[Human mobility and the current epidemiology of syphilis].
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Epidemiologic Methods↗
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NAQ Forum: Staffing. Mobilizing human resources.
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Nursing Service, Hospital↗
Identification, purification, and characterization of subunits of cAMP-dependent protein kinase in human testis. Reverse mobilities of human RII alpha and RII beta on sodium dodecyl sulfate-polyacrylamide gel electrophoresis compared with rat and bovine RIIs.
We have previously identified and characterized regulatory (R) subunits of cyclic AMP-dependent protein kinase, particularly the RII subunits in rat tissues (Jahnsen, T., Lohmann, S. M., Walter, U., Hedin, L., and Richards, J. S. (1985) J. Biol. Chem. 260, 15980-15987; Jahnsen, T., Hedin, L., Lohmann, S. M., Walter, U., and Richards, J. S. (1986) J. Biol. Chem. 261, 6637-6639; Jahnsen, T., Hedin, L., Kidd, V. J., Beattie, W. G., Lohmann, S. M., Walter, U., Durica, J., Schulz, T. Z., Schiltz, E., Browner, M., Lawrence, C. B., Goldman, D., Ratoosh, S. L., and Richards, J. S. (1986) J. Biol. Chem. 261, 12352-12361). These studies showed that rat RII alpha and RII beta had apparent molecular masses of 54 and 52 kDa, respectively. The aim of the present study was to purify and characterize cAMP-dependent protein kinase R subunits in human testis and to examine which of the subunits (mRNAs and proteins) are present in this tissue. Our results show that human testis contains mRNAs for five out of the seven known subunits of cAMP-dependent protein kinase. We observed strong expression of mRNAs for RI alpha (1.5 and 3.2 kilobases (kb)), RII alpha (2.2, 2.4, and 7.0 kb), and RII beta (3.3 kb). We also demonstrated mRNAs for two of the three catalytic subunits, C alpha (2.7 kb) and C gamma (1.7 kb). Purification of R subunits by DEAE-cellulose and cAMP affinity chromatography revealed three distinct forms with apparent molecular masses of 49, 51, and 53 kDa, respectively. Characterization of these R subunits by their 8-azido-cAMP photoaffinity labeling and immunoreactivity, as well as by a phosphorylation-dependent mobility shift on sodium dodecyl sulfate-polyacrylamide gel electrophoresis (SDS-PAGE), indicated subunit sizes of RII beta (53 kDa) greater than RII alpha dephosphoform (51 kDa) greater than RI alpha (49 kDa). This conclusion was verified by the analysis of RII subunits produced by in vitro transcription/translation of full-length cDNAs for both human RII alpha and RII beta in wheat germ lysates. The in vitro translated products were the same size as the purified human testis subunits, and only the smallest RII subunit (RII alpha) revealed a distinct mobility shift on SDS-PAGE after phosphorylation/dephosphorylation. This study supports the conclusion that the mobilities of human RII subunits (RII alpha, RII beta) on SDS-PAGE are reversed in contrast with those of other species such as rat and bovine.(ABSTRACT TRUNCATED AT 400 WORDS)
Animals↗
Effect of protein kinase C inhibitors on calcium ionophore-induced arachidonic acid mobilization in human leukocytes.
Arachidonic acid mobilization in human polymorphonuclear leukocytes stimulated with calcium ionophore A23187 was amplified by synthetic diacylglycerol and, to a much lesser extent, by phorbol ester. The effect was synergistic and dependent upon influx of calcium ions. Thin layer chromatographic analysis of phospholipids of stimulated cells revealed a loss of arachidonic acid associated with phosphatidylinositol and phosphatidylcholine. The synergistic response was unaffected by treatment of cells with two inhibitors of protein kinase C, namely, polymyxin B and 1-(5-isoquinolinylsulfonyl)-2-methylpiperazine. Moreover, both agents consistently augmented the cellular response to A23187 alone. These findings suggest that A23187-induced arachidonic acid mobilization in leukocytes is independent of protein kinase C activity.
