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Defense Mechanisms (defense + mechanism)
Kinds of Defense Mechanisms Selected AbstractsDefense Mechanisms and Physiological Reactivity to StressJOURNAL OF PERSONALITY, Issue 2 2003Phebe Cramer The relation between the use of defense mechanisms and autonomic nervous system reactivity, under conditions of laboratory stress, was studied in 78 men and women. Both diastolic blood pressure (DBP) and skin conductance level (SCL) were monitored during exposure to ten stress tasks; concurrently, the use of three defense mechanisms was assessed by coding Thematic Apperception Test stories. Autonomic reactivity was found to be related to defenses; the nature of that relation differed across the defenses. DBP, typically found to be associated with cognitive work, was higher in those individuals who used more Identification, a defense that requires greater cognitive activity. The use of Projection, on the other hand, was associated with lower DBP. In addition, the use of Identification showed a tendency to be associated with lower SCL. [source] Hope, Defense Mechanisms, and Adjustment: Implications for False Hope and Defensive HopelessnessJOURNAL OF PERSONALITY, Issue 2 2002Paul Kwon ABSTRACT Two studies replicated and expanded an earlier finding that defense style plays a crucial role in the relation between hope and dysphoria (Kwon, 2000). Lower hope and higher defense style immaturity were each associated with greater dysphoria, depression proneness, and maladjustment. Individuals with low hope and low defense immaturity did not have poor outcomes, supporting the existence of a subtype of low hope (defensive hopelessness) that may have adaptive value. The combination of high hope and high defense immaturity was not associated with maladaptive outcomes, arguing against the false hope construct. Additionally, the findings remained after controlling for levels of anxiety. Thus, it appears that the results are not attributable to general distress or negative affectivity. Finally, domain-specific hope was shown to correlate most strongly with matching areas of adjustment, providing evidence for the validity of the construct. [source] Immature Defense Mechanisms Are Associated with Lesser Vaginal Orgasm Consistency and Greater Alcohol Consumption before SexTHE JOURNAL OF SEXUAL MEDICINE, Issue 2pt1 2010Rui Miguel Costa MA ABSTRACT Introduction., Disturbances of emotional and physical awareness can impair female sexual function. Previous research revealed that immature psychological defense mechanisms (impairing emotional awareness) are associated specifically with impaired vaginal orgasm (orgasm triggered solely by penile,vaginal stimulation). Alcohol consumed before sex (ACBS) might impair vaginal orgasm or lead to avoiding the opportunity for it, but research examining immature defenses, ACBS, and specific sexual behaviors has been lacking. Aim., To test the hypothesis that greater use of immature defenses and greater ACBS are inversely associated with vaginal orgasm consistency, but unrelated or positively correlated with greater frequency of other sexual behaviors. Methods., Three hundred twenty-three coitally experienced women (predominantly Scottish) responded to an online survey reporting their frequency of various sexual activities (and corresponding orgasms) and their ACBS, and completed the Defense Style Questionnaire DSQ-40. Main Outcome Measures., Univariate and multivariate correlations of immature defenses, ACBS, and various sexual behaviors. Results., Both immature defenses and ACBS were associated with less vaginal orgasm consistency, but unrelated or positively correlated with frequency of other sexual behaviors (including clitoral masturbation during penile,vaginal intercourse). Immature defenses were associated with more ACBS. Immature defenses explained the association between ACBS and both lack of vaginal orgasm and greater frequency of other sexual behaviors. Conclusions., The results provide further evidence that difficulty in having a vaginal orgasm is associated with immature defenses (and associated disturbances of sensibility), among other indicators of poorer health and relatedness. ACBS might impair vaginal orgasm or increase the likelihood of choosing other sexual activities, but this effect might be somewhat contingent on immature defenses. Based on various empirical studies, we call for examination of the possibility that lack of vaginal orgasm (given an adequate man) should qualify as a female sexual dysfunction. Costa RM, and Brody S. Immature defense mechanisms are associated with lesser vaginal orgasm consistency and greater alcohol consumption before sex. J Sex Med 2010;7:775,786. [source] Defense mechanism to oxidative DNA damage in glial cellsNEUROPATHOLOGY, Issue 2 2004Takashi Iida Astrocytosis is a sequential morphological change of astrocytic reaction to tissue damage, and is associated with regulation of antioxidant defense mechanisms to reduce oxidative damage. The repair enzymes to oxidative DNA damage, oxidized purine-nucleoside triphosphatase (hMTH1) and a mitochondrial type of 8-oxoguanine DNA glycosylase (hOGG1,2a) in brain tumors and neurons of Alzheimer's disease, were previously reported. In the present study, glial expression of these repair enzymes under such pathological conditions as cerebrovascular diseases and metastatic brain tumors, were investigated. Furthermore, an in-vitro experiment using a glioma cell-line under oxidative stress was performed to verify the immunohistochemical results of post-mortem materials. As a result, hOGG1,2a immunoreactivities in reactive astrocytes were more intense than those to hMTH1. Oligodendrocytes of acute or subacute stage of brain infarction were strongly immunoreactive to both repair enzymes. In-vitro study revealed that, hOGG1,2a is constitutively expressed in both untreated glioma cells and the glioma cells under oxidative stress. However, although no immunoreactivity to hMTH1 was found in the control cells, accumulation of hMTH1 was rapidly induced by oxidative stress. These results indicate that the two repair enzymes to oxidative DNA damage are differentially regulated in glial cells, and that there is a