The Variation of Amplitude in a Money-Winning Paradigm in Children

In the present study the influence on amplitude of monetary payoff values linked to stimuli was investigated. Eight school boys (aged 11–13 yrs) were presented with random series of four equally frequent visual numeric stimuli (0, 2, 10, and 50). In the payoff condition (PC) subjects were told that each number would indicate the number of German pennies as a winning. In the no-payoff condition (NPC) subjects only had to attend to the stimuli. The amplitude of a late positive component (P440–540) of the visual evoked potential (identified as a representation of the in this age group) was significantly larger in PC than in NPC. The amplitude was also influenced by the amount of monetary payoff, being significantly largest after presentation of the ‘50’stimulus. Results are discussed in terms of the relevance of information provided by the stimulus, internal categorization, and subjective probabilities of the stimuli.     

LPS致敏巨噬细胞产生及其信号机制

目的探讨LPS诱导的巨噬细胞(Mφ)致敏及其信号机制.方法巨噬细胞样细胞株RAW 264.7以10μg/L LPS预处理1 h后洗去,再以1 mg/LPMA、1μmmol/LfMLP、100μg/L LPS、1 g/LZyms和15mg/L MDP攻击1h,检测上清中超氧阴离子(O-2)的产生,并用荧光显微成像系统检测细胞内游离钙离子浓度([Ca2+]i),探讨[Ca2+]i与LPS致敏Mφ产生O-2的关系.结果LPS预处理后以上述刺激剂攻击1 h均能不同程度致敏O-2的产生,且致敏程度在一定范围内与LPS剂量和作用时间相关;细胞内静息态[Ca2+]i也呈LPS剂量和时间依赖性升高,均显著相关.且LPS预处理后用PMA攻击,细胞内瞬时[Ca2+]i升高幅度明显高于LPS未处理组.用A23187使细胞内[Ca2+]i升高可代替LPS致敏O-2的产生,而预先用BAPTA和EGTA降低细胞内[Ca2+]i则可阻断LPS致敏O-2的作用.结论LPS可致敏Mφ产生O-2;LPS预处理后细胞内静态[Ca2+]i的升高是LPS诱导O-2致敏的重要原因.     

Electrochemical study of corrosion in NiCr dental alloys

The anodic behaviour of Ni-Cr dental alloys used as porcelain substrates has been investigated in both as-cast and thermal treated conditions. Polarization curves and scratching at constant potentials in synthetic salivas have shown that breakdown potentials are not influenced by the elimination of passive films covering the samples. Thermal treatments used to reproduce the microstructure of the alloys in dental crowns have not shown detectable effects on the electrochemical behaviour. Selective corrosion occurs by dissolution of Ni-rich interdendritic regions formed during solidification.     

-Deprenyl attenuates stress ulcer formation in rats

Both intraperitoneal and intracerebroventricular (i.c.v.) administration of the monoamine oxidase-B inhibitor -deprenyl markedly attenuated restraint stress-induced gastric ulcers in rats. -Deprenyl given i.c.v. attenuated stress ulcers in microgram doses and virtually abolished ulcer formation at a dose of 2.0 μg. These data suggest that intact or augmented central dopaminergic function may be an essential component of gastric mucosal protection.     

Diabetes‐induced Changes in Mannan‐binding Lectin Levels and Complement Activation in a Mouse Model of Type 1 Diabetes

Circulating mannan‐binding lectin (MBL) levels are elevated in type 1 diabetes. Further, high MBL levels are associated with the development of diabetic nephropathy. In animals, a direct effect of MBL on diabetic kidney changes is observed. We hypothesized that MBL levels and detrimental complement activation increase as a consequence of diabetes. We measured plasma MBL before and 7 weeks after inducing diabetes by streptozotocin. Mice have two MBLs, MBL‐A and MBL‐C. Diabetes induction led to an increase in MBL‐C concentration, whereas no change during the study was found in the control group. The increase in MBL‐C was associated with the increasing plasma glucose levels. In accordance with the observed changes in circulating MBL levels, liver expression of Mbl2mRNA (encoding MBL‐C) was increased in diabetes. Mbl1expression (encoding MBL‐A) did not differ between diabetic and control animals. The estimated half‐life of recombinant human MBL was significantly prolonged in mice with diabetes compared with control mice. Complement activation in plasma and glomeruli did not differ between groups. We demonstrate for the first time that MBL levels increase after induction of diabetes and in parallel with increasing plasma glucose. Our findings support the previous clinical observations of increased MBL in type 1 diabetes. This change may be explained by alternations in both MBL production and turnover.     