1-(5-Isoquinolinesulfonyl)-2-Methylpiperazine↗
Human retinal pigment epithelial cells possess muscarinic receptors coupled to calcium mobilization.
Human retinal pigment epithelial (RPE) cells in culture demonstrated saturable specific binding of [3H]quinuclidinyl benzilate (QNB). Specific binding represents about 75% of total binding. Scatchard analysis yields a Kd of 0.178 nM and Bmax of 42 fmol/mg protein. Atropine and carbachol show typical displacement curves, and a Hill plot has a slope of 0.96, suggesting a homogeneous population of receptors. Muscarinic agonists have no effect on intracellular cyclic adenosine monophosphate levels in RPE cells measured by radioimmunoassay, nor do they alter the isoproterenol-induced stimulation of adenylate cyclase. However, both acetylcholine and carbachol cause a rapid increase in intracellular calcium concentration measured by the fluorescent indicator quin 2. Atropine reverses the calcium rise when added after agonist and prevents the rise when added prior to agonist. These data suggest that human RPE cells possess muscarinic receptors coupled to calcium mobilization.
Atropine↗
Role of glucose, insulin, and glucagon in glycogen mobilization in human hepatocytes.
This study investigated the role of glucose, insulin, and glucagon in the activation of glycogen catabolism in cultured human hepatocytes. Basal glycogenolysis in unstimulated human hepatocytes was low (only 19% of initial glycogen content was degraded in a 4-h incubation) and insensitive to changes in external glucose concentration (from 10 to 0 mM). Both glycogenolysis and glucose output could be significantly stimulated by 35 ng/L glucagon or 10(5) pM dibutyryl cAMP; half-maximal effect was found with 28 x 10(2) ng/L glucagon and 4 x 10(5) pM dibutyryl cAMP. After a 3-h exposure to 35 x 10(3) ng/L glucagon, greater than 90% of glycogen content of human hepatocytes was mobilized. This caused a 4.6-fold increase in the rate of glucose output to the medium compared with nonstimulated cells. About 85% of degraded glycogen rendered glucose to the medium. Insulin (10(4) pM) was able to totally suppress basal glycogenolysis; insulin was also essential to reverse the action of glucagon in hepatocytes incubated with glucagon, whereas glucose alone, even at postprandial concentration, was unable to reverse glucagon action. In summary, these experiments show that the mobilization of glycogen stores of human hepatocytes, as it occurs during the postabsorptive periods in humans, is largely dependent on the presence of glucagon and is not simply due to a decrease of external glucose. Insulin, on the other hand, was essential to suppress both basal and glucagon-activated glycogenolysis.
Bucladesine↗
Comparison of multiple forms of the high mobility group I proteins in rodent and human cells. Identification of the human high mobility group I-C protein.
The class I of the high mobility group (HMG) proteins is formed by phosphoproteins which are associated with AT-rich DNA sequences in the nucleus. Three HMGI proteins have previously been described in proliferating rodent cells (HMG Y, HMG I and HMGI-C). All three proteins exhibit microheterogeneity. The microheterogeneity of mouse HMG Y has been investigated in detail and shown to be due to phosphorylation of the protein which is sensitive to alkaline-phosphatase treatment. HMG I is similarly modified. Human cells have up to now only been found to contain HMG Y and HMG I. A search for the third protein, HMGI-C, in human cells was carried out and the protein was found in a hepatoma cell line, but not in normal or transformed T-cells. This HMGI-C protein was found to be modified by phosphorylation, part of which was found to be phosphatase insensitive. An unexpected additional finding in this study was that human cells contain two HMG17 proteins which differ in their N-terminal primary sequences.
Alkaline Phosphatase↗
The role of intracellular acidification in calcium mobilization in human neutrophils.
