminal portion and ducts were covered by a number of extensive myoepithelial cellular processes expressing podoplanin, and the immunostaining level with anti-podoplanin antibody to myoepithelial cells completely coincided with the immunostaining level with anti-α-SMA antibody. These findings suggest that podoplanin is a salivary gland myoepithelial cell antigen, and that the detection level directly reflects the myoepithelial cell distribution. In immunoelectron microscopic study, a number of reaction products with anti-podoplanin antibody were found at the Golgi apparatus binding to the endoplasmic reticulum in the cytoplasm of myoepithelial cells between sublingual gland acinar cells, and were also found at the myoepithelial cell membrane. These findings suggest that salivary gland myoepithelial cells constantly produce podoplanin and glycosylate at the Golgi apparatus, and transport them to the cell membrane. Podoplanin may be involved in maintaining the homeostasis of myoepithelial cells through its characteristic as a mucin-type transmembrane glycoprotein

Osteoprotegerin Contributes to the Metastatic Potential of Cells with a Dysfunctional TSC2 Tumor-Suppressor Gene

In addition to its effects on bone metabolism, osteoprotegerin (OPG), a soluble member of the tumor necrosis factor family of receptors, promotes smooth muscle cell proliferation and migration and may act as a survival factor for tumor cells. We hypothesized that these cellular mechanisms of OPG may be involved in the growth and proliferation of lymphangioleiomyomatosis (LAM) cells, abnormal smooth muscle-like cells with mutations in one of the tuberous sclerosis complex tumor-suppressor genes (TSC1/TSC2) that cause LAM, a multisystem disease characterized by cystic lung destruction, lymphatic infiltration, and abdominal tumors. Herein, we show that OPG stimulated proliferation of cells cultured from explanted LAM lungs, and selectively induced migration of LAM cells identified by the loss of heterozygosity for TSC2. Consistent with these observations, cells with TSC2 loss of heterozygosity expressed the OPG receptors, receptor activator of NF-κB ligand, syndecan-1, and syndecan-2. LAM lung nodules showed reactivities to antibodies to tumor necrosis factor–related apoptosis-inducing ligand, receptor activator of NF-κB ligand, syndecan-1, and syndecan-2. LAM lung nodules also produced OPG, as shown by expression of OPG mRNA and colocalization of reactivities to anti-OPG and anti-gp100 (HMB45) antibodies in LAM lung nodules. Serum OPG was significantly higher in LAM patients than in normal volunteers. Based on these data, it appears that OPG may have tumor-promoting roles in the pathogenesis of lymphangioleiomyomatosis, perhaps acting as both autocrine and paracrine factors

Time evolution in visible light emission from high-power Ar pulse-modulated induction thermal plasmas

Transient behavior of a 15-kW Ar pulse-modulated induction thermal plasma (PMITP) at a pressure of 31 kPa was observed using a high-speed video camera. The PMITP method is one of new techniques for controlling temperature and radical density in time-domain in high-power thermal plasmas. The adoption of a high-power metal-oxide-semiconductor field-effect transistor (MOSFET) inverter power supply makes it possible to sustain PMITPs with high power-conversion efficiency. The high-speed video pictures provide two-dimensional, time-dependent radiation intensity distributions from PMITPs, which are useful for understanding an unique transition behavior of PMITPs

Direct observation of a surface induced disordering process in magnetic nanoparticles

We present experimental evidence of surface induced disordering at magnetic FeCoPd nanoparticles during the L1₀-A1 phase transition using high-resolution aberration-corrected electron microscopy and strain mapping. In situ electron diffraction studies show a narrow temperature range of fully ordered L1₀ structure. The order-disorder transition is size dependent and induces strong lattice deformation in outer part of the nanocrystals. The formation of unusually large strain of 20% is discussed in terms of core-shell structure formation with surface disordered layer and ordered core. © 2009 The American Physical Society.András Kovács, Kazuhisa Sato, Vlado K. Lazarov, Pedro L. Galindo, Toyohiko J. Konno, and Yoshihiko Hirotsu, Phys. Rev. Lett. 103, 115703, 2009

Analog peptides of type II collagen can suppress arthritis in HLA-DR4 (DRB1*0401) transgenic mice

Rheumatoid arthritis (RA) is an autoimmune disease associated with the recognition of self proteins secluded in diarthrodial joints. We have previously established that mice transgenic for the human DR genes associated with RA are susceptible to collagen-induced arthritis (CIA) and we have identified a determinant of type II collagen (CII(263–270)) that triggers T-cell immune responses in these mice. We have also determined that an analog of CII(263–270 )would suppress disease in DR1 transgenic mice. Because the immunodominant determinant is the same for both DR1 transgenic and DR4 transgenic mice, we attempted to determine whether the analog peptide that was suppressive in DR1 transgenic mice would also be effective in suppressing CIA in DR4 transgenic mice. We treated DR4 transgenic mice with two analog peptides of CII that contained substitutions in the core of the immunodominant determinant: CII(256–276 )(F263N, E266D) and CII(256–270 )(F263N, E266A). Mice were observed for CIA, and T-cell proliferative responses were determined. Either peptide administered at the time of immunization with CII significantly downregulated arthritis. Binding studies demonstrated that replacement of the phenylalanine residue in position 263 of the CII peptide with asparagine significantly decreased the affinity of the peptide for the DR4 molecule. In contrast, replacement of the glutamic acid residue in position 266 with aspartic acid or with alanine had differing results. Aspartic acid reduced the affinity (35-fold) whereas alanine did not. Both peptides were capable of suppressing CIA. With the use of either peptide, CII(256–276 )(F263N, E266D) or CII(256–270 )(F263N, E266A), the modulation of CIA was associated with an increase in T-cell secretion of IL-4 together with a decrease in IFN-γ. We have identified two analog peptides that are potent suppressors of CIA in DR4 transgenic mice. These experiments represent the first description of an analog peptide of CII recognized by T cells in the context of HLA-DR4 that can suppress autoimmune arthritis