difference in the expression of the repair enzymes between reactive astrocytes and oligodendrocytes. [source] Defense mechanisms against grazing: a study of trypsin inhibitor responses to simulated grazing in the sedge Carex bigelowiiOIKOS, Issue 9 2007Åsa Lindgren Trypsin inhibitors have been suggested to constitute an inducible defense in the sedge Carex bigelowii, and some former studies suggest that this might be a cause for the cyclic population dynamics in many alpine and arctic small mammals, for example lemmings (Lemmus lemmus). We investigated this further by using a method of simulated grazing (clipping) at different intensities, in three different habitats with varying resource availability, with different harvest times (hours after clipping), and two different stages of ramets (reproductive/vegetative) in a study from the Swedish mountain range. Our results do not indicate that C. bigelowii has an inducible defense constituted by an increase in trypsin inhibitor activity (TIA), but rather that the amount of soluble plant proteins (SPP) is lowered in wounded plants. The responses were somewhat different in the three habitats, with ramets growing in the marsh showing the highest ratio of TIA to SPP, due to low amounts of SPP. We did not find any significant effects of harvest time, or of the stage of the ramet that could support the hypothesis of an inducible defense. To conclude, we could not find any evidence for an inducible defense consisting of trypsin inhibitors in Carex bigelowii ramets, but we did find variations in the amount of SPP that may have nutritional consequences for herbivores. [source] The ubiquitin-proteasome system and its role in ethanol-induced disordersADDICTION BIOLOGY, Issue 1 2002Terrence M. Donohue Jr The levels of these proteins are controlled by their rates of degradation. Similarly, protein catabolism plays a crucial role in prolonging cellular life by destroying damaged proteins that are potentially cytotoxic. A major player in these catabolic reactions is the ubiquitin-proteasome system, a novel proteolytic system that has become the primary proteolytic pathway in eukaryotic cells. Ubiquitin-mediated proteolysis is now regarded as the major pathway by which most intracellular proteins are destroyed. Equally important, from a toxicological standpoint, is that the ubiquitin-proteasome system is also widely considered to be a cellular defense mechanism, since it is involved in the removal of damaged proteins generated by adduct formation and oxidative stress. This review describes the history and the components of the ubiquitin-proteasome system, its regulation and its role in pathological states, with the major emphasis on ethanol-induced organ injury. The available literature cited here deals mainly with the effects of ethanol consumption on the ubiquitin-proteasome pathway in the liver. However, since this proteolytic system is an essential pathway in all cells it is an attractive experimental model and therapeutic target in extrahepatic organs such as the brain and heart that are also affected by excessive alcohol consumption. [source] In case of death, cling to the ingroupEUROPEAN JOURNAL OF SOCIAL PSYCHOLOGY, Issue 4 2004Emanuele Castano An experiment investigated whether the enhanced importance of the ingroup as a consequence of the salience of death thoughts is a unconscious defense mechanism. Scottish participants were subliminally primed with either the word death or field. Subsequently, they were asked to classify a series of pictures as either English or Scottish, and to state whether a series of negative traits applied to the English or not. Results showed that participants primed with the word death were more likely to exclude targets that looked more like outgroup than ingroup members, than participants in the field (control) prime condition. The pattern observed on the categorization-latency also supported the claim that death-prime participants are more careful in classifying targets. Finally, death-prime participants also conveyed more negative, stereotypical judgments of the English in a trait attribution task. The implications of the results are discussed in relation to terror management theory and social identification phenomena. Copyright © 2004 John Wiley & Sons, Ltd. [source] Expression and functional characterization of P2Y1 and P2Y12 nucleotide receptors in long-term serum-deprived glioma C6 cellsFEBS JOURNAL, Issue 8 2007Patryk Krzemi We characterized the expression and functional properties of the ADP-sensitive P2Y1 and P2Y12 nucleotide receptors in glioma C6 cells cultured in medium devoid of serum for up to 96 h. During this long-term serum starvation, cell morphology changed from fibroblast-like flat to round, the adhesion pattern changed, cell-cycle arrest was induced, extracellular signal-regulated kinase (ERK1/2) phosphorylation was reduced, Akt phosphorylation was enhanced, and expression of the P2Y12 receptor relative to P2Y1 was increased. These processes did not reflect differentiation into astrocytes or oligodendrocytes, as expression of glial fibrillary acidic protein and NG2 proteoglycan (standard markers of glial cell differentiation) was not increased during the serum deprivation. Transfer of the cells into fresh medium containing 10% fetal bovine serum reversed the changes. This demonstrates that serum starvation caused only temporary growth arrest of the glioma C6 cells, which were ready for rapid division as soon as the environment became more favorable. In cells starved for 72 and 96 h, expression of the P2Y1 receptor was low, and the P2Y12 receptor was the major player, responsible for ADP-evoked signal transduction. The P2Y12 receptor activated ERK1/2 kinase phosphorylation (a known cell proliferation regulator) and stimulated Akt activity. These effects were reduced by AR-C69931MX, a specific antagonist of the P2Y12 receptor. On the other hand, Akt phosphorylation increased in parallel with the low expression of the P2Y1 receptor, indicating the inhibitory role of P2Y1 in Akt pathway signaling. The shift in nucleotide receptor expression from P2Y1 to P2Y12 would appear to be a new and important self-regulating mechanism that promotes cell growth rather