Propionic acid induces a calcium mobilization in human neutrophils which is prevented by pretreatment with phorbol ester or pertussis toxin. The effect is reminiscent of that of chemotactic factors and leukotriene B4 and was attributed to cytoplasmic acidification (Naccache, P.H. et al. (1988) J. Cell. Physiol. 136, 118-124). We show there that other weak acids also induced cytoplasmic alkalinization and calcium mobilization. However, addition of trimethylamine together with propionic acid prevented the cytoplasmic acidification without modifying the calcium mobilization. Propionic acid increased the production of inositol phosphates but this effect was largely prevented by the joint addition of trimethylamine. The ionophores nigericin and monensin can both be forced to produce either cytoplasmic acidification or alkalinization by manipulating the extracellular concentrations of Na+, K+ or H+. Both ionophores produced calcium mobilization in all the cases, irrespective of the direction of the cytoplasmic pH shift. The ionophores were documented to collapse existing pH gradients among the cytoplasm and intracellular compartments. We conclude that the calcium-mobilizing effect of propionic acid and other weak acids is not due to the acidification of the cytoplasm. Our results are consistent, however, with calcium mobilization induced by weak acids and ionophores arising from acidification of an alkaline intracellular compartment.
Calcium↗
Effects of human chorionic gonadotropin and antithymocyte-globulin on the electrophoretic mobility of human lymphocytes.
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ABO Blood-Group System↗
Histamine-induced lipid mobilization in humans and dogs.
The effect of histamine on serum free fatty acid (FFA) and glycerol levels was examined in humans and dogs in vivo. By the end of a 15-minute infusion of histamine diphosphate (11 mug of histamine per min i.v.), FFA levels in six male human volunteers had risen from basal values of 424 +/- 41 (mean +/- S.E.M.) to 909 +/- 45 muEq/1, and glycerol levels had risen from 66 +/- 5.5 to 124 +/- 9.3 mumol/1. These effects in man were not blocked by diphenhydramine, an H1-receptor antagonist, but were entirely blocked by propranolol, a beta adrenergic antagonist. Similar infusions of histamine (11 mug/min i.v.) in six anesthetized dogs caused FFA levels to rise from 189 +/- 13 to 461 +/- 92 muEq/1 and glycerol levels to rise from 58 +/- 3.7 to 157 +/- 22.4 mumol/1. These effects in the dog were not blocked by diphenhydramine or by propranolol but were entirely blocked by metiamide, an H2-receptor antagonist. These observations illustrate that low levels of histamine in vivo can produce significant elevations of serum FFA and glycerol levels in both humans and dogs. These results further suggest that the action of histamine in humans is indirect whereas the effect in dogs may be due to a direct action of histamine at the H2-receptor in canine adipose tissue.
Adult↗
Age-dependent changes in the electrophoretic mobilities of human blood lymphocytes.
The distribution of the anodic electrophoretic mobilities (EPM) of human peripheral blood lymphocytes was determined for lymphocytes isolated from umbilical cord blood and from blood of individuals 6 months to 93 years of age. The distribution was bimodal in infants up to 2 years of age and suggested a small percentage of cells with a mobility of 0.95 micrometer s-1 V-1 cm. this value was chosen to discriminate between low-mobility cells (LMCs) and high-mobility cells (HMCs). The relative percentage of LMCs increased from birth to 2 years and two types of LMCs could be distinguished. The distribution was unimodal and asymmetric in children and adults and nearly Gaussian in aged people. Substantial differences between the distributions of the lymphocyte EPMs were seen on comparison of the histograms for individuals of similar ages. The analysis of the distribution of the lymphocyte EPMs on cell suspensions enriched in, or depleted of T or B cells confirmed the mobility of most T cells to be higher than the mobility of most B cells, whatever the age of the individual. The distribution of lymphocyte EPMs determined in the same adult over a 6 year period showed minor variations.
Adolescent↗
The relationship between the mobility of human teeth and their supracrestal fiber support.
A method to study the relationship between the mobility of human teeth and their supracrestal fiber support was developed. The results of this study would indicate that: (1) The supracrestal fibers do not contribute significantly to the support of a normal premolar tooth. (2) As a human premolar tooth develops moderate to severe loss of osseous support, the relative contribution of the supracrestal fibers to the support of the tooth increases significantly.
