Showing papers by "Osaka University published in 1997"
TL;DR: This work was supported in part by Grants-in-Aid from the Ministry of Education, Science, and Culture of Japan and by a Research Grant from the Princess Takamatsu Cancer Research Fund, and performed in part through Special Coordination Funds of the Science and Technology Agency of the Japanese Government.
5,054 citations
TL;DR: The data suggest that both intramembranous and endochondral ossification were completely blocked, owing to the maturational arrest of osteoblasts in the mutant mice, and demonstrate that Cbfa1 plays an essential role in osteogenesis.
4,196 citations
TL;DR: A new gene, termed klotho, has been identified that is involved in the suppression of several ageing phenotypes in the mouse, and may function as part of a signalling pathway that regulates ageing in vivo and morbidity in age-related diseases.
Abstract: A new gene, termed klotho, has been identified that is involved in the suppression of several ageing phenotypes. A defect in klotho gene expression in the mouse results in a syndrome that resembles human ageing, including a short lifespan, infertility, arteriosclerosis, skin atrophy, osteoporosis and emphysema. The gene encodes a membrane protein that shares sequence similarity with the β-glucosidase enzymes. The klotho gene product may function as part of a signalling pathway that regulates ageing in vivo and morbidity in age-related diseases.
3,025 citations
TL;DR: Transgenic mouse lines with an ‘enhanced’ GFP (EGFP) cDNA under the control of a chicken beta‐actin promoter and cytomegalovirus enhancer were produced and all of the tissues from these transgenic lines, with the exception of erythrocytes and hair, were green under excitation light.
2,626 citations
TL;DR: The authors present an overview of new multiple access schemes based on a combination of code division and multicarrier techniques, such as multicarrier code-division multiple access (MC-CDMA), multicarriers direct sequence CDMA, and multitone CDMA.
Abstract: The authors present an overview of new multiple access schemes based on a combination of code division and multicarrier techniques, such as multicarrier code-division multiple access (MC-CDMA), multicarrier direct sequence CDMA (multicarrier DS-CDMA), and multitone CDMA (MT-CDMA).
2,137 citations
TL;DR: The usefulness of the proposed method for three-dimensional microfabrication with photopolymerization stimulated by two-photon absorption with a pulsed infrared laser has been verified by fabrication of several kinds of microstructure by use of a resin consisting of photoinitiators, urethane acrylate monomers, and urethanacrylate oligomers.
Abstract: We propose a method for three-dimensional microfabrication with photopolymerization stimulated by two-photon absorption with a pulsed infrared laser An experimental system for the microfabrication has been developed with a Ti:sapphire laser whose oscillating wavelength and pulse width are 790 nm and 200 fs, respectively The usefulness of the proposed method has been verified by fabrication of several kinds of microstructure by use of a resin consisting of photoinitiators, urethane acrylate monomers, and urethane acrylate oligomers
1,660 citations
TL;DR: This paper reviews recent progress in the study of the interleukin-6 family of cytokines and gp130 and describes how the dimerization of gp130 leads to activation of associated cytoplasmic tyrosine kinases and subsequent modification of transcription factors.
Abstract: Receptors for most interleukins and cytokines that regulate immune and hematopoietic systems belong to the class I cytokine receptor family. These molecules form multichain receptor complexes in order to exhibit high-affinity binding to, and mediate biological functions of, their respective cytokines. In most cases, these functional receptor complexes share common signal transducing receptor components that are also in the class I cytokine receptor family, i.e. gp130, common beta, and common gamma molecules. Interleukin-6 and related cytokines, interleukin-11, leukemia inhibitory factor, oncostatin M, ciliary neurotrophic factor, and cardiotrophin-1 are all pleiotropic and exhibit overlapping biological functions. Functional receptor complexes for this interleukin-6 family of cytokines share gp130 as a component critical for signal transduction. Unlike cytokines sharing common beta and common gamma chains that mainly function in hematopoietic and lymphoid cell systems, the interleukin-6 family of cytokines function extensively outside these systems as well, e.g. from the cardiovascular to the nervous system, owing to ubiquitously expressed gp130. Stimulation of cells with the interleukin-6 family of cytokines triggers homo- or hetero-dimerization of gp130. Although gp130 and its dimer partners possess no intrinsic tyrosine kinase domain, the dimerization of gp130 leads to activation of associated cytoplasmic tyrosine kinases and subsequent modification of transcription factors. This paper reviews recent progress in the study of the interleukin-6 family of cytokines and gp130.