than differentiation and is a defense mechanism against effects of serum deprivation. [source] Productive Chlamydia trachomatis lymphogranuloma venereum 434 infection in cells with augmented or inactivated autophagic activitiesFEMS MICROBIOLOGY LETTERS, Issue 2 2009Niseema Pachikara Abstract Autophagy, a eukaryotic cellular activity leading to the degradation of cellular components, serves as a defense mechanism against facultative intracellular bacteria as well as a growth niche for the obligate intracellular bacterium Coxiella burnetii. We here demonstrate that the obligate intracellular bacterial pathogen Chlamydia trachomatis lymphogranuloma venereum strongly induced autophagy in the middle of the chlamydial developmental cycle (24 h after infection), a time point with maximal level of chlamydial replication, but not during the early stages with low overall chlamydial metabolism (before 8 h). No autophagy induction was evident in cells exposed to heat- and UV-inactivated elementary bodies (EBs, the infectious form of Chlamydia) or to inocula from which EBs had been removed before inoculation. Blocking chlamydial development with chloramphenicol also prevented autophagy induction in cells infected with infectious EBs. It appears that autophagy is activated primarily in response to the metabolic stress consequent to chlamydial replication. However, autophagy-defective ATG5,/, cells supported chlamydial development as efficiently as autophagy-proficient ATG5+/+ cells. [source] Biliverdin therapy protects rat livers from ischemia and reperfusion injuryHEPATOLOGY, Issue 6 2004Constantino Fondevila Heme oxygenase (HO-1) provides a cellular defense mechanism during oxidative stress and catalyzes the rate-limiting step in heme metabolism that produces biliverdin (BV). The role of BV and its potential use in preventing ischemia/reperfusion injury (IRI) had never been studied. This study was designed to explore putative cytoprotective functions of BV during hepatic IRI in rat liver models of ex vivo perfusion and orthotopic liver transplantation (OLT) after prolonged periods of cold ischemia. In an ex vivo hepatic IRI model, adjunctive BV improved portal venous blood flow, increased bile production, and decreased hepatocellular damage. These findings were correlated with amelioration of histological features of IRI, as assessed by Suzuki's criteria. Following cold ischemia and syngeneic OLT, BV therapy extended animal survival from 50% in untreated controls to 90% to 100%. This effect correlated with improved liver function and preserved hepatic architecture. Additionally, BV adjuvant after OLT decreased endothelial expression of cellular adhesion molecules (P-selectin and intracellular adhesion molecule 1), and decreased the extent of infiltration by neutrophils and inflammatory macrophages. BV also inhibited expression of inducible nitric oxide synthase and proinflammatory cytokines (interleukin 1,, tumor necrosis factor ,, and interleukin 6) in OLTs. Finally, BV therapy promoted an increased expression of antiapoptotic molecules independently of HO-1 expression, consistent with BV being an important mediator through which HO-1 prevents cell death. In conclusion, this study documents and dissects potent cytoprotective effects of BV in well-established rat models of hepatic IRI. Our results provide the rationale for a novel therapeutic approach using BV to maximize the function and thus the availability of donor organs. (HEPATOLOGY 2004;40:1333,1341.) [source] The Impact of Interferon Gamma Receptor Expression on the Mechanism of Escape From Host Immune Surveillance in Hepatocellular CarcinomaHEPATOLOGY, Issue 3 2000Mitsuo Nagao M.D. Interferon gamma (IFN-,) plays an important role in host defense mechanism and participates in the progression of chronic liver disease. IFN-, exerts its pleiotrophic effects by transcriptional regulation of expression of numerous genes, such as major histocompatibility complex (MHC) class I and Fas, through interaction with IFN-, receptor (IFN-,-R). Although hepatocytes in normal liver express weak or no IFN-,-R, those in acute and chronic liver disease up-regulate its expression. A study using IFN-,-R ,-chain knock-out mice revealed the actions of IFN-, on tumor cells as an extrinsic tumor-suppressor mechanism. However, it is unclear whether or how hepatocellular carcinoma (HCC) blocks the signal transduction of IFN-, to evade host immune surveillance. We examined the expression of IFN-,-R and IFN-,,inducible genes in 44 cases with HCC using real-time reverse-transcriptase polymerase chain reaction (RT-PCR) and immunohistochemistry. In noncancerous liver tissues (n = 38), IFN-,-R expression on the cell surface was up-regulated in 27 cases. In IFN-,-R,negative cases (n = 15), tumor size was larger (P = .032), serum ,-fetoprotein (AFP) level was higher (P = .001), intrahepatic and extrahepatic metastasis was more common (P = .044 and .013, respectively), and Ki-67 labeling index (LI) was higher (P = .041), compared with IFN-,-R,positive cases. Accordingly, the evasion mechanism may play an important role in progression, especially metastasis, in HCC. The significant correlation between the status of IFN-,-R and the expression of Fas and MHC implies that the loss of IFN-,-R might contribute to the mechanism of escape from host immune rejection in HCC. [source] Radiation-induced gene expression profile of human cells deficient in 8-hydroxy-2,-deoxyguanine glycosylaseINTERNATIONAL JOURNAL OF CANCER, Issue 3 2006M. Ahmad Chaudhry Abstract The human OGG1 gene encodes a DNA glycosylase that is involved in the base excision repair of 8-hydroxy-2,-deoxyguanine (8-OH-dG) from oxidatively damaged DNA. Cellular 8-OH-dG levels accumulate in the absence of this activity and could be deleterious for the cell. To assess the role of 8-oxoguanine glycosylase (OGG1) in the cellular defense mechanism in a specific DNA repair defect background, we set out to determine the expression pattern of base excision repair genes and other cellular genes not involved in the base excision pathway in OGG1-deficient human KG-1 cells after ionizing radiation exposure. KG-1 cells have lost OGG1 activity due to a homozygous mutation of Arg229Gln. Gene