-Tocopherol attenuates alcohol-induced cerebral vascular damage in rats: possible role of oxidants in alcohol brain pathology and stroke

Effects of chronic (14 day) pretreatment of timed-release of -tocopherol (1.25–5 mg/day) on alcohol-induced venular cerebrovasospasm, microvessel rupture and micro-hemorrhaging was studied by direct, quantitative in-vivo high-resolution TV microscopy of the intact rat brain. Sham animals chronically treated with placebo exhibited concentration-dependent venular cerebrovasospasm, microvessel rupture and focal hemorrhages, irrespective of route (i.e. perivascular, systemic) of ethanol administration. -Tocopherol pretreatment either prevented or ameliorated greatly the cerebrovasospasm and vascular damage induced by ethanol. These results suggest that alcohol-induced cerebral vascular and brain damage by reperfusion injury events triggers lipid peroxidation of vascular smooth muscle and endothelial cell membranes; these pro-oxidant events could play a crucial role in the pathogenesis of alcohol-induced cerebral ischemia and stroke.     

Differential effects of -trytophan and buspirone on biogenic amine contents and metabolism in Lurcher mice cerebellum

The effects of serotoninergic stimulation on monoamines were studied in the heterozygous Lurcher (Lc/+) mutant mouse, a model of human cerebellar ataxia. Wild type (+/+) and Lc/+ mice were treated for 40 days with -tryptophan or buspirone, and serotonin (5-HT), dopamine (DA), noradrenaline (NA) and their main metabolites were measured in the cerebellum. In +/+ mice, only buspirone increased concentrations of 5-HT metabolites. In the hypoplastic Lc/+ cerebellum, indoleamines were higher, and increased further after both treatments. The 5-HT turnover index was increased in +/+ mice by buspirone, while in Lc/+ mutants it increased after -tryptophan but was decreased by buspirone, indicating that in the mutants nerve terminals synthesize and accumulate 5-HT, but may not utilize it efficiently. Catecholamine contents remained unchanged in +/+ mice, but in Lc/+ mutants with higher endogenous NA, -tryptophan further increased NA and 3,4-dihydroxy-phenylacetic acid (DOPAC), and buspirone augmented NA, DA and DOPAC levels.     

Potassium Humate Inhibits Complement Activation and the Production of Inflammatory Cytokines <Emphasis Type="Italic">In Vitro</Emphasis>

The effects of brown coal derived potassium humate on lymphocyte proliferation, cytokine production and complement activation were investigated in vitro. Potassium humate increased lymphocyte proliferation of phytohaemaglutinin A (PHA) and pokeweed mitogen (PWM) stimulated mononuclear lymphocytes (MNL) in vitro from concentrations of 20 to 80 μg/ml, in a dose dependant manner. On the other hand potassium humate, at 40 μg/ml, significantly inhibited the release of TNF-α, IL-1β, IL-6 and IL-10 by PHA stimulated MNL. Regarding complement activation it was found that potassium humate inhibits the activation of both the alternative and classical pathways without affecting the stability of the red blood cell membranes. These results indicate that the anti-inflammatory potential of potassium humate could be partially due to the inhibition of pro-inflammatory cytokines responsible for the initiation of these reactions as well as inhibition of complement activation. The increased lymphocyte proliferation observed, might be due to increased IL-2 production as previously been documented.     

Influence of the N-methyl- -aspartate antagonist memantine on human motor cortex excitability

The aim of our study was to investigate the effect of the N-methyl- -aspartate (NMDA) antagonist memantine on motor excitability in humans. Seven healthy volunteers received memantine or placebo, respectively, over a period of 8 days. At day 8, transcranial magnetic stimulation (TMS) was performed using a paired pulses paradigm in order to assess intracortical inhibition and facilitation. Additionally, motor threshold and silent period duration after TMS were measured as well as M waves, F waves and peripheral silent period after electrical peripheral nerve stimulation. Intracortical inhibition was enhanced, and intracortical facilitation reduced after memantine ingestion in comparison to placebo, whereas no significant difference could be observed regarding the other neurophysiological parameters. We conclude that the NMDA receptor is involved in the regulation of excitability of intracortical interneuronal circuits.     