1,514 citations
TL;DR: A new SH2-domain-containing protein is isolated, JAB, which is a JAK-binding protein that interacts with the Jak2 tyrosine-kinase JH1 domain, and JAB and CIS appear to function as negative regulators in the JAK signalling pathway.
Abstract: The proliferation and differentiation of cells of many lineages are regulated by secreted proteins known as cytokines. Cytokines exert their biological effect through binding to cell-surface receptors that are associated with one or more members of the JAK family of cytoplasmic tyrosine kinases. Cytokine-induced receptor dimerization leads to the activation of JAKs, rapid tyrosine-phosphorylation of the cytoplasmic domains, and subsequent recruitment of various signalling proteins, including members of the STAT family of transcription factors, to the receptor complex. Using the yeast two-hybrid system, we have now isolated a new SH2-domain-containing protein, JAB, which is a JAK-binding protein that interacts with the Jak2 tyrosine-kinase JH1 domain. JAB is structurally related to CIS, a cytokine-inducible SH2 protein. Interaction of JAB with Jak1, Jak2 or Jak3 markedly reduces their tyrosine-kinase activity and suppresses the tyrosine-phosphorylation and activation of STATs. JAB and CIS appear to function as negative regulators in the JAK signalling pathway.
1,436 citations
TL;DR: It is demonstrated that constitutive expression of COX-2 can lead to phenotypic changes that alter the metastatic potential of colorectal cancer cells and be reversed by treatment with sulindac sulfide, a known COX inhibitor.
Abstract: Recent epidemiologic studies have shown a 40–50% reduction in mortality from colorectal cancer in individuals who take nonsteroidal antiinflammatory drugs on a regular basis compared with those not taking these agents. One property shared by all of these drugs is their ability to inhibit cyclooxygenase (COX), a key enzyme in the conversion of arachidonic acid to prostaglandins. Two isoforms of COX have been characterized, COX-1 and COX-2. COX-2 is expressed at high levels in intestinal tumors in humans and rodents. Human colon cancer cells (Caco-2) were permanently transfected with a COX-2 expression vector or the identical vector lacking the COX-2 insert. The Caco-2 cells, which constitutively expressed COX-2, acquired increased invasiveness compared with the parental Caco-2 cells or the vector transfected control cells. Biochemical changes associated with this phenotypic change included activation of metalloproteinase-2 and increased RNA levels for the membrane-type metalloproteinase. Increased invasiveness and prostaglandin production were reversed by treatment with sulindac sulfide, a known COX inhibitor. These studies demonstrate that constitutive expression of COX-2 can lead to phenotypic changes that alter the metastatic potential of colorectal cancer cells.
1,427 citations
TL;DR: It is found that SSI-1 messenger RNA was induced by the cytokines interleukins 4 and 6, leukaemia-inhibitory factor (LIF), and granulocyte colony-stimulating factor (G-CSF), and these findings indicate that SSi-1 is responsible for negative-feedback regulation of the JAK–STAT pathway induced by cytokine stimulation.