expression alterations were monitored at 4, 8, 12 and 24 hr in 2 Gy irradiated cells. Large-scale gene expression profiling was assessed with DNA microarray technology. Gene expression analysis identified a number of ionizing radiation-responsive genes, including several novel genes. There were 2 peaks of radiation-induced gene induction or repression: one at 8 hr and the other at 24 hr. Overall the number of downregulated genes was higher than the number of upregulated genes. The highest number of downregulated genes was at 8 hr postirradiation. Genes corresponding to cellular, physiologic, developmental and extracellular processes were identified. The highest number of radiation-induced genes belonged to the signal transduction category, followed by genes involved in transcription and response to stress. Microarray gene expression data were independently validated by relative quantitative RT-PCR. Surprisingly, none of the genes involved in the base excision repair of radiation-induced DNA damage showed altered expression. © 2005 Wiley-Liss, Inc. [source] Modulation of inflammation in brain: a matter of fatJOURNAL OF NEUROCHEMISTRY, Issue 3 2007Akhlaq A. Farooqui Abstract Neuroinflammation is a host defense mechanism associated with neutralization of an insult and restoration of normal structure and function of brain. Neuroinflammation is a hallmark of all major CNS diseases. The main mediators of neuroinflammation are microglial cells. These cells are activated during a CNS injury. Microglial cells initiate a rapid response that involves cell migration, proliferation, release of cytokines/chemokines and trophic and/or toxic effects. Cytokines/chemokines stimulate phospholipases A2 and cyclooxygenases. This results in breakdown of membrane glycerophospholipids with the release of arachidonic acid (AA) and docosahexaenoic acid (DHA). Oxidation of AA produces pro-inflammatory prostaglandins, leukotrienes, and thromboxanes. One of the lyso-glycerophospholipids, the other products of reactions catalyzed by phospholipase A2, is used for the synthesis of pro-inflammatory platelet-activating factor. These pro-inflammatory mediators intensify neuroinflammation. Lipoxin, an oxidized product of AA through 5-lipoxygenase, is involved in the resolution of inflammation and is anti-inflammatory. Docosahexaenoic acid is metabolized to resolvins and neuroprotectins. These lipid mediators inhibit the generation of prostaglandins, leukotrienes, and thromboxanes. Levels of prostaglandins, leukotrienes, and thromboxanes are markedly increased in acute neural trauma and neurodegenerative diseases. Docosahexaenoic acid and its lipid mediators prevent neuroinflammation by inhibiting transcription factor NF,B, preventing cytokine secretion, blocking the synthesis of prostaglandins, leukotrienes, and thromboxanes, and modulating leukocyte trafficking. Depending on its timing and magnitude in brain tissue, inflammation serves multiple purposes. It is involved in the protection of uninjured neurons and removal of degenerating neuronal debris and also in assisting repair and recovery processes. The dietary ratio of AA to DHA may affect neurodegeneration associated with acute neural trauma and neurodegenerative diseases. The dietary intake of docosahexaenoic acid offers the possibility of counter-balancing the harmful effects of high levels of AA-derived pro-inflammatory lipid mediators. [source] Protective role of COMP-Ang1 in ischemic rat brainJOURNAL OF NEUROSCIENCE RESEARCH, Issue 5 2010Hye Young Shin Abstract In cerebral ischemia, the induction of angiogenesis may represent a natural defense mechanism that enables the hypoxic brain to avoid progression into infarction. Angiopoietin-1 (Ang1) is known to produce non-leaky and stable blood vessel formation mainly by the Tie2 receptor. Therefore, we envisioned that the application of cartilage oligomeric matrix protein-Ang1 (COMP-Ang1), a soluble, stable, and potent form of Ang1, would promote angiogenesis and provide a protective effect following unilateral middle cerebral artery occlusion (MCAO) in rats. To this end, we employed a 2-hour-MCAO model, and treated rats with adenovirus encoding COMP-Ang1 (Ade-COMP-Ang1) or control virus encoding ,-gal (Ade-,-gal). Time course magnetic resonance images (MRIs) revealed significantly reduced infarct volume in the rats treated with Ade-COMP-Ang1 with an improvement of post-ischemic neurological deficits compared with rats treated with Ade-,-gal. Moreover, compared to the rats treated with Ade-,-gal, the rats treated with Ade-COMP-Ang1 showed an increase in blood vessels, especially in the border zone adjacent to the infarction, increased number of endogenous neuronal progenitor cells in the ischemic brain, and decreased number of TUNEL-positive cells. Taken together, COMP-Ang1 reduced infarct volume and consequently attenuated post-ischemic neurological deficits through enhanced angiogenesis and increased viable cell mass of neuronal cells. © 2009 Wiley-Liss, Inc. [source] Extracellular neutrophil traps in periodontitisJOURNAL OF PERIODONTAL RESEARCH, Issue 5 2009L. Vitkov Background and Objective:, Chronic periodontitis, the chronic inflammatory disease of the periodontium, is caused by bacteria and is characterized by an influx of neutrophils into the gingival crevice. Recently, a ,new' extracellular neutrophil defense mechanism , neutrophil extracellular traps , has been described. However, their role in periodontitis has not yet been investigated. Material and Methods:, Clinical examinations, transmission and scanning electron microscopy, as well as cytology and confocal laser-scanning microscopy, were employed to analyze gingiva biopsies and crevicular exudate from patients with chronic periodontitis. Results:, An abundance of neutrophil extracellular traps and some phagocytic neutrophils was found on the gingival pocket surface and in the purulent crevicular exudate. Finding neutrophil extracellular traps in the spontaneously effused purulent crevicular exudate clearly indicated that they are flushed from the pocket by the crevicular exudate. In cases of dispersal of subgingival plaque bacteria, their trapping by neutrophil extracellular traps in purulent crevicular