A time course analysis of the synesthetic colour priming effect.

Author(s):  
Adriaan Spruyt ◽  
Johannes Koch ◽  
Heleen Vandromme ◽  
Dirk Hermans ◽  
Paul Eelen
Keyword(s):  
2001 ◽  
Vol 15 (2) ◽  
pp. 143-165 ◽  
Author(s):  
Dirk Hermans ◽  
Jan De Houwer ◽  
Paul Eelen

2016 ◽  
pp. 311-320 ◽  
Author(s):  
R. A. HART ◽  
R. C. DOBOS ◽  
L. L. AGNEW ◽  
R. L. TELLAM ◽  
J. R. MCFARLANE

Pharmacokinetics of leptin in mammals has received limited attention and only one study has examined more than two time points and this was in ob/ob mice. This study is the first to observe the distribution of leptin over a time course in female mice. A physiologic dose (12 ng) of radiolabelled leptin was injected in adult female mice via the lateral tail vein and tissues were dissected out and measured for radioactivity over a time course up to two hours. Major targets for administered leptin included the liver, kidneys, gastrointestinal tract and the skin while the lungs had high concentrations of administered leptin per gram of tissue. Leptin was also found to enter the lumen of the digestive tract intact from the plasma. Very little of the dose (<1 %) was recovered from the brain at any time. Consequently we confirm that the brain is not a major target for leptin from the periphery, although it may be very sensitive to leptin that does get to the hypothalamus. Several of the major targets (GI tract, skin and lungs) for leptin form the interface for the body with the environment, and given the ability of leptin to modulate immune function, this may represent a priming effect for tissues to respond to damage and infection.


1981 ◽  
Vol 240 (3) ◽  
pp. E297-E301
Author(s):  
L. K. Tang ◽  
F. Y. Tang

Effects of 17 beta-estradiol (E2) on adenosine 3',5'-cyclic monophosphate (cAMP) binding and luteinizing hormone (LH) and prolactin (PRL) responses to N6-O-2'-dibutyryl cAMP (DBcAMP) were examined in pituitary monolayer cultures prepared from female rats. Incubation with 8 mM DBcAMP for 4 h significantly (P less than 0.05) increased both LH and PRL release into medium by two- to threefold. E2 pretreatment augmented the DBcAMP-induced LH release but not PRL release to 160% of the non-E2-treated controls. However, the cellular and total accumulation of both LH and PRL were significantly increased in cultures pretreated with E2. The effect of E2 was time dependent, and the maximal effect was observed after 3 days of treatment. Furthermore, E2 treatment significantly increased cAMP-binding activities to 254% of the non-E2-treated controls. The time course of the E2 effect on cAMP-binding activities closely resembled the time course of the E2 effect on LH and PRL accumulation as well as the DBcAMP-induced LH release. These results suggest that the priming effect of E2 on pituitary LH and PRL responses to DBcAMP is associated with increased hormone synthesis and cAMP binding stimulated by E2 pretreatment.


Blood ◽  
1996 ◽  
Vol 88 (11) ◽  
pp. 4330-4337 ◽  
Author(s):  
E Kitchen ◽  
AG Rossi ◽  
AM Condliffe ◽  
C Haslett ◽  
ER Chilvers

Abstract Exposure of neutrophils to agents such as lipopolysaccharide, tumor necrosis factor-alpha (TNF-alpha), and the granulocyte-macrophage colony-stimulating factor causes a major upregulation of subsequent agonist-induced NADPH oxidase activation. This priming effect is a prerequisite for neutrophil-mediated tissue damage and has been widely considered to be an irreversible process. We have investigated the potential for neutrophils to recover from a priming stimulus by studying the effects of platelet-activating factor (PAF). PAF did not stimulate respiratory burst activity directly, but caused a rapid (maximal at 10 minutes) and concentration-dependent (EC50 50.2 nmol/L) increase in N-formyl-methionyl-leucyl-phenylalanine (fMLP)-stimulated superoxide anion release. At time-points > 10 minutes, this priming effect spontaneously declined, with return to basal levels of fMLP- stimulated superoxide anion generation by 120 minutes. An identical priming time-course was observed with N-methyl carbamyl PAF, a nonmetabolizable analogue of PAF, indicating that the transient nature of PAF-induced priming was not secondary to PAF metabolism. Two structurally diverse PAF receptor antagonists (UK-74,505 and WEB 2086), added 10 minutes after PAF addition, increased the rate of decay of the priming effect. In contrast, TNF-alpha-induced priming, which was of a similar magnitude to that observed for PAF, was slower to evolve (maximal at 30 minutes) and remained constant for at least 120 minutes. The reversible nature of PAF-induced priming was confirmed by demonstrating that PAF-, but not TNF-alpha-, induced cell polarization (shape change) and CD11b-dependent neutrophil binding of albumin-coated latex beads was also transient, with return to basal, unstimulated levels by 120 minutes. Furthermore, cells that had spontaneously deprimed following PAF exposure retained their capacity to be fully reprimed by a subsequent addition of either PAF or TNF-alpha. These data imply that neutrophil priming is not an irreversible event: the demonstration of a cycle of complete priming, depriming, and repriming offers the potential for functional recycling of neutrophils at sites of inflammation.


