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Of Stimuli (of + stimulus)
Kinds of Of Stimuli Selected AbstractsManipulation of NK cytotoxicity by the IAP family member LivinEUROPEAN JOURNAL OF IMMUNOLOGY, Issue 12 2007Boaz Nachmias Abstract Natural killer (NK) cells are part of the innate immune system, capable of killing tumor and virally infected cells. NK cells induce apoptosis in the target cell by either granule- or receptor-mediated pathways. A set of inhibitory and activation ligands governs NK cell activation. As transformed cells often attempt to evade NK cell killing, up-regulation of a potential anti-apoptotic factor should provide a survival advantage. The inhibitor of apoptosis protein (IAP) family can inhibit apoptosis induced by a variety of stimuli. We have previously described a new IAP family member, termed Livin, which has two splice variants (, and ,) with differential anti-apoptotic activities. In this study, we explore the ability of Livin to inhibit NK cell-induced killing. We demonstrate that Livin,, moderately protects against NK cell killing whereas Livin,, augments killing. We show that Livin,, inhibition in Jurkat cells is apparent upon concomitant activation of an inhibitory signal, suggesting that Livin augments an extrinsic inhibitory signal rather than functioning as an independent inhibitory mechanism. Finally, we demonstrate that detection of both Livin isoforms in melanoma cells correlates with a low killing rate. To date, this is the first evidence that directly demonstrates the ability of IAP to protect against NK cell-induced apoptosis. [source] Multiresponsive PEDOT,Ionic Liquid Materials for the Design of Surfaces with Switchable WettabilityADVANCED FUNCTIONAL MATERIALS, Issue 20 2009Markus Döbbelin Abstract Among the different types of stimuli-responsive polymers, conjugated polymers reveal unique multiresponsive behavior. In this work, the synthesis and characterization of new functional poly(3,4-ethylenedioxythiophenes) (PEDOT) bearing imidazolium ionic-liquid moieties (PEDOT-Im) is reported. PEDOT-Im polymers show multiresponsive properties to a variety of stimuli, such as temperature, pH, oxidative doping, and presence of anions. These stimuli provoke different changes in PEDOT-Im, such as changes in color, oxidation state, and, wetting behavior. In all cases, a reversible effect is observed, and the polymers reveal responsive properties in solution as well as in the form of thin films. Whereas sensitiveness to pH and oxidative doping are known phenomena for other PEDOT derivatives, responsiveness to temperature and to anions is a unique property of PEDOT-Im. The anion exchange is further investigated by means of the Quartz Crystal Microbalance with dissipation. Anion exchanges induce fast, adjustable, and reversible contact angle changes between 24° and 107°. As a potential application, surfaces with switchable wettability triggered by anion solutions are prepared by spin-coating PEDOT-Im films onto different substrates. [source] Ca2+ entry through TRPC1 channels contributes to intracellular Ca2+ dynamics and consequent glutamate release from rat astrocytesGLIA, Issue 8 2008Erik B. Malarkey Abstract Astrocytes can respond to a variety of stimuli by elevating their cytoplasmic Ca2+ concentration and can in turn release glutamate to signal adjacent neurons. The majority of this Ca2+ is derived from internal stores while a portion also comes from outside of the cell. Astrocytes use Ca2+ entry through store-operated Ca2+ channels to refill their internal stores. Therefore, we investigated what role this store-operated Ca2+ entry plays in astrocytic Ca2+ responses and subsequent glutamate release. Astrocytes express canonical transient receptor potential (TRPC) channels that have been implicated in mediating store-operated Ca2+ entry. Here, we show that astrocytes in culture and freshly isolated astrocytes from visual cortex express TRPC1, TRPC4, and TRPC5. Indirect immunocytochemistry reveals that these proteins are present throughout the cell; the predominant expression of functionally tested TRPC1, however, is on the plasma membrane. Labeling in freshly isolated astrocytes reveals changes in TRPC expression throughout development. Using an antibody against TRPC1 we were able to block the function of TRPC1 channels and determine their involvement in mechanically and agonist-evoked Ca2+ entry in cultured astrocytes. Blocking TRPC1 was also found to reduce mechanically induced Ca2+ -dependent glutamate release. These data indicate that Ca2+ entry through TRPC1 channels contributes to Ca2+ signaling in astrocytes and the consequent glutamate release from these cells. © 2008 Wiley-Liss, Inc. [source] Systemic and local effects of long-term exposure to alkaline drinking water in ratsINTERNATIONAL JOURNAL OF EXPERIMENTAL PATHOLOGY, Issue 4 2001Marina E.T. Merne Alkaline conditions in the oral cavity may