exudate and on the gingival surface was demonstrated. Conclusion:, Trapping the crevicular bacteria prevents their adhesion to and invasion of the gingiva. The combination of neutrophil extracellular traps and crevicular exudate outflow appears to be a ,novel' defense mechanism for the clearance of crevicular bacteria in chronic periodontitis. [source] Lipid Peroxidation and Antioxidant Activities Involved in Resistance Response against Downy Mildew in Opium PoppyJOURNAL OF PHYTOPATHOLOGY, Issue 2 2010Mukesh K. Dubey Abstract The aim of this study was to observe the lipid peroxidation (LP) of cell membranes and antioxidant systems in response to inoculation of Peronospora arborescens causing downy mildew (DM) in opium poppy. Contents of the LP product, malondialdehyde (MDA) and antioxidant glutathione (GSH) were determined in leaves of two opium poppy genotypes, Pps-1 (highly resistant to DM) and Jawahar-16 (highly susceptible to DM) at different time intervals after inoculation (12 h, 24 h, 48 h and 72 h). The provided GSH content corresponded to that of total non-protein sulfhydryl groups. In leaves of Jawahar-16, a significant decrease in concentration of GSH and a persistent increase in concentration of MDA were recorded after inoculation in comparison to leaves of control plants. The continuous decrease in GSH content contributed to damage of cell membranes leading to disease development in Jawahar-16. On the other hand in a resistant genotype (Pps-1), initially at 12 h after inoculation (hai) the level of GSH was found to be high, but a transient and highly significant decrease in content of GSH and increase in content of MDA was observed at 24 hai in comparison to control plants of same genotype and also in comparison to inoculated plants of susceptible genotype (Jawahar-16). These results indicate that generation of GSH and MDA is negatively correlated during the infection process as found in the case of DM-resistant genotype Pps-1 at 24hai, which also suggests an increased need by the host plant for oxidative stress, required for hypersensitive response mediated defense mechanism. [source] Storage and ultraviolet-induced tissue stress effects on fresh-cut pineapple,JOURNAL OF THE SCIENCE OF FOOD AND AGRICULTURE, Issue 14 2004Olusola Lamikanra Abstract The effect of UV-induced stress on the volatile aroma compounds in cut pineapple was compared with that of storage at 4 °C for 24 h. Eighteen volatile compounds were identified by solid-phase microextraction (SPME) in fresh-cut pineapple. Methyl-2-methylbutanoate, methyl hexanoate, methyl 5-hexenoate, ethyl hexanoate and ethyl 5-hexenoate were the major aroma compounds. Storage at 4 °C for 24 h, and exposure of cut fruit to UV radiation for 15 min caused a considerable decrease in the concentration of esters and increase in the relative amount of copaene. This sesquiterpene, when added to crushed cantaloupe melon (0.1 mg g,1), inhibited microbial growth in the fruit over a period of 24 h at 20 °C. Cis - and trans -ocimene were present in the fruit but their production was not photo-induced by UV irradiation. Ocimene, however, was a potent antimicrobial agent that killed microorganisms when added to the crushed fruit and stored at 20 °C for 24 h. The results indicate that sesquiterpene phytoalexins could contribute to the defense mechanism in wounded pineapple tissue. Published in 2004 for SCI by John Wiley & Sons, Ltd. [source] Mild hypothermia inhibits IL-10 production in peripheral blood mononuclear cellsACTA ANAESTHESIOLOGICA SCANDINAVICA, Issue 2 2004T. Matsui Background:, Hypothermia is often associated with compromised host defenses and infections. Deterioration of immune functions related to hypothermia have been investigated, but the involvement of cytokines in host defense mechanisms and in infection remains unclear. Therefore, we determined whether mild hypothermia affects the production of several types of cytokines in peripheral blood mononuclear cells (PBMCs), and the balance between pro-inflammatory and anti-inflammatory states. Methods:, PBMCs obtained from 12 healthy humans were cultured with phytohemagglutinin (PHA) in normothermic (37°C: control) or hypothermic (33°C) conditions for 24 h. The production levels of tumor necrosis factor (TNF)-,, the interleukins (ILs) IL-6, IL-8 and IL-10, and interferon (IFN)-, in the culture supernatants were measured by means of enzyme-linked immunosorbent assay (ELISA). Results:, Under hypothermic conditions (33°C), PHA-induced production of IL-10 and IFN-, in PBMCs was significantly lower, by 34% and 84%, respectively, when compared with controls, while production of TNF-,, IL-6 and IL-8 did not change. The magnitude of reduction of IL-10 in hypothermic conditions resulted in IL-10/pro-inflammatory cytokine ratios decreasing to approximately 30,45% of those of controls. Conclusions:, The present study clearly demonstrates that mild hypothermia (33°C) inhibits IL-10 and IFN-, production in cultured PBMCs. The profound inhibition of IL-10 and the pro-inflammatory reaction-dominated state induced suggests that the host defense mechanism against secondary infection may be maintained rather than inhibited in hypothermia. Thus, the reduction of IL-10 could be an important characteristic of immune responses in mild hypothermia. [source] Apoptosis of circulating lymphocyte in rats with unilateral ureteral obstruction: Role of angiotensin IINEPHROLOGY, Issue 5 2005SOMCHIT EIAM-ONG SUMMARY: Background: Unilateral ureteral obstruction (UUO) could induce increased renal angiotensin II (ANG II), which enhances apoptosis of renal tubular cells and renal tissue loss. Systemic ANG II is also increased in UUO. There are no data available about whether UUO can induce apoptosis of circulating lymphocytes or not. Methods: UUO or sham-operated male Wistar rats (n = 8 in each group) were fed a drinking solution containing water, angiotensin II receptor type 1 antagonist (ARA; losartan, 500 mg/L) or angiotensin-converting enzyme inhibitor (ACEI; enalapril: 200 mg/L) for 1 day or 7 days. Blood samples were collected and circulating lymphocyte cells were separated. The apoptotic cells were detected by in situ terminal deoxynucleotidyl transferase (TdT