2001 ◽  
Vol 15 (2) ◽  
pp. 143-165 ◽  
Author(s):  
Dirk Hermans ◽  
Jan De Houwer ◽  
Paul Eelen

Blood ◽  
1996 ◽  
Vol 88 (11) ◽  
pp. 4330-4337 ◽  
Author(s):  
E Kitchen ◽  
AG Rossi ◽  
AM Condliffe ◽  
C Haslett ◽  
ER Chilvers

Exposure of neutrophils to agents such as lipopolysaccharide, tumor necrosis factor-alpha (TNF-alpha), and the granulocyte-macrophage colony-stimulating factor causes a major upregulation of subsequent agonist-induced NADPH oxidase activation. This priming effect is a prerequisite for neutrophil-mediated tissue damage and has been widely considered to be an irreversible process. We have investigated the potential for neutrophils to recover from a priming stimulus by studying the effects of platelet-activating factor (PAF). PAF did not stimulate respiratory burst activity directly, but caused a rapid (maximal at 10 minutes) and concentration-dependent (EC50 50.2 nmol/L) increase in N-formyl-methionyl-leucyl-phenylalanine (fMLP)-stimulated superoxide anion release. At time-points > 10 minutes, this priming effect spontaneously declined, with return to basal levels of fMLP- stimulated superoxide anion generation by 120 minutes. An identical priming time-course was observed with N-methyl carbamyl PAF, a nonmetabolizable analogue of PAF, indicating that the transient nature of PAF-induced priming was not secondary to PAF metabolism. Two structurally diverse PAF receptor antagonists (UK-74,505 and WEB 2086), added 10 minutes after PAF addition, increased the rate of decay of the priming effect. In contrast, TNF-alpha-induced priming, which was of a similar magnitude to that observed for PAF, was slower to evolve (maximal at 30 minutes) and remained constant for at least 120 minutes. The reversible nature of PAF-induced priming was confirmed by demonstrating that PAF-, but not TNF-alpha-, induced cell polarization (shape change) and CD11b-dependent neutrophil binding of albumin-coated latex beads was also transient, with return to basal, unstimulated levels by 120 minutes. Furthermore, cells that had spontaneously deprimed following PAF exposure retained their capacity to be fully reprimed by a subsequent addition of either PAF or TNF-alpha. These data imply that neutrophil priming is not an irreversible event: the demonstration of a cycle of complete priming, depriming, and repriming offers the potential for functional recycling of neutrophils at sites of inflammation.


Author(s):  
K.W. Lee ◽  
R.H. Meints ◽  
D. Kuczmarski ◽  
J.L. Van Etten

The physiological, biochemical, and ultrastructural aspects of the symbiotic relationship between the Chlorella-like algae and the hydra have been intensively investigated. Reciprocal cross-transfer of the Chlorellalike algae between different strains of green hydra provide a system for the study of cell recognition. However, our attempts to culture the algae free of the host hydra of the Florida strain, Hydra viridis, have been consistently unsuccessful. We were, therefore, prompted to examine the isolated algae at the ultrastructural level on a time course.