<Emphasis Type="Italic">S</Emphasis>-Methylisothiourea Induces Apoptosis of Herpes Simplex Virus-1-Infected Microglial Cells

Our study showed that S-methylisothiourea (SMT) had anti-inflammatory effects in treating herpes simplex encephalitis in mice, and SMT also induced apoptosis of herpes simplex virus (HSV-1)-infected microglial cells. Both animal and cell models were employed in this study. Both models included the following five groups: a normal control group, a virus group (HSV-1 infected), an SMT group (HSV-1-infected + SMT (0.1 mg/10 g)), a dexamethasone group (HSV-1 infected + dexamethasone (2 μg/10 g)), and an APS group (HSV-1-infected + APS (0.8 mg/10 g)). ELISA was used to measure tumor necrosis factor (TNF)-α, interleukin (IL)-1β, and IL-10, and Greiss method was used for measuring nitric oxide (NO) secretion. HE staining was performed for detecting changes in mice brain. Flow cytometry assay for caspase-3, caspase-8, caspase-9, and caspase-12 expressions was also carried out to assess apoptosis. Expressions of TNF-α, IL-1β, and NO were significantly elevated after stimulation of microglial cells with HSV-1. Following SMT intervention, TNF-α, IL-1β, and NO levels were significantly decreased. The inflammatory changes in HSV-1-infected murine brain tissues were also reduced. SMT induction of apoptosis of HSV-stimulated microglia seemed to be through three pathways: the death receptor, mitochondrially gated, and endoplasmic reticulum. SMT can reduce HSV-induced inflammatory insult to the brain. Its mechanism of action is most probably due to the induction of microglial cell apoptosis.     

Kinetic Analysis of the Interaction between Recombinant Human FcRIα and Serum IgEs from Allergic Patients

Binding of IgE to the high-affinity IgE receptor (FcεRI) is the essential event for allergic reaction. Although there are many reports on binding kinetics between myeloma IgE and FcεRI, little is known about the kinetics between heterogeneous polyclonal IgE in the serum and FcεRIα. To elucidate the binding characteristics of heterogeneous serum IgE, we measured kinetic parameters of binding between IgE from allergic patients and a recombinant ectodomain of the human FcεRIα subunit by real-time interaction analysis based on surface plasmon resonance. Purified IgE monomer from the plasma of allergic patients displayed kinetics for the interaction with FcεRIα similar to those of myeloma IgE. In the case of crude IgE samples from allergic patients, one of seven specimens showed significantly higher affinity than highly purified IgE, suggesting that it is possible for IgEs in this specimen to form complexes of higher molecular weight.     

The Enzyme Cyp26b1 Mediates Inhibition of Mast Cell Activation by Fibroblasts to Maintain Skin-Barrier Homeostasis

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Exposure to Organic Dust Causes Activation of Human Plasma Complement Factors C3 and B and the Synthesis of Factor C3 by Lung Epithelial Cells <Emphasis Type="Italic">In Vitro</Emphasis>

Exposure in swine confinement buildings induces an intense airway inflammation. Twenty-two volunteers, of whom eleven wore a half-mask, were exposed for 3 hr in a swine barn. Blood samples were drawn before and after exposure. The ratio C3b/totalC3 in plasma decreased from 6.8 to 5.0% (p = 0.02) without mask and from 6.6 to 5.9% (p = 0.01) with mask (p = 0.67 between groups). The ratio Bb/totalB decreased from 14.5 to 13.5% (p < 0.01) without and 14.6–13.3% (p = 0.09) with mask (p = 0.25 between groups). Epithelial cells (A549) incubated up to 24 hr with 0.1 mg/mL dust suspensions were analysed for C3, IL-6 and IL-8 secretion. Cumulative C3 synthesis of dust stimulated cell cultures was 43,000 pg/mL compared to 25,000 pg/mL in unstimulated cells. Cumulative dust-induced IL-6 and IL-8 secretion was 200 and 3000 pg/mL, respectively and below detection in unstimulated cells.The activation of complement in vivo and induced C3 synthesis by epithelial cells suggests a role of complement in the airway reaction to organic dust exposure.     