assay)-mediated digoxigenin/antidigoxigenin conjugated fluorescein method and counted under a fluorescence microscope. The apoptotic index was calculated. Results: UUO caused marked increases in the apoptotic index of circulating lymphocytes in UUO rats at both 1 day and 7 days when compared with the respective sham groups (P < 0.001). Neither ARA nor ACEI treatment had an effect on the apoptotic index values in the UUO rats at 1 day. In the UUO rats at 7 days, the apoptosis of circulating lymphocytes was markedly decreased from 29.2 ± 2.7% to 11.9 ± 2.7% (P < 0.01) in the ARA-treated rats and to 7.6 ± 2.7% (P < 0.001) in the ACEI-treated rats. Conclusion: UUO, via stimulation of ANG II, could promptly enhance apoptosis of circulating lymphocytes. The apoptosis persisted throughout the 7 days of the study. Prolonged UUO would impair lymphocyte cell immunity and the host defense mechanism. Continuous treatment with either ARA or ACEI could abrogate ANG II-stimulated circulating lymphocyte apoptosis. [source] Molecular Responses to Stress Induced in Normal Human Caucasian Melanocytes in Culture by Exposure to Simulated Solar UV,PHOTOCHEMISTRY & PHOTOBIOLOGY, Issue 2 2005Laurent Marrot ABSTRACT Melanocytes play a central role in the response of skin to sunlight exposure. They are directly involved in UV-induced pigmentation as a defense mechanism. However, their alteration can lead to melanoma, a process where the role of sun overexposure is highly probable. The transformation process whereby UV damage may result in melanoma initiation is poorly understood, especially in terms of UV-induced genotoxicity in pigmented cells, where melanin can act either as a sunscreen or as a photosensitizer. The aim of this study was to analyze the behavior of melanocytes from fair skin under irradiation mimicking environmental sunlight in terms of spectral power distribution. To do this, normal human Caucasian melanocytes in culture were exposed to simulated solar UV (SSUV, 300,400 nm). Even at relatively high doses (until 20 min exposure, corresponding to 12 kJ/m2 UV-B and 110 kJ/m2 UV-A), cell death was limited, as shown by cell viability and low occurrence of apoptosis (caspase-3 activation). Moreover, p53 accumulation was three times lower in melanocytes than in unpigmented cells such as fibroblasts after SSUV exposure. However, an important fraction of melanocyte population was arrested in G2-M phase, and this correlated well with a high induction level of the gene GADD45, 4 h after exposure. Among the genes involved in DNA repair, gene XPC was the most inducible because its expression increased more than two-fold 15 h after a 20 min exposure, whereas expression of P48 was only slightly increased. In addition, an early induction of Heme Oxygenase 1 (HO1) gene, a typical response to oxidative stress, was also observed for the first time in melanocytes. Interestingly, this induction remained significant when melanocytes were exposed to UV-A radiation only (320,400 nm), and stimulation of melanogenesis before irradiation further increased HO1 induction. These results were obtained with normal human cells after exposure to SSUV radiation, which mimicked natural sunlight. They provide new data related to gene expression and suggest that melanin in light skin could contribute to sunlight-induced genotoxicity and maybe to melanocyte transformation. [source] Proteomic analysis of bacterial-blight defense-responsive proteins in rice leaf bladesPROTEINS: STRUCTURE, FUNCTION AND BIOINFORMATICS, Issue 22 2006Tariq Mahmood Abstract Plants exhibit resistance against incompatible pathogens, via localized and systemic responses as part of an integrated defense mechanism. To study the compatible and incompatible interactions between rice and bacteria, a proteomic approach was applied. Rice cv. Java 14 seedlings were inoculated with compatible (Xo7435) and incompatible (T7174) races of Xanthomonasoryzae pv. oryzae (Xoo). Cytosolic and membrane proteins were fractionated from the leaf blades and separated by 2-D PAGE. From 366 proteins analyzed, 20 were differentially expressed in response to bacterial inoculation. These proteins were categorized into classes related to energy (30%), metabolism (20%), and defense (20%). Among the 20 proteins, ribulose-1,5-bisphosphate carboxylase/oxygenase large subunit (RuBisCO LSU) was fragmented into two smaller proteins by T7174 and Xo7435 inoculation. Treatment with jasmonic acid (JA), a signaling molecule in plant defense responses, changed the level of protein accumulation for 5 of the 20 proteins. Thaumatin-like protein and probenazole-inducible protein (PBZ) were commonly up-regulated by T7174 and Xo7435 inoculation and JA treatment. These results suggest that synthesis of the defense-related thaumatin-like protein and PBZ are stimulated by JA in the defense response pathway of rice against bacterial blight. [source] Saliva of the graminivorous Theropithecus gelada lacks proline-rich proteins and tannin-binding capacityAMERICAN JOURNAL OF PRIMATOLOGY, Issue 8 2009Marcus Mau Abstract Gelada baboons are the sole survivors of the genus Theropithecus and the only known graminivorous primates. They developed special adaptations to their diet such as high-crowned teeth for processing hard and abrasive feed. The fine-tuning of salivary protein composition might be another key mechanism that is used by species for adapting to the environment and competing with rivals for exploiting new ecological niches. In order to test whether gelada (graminivorous) and hamadryas baboons (omnivorous) differ in their salivary protein composition, we compared whole saliva samples of captive Theropithecus gelada and Papio hamadryas using gel electrophoresis and tannin-binding assay. We hypothesized that the amount of proline-rich salivary proteins with tannin-binding capacity is higher in baboons consuming a feed with high dicot/monocot rations. Dicots produce tannins as a chemical defense system, discouraging animals from eating them. In contrast to dicots, monocots do not synthesize tannins. The presence of tannin-binding proteins in saliva should effectively inactivate the dicot tannin-based defense mechanism and increase the dietary breadth and/or the capability to switch between monocots and dicot leaves. The lack of such tannin-binding proteins in saliva would indicate a narrow dietary spectrum more restricted to monocots. We found T. gelada to completely lack proline-rich proteins (PRPs) and tannin-binding capacity similar to a great variety of other grazing mammals. In contrast, P. hamadryas does possess PRPs with tannin-binding activity. The findings support a growing body of evidence suggesting a high-level specialization of T. gelada to grass diets. However, it remains unclear, whether loss of salivary tannin-binding capacity drove the gelada into its narrow feeding niche, or whether this loss is the result of a long process of increased specialization. Thus, from an ecological point of view, T. gelada appears to be more vulnerable to environmental changes than other baboon species owing to its narrow dietary traits. Am. J. Primatol. 