Abstract: The signalling pathway that comprises JAK kinases and STAT proteins (for signal transducer and activator of transcription) is important for relaying signals from various cytokines outside the cell to the inside. The feedback mechanism responsible for switching off the cytokine signal has not been elucidated. We now report the cloning and characterization of an inhibitor of STAT activation which we name SSI-1 (for STAT-induced STAT inhibitor-1). We found that SSI-1 messenger RNA was induced by the cytokines interleukins 4 and 6 (IL-4, IL-6), leukaemia-inhibitory factor (LIF), and granulocyte colony-stimulating factor (G-CSF). Stimulation by IL-6 or LIF of murine myeloid leukaemia cells (M1 cells) induced SSI-1 mRNA expression which was blocked by transfection of a dominant-negative mutant of Stat3, indicating that the SSI-1 gene is a target of Stat3. Forced overexpression of SSI-1 complementary DNA interfered with IL-6- and LIF-mediated apoptosis and macrophage differentiation of M1 cells, as well as IL-6 induced tyrosine-phosphorylation of a receptor glycoprotein component, gp130, and of Stat3. When SSI-1 is overexpressed in COS7 cells, it can associate with the kinases Jak2 and Tyk2. These findings indicate that SSI-1 is responsible for negative-feedback regulation of the JAK-STAT pathway induced by cytokine stimulation.
1,309 citations
Journal Article•
TL;DR: This study addressed the question of whether apoptosis depends on intracellular ATP levels, since longer incubation under ATP-depleting conditions results in necrotic cell death, and indicated that ATP levels are a determinant of manifestation of cell death.
Abstract: Although apoptosis and necrosis are morphologically distinct manifestations of cell death, apoptosis and some necroses share common features in the death signaling pathway involving functional steps of death-driving interleukin 1beta-converting enzyme family proteases and anti-cell death protein Bcl-2. One evident physiological difference in cells undergoing apoptosis versus necrosis is in intracellular levels of ATP. In this study, we specifically addressed the question of whether apoptosis depends on intracellular ATP levels, since longer incubation under ATP-depleting conditions results in necrotic cell death. Incubation of cells in glucose-free medium with an inhibitor of mitochondrial F0F1-ATPases reduces intracellular ATP levels and completely blocks Fas/Apo-1-stimulated apoptosis. ATP supplied through glycolysis or oxidative phosphorylation restores the apoptotic cell death pathway. ATP depletion also leads to a block in Fas-induced activation of CPP32/Yama(-like) proteases, and when ATP is depleted after the activation of the proteases, subsequent apoptosis is significantly blocked. Thus, ATP-dependent steps exist both upstream and downstream of CPP32/Yama(-like) protease activation in apoptotic signal transduction. Treatment with the calcium ionophore induces apoptosis under ATP-supplying conditions but induces necrotic cell death under ATP-depleting conditions, indicating that ATP levels are a determinant of manifestation of cell death.
Chugai Pharmaceutical Co.1, University of Tokyo2, Kumamoto University3, Osaka University4, Japanese Foundation for Cancer Research5, Obihiro University of Agriculture and Veterinary Medicine6, Leiden University7, University of British Columbia8, University of North Carolina at Chapel Hill9, University of Oxford10
TL;DR: It is shown that targeted disruption of the MSR-A gene in mice results in a reduction in the size of atherosclerotic lesions in an animal deficient in apolipoprotein E, indicating that MSr-A may play a part in host defence against pathogens.
Abstract: Macrophage type-I and type-II class-A scavenger receptors (MSR-A) are implicated in the pathological deposition of cholesterol during atherogenesis as a result of receptor-mediated uptake of modified low-density lipoproteins (mLDL)1–6. MSR-A can bind an extraordinarily wide range of ligands, including bacterial pathogens7, and also mediates cation-independent macrophage adhesion in vitro8. Here we show that targeted disruption of the MSR-A gene in mice results in a reduction in the size of atherosclerotic lesions in an animal deficient in apolipoprotein E. Macrophages from MSR-A-deficient mice show a marked decrease in mLDL uptake in vitro, whereas mLDL clearance from plasma occurs at a normal rate, indicating that there may be alternative mechanisms for removing mLDL from the circulation. In addition, MSR-A-knockout mice show an increased susceptibility to infection with Listeria monocytogenes or herpes simplex virus type-1, indicating that MSR-A may play a part in host defence against pathogens.