be caused by a variety of stimuli, including tobacco products, antacids, alkaline drinking water or bicarbonate toothpaste. The effects of alkaline pH on oral mucosa have not been systematically studied. To assess the systemic (organ) and local (oral mucosal) effects of alkalinity, drinking water supplemented with Ca(OH)2 or NaOH, with pH 11.2 or 12 was administered to rats (n = 36) for 52 weeks. Tissues were subjected to histopathological examination; oral mucosal biopsy samples were also subjected to immunohistochemical (IHC) analyses for pankeratin, CK19, CK5, CK4, PCNA, ICAM-1, CD44, CD68, S-100, HSP 60, HSP70, and HSP90. At completion of the study, animals in the study groups had lower body weights (up to 29% less) than controls despite equal food and water intake, suggesting a systemic response to the alkaline treatment. The lowest body weight was found in rats exposed to water with the highest pH value and starting the experiment when young (6 weeks). No histological changes attributable to alkaline exposure occurred in the oral mucosa or other tissues studied. Alkaline exposure did not affect cell proliferation in the oral epithelium, as shown by the equal expression of PCNA in groups. The up-regulation of HSP70 protein expression in the oral mucosa of rats exposed to alkaline water, especially Ca(OH)2 treated rats, may indicate a protective response. Intercellular adhesion molecule-1 (ICAM-1) positivity was lost in 6/12 rats treated with Ca(OH)2 with pH 11.2, and loss of CD44 expression was seen in 3/6 rats in both study groups exposed to alkaline water with pH 12. The results suggest that the oral mucosa in rats is resistant to the effects of highly alkaline drinking water. However, high alkalinity may have some unknown systemic effects leading to growth retardation, the cause of which remains to be determined. [source] How do nonhuman animals perceptually integrate figural fragments?1JAPANESE PSYCHOLOGICAL RESEARCH, Issue 3 2004KAZUO FUJITA Abstract:, Visual information available from the environment is often fragmented in time and space. Integrating such fragmentary information is essential for animals to recognize meaningful objects surrounding them. It has been well-documented that humans perceptually organize visual inputs. In nonhumans, on the other hand, little has been known about their process of perceptual organization. This paper focuses amodal completion in nonhuman species as one of such processes. So far, several nonhuman species including primates, rodents, and birds have been tested for amodal completion of a variety of stimuli. Positive results have been obtained in most of the species tested. In particular, nonhuman primates have been suggested to share many characteristics of this process with humans; a notable exception is pigeons. They have been shown to fail to complete with a variety of stimuli in a variety of procedures. However, this may be understood as a nature of this species adapted to their ecology. Surprising differences in perception in species that share many cognitive characteristics such as memory, concept formation, figure recognition, and so on, advises us to pay more attention to the correlation of perceptual systems and the way the species live in. [source] When scientific knowledge becomes scientific discovery: The disappearance of classical conditioning before PavlovJOURNAL OF THE HISTORY OF THE BEHAVIORAL SCIENCES, Issue 4 2002Biology, Cheryl A. Logan Professor of Psychology In the nineteenth century, scientific materials in experimental physiology changed dramatically. In this context, phenomena that had been widely accepted were lost, sometimes to be reintroduced later as "discoveries." I describe the loss of the phenomenon of classical conditioning, later rediscovered by Ivan Pavlov. In 1896, Austrian physiologist Alois Kreidl demonstrated experimentally that animals anticipate the occurrence of food that is cued by a variety of stimuli. Kreidl stated, moreover, that the fact that animals can be called to food had been widely known to science since the 1830s. I describe Kreidl's work and discuss several factors that may have led to the disappearance of conditioning prior to its rediscovery by Pavlov. © 2002 Wiley Periodicals, Inc. [source] Platelet nitric oxide synthase is activated by tyrosine dephosphorylation: possible role for SHP-1 phosphataseJOURNAL OF THROMBOSIS AND HAEMOSTASIS, Issue 11 2006B. PATEL Summary.,Background:,Endothelial nitric oxide synthase (eNOS) activity in endothelial cells is regulated by post-translational phosphorylation of critical serine, threonine and tyrosine residues in response to a variety of stimuli. However, the post-translational regulation of eNOS in platelets is poorly defined. Objectives:,We investigated the role of tyrosine phosphorylation in the regulation of platelet eNOS activity. Methods:,Tyrosine phosphorylation of eNOS and interaction with the