71:663,669, 2009. © 2009 Wiley-Liss, Inc. [source] Chemical stress induces the unfolded protein response in olfactory sensory neuronsTHE JOURNAL OF COMPARATIVE NEUROLOGY, Issue 10 2010Neeraja Sammeta Abstract More than any other neuron, olfactory sensory neurons are exposed to environmental insults. Surprisingly, their only documented response to damaging stress is apoptosis and subsequent replacement by new neurons. However, they expressed unfolded protein response genes, a transcriptionally regulated defense mechanism activated by many types of insults. The unfolded protein response transcripts Xbp1, spliced Xbp1, Chop (Ddit3), and BiP (Hspa5) were decreased when external access of stressors was reduced by blocking a nostril (naris occlusion). These transcripts and Nrf2 (Nfe2l2) were increased by systemic application of tunicamycin or the selective olfactotoxic chemical methimazole. Methimazole's effects overcame naris occlusion, and the unfolded protein response was independent of odor-evoked neuronal activity. Chemical stress is therefore a major and chronic activator of the unfolded protein response in olfactory sensory neurons. Stress-dependent repression of the antiapoptotic gene Bcl2 was absent, however, suggesting a mechanism for disconnecting the UPR from apoptosis and tolerating a chronic unfolded protein response. Environmental stressors also affect both the sustentacular cells that support the neurons and the respiratory epithelia, because naris occlusion decreased expression of the xenobiotic chemical transformation enzyme Cyp2a5 in sustentacular cells, and both naris occlusion and methimazole altered the abundance of the antibacterial lectin Reg3g in respiratory epithelia. J. Comp. Neurol. 518:1825,1836, 2010. © 2009 Wiley-Liss, Inc. [source] History and Update on Host Defense Against Vaginal CandidiasisAMERICAN JOURNAL OF REPRODUCTIVE IMMUNOLOGY, Issue 1 2007Paul L. Fidel Jr Vulvovaginal candidiasis (VVC), caused by Candida albicans, remains a significant problem in women of childbearing age. While cell-mediated immunity is considered the predominant host defense mechanism against mucosal candidal infections, two decades of research from animal models and clinical studies have revealed a lack of a protective role for adaptive immunity against VVC caused by putative immunoregulatory mechanisms. Moreover, natural protective mechanisms and factors associated with susceptibility to infection have remained elusive. That is until recently, when through a live challenge model in humans, it was revealed that protection against vaginitis coincides with a non-inflammatory innate presence, whereas symptomatic infection correlates with a neutrophil infiltrate in the vaginal lumen and elevated fungal burden. Thus, instead of VVC being caused by a putative deficient adaptive immune response, it is now being considered that symptomatic vaginitis is caused by an aggressive innate response. [source] Plastid ,3-fatty acid desaturase-dependent accumulation of a systemic acquired resistance inducing activity in petiole exudates of Arabidopsis thaliana is independent of jasmonic acidTHE PLANT JOURNAL, Issue 1 2008Ratnesh Chaturvedi Summary Systemic acquired resistance (SAR) is an inducible defense mechanism that is activated throughout the plant, subsequent to localized inoculation with a pathogen. The establishment of SAR requires translocation of an unknown signal from the pathogen-inoculated leaf to the distal organs, where salicylic acid-dependent defenses are activated. We demonstrate here that petiole exudates (PeXs) collected from Arabidopsis leaves inoculated with an avirulent (Avr) Pseudomonas syringae strain promote resistance when applied to Arabidopsis, tomato (Lycopersicum esculentum) and wheat (Triticum aestivum). Arabidopsis FATTY ACID DESATURASE7 (FAD7), SUPPRESSOR OF FATTY ACID DESATURASE DEFICIENCY1 (SFD1) and SFD2 genes are required for accumulation of the SAR-inducing activity. In contrast to Avr PeX from wild-type plants, Avr PeXs from fad7, sfd1 and sfd2 mutants were unable to activate SAR when applied to wild-type plants. However, the SAR-inducing activity was reconstituted by mixing Avr PeXs collected from fad7 and sfd1 with Avr PeX from the SAR-deficient dir1 mutant. Since FAD7, SFD1 and SFD2 are involved in plastid glycerolipid biosynthesis and SAR is also compromised in the Arabidopsis monogalactosyldiacylglycerol synthase1 mutant we suggest that a plastid glycerolipid-dependent factor is required in Avr PeX along with the DIR1- encoded lipid transfer protein for long-distance signaling in SAR. FAD7 -synthesized lipids provide fatty acids for synthesis of jasmonic acid (JA). However, co-infiltration of JA and methylJA with Avr PeX from fad7 and sfd1 did not reconstitute the SAR-inducing activity. In addition, JA did not co-purify with the SAR-inducing activity confirming that JA is not the mobile signal in SAR. [source] Mature monomeric forms of Hop stunt viroid resist RNA silencing in transgenic plantsTHE PLANT JOURNAL, Issue 6 2007G. Gómez Summary Viroids, small non-coding pathogenic RNAs, are able to induce RNA silencing, a phenomenon that has been associated with the pathogenesis and evolution of these small RNAs. It has been recently suggested that viroids may resist this plant defense mechanism. However, the simultaneous degradation