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Enhanced Formation (enhanced + formation)
Selected AbstractsEnhanced Formation of Azoxymethane-induced Colorectal Adenocarcinoma in ,, T Lymphocyte-deficient MiceCANCER SCIENCE, Issue 8 2001Shunji Matsuda T cell receptor (TCR) ,, -positive T lymphocytes, which are localized mostly within the intraepithe-lial space of intestinal epithelium, have been suggested to play a role in maintaining the normal configuration of intestinal epithelium. However, the role of TCR,, -positive T lymphocytes in the formation and progression of colorectal adenocarcinoma that originates from colorectal epithelial cells remains to be elucidated. In this study, TCR,, and TCR,, -positive T lymphocyte-deficient mice (homozygous TCR, and TCR,-gene knockout mice) and the background wild-type mice were administered azoxymethane, and the formation of macroscopic tumors and microscopic aberrant crypt foci in colorectal mucosa were compared among the three types of mice. Well-differentiated adenocarcinoma appeared 5 months after 5 administrations of azoxymethane (10 mg/kg weight) only in a few TCR,-gene knockout mice and the frequency of the carcinoma-bearing mice was increased at 7 and 9 months after the administration. Aberrant crypt foci were also detected in the colorectal mucosa of TCR,-gene knockout mice to a greater extent than in colorectal mucosa of TCR,-gene knockout mice 1 month after the azoxymethane administration. These results suggest that TCR,, -positive T lymphocytes, which are present mainly in the intraepithelial space, play a role in suppression of the formation and progression of colorectal adenocarcinoma in mice. [source] Optical studies of defects generated in neutron-irradiated Cz-Si during HP-HT treatmentCRYSTAL RESEARCH AND TECHNOLOGY, Issue 4-5 2005B. Surma Abstract Neutron-irradiated Czochralski grown silicon subjected to heat treatment (HT) at 350 °C and 1000 °C under enhanced hydrostatic pressure (HP) was studied in this work. It has been shown that external hydrostatic pressure enhances the creation of VO2 defects in neutron irradiated silicon subjected to the HP - HT treatment at 350 °C. Enhanced formation of platelet-like oxygen precipitates was found in the samples treated at 1000 °C under 1.1 GPa. This effect was more pronounced in the samples with VO2 defects. Presented results seem to suggest that probably HP helps to transform VO2 to some kind of defects or change alone VO2 defects in the form that can act as an additional nucleus for an additional oxygen precipitation at 1000°C. No correlation between the plate-like oxygen precipitates related absorption at 1225 cm -1 and dislocation-related emission has been confirmed. (© 2005 WILEY-VCH Verlag GmbH & Co. KGaA, Weinheim) [source] Enhanced formation of advanced oxidation protein products in IBDINFLAMMATORY BOWEL DISEASES, Issue 6 2008Malgorzata Krzystek-Korpacka PhD Abstract Background: Advanced oxidation protein products (AOPPs) are new protein markers of oxidative stress with pro-inflammatory properties, accumulated in many pathological conditions. The issue of their enhanced formation in IBD has not been addressed yet. Methods: The concentration of relative AOPPs (rAOPP; concentration of AOPPs divided by albumin level) were measured in 68 subjects with ulcerative colitis (UC), 50 subjects with Crohn's disease (CD) and 45 healthy volunteers, and related to disease phenotype, clinical and biochemical activity, and therapeutic strategy. Diagnostic utility of rAOPP was evaluated by ROC analysis. Results: In comparison with controls (1.367 ,mol/g), rAOPP were increased in inactive (1.778 ,mol/g, P = 0.053) and active (1.895 ,mol/g, P = 0.013) UC and in active (1.847 ,mol/g, P = 0.003) CD. In CD, but not UC, rAOPP correlated with disease activity (r = 0.42, P = 0.013). Significant correlations with the inflammatory/malnutrition indices-erythrocyte sedimentation rate (ESR) (r = 0.53), leukocytes (r = 0.33), platelets (r = 0.38), IL-6 (r = 0.36), and transferrin (r = ,0.35) were demonstrated in CD. In UC, rAOPP correlated only with ESR (r = 0.35) and IL-6 (r = 0.30). Instead, associations with antioxidant dismutase (r = 0.29) and catalase (r = 0.22) were observed. The diagnostic power of rAOPP in discriminating diseased from non-diseased subjects was less than that of C-reactive protein (CRP). Simultaneous determination of rAOPP and CRP did not significantly improve the power of single CRP determination. Conclusions: IBD was associated with enhanced formation of AOPP, which differed between C and UC with respect to the relationship between rAOPP and disease activity, inflammatory and antioxidant response. These differences may reflect divergent ways that oxidative stress develops in CD and UC. The diagnostic power of rAOPP was insufficient for its clinical application. (Inflamm Bowel Dis 2008) [source] Selective mitochondrial glutathione depletion by ethanol enhances acetaminophen toxicity in rat liverHEPATOLOGY, Issue 2 2002Ping Zhao Chronic alcohol consumption may potentiate acetaminophen (APAP) hepatotoxicity through enhanced formation of N -acetyl- p -benzoquinone imine (NAPQI) via induction of cytochrome P450 2E1 (CYP2E1). However, CYP2E1 induction appears to be insufficient to explain the claimed magnitude of the interaction. We assessed the role of selective depletion of liver mitochondrial glutathione (GSH) by chronic ethanol. Rats were fed the Lieber-DeCarli diet for 10 days or 6 weeks. APAP toxicity in liver slices (% glutathione- S -transferase , released to the medium, GST release) and NAPQI toxicity in isolated liver mitochondria (succinate dehydrogenase inactivation, SDH) from these rats were compared with pair-fed controls. Ethanol induced CYP2E1 in both the 10-day and 6-week groups by ,2-fold. APAP toxicity in liver slices was higher in the 6-week ethanol group than the 10-day ethanol group. Partial inhibition of NAPQI formation by CYP2E1 inhibitor diethyldithiocarbamate to that of pair-fed controls abolished APAP toxicity in the 10-day ethanol group only. Ethanol selectively depleted liver mitochondrial GSH only in the 6-week group (by 52%) without altering cytosolic GSH. Significantly greater GSH loss and APAP covalent binding were observed in liver slice mitochondria of the 6-week ethanol group. Isolated mitochondria of the 6-week ethanol group were ,50% more susceptible to NAPQI (25-165 ,mol/L) induced SDH inactivation. This increased susceptibility was reproduced in pair-fed control mitochondria pretreated with diethylmaleate. In conclusion, 10-day ethanol feeding enhances APAP toxicity through CYP2E1 induction, whereas 6-week ethanol feeding potentiates APAP hepatotoxicity by inducing CYP2E1 and selectively depleting mitochondrial GSH. [source] Enhanced formation of advanced oxidation protein products in IBDINFLAMMATORY BOWEL DISEASES, Issue 6 2008Malgorzata Krzystek-Korpacka PhD Abstract Background: Advanced oxidation protein products (AOPPs) are new protein markers of oxidative stress with pro-inflammatory properties, accumulated in many pathological conditions. The issue of their enhanced formation in IBD has not been addressed yet. Methods: The concentration of relative AOPPs (rAOPP; concentration of AOPPs divided by albumin level) were measured