Adolescent↗
Inhibitory effect of antibiotic cerulenin on the respiratory burst in phagocytes. II. Inhibition by cerulenin of intracellular calcium mobilization in human neutrophils.
Generation of superoxide anion (O2-) and mobilization of intracellular Ca2+ in human neutrophils upon exposure to stimuli such as N-formylmethionylleucylphenylalanine (fMLP) were inhibited by the antibiotic cerulenin, which inhibits fatty acid and cholesterol biosynthesis. The inhibition of O2- generation and Ca2+-mobilization required certain periods of incubation with cerulenin and both abilities of the cells were gradually lost following a similar time-course. In contrast, significant Ca2+-influx from the medium was observed in cerulenin-treated cells as well as untreated cells. The results suggest that an event which coincides with the Ca2+-mobilization and not Ca2+ per se is important for the induction of O2- generation in the fMLP-stimulated cells and that this step is blocked in cerulenin-treated cells. Phorbol myristate acetate or synthetic 1-oleoyl-2-acetylglycerol were able to bypass the block and induced O2- generation in cerulenin-treated cells.
Antifungal Agents↗
Lateral mobility of human erythrocyte integral membrane proteins.
Fluorescein isothiocyanate-labelled integral membrane proteins are mobile in the membranes of human erythrocytes that have fused (and haemolysed) by Sendai virus or polyethylene glycol. Minimum diffusion coefficients are of the order of 10(-11) cm2 s-1 at 37 degrees C. This mobility is reduced several-fold at room temperature, not detected at 0 degrees C, and is significantly greater in fresh than in aged blood. Mobility was assessed by observing the spread of fluorescence on labelled cells which had been fused with unlabelled cells; neither intramembrane particle aggregation nor spectrin release occurred during this process.
Adenosine Triphosphate↗
Effect of benzyl alcohol on phospholipid transverse mobility in human erythrocyte membrane.
The effect of benzyl alcohol on the transverse mobility and repartition of phospholipids in the human erythrocyte membrane was investigated using electron spin resonance and morphological modification of red blood cells. Transmembrane internalization rates and equilibrium distribution in red blood cells of short-chain spin-labeled phosphatidylcholine, phosphatidylethanolamine and phosphatidylserine were strongly modified by treatment with 10-70 mM benzyl alcohol. A dual effect was observed: (a) at 4 degrees C and 37 degrees C there was an N-ethylmaleimide-sensitive, long lasting and fully reversible increase in the spin-labeled phosphatidylserine and phosphatidylethanolamine internalization rate; (b) at 37 degrees C, an enhancement of N-ethylmaleimide-insensitive fluxes of all the labeled phospholipids through the membrane occurred. Both effects were dose-dependent. Erythrocytes submitted to benzyl alcohol incubation also showed dose-dependent shape changes: an immediate one from discocytes to echinocytes, followed by a slower N-ethylmaleimide- and ATP-dependent change to stomatocytes. Moreover, benzyl alcohol treatment was shown to lead to enhanced hydrolysis of intracellular ATP. All the effects of benzyl alcohol can be described as an accumulation of labeled phosphatidylethanolamine (and labeled phosphatidylcholine at 37 degrees C) in the inner leaflet. This can be interpreted as a perturbation of the erythrocyte membrane, leading to an energy-consuming specific increase in aminophospholipid translocase activity, in addition to a slow and passive bidirectional flux of all phospholipids at 37 degrees C.
Adenosine Triphosphate↗
Effect of procaine hydrochloride on the electrophoretic mobility of human red blood cells.