08 Feb 1997
TL;DR: The Robot World Cup Initiative (R, oboCup) is attempt to foster AI and intelligent rohoties research by providing a standard problem where wide range of technologies especially concerning multi-agent research can be integrated and examined.
Abstract: The Robot World Cup Initiative (R, oboCup) is attempt to foster AI and intelligent rohoties research by providing a standard problem where wide range of technologies especially concerning multi-agent research (:an be integrated and examined. The first RoboCup competition is to be, heht at. IJCAI-97, Nagoya. In order for a robot team to actually perform a soccer game. various technologies must I)e incorl)orated including: design principles of autononmus agents, multi-agent collaboration, strategy acquisition, real-time rea.~oning, robotics, and sensor-fllsion. Unlike AAAI robot competition, which is tuned for a single heavy-duty slow-moving robot. RoboCup is a task for a team of multiple f‘ast-moving robots under a dynamic environmen(. Although RoboCnp’s final target is a worhl cup with real robots, RoboCup offers a soft.ware platform for reseaxch on the software aspects of RoboCup. This paper describes teclini(’M challenges involw~d in RoboCup, rules, and simulation environment.
TL;DR: The concept of a one-dimensional optical wave and its waveguides are proposed for what is to the authors' knowledge the first time and the applications of the waveguide to optical devices in the nanometer range are discussed.
Abstract: The concept of a one-dimensional optical wave and its waveguides are proposed for what is to our knowledge the first time. The proposed waveguides are principally new and named for one-dimensional optical waveguides. One-dimensional optical waveguides make it possible to guide very thin optical beams in the visible or the near-infrared region with a diameter in the nanometer range. The propagation properties are analyzed theoretically. The applications of the waveguides to optical devices in the nanometer range are discussed.
TL;DR: In this article, the plasmon LO-phonon coupled modes whose spectral profiles are used to evaluate the carrier concentration and mobility of SiC crystals are discussed, and anisotropic electronic properties of α-SiC and characteristics of heavily doped crystals are also treated.
Abstract: It has been recognized that Raman scattering spectroscopy is a powerful tool to characterize SiC crystals non-destructively. We review recent significant developments in the use of Raman scattering to study structural and electronic properties of SiC crystals. The areas to be discussed in the first part include polytype identification, evaluation of stacking disorder and ion-implantation damages, and stress evaluation. The Raman scattering by electronic transitions is discussed in the second part of this article. We concentrate on the plasmon LO-phonon coupled modes whose spectral profiles are used to evaluate the carrier concentration and mobility. Anisotropic electronic properties of α-SiC and characteristics of heavily doped crystals are discussed. Semiconductor-to-metal transition and Fano interference effect are also treated.
TL;DR: It is suggested that Y-STR loci are useful markers to identify males and male lineages in forensic practice and recommended for the forensic application of a basic set of 7 STRs for standard Y-haplotyping in forensic and paternity casework.
Abstract: A multicenter study has been carried out to characterize 13 polymorphic short tandem repeat (STR) systems located on the male specific part of the human Y chromosome (DYS19, DYS288, DYS385, DYS388, DYS389I/II, DYS390, DYS391, DYS392, DYS393, YCAI, YCAII, YCAIII, DXYS156Y). Amplification parameters and electrophoresis protocols including multiplex approaches were compiled. The typing of non-recombining Y loci with uniparental inheritance requires special attention to population substructuring due to prevalent male lineages. To assess the extent of these subheterogeneities up to 3825 unrelated males were typed in up to 48 population samples for the respective loci. A consistent repeat based nomenclature for most of the loci has been introduced. Moreover we have estimated the average mutation rate for DYS19 in 626 confirmed father-son pairs as 3.2 × 10–3 (95% confidence interval limits of 0.00041–0.00677), a value which can also be expected for other Y-STR loci with similar repeat structure. Recommendations are given for the forensic application of a basic set of 7 STRs (DYS19, DYS389I, DYS389II, DYS390, DYS391, DYS392, DYS393) for standard Y-haplotyping in forensic and paternity casework. We recommend further the inclusion of the highly polymorphic bilocal Y-STRs DYS385, YCAII, YCAIII for a nearly complete individualisation of almost any given unrelated male individual. Together, these results suggest that Y-STR loci are useful markers to identify males and male lineages in forensic practice.