tyrosine phosphatase SHP-1 were investigated by coimmunoprecipitation and immunoblotting. An in vitro immunoassay was used to determine eNOS activity together with the contribution of protein tyrosine phosphorylation. Results:,We found platelet eNOS was tyrosine phosphorylated under basal conditions. Thrombin induced a dose- and time-dependent increase in eNOS activity without altering overall level of tyrosine phosphorylation, although we did observe evidence of minor tyrosine dephosphorylation. In vitro tyrosine dephosphorylation of platelet eNOS using a recombinant protein tyrosine phosphatase enhanced thrombin-induced activity compared to thrombin alone, but had no effect on endothelial eNOS activity either at basal or after stimulation with bradykinin. Having shown that dephosphorylation could modulate platelet eNOS activity we examined the role of potential protein phosphatases important for platelet eNOS activity. We found SHP-1 protein tyrosine phosphatase, co-associated with platelet eNOS in resting platelets, but does not associate with eNOS in endothelial cells. Stimulation of platelets with thrombin increased SHP-1 association with eNOS, while inhibition of SHP-1 abolished the ability of thrombin to induce elevated eNOS activity. Conclusions:,Our data suggest a novel role for tyrosine dephosphorylation in platelet eNOS activation, which may be mediated by SHP-1. [source] Inhibition of p38 MAPK improves intestinal disturbances and oxidative stress induced in a rabbit endotoxemia modelNEUROGASTROENTEROLOGY & MOTILITY, Issue 5 2010S. Gonzalo Abstract Background, Lipopolysaccharide (LPS) decreases intestinal contractility and induces the release of reactive oxygen species, which play an important role in the pathogenesis of sepsis. p38 mitogen-activated protein kinase (MAPK) can be activated by a variety of stimuli such as LPS. The aims of this study were: (i) to investigate the role of p38 MAPK in the effect of LPS on (a) the acetylcholine, prostaglandin E2 and KCl-induced contractions of rabbit duodenum and (b) the oxidative stress status; (ii) to localize the active form of p38 in the intestine. Methods, Rabbits were injected with (i) saline, (ii) LPS, (iii) SB203580, a specific p38 MAPK inhibitor or (iv) SB203580 + LPS. Duodenal contractility was studied in an organ bath. SB203580 was also tested in vitro. The protein expression of p-p38 and total p38 was measured by Western blot and p-p38 was localized by inmunohistochemistry. The formation of products of oxidative damage to proteins (carbonyls) and lipids (MDA+4-HDA) was quantified in intestine and plasma. Key Results, ACh, PGE2 and KCl-induced contractions decreased with LPS. LPS increased phospho-p38 expression and the levels of carbonyls and MDA+4-HDA. SB203580 blocked the effect of LPS on the ACh, PGE2 and KCl-induced contractions in vivo and in vitro and the levels of carbonyls and MDA+4-HDA. P-p38 was detected in neurons of the myenteric plexus and smooth muscle cells of duodenum. Conclusions & Inferences, Lipopolysaccharide decreases the duodenal contractility in rabbits and increases the production of free radicals. p38 MAPK is a mediator of these effects. [source] REVIEW ARTICLE: Placental Apoptosis in Health and DiseaseAMERICAN JOURNAL OF REPRODUCTIVE IMMUNOLOGY, Issue 3 2010Andrew N. Sharp Citation Sharp AN, Heazell AEP, Crocker IP, Mor G. Placental apoptosis in health and disease. Am J Reprod Immunol 2010; 64: 159,169 Apoptosis, programmed cell death, is an essential feature of normal placental development but is exaggerated in association with placental disease. Placental development relies upon effective implantation and invasion of the maternal decidua by the placental trophoblast. In normal pregnancy, trophoblast apoptosis increases with placental growth and advancing gestation. However, apoptosis is notably exaggerated in the pregnancy complications, hydatidiform mole, pre-eclampsia, and intrauterine growth restriction (IUGR). Placental apoptosis may be initiated by a variety of stimuli, including hypoxia and oxidative stress. In common with other cell-types, trophoblast apoptosis follows the extrinsic or intrinsic pathways culminating in the activation of caspases. In contrast, the formation of apoptotic bodies is less clearly identified, but postulated by some to involve the clustering of apoptotic nuclei and liberation of this material into the maternal circulation. In addition to promoting a favorable maternal immune response, the release of this placental-derived material is thought to provoke the endothelial dysfunction of pre-eclampsia. Widespread apoptosis of the syncytiotrophoblast may also impair trophoblast function leading to the reduction in nutrient transport seen in IUGR. A clearer understanding of placental apoptosis and its regulation may provide new insights into placental pathologies, potentially suggesting therapeutic targets. [source] | |||||||||||||