of non-replicating full-length viroid RNA, and the resistance of mature forms of viroids to RNA silencing, have not been experimentally demonstrated. Transgenic Nicotiana benthamiana plants expressing a dimeric form of Hop stunt viroid (HSVd) that have the capability to cleave and circularize this viroid RNA were used to address this question. A reporter construct, consisting of a full-length HSVd RNA fused to GFP-mRNA, was agroinfiltrated in these plants and its expression was suppressed. Interestingly, both circular and linear HSVd molecules were stable and able to traffic through grafts in these restrictive conditions, indicating that the mature forms of HSVd are able, in some way, to resist the RNA-silencing mechanism. The observation that a full-length HSVd RNA fused to GFP-mRNA, but not circular and/or linear viroid forms, was fully susceptible to RNA degradation strongly suggests that structures adopted by the free mature monomer protect the pathogenesis-associated forms of the viroid from RNA silencing. [source] Isolation and characterisation of crocosin, an antibacterial compound from crocodile (Crocodylus siamensis) plasmaANIMAL SCIENCE JOURNAL, Issue 3 2010Sutthidech PREECHARRAM ABSTRACT An antibacterial compound from crocodile blood was partially purified and functionally characterised. The freshwater crocodile (Crocodylus siamensis) plasma with antibacterial activity was partially purified by using a centrifugal concentrator and reverse phase high powered liquid chromatography, and designated as crocosin. Crocosin exhibits antibacterial activity toward Salmonella typhi and Staphylococcus aureus. Crocosin is thermostable and resistant to pronase digestion. The structure of crocosin analyzed by mass spectrometry contains repeating units of 94 and 136 m/z. Scanning electron microscopy indicates that crocosin probably penetrates progressively into cytoplasm space, perturbing and damaging bacterial membranes. Crocosin may provide an early defense mechanism toward bacterial infection in freshwater. [source] Clinical characteristics of inpatient adolescents with severe obsessive,compulsive disorderDEPRESSION AND ANXIETY, Issue 2 2006Gal Shoval M.D. Abstract Obsessive,compulsive disorder (OCD) is a common disorder in adolescents, usually treated in the outpatient setting. Our aim in this study was to evaluate the clinical characteristics of adolescents with severe OCD that required hospitalization. A total of 342 patients consecutively admitted to a psychiatric adolescent inpatient unit and 87 healthy volunteers were assessed by a semistructured interview for clinical diagnosis, suicide risk factors, aggression, ego defense mechanisms, and intelligence. Patients with OCD (n=40) were compared to other four diagnostic patient groups with psychotic, affective, conduct, and eating disorders, as well as to normal controls. Adolescent inpatients with OCD experienced less separation anxiety than all the other psychiatric groups (P < .01) and were less impulsive than controls (P < .001). They differed in aggressive/impulsive traits and hospital-related behaviors from other diagnostic groups. Adolescent inpatients with OCD consist of a unique subgroup in the inpatient unit in terms of their clinical characteristics and risk factors for suicide. These characteristics should be taken into account when developing a treatment plan for these difficult-to-treat inpatients. Depression and Anxiety 23:62,70, 2006. © 2006 Wiley-Liss, Inc. [source] Improved Comet assay for the assessment of UV genotoxicity in Mediterranean sea urchin eggsENVIRONMENTAL AND MOLECULAR MUTAGENESIS, Issue 5 2008Sarah Nahon Abstract Gametes and embryos of broadcast spawners are exposed to a wide range of chemical and physical stressors which may alone, or in conjunction, have serious consequences on reproductive outcomes. In this study, two Mediterranean echinoid species, Paracentrotus lividus and Sphaerechinus granularis, were chosen as models to study the genotoxicity of UV radiation (UVR) on the eggs of broadcast-spawning marine invertebrates. The single cell gel electrophoresis, or Comet assay, was successfully adapted to assess DNA strand breakage in sea urchin eggs. The results demonstrated that the genetic material of sea urchin eggs is susceptible to environmentally realistic UV exposure. The induction of DNA damage in the irradiated unfertilized eggs suggests that the previously described defense mechanisms in sea urchin eggs do not completely protect the egg's DNA against UV toxicity. Taken together, our results suggest that UV-impairment of the genetic integrity of the eggs might have a role in postfertilization failures and abnormal embryonic development. Although both species were vulnerable to UVR, embryonic development was less dramatically impaired in P.Lividus. This observation supports the postulation that species inhabiting shallower environments possess more efficient mechanisms to overcome UV-induced DNA alterations. The present demonstration of the utility and sensitivity of the Comet assay to evaluate DNA integrity in eggs from marine invertebrates opens new perspectives for monitoring the long-term effects of environmental exposure on populations and for the routine screening of substances for genotoxicity in marine systems. Environ. Mol. Mutagen., 2008. © 2008 Wiley-Liss, Inc. [source] Influence of deltamethrin on nonspecific cellular and humoral defense mechanisms in rainbow trout (Oncorhynchus mykiss),ENVIRONMENTAL TOXICOLOGY & CHEMISTRY, Issue 3 2010Andrzej K. Siwicki Abstract The influence of deltamethrin on the innate immunity in rainbow trout was examined. Fish were immersed in deltamethrin at doses of 1, 2, and 4,µg/L for 30 min. The results showed that deltamethrin at doses of 2 and 4,µg/L decreased phagocytic activity of spleen macrophages and proliferative response of pronephros lymphocytes at days 1, 2, and 5 after immersion. Deltamethrin at these doses decreased the lysozyme activity, total protein, and immunoglobulin levels in serum. The greatest immunosuppressive influence of deltamethrin at dose 4,µg/L was observed at the end of the study. Environ. Toxicol. Chem. 2010;29:489,491. © 2009 SETAC [source] | |||||||||||||||||||||||||||||||||||||