TL;DR: PSD-95 is a component of postsynaptic densities in central synapses that contains three PDZ domains that localize N-methyl-D-aspartate receptor subunit 2 (NMDA2 receptor) and K+ channels to synapses and may recruit ion channels and neurotransmitter receptors to intercellular junctions formed between neurons by neuroligins and beta-neurexins.
Abstract: PSD-95 is a component of postsynaptic densities in central synapses. It contains three PDZ domains that localizeN-methyl-d-aspartate receptor subunit 2 (NMDA2 receptor) and K+ channels to synapses. In mouse forebrain, PSD-95 bound to the cytoplasmic COOH-termini of neuroligins, which are neuronal cell adhesion molecules that interact with β-neurexins and form intercellular junctions. Neuroligins bind to the third PDZ domain of PSD-95, whereas NMDA2 receptors and K+ channels interact with the first and second PDZ domains. Thus different PDZ domains of PSD-95 are specialized for distinct functions. PSD-95 may recruit ion channels and neurotransmitter receptors to intercellular junctions formed between neurons by neuroligins and β-neurexins.
TL;DR: It is demonstrated that C/EBPβ and C-EBPδ have a synergistic role in terminal adipocyte differentiation in vivo, but co‐expression of C‐EBPα and PPARγ is not sufficient for complete adipocyte differentiate in the absence of C/ EBP β and C/C/E BPδ.
Abstract: To investigate the role of C/EBP family members during adipocyte differentiation in vivo, we have generated mice lacking the C/EBPbeta and/or C/EBPdelta by gene targeting. Approximately 85% of C/EBPbeta(-/-).delta(-/-) mice died at the early neonatal stage. By 20 h after birth, brown adipose tissue of the interscapular region in wild-type mice contained many lipid droplets, whereas C/EBPbeta(-/-).delta(-/-) mice did not accumulate droplets. In addition, the epidydimal fat pad weight of surviving adult C/EBPbeta(-/-).delta(-/-) mice was significantly reduced compared with wild-type mice. However, these adipose tissues in C/EBPbeta(-/-).delta(-/-) mice exhibit normal expression of C/EBPalpha and PPARgamma, despite impaired adipogenesis. These results demonstrated that C/EBPbeta and C/EBPdelta have a synergistic role in terminal adipocyte differentiation in vivo. The induction of C/EBPalpha and PPARgamma does not always require C/EBPbeta and C/EBPdelta, but co-expression of C/EBPalpha and PPARgamma is not sufficient for complete adipocyte differentiation in the absence of C/EBPbeta and C/EBPdelta.
TL;DR: Findings suggest that Gli, and probably also Gli2, are good candidates for transcriptional activators of the HNF-3beta floor plate enhancer, and the binding site for Gli proteins is a key element for response to Shh signalling.