The interaction of cationic anesthetics with biological membranes and the resulting alterations of membrane electrokinetic properties continue to be of current interest. The present study was designed to examine the effects of procaine hydrochloride (PRHCL) on the mobility of human red blood cells (RBC); electrophoretic measurements were made on RBC suspended in phosphate-buffered saline (PBS, pH = 5.0, 7.4, or 9.2), autologous plasma or 3 g% dextran T70/PBS (pH = 7.4), with PRHCL concentrations from 8 x 10(-6) to 8 x 10(-2) M. Low concentrations of PRHCL (8 x 10(-5)-8 x 10(-3) M) significantly (p less than 0.001) increased RBC mobility, with a maximal increase of 8.2% at 8 x 10(-4) M. Conversely, a higher PRHCL concentration (8 x 10(-2) M significantly (p less than 0.001) decreased RBC mobility. Both glutaraldehyde fixation and lipid extraction abolished any PRHCL-induced increase in RBC mobility; the observed increases in mobility for normal cells are, thus, consistent with a mechanism based on expansion of the RBC membrane glycocalyx. Microelectrophoretic methods were also used to study the effect of PRHCL (8 x 10(-4) and 8 x 10(-2) M) on RBC membrane calcium binding, with the results indicating that PRHCL competes with calcium for neuraminate binding sites. We conclude that the observed changes in RBC electrokinetic properties reflect incorporation of PRHCL into the RBC membrane; such changes may be of importance in modulating cell-cell interactions.
Binding, Competitive↗
Priming of calcium mobilization in human neutrophils by granulocyte-macrophage colony-stimulating factor: evidence for an involvement of phospholipase D-derived phosphatidic acid.
Human neutrophils pre-incubated with granulocyte-macrophage-colony-stimulating factor (GM-CSF) exhibit an enhanced mobilization of calcium in response to secondary stimuli such as chemotactic factors. The mechanisms underlying this priming effect of GM-CSF were examined. It was first demonstrated that the additional calcium mobilized by chemotactic factors in GM-CSF-treated cells was derived from intracellular stores and was associated neither with an increased permeability to calcium nor with production of inositol 1,4,5-trisphosphate. These results indicated that GM-CSF called upon a novel mechanism in order to enhance the mobilization of calcium in human neutrophils. The growth factor has recently been shown to prime phospholipase D leading to an enhanced activation by chemotactic factors and an augmented production of phosphatidic acid. Furthermore the ability of exogenous phosphatidic acid to mobilize calcium in cell types other than neutrophils has been previously demonstrated. Therefore, we examined the potential involvement of phospholipase D in the priming of the calcium response by GM-CSF in human neutrophils. Inhibition of the production of the fMet-Leu-Phe-stimulated production of phosphatidic acid by ethanol or wortmannin had only marginal effects on the concurrent mobilization of calcium. However, the priming of the mobilization of calcium by GM-CSF was greatly decreased in cells treated with either ethanol or wortmannin. These results provide strong support for the hypothesis that the production of phosphatidic acid, which is enhanced in GM-CSF-treated cells, is linked to an increased mobilization of intracellular calcium. These results may have relevance to the mechanism of action of GM-CSF in mature haematopoeitic cells as well to the mitogenic activity of other growth factors.
Adult↗
Inhibition of superoxide production and Ca2+ mobilization in human neutrophils by halothane, enflurane, and isoflurane.
The inhibitory effects of three inhalation anesthetics, i.e., halothane, enflurane, and isoflurane, on superoxide production and the intracellular mobilization of calcium in human neutrophils were studied. The superoxide production induced by N-formyl-methionyl-leucyl-phenylalanine (FMLP) was inhibited by the anesthetics, but the binding of FML[3H]P to the cells and the superoxide-forming NADPH oxidase of the phagocytic vesicles were not inhibited. The inhibition of the cellular superoxide production was partially reversed by the addition of a calcium ionophore, A23187. The increase in intracellular free calcium monitored by a calcium-sensitive fluorescent probe, quin-2 and the release of calcium from hydrophobic environment monitored by chlortetracycline were inhibited dose dependently by the anesthetics. These observations suggest that decreased mobilization of intracellular Ca2+ is one of the mechanisms by which the anesthetics inhibited the superoxide production of human neutrophils stimulated by FMLP.
Calcimycin↗