Author(s):  
P. Maupin-Szamier ◽  
T. D. Pollard

We have studied the destruction of rabbit muscle actin filaments by osmium tetroxide (OSO4) to develop methods which will preserve the structure of actin filaments during preparation for transmission electron microscopy.Negatively stained F-actin, which appears as smooth, gently curved filaments in control samples (Fig. 1a), acquire an angular, distorted profile and break into progressively shorter pieces after exposure to OSO4 (Fig. 1b,c). We followed the time course of the reaction with viscometry since it is a simple, quantitative method to assess filament integrity. The difference in rates of decay in viscosity of polymerized actin solutions after the addition of four concentrations of OSO4 is illustrated in Fig. 2. Viscometry indicated that the rate of actin filament destruction is also dependent upon temperature, buffer type, buffer concentration, and pH, and requires the continued presence of OSO4. The conditions most favorable to filament preservation are fixation in a low concentration of OSO4 for a short time at 0°C in 100mM sodium phosphate buffer, pH 6.0.


Author(s):  
Nancy R. Wallace ◽  
Craig C. Freudenrich ◽  
Karl Wilbur ◽  
Peter Ingram ◽  
Ann LeFurgey

The morphology of balanomorph barnacles during metamorphosis from the cyprid larval stage to the juvenile has been examined by light microscopy and scanning electron microscopy (SEM). The free-swimming cyprid attaches to a substrate, rotates 90° in the vertical plane, molts, and assumes the adult shape. The resulting metamorph is clad in soft cuticle and has an adult-like appearance with a mantle cavity, thorax with cirri, and incipient shell plates. At some time during the development from cyprid to juvenile, the barnacle begins to mineralize its shell, but it is not known whether calcification occurs before, during, or after ecdysis. To examine this issue, electron probe x-ray microanalysis (EPXMA) was used to detect calcium in cyprids and juveniles at various times during metamorphosis.Laboratory-raised, free-swimming cyprid larvae were allowed to settle on plastic coverslips in culture dishes of seawater. The cyprids were observed with a dissecting microscope, cryopreserved in liquid nitrogen-cooled liquid propane at various times (0-24 h) during metamorphosis, freeze dried, rotary carbon-coated, and examined with scanning electron microscopy (SEM). EPXMA dot maps were obtained in parallel for qualitative assessment of calcium and other elements in the carapace, wall, and opercular plates.


2019 ◽  
Vol 476 (22) ◽  
pp. 3521-3532
Author(s):  
Eric Soubeyrand ◽  
Megan Kelly ◽  
Shea A. Keene ◽  
Ann C. Bernert ◽  
Scott Latimer ◽  
...  

Plants have evolved the ability to derive the benzenoid moiety of the respiratory cofactor and antioxidant, ubiquinone (coenzyme Q), either from the β-oxidative metabolism of p-coumarate or from the peroxidative cleavage of kaempferol. Here, isotopic feeding assays, gene co-expression analysis and reverse genetics identified Arabidopsis 4-COUMARATE-COA LIGASE 8 (4-CL8; At5g38120) as a contributor to the β-oxidation of p-coumarate for ubiquinone biosynthesis. The enzyme is part of the same clade (V) of acyl-activating enzymes than At4g19010, a p-coumarate CoA ligase known to play a central role in the conversion of p-coumarate into 4-hydroxybenzoate. A 4-cl8 T-DNA knockout displayed a 20% decrease in ubiquinone content compared with wild-type plants, while 4-CL8 overexpression boosted ubiquinone content up to 150% of the control level. Similarly, the isotopic enrichment of ubiquinone's ring was decreased by 28% in the 4-cl8 knockout as compared with wild-type controls when Phe-[Ring-13C6] was fed to the plants. This metabolic blockage could be bypassed via the exogenous supply of 4-hydroxybenzoate, the product of p-coumarate β-oxidation. Arabidopsis 4-CL8 displays a canonical peroxisomal targeting sequence type 1, and confocal microscopy experiments using fused fluorescent reporters demonstrated that this enzyme is imported into peroxisomes. Time course feeding assays using Phe-[Ring-13C6] in a series of Arabidopsis single and double knockouts blocked in the β-oxidative metabolism of p-coumarate (4-cl8; at4g19010; at4g19010 × 4-cl8), flavonol biosynthesis (flavanone-3-hydroxylase), or both (at4g19010 × flavanone-3-hydroxylase) indicated that continuous high light treatments (500 µE m−2 s−1; 24 h) markedly stimulated the de novo biosynthesis of ubiquinone independently of kaempferol catabolism.


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