Abstract: The floor plate plays important roles in ventral pattern formation and axonal guidance within the neural tube of vertebrate embryos. A critical event for floor plate development is the induction of a winged helix transcription factor, Hepatocyte Nuclear Factor-3beta (HNF-3beta). The enhancer for floor plate expression of HNF-3beta is located 3' of the transcription unit and consists of multiple elements. HNF-3beta induction depends on the notochord-derived signal, Sonic hedgehog (Shh). Genetic analysis in Drosophila has led to the identification of genes involved in the Hh signalling pathway, and cubitus interruptus (ci), encoding a protein with five zinc finger motifs, was placed downstream. In the present work, we test the involvement of Gli proteins, the mouse homologues of Ci, in activation of the floor plate enhancer of HNF-3beta. Transgenic analysis shows that a Gli-binding site is required for the activity of the minimal floor plate enhancer of HNF-3beta in vivo. Three Gli genes are differentially expressed in the developing neural tube. Gli expression is restricted to the ventral part, while Gli2 and Gli3 are expressed throughout the neural tube and dorsally, respectively. Strong Gli and Gli2, and weak Gli3 expressions transiently overlap with HNF-3beta at the time of its induction. Consistent with ventrally localized expression, Gli expression can be up-regulated by Shh in a cell line. Finally, the Gli-binding site acts as a Shh responsive element, and human GLI, but not GLI3, can activate this binding site in tissue culture. Taken together, these findings suggest that Gli, and probably also Gli2, are good candidates for transcriptional activators of the HNF-3beta floor plate enhancer, and the binding site for Gli proteins is a key element for response to Shh signalling. These results also support the idea that Gli/Ci are evolutionary conserved transcription factors in the Hedgehog signalling pathway.
TL;DR: Results indicate that cytosolic PLA2 plays a non-redundant role in allergic responses and reproductive physiology and is activated by submicromolar concentrations of Ca2+ ions and by phosphorylation by mitogen-activated protein kinases (MAP kinases).
Abstract: Phospholipase A2 (PLA2) comprises a superfamily of enzymes that hydrolyse the ester bond of phospholipids at the sn-2 position1,2,3. Among the members of this superfamily, cytosolic PLA2 has attracted attention because it preferentially hydrolyses arachidonoyl phospholipids and is activated by submicromolar concentrations of Ca2+ ions and by phosphorylation by mitogen-activated protein kinases (MAP kinases)4,5,6,7,8. Here we investigate the function of cytosolic PLA2 in vivo by using homologous recombination to generate mice deficient in this enzyme. These mice showed a marked decrease in their production of eicosanoids and platelet-activating factor in peritoneal macrophages. Their ovalbumin-induced anaphylactic responses were significantly reduced, as was their bronchial reactivity to methacholine. Female mutant mice failed to deliver offspring, but these could be rescued by administration of a progesterone-receptor antagonist to the mother at term. Considered together with previous findings9,10,11,12,13,14,15, our results indicate that cytosolic PLA2 plays a non-redundant role in allergic responses and reproductive physiology.
TL;DR: It is shown that the solvability of a set of matrix inequalities is necessary and sufficient to the existence of a proper controller that satisfies a prescribed H ∞ norm condition as well as stabilizing the closed-loop system and eliminating all impulsive modes.
TL;DR: The first successful in vivo transfer of NFκB decoy oligodeoxynucleotides to reduce the extent of myocardial infarction following reperfusion is reported, providing a new therapeutic strategy for myocardia infarctions.
Abstract: The transcriptional factor nuclear factor-kappaB (NFkappaB) plays a pivotal role in the coordinated transactivation of cytokine and adhesion molecule genes that might be involved in myocardial damage after ischemia and reperfusion. Therefore, we hypothesized that synthetic double-stranded DNA with high affinity for NFkappaB could be introduced in vivo as "decoy" cis elements to bind the transcriptional factor and to block the activation of genes mediating myocardial infarction, thus providing effective therapy for myocardial infarction. Treatment before and after infarction by transfection of NFkappaB decoy, but not scrambled decoy, oligodeoxynucleotides before coronary artery occlusion or immediately after reperfusion had a significant inhibitory effect on the area of infarction. Here, we report the first successful in vivo transfer of NFkappaB decoy oligodeoxynucleotides to reduce the extent of myocardial infarction following reperfusion, providing a new therapeutic strategy for myocardial infarction.
TL;DR: The results suggest that the Rho subfamily is necessary for the formation of both the cadherin-based cell– cell adhesion and the tight junction, but not essential for the Rac subfamily-regulated, cadherIn-basedCell–cell adhesion.
