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At least 721 records · Page 40Linked to original sources
PubMed1980

Ionophore-mediated cation translocation in artificial systems. II. - X537A-mediated calcium and sodium translocation.

The ionophore X537A translocates both calcium and sodium from an aqueous into an organic solution. At non saturating cationic concentrations, each atom of calcium seems to react with two molecules of ionophore, whereas each atom of sodium apparently reacts with only one molecule of X537A. The phenomena of sodium and calcium translocation, respectively, are competitive and are both inhibited when the pH of the aqueous phase is decreased.

Binding Sites↗
PubMed1979

Ionophore-mediated cation translocation in artificial systems. I. A23187-mediated calcium translocation.

The inophore A23187 stimulates the translocation of calcium from an aqueous Hepes buffer into an organic immiscible phase. At saturating calcium concentrations, 2 molecules of ionophore seem to complex each atom of calcium. Consistent with such a stoichiometric behaviour, the apparent ratio of calcium-ionophore association to dissociation rate constants increases as the concentration of ionophore is raised. As a result, at low calcium concentrations, the amount of translocated calcium increases as a power function of A23187 concentration. When allowance is made for such a phenomenon, the relation between calcium translocation and concentration is characterized by usual substrate-receptor binding kinetics.

Anti-Bacterial Agents↗
PubMed1999

Allogeneic cell-mediated immunotherapy for eradication of minimal residual disease: comparison of T-cell and IL-2 activated killer (LAK) cell-mediated adoptive immunotherapy in murine models.

In the course of allogeneic bone marrow transplantation (BMT), avoiding graft-versus-host disease (GVHD) while retaining the antileukemic effects of the T cells remains a major challenge. T-cell depletion (TCD) reduces the incidence of GVHD but increases the relapse rate after allogeneic BMT. We attempted to develop a regimen that would retain or increase the graft-versus-leukemia effect induced by donor T cells while preventing GVHD. Immunosuppressed mice were given immunocompetent donor cells, i.e., fresh lymphocytes or lymphokine-activated killer (LAK) cells differing from the host in major (MHC) or minor (MiHC) histocompatibility antigens. Engraftment of donor cells was documented by polymerase chain reaction analysis. Administration of MHC- and MiHC-incompatible allogeneic LAK cells, especially in conjunction with recombinant interleukin-2 (rIL-2), increased disease manifestations and mortality associated with GVHD. On the other hand, irradiated LAK cells or TCD-LAK cells prevented GVHD in both mice models studied. Phenotypic analysis of LAK cells demonstrated that CD8(+)-equivalent (Lyt-2) T cells are of significance in aggravation of GVHD. The in vitro cytotoxic capacity of LAK cells against MHC-nonrestricted target cells was not reduced by either irradiation or TCD. These results provide the background for designing improved protocols for immunotherapy of residual disease after BMT. In addition, the data imply that antitumor effects may be retained by irradiated rIL-2-activated allogeneic cells without causing GVHD. Whereas unmodified allogeneic LAK cells can induce more effective graft-versus-leukemia effects at the cost of GVHD, irradiated allogeneic donor LAK cells might play some role in eradication of minimal residual disease following autologous or allogeneic BMT without causing GVHD.

Animals↗
PubMed2002

Alpha(1)-adrenoceptor-mediated depolarization and beta-mediated hyperpolarization in cultured rat dorsal root ganglion neurones.

The mechanism of sympathetic - sensory coupling after nerve injury is still not well understood. We have studied the changes in resting potential and excitability of sensory neurones induced by adrenergic stimulation, using whole-cell and perforated-patch recordings in cultured dorsal root ganglion neurones from normal rats. Adrenaline (1-100 microM) depolarized 18 of 39 neurones (46%) and hyperpolarized seven neurones (18%); excitability was increased and decreased, respectively. Stimulating the neurones with 10 microM phenylephrine (alpha(1)-agonist) induced depolarization and increased excitability, while 10 microM isoprenaline (beta-agonist) induced hyperpolarization and reduced excitability. We conclude that alpha(1)- and beta-receptors have opposing effects on membrane potential and excitability in cultured dorsal root ganglion neurones, and the differing effects of adrenaline can be explained by different degrees of expression of each receptor type.

Action Potentials↗
PubMed1998

Increased induction of Ca2+-mediated differentiation by gamma ray is mediated by endogenous activation of the protein kinase C signaling pathways in mouse epidermal cells.

PURPOSE: The aim of this study was to determine whether gamma-rays can affect Ca2+-induced differentiation in normal and neoplastic mouse epidermal cells. METHODS AND MATERIALS: After gamma-ray irradiation, primary and v-rasHa transformed mouse keratinocytes were cultured for 48 h in 0.12 mM Ca2+-containing media, and cellular translocation from cytosolic to particulated fraction of each PKC isozyme and expressions of differentiation markers were examined. RESULTS: Morphological difference was seen at 48 h after irradiation in both Ca2+-shifted normal and v-rasHa transformed cells; v-rasHa cells were more resistant to the radiation than normal cells. Radiation potentiated granular cell-differentiation marker expressions (filaggrin, loricrin, and SPR-1) in both normal and v-rasHa transformed cells. In the case of spinous cell markers, the expression of keratins K1 and K10, which are usually blocked in v-rasHa cells was increased after irradiation. However, there was no change of K8 expression level, which can be seen only after v-rasHa transfection. Cellular fractionation and immunoblot analysis with antibodies against PKCalpha, delta, epsilon, eta, and xi revealed that PKCalpha was responsible for the differentiation marker expression. CONCLUSIONS: These findings suggest that PKCalpha is an important component of the signaling pathway regulating radiation-induced differentiation in both normal and neoplastic epidermal cells.