Involvement of the AIM2, NLRC4, and NLRP3 Inflammasomes in Caspase-1 Activation by <Emphasis Type="Italic">Listeria monocytogenes</Emphasis>

Infection with Listeria monocytogenes can cause meningitis and septicemia in newborn, elderly, or immunocompromised individuals. Pregnant women are particularly susceptible to Listeria, leading to a potentially fatal infection. Cytosolic Listeria activates the proinflammatory caspase-1 and induces the processing and secretion of interleukins IL-1β and IL-18 as well as caspase-1-dependent pyroptosis. This study elucidates the role of various inflammasome components of host macrophages in the proinflammatory response to infection with Listeria. Here, we have used macrophages from AIM2-, NLRC4-, NLRP3-, and ASC-deficient mice to demonstrate that AIM2, NLRC4, and NLRP3 inflammasomes as well as the adaptor protein ASC all contribute to activation of caspase-1 in Listeria-infected macrophages. We show that Listeria DNA, which escapes into the cytosol of infected macrophages, triggers AIM2 oligomerization, caspase-1 activation, and pyroptosis. Interestingly, we found that flagellin-deficient Listeria, like Francisella tularensis, is recognized primarily by the AIM2 inflammasome, as no caspase-1 activation or cell death was observed in AIM2-deficient macrophages infected with this Listeria mutant. We further show that prior priming of NLRC4-deficient macrophages with LPS is sufficient for Listeria-induced caspase-1 activation in these macrophages, suggesting that TLR4 signaling is important for activation of the AIM2 and NLRP3 inflammasomes by Listeria in the absence of NLRC4. Taken together, our results indicate that Listeria infection is sensed by multiple inflammasomes that collectively orchestrate a robust caspase-1 activation and proinflammatory response.     

Differential Induction of Immunoregulatory Circuits of Phagocytic Cells by Gal/Gal NAc Lectin from Pathogenic and Nonpathogenic <Emphasis Type="Italic">Entamoeba</Emphasis>

INTRODUCTION: Amoebic liver abscess (ALA) is an acute inflammatory disease caused by Entamoeba histolytica. MATERIALS AND METHODS: The key player in the pathogenesis and immunoprotection is the Gal/GalNAc inhibitable lectin, possessed by both pathogenic (Entamoeba histolytica) and nonpathogenic (Entamoeba dispar) strains, but only E. histolytica infection is associated with an acute inflammation and subsequently the disease. RESULTS AND DISCUSSION: The stimulation with the lectin induces the secretion of various proinflammatory cytokines/chemokines from intestinal epithelial cells. The differential induction of cytokine/chemokine network by the two strains can further regulate the immunoregulatory functions of the immune cells (monocytes and neutrophils) of the host. The soluble levels of IL-1beta, IL-6, IL-8, IL-10, MIP-1alpha, MCP-1, RANTES, GRO-alpha, GMCSF were quantitated to be significantly higher in pathogenic lectin-induced conditioned media (LCM) compared to nonpathogenic LCM (NP-LCM). The monocytes from ALA patients responded to the presence of pathogenic-LCM (P-LCM) by lowering of intracellular Ca(2+) (which was still higher than control). The proinflammatory MCP-1, GRO-alpha, and GMCSF levels in the monocytes were recorded both (quantitatively and mRNA quantitation) to be tremendously higher along with their respective receptors, with P-LCM compared to NP-LCM. A significant increase in the reactive oxygen intermediates and chemotactic index (CI) was observed in the monocytes when treated with P-LCM. Similarly, in neutrophils of ALA patients, an increase in intracellular Ca(2+), ROS and chemotaxis was observed with P-LCM. OBJECTIVES: The study is a step towards understanding the mechanism of immunopathogenesis of amoebiasis, on one hand, and points to the central role of cytokine/chemokine network in the process, on the other hand.