Abstract: The Rho small G protein family, consisting of the Rho, Rac, and Cdc42 subfamilies, regulates various cell functions, such as cell shape change, cell motility, and cytokinesis, through reorganization of the actin cytoskeleton We show here that the Rac and Rho subfamilies furthermore regulate cell–cell adhesion We prepared MDCK cell lines stably expressing each of dominant active mutants of RhoA (sMDCK-RhoDA), Rac1 (sMDCK-RacDA), and Cdc42 (sMDCK-Cdc42DA) and dominant negative mutants of Rac1 (sMDCK-RacDN) and Cdc42 (sMDCK-Cdc42DN) and analyzed cell adhesion in these cell lines The actin filaments at the cell–cell adhesion sites markedly increased in sMDCK-RacDA cells, whereas they apparently decreased in sMDCK-RacDN cells, compared with those in wild-type MDCK cells Both E-cadherin and β-catenin, adherens junctional proteins, at the cell–cell adhesion sites also increased in sMDCK-RacDA cells, whereas both of them decreased in sMDCK-RacDN cells The detergent solubility assay indicated that the amount of detergent-insoluble E-cadherin increased in sMDCK-RacDA cells, whereas it slightly decreased in sMDCK-RacDN cells, compared with that in wild-type MDCK cells In sMDCK-RhoDA, -Cdc42DA, and -Cdc42DN cells, neither of these proteins at the cell–cell adhesion sites was apparently affected ZO-1, a tight junctional protein, was not apparently affected in any of the transformant cell lines Electron microscopic analysis revealed that sMDCK-RacDA cells tightly made contact with each other throughout the lateral membranes, whereas wild-type MDCK and sMDCK-RacDN cells tightly and linearly made contact at the apical area of the lateral membranes These results suggest that the Rac subfamily regulates the formation of the cadherin-based cell– cell adhesion Microinjection of C3 into wild-type MDCK cells inhibited the formation of both the cadherin-based cell–cell adhesion and the tight junction, but microinjection of C3 into sMDCK-RacDA cells showed little effect on the localization of the actin filaments and E-cadherin at the cell–cell adhesion sites These results suggest that the Rho subfamily is necessary for the formation of both the cadherin-based cell– cell adhesion and the tight junction, but not essential for the Rac subfamily-regulated, cadherin-based cell– cell adhesion
TL;DR: In this article, the long-lived charge-transfer state of the C 60 -porphyrin dyad was successfully converted to photocurrent using a self-assembled monolayer technique.
Abstract: Redox-active fullerenes can be covalently bound to a variety of donors; their photophysical properties have been investigated. Their photochemical processes, including electron transfer and energy transfer, are varied, depending on the donor, linkage between the donor and C 60 , and solvent. Regardless of the solvent and linkage, the charge-separated state is produced efficiently in zinc porphyrin-C 60 systems, showing that C 60 is a good electron acceptor. The most intriguing characteristic of C 60 in electron transfer is that C 60 accelerates photoinduced charge separation and retards charge recombination in the dark. The long-lived charge-transfer state of the C 60 -porphyrin dyad was successfully converted to photocurrent using a self-assembled monolayer technique. These findings will provide a new strategy for the design and synthesis of artificial photosynthethic systems and photoactive materials using C 60 as a building block.
TL;DR: 2′-O,4′-C-Methyleneuridine and -cytidine, novel bicyclic nucleoside analogs having a typical C3′-endo sugar puckering, were synthesized starting from uridine via a several-step sequence.
TL;DR: A transgenic mouse line carrying the CAG-cre transgene in which the cre gene is under control of the cytomegalovirus immediate early enhancer-chicken beta-actin hybrid (CAG) promoter is developed, and Cre mRNA and/or protein are retained in mature oocytes irrespective of the transmission of the C AG-cre Transgene, resulting in efficient Cre-mediated recombination of paternally derived target genes upon fertilization.
TL;DR: It is demonstrated that membrane-bound Fas ligand (FasL) kills both fresh and in vitro–activated PBT, indicating that the Fas expressed on fresh PBT is functional and that the shedding of FasL from the membrane is a mechanism for downregulating at least part of its killing activity.
Abstract: It has been believed that the Fas expressed on human peripheral blood T cells (PBT) is nonfunctional, because these cells are insensitive to agonistic anti-Fas/Apo-1 mAbs that efficiently kill in vitro–activated T cells and many Fas-expressing cell lines. Here, we demonstrate that membrane-bound Fas ligand (FasL) kills both fresh and in vitro–activated PBT, indicating that the Fas expressed on fresh PBT is functional. In contrast, soluble FasL kills only the latter. Naive T cells in umbilical cord blood do not express Fas, but can be induced to express Fas by IFN-γ or by a combination of IL-2 and anti-CD28 mAb, after which they acquire sensitivity to membrane but not to soluble FasL. Soluble FasL inhibited the killing of fresh PBT by membrane FasL. These results indicate that the shedding of FasL from the membrane is a mechanism for downregulating at least part of its killing activity.
19 Mar 1997
TL;DR: A line-enhancement filter based on the eigenvalues of Hessian matrix aiming at both the discrimination of line structures from other structures and the recovery of original line structuresfrom corrupted ones is developed.
Abstract: This paper describes a method for the enhancement of curvilinear structures like vessels and bronchi in 3D medical images. We develop a line-enhancement filter based on the eigenvalues of Hessian matrix aiming at both the discrimination of line structures from other structures and the recovery of original line structures from corrupted ones. The multi-scale responses of the line filters are integrated based on the equalization of noise level at each scale. The resulted multi-scale line filtered images provide significantly improved segmentation of curvilinear structures. The line-filtered images are also useful for the direct visualization of curvilinear structures by combining with a volume rendering technique even from conventional MR images. We show the usefulness of the method through the segmentation and visualization of vessels from MRA and MR images, and bronchi from CT images.
TL;DR: It is demonstrated that E6 proteins can bind to the second PDZ domain of the human homologue of the Drosophila discs large tumor suppressor protein (hDLG) through their C-terminal XS/TXV/L motif, similar to the interaction between the adenomatous polyposis coli gene product and hDLG.
Abstract: In the majority of cervical cancers, DNAs of high-risk mucosotpropic human papillomaviruses (HPVs), such as type 16, are maintained so as to express two viral proteins, E6 and E7, suggesting an essential importance to carcinogenesis. The high-risk HPV E6 proteins are known to inactivate p53 tumor suppressor protein but appear to have an additional, molecularly unknown function(s). In this study, we demonstrate that these E6 proteins can bind to the second PDZ domain of the human homologue of the Drosophila discs large tumor suppressor protein (hDLG) through their C-terminal XS/TXV/L (where X represents any amino acid, S/T serine or threonine, and V/L valine or leucine) motif. This finding is similar to the interaction between the adenomatous polyposis coli gene product and hDLG. E6 mutants losing the ability to bind to hDLG are no longer able to induce E6-dependent transformation of rodent cells. These results suggest an intriguing possibility that interaction between the E6 protein and hDLG or other PDZ domain-containing proteins could be an underlying mechanism in the development of HPV-associated cancers.
TL;DR: A theoretical analysis of the energy balance in the laser - metal interaction zone is carried out in this article, where heat transfer due to the recoil-pressure-induced melt flow is taken into consideration.
Abstract: A theoretical analysis of the energy balance in the laser - metal interaction zone is carried out. The heat transfer due to the recoil-pressure-induced melt flow is taken into consideration. It is shown that, for the absorbed laser intensities typical in welding and cutting, the recoil pressure induces high-velocity melt-flow ejection from the interaction zone. This melt flow carries away from the interaction zone a significant portion of the absorbed laser intensity (about 70 - 90% at low laser intensities); thus, convection-related terms can be ignored neither in calculations of the energy balance in the interaction zone nor in calculations of the thermal field in the vicinity of the weld pool or cutting front.