Animals↗
PubMed2003

Different mechanisms of adhesion molecule expression in human dermal microvascular endothelial cells by xanthoma tissue-mediated and copper-mediated oxidized low density lipoproteins.

BACKGROUND: Oxidation of low density lipoprotein (LDL) has been implicated in infiltration of foam cells derived from circulating monocytes. Monocyte adhesion to endothelial cells and migration into dermis are essential steps for infiltration of foam cells. OBJECTIVE: We investigated the role of adhesion molecules contributing to the process of monocyte adhesion to human dermal microvascular endothelial cells (HDMEC). Special attention was paid to the signal transduction for adhesion molecule expression induced by two distinct types of oxidized LDL. METHODS: HDMEC were incubated with xanthoma tissue-modified LDL (x-LDL), a model of extravasated LDL oxidized in xanthoma lesions, or Cu(2+)-treated LDL (Cu-LDL), a model of oxidized LDL. Adhesion of U937 cells, a human monocytic leukemia cell line, to HDMEC and expression of endothelial cell adhesion molecules on HDMEC were examined. Signal transduction pathways for the adhesion molecule expression were evaluated by employing specific inhibitors. RESULTS: x-LDL induced adhesion of U937 cells to HDMEC through vascular cell adhesion molecule-1 (VCAM-1) and E-selectin by activating tyrosine kinase pathway. Cu-LDL up-regulated the adhesion through not only VCAM-1 and E-selectin but also intercellular cell adhesion molecule-1 (ICAM-1) by activating G(i) protein pathway. CONCLUSION: Extravasated and oxidized LDL in xanthoma lesions contributes to foam cell recruitment by activating tyrosine kinase pathway and inducing adhesion of monocytes to HDMEC through VCAM-1 and E-selectin. Cu-LDL, on the other hand, activates G(i) protein pathway and induces the adhesion through ICAM-1, VCAM-1 and E-selectin.

Cell Adhesion↗
PubMed2004

Prostaphopain B structure: a comparison of proregion-mediated and staphostatin-mediated protease inhibition.

Prostaphopain B is the precursor of staphopain B, a papain-type secreted cysteine protease from the pathogen Staphylococcus aureus. Here, we describe the 2.5 A crystal structure of the proenzyme. Its 21 kDa proregion is organized around a central half-barrel or barrel-sandwich hybrid and occludes primed, but not nonprimed, sites in the active site cleft of the protease. The structure of the mature part of the protease is similar to previously reported staphopain structures, and no distortion of the catalytic residues is apparent at 2.5 A resolution. A comparison of prostaphopain B with the staphopain B-staphostatin B complex shows that the proregion and the inhibitor interact with largely nonoverlapping parts of the protease surface. In a modeled complex of prostaphopain B with staphostatin B, clashes occur both inside and outside the active site cleft, but involve mostly poorly ordered regions of the protein that may be mobile.

Bacterial Proteins↗
PubMed1993

Phenytoin-lipid conjugates: chemical, plasma esterase-mediated, and pancreatic lipase-mediated hydrolysis in vitro.

Phenytoin-lipid conjugates obtained by covalent binding of hydroxymethylphenytoin to diacylglycerides and to 3-acyloxy-2-acyl-oxymethylpropionic acids formed dispersions with a particle size of 10-200 microns when briefly sonicated in a sodium taurodeoxycholate-containing ethanol-water mixture. In contrast to the corresponding bis-deacyl derivatives, the lipids were not significantly hydrolyzed in aqueous buffers and in plasma. Incubation with pancreatic lipase yielded primarily the bis-deacyl compounds, which are comparable to monoglycerides, and subsequently liberated phenytoin. The glyceride-derived prodrugs were better substrates for the enzyme than the 3-acyloxy-2-acyloxymethyl-propionic acid derivatives. It is concluded that the phenytoin lipid conjugates are hydrolyzed by pancreatic lipase in a similar manner as natural triglycerides.

Chromatography, High Pressure Liquid↗
PubMed1993

Personality effects on children's speech in everyday life: sociability-mediated exposure and shyness-mediated reactivity to social situations.

Speech and heart rate were continuously monitored during 7 days from morning to evening in 41 Grade 2 children selected for high or low parental judgments of sociability and shyness. Children attended school in the mornings and were free in the afternoons; the child's social situations in the afternoon were reconstructed with the child and a caretaker. During the afternoons sociable children spent more time in conversations than unsociable children, but the groups did not differ in their verbal participation within conversations. Shy children spent as much time in conversations and spoke as much in familiar situations as nonshy children but spoke less in moderately unfamiliar situations. Neither sociability nor shyness had an effect on heart rate reactivity. The results show that sociability affects the exposure, and shyness the reactivity, to situations and that these traits are clearly distinct despite some similarity in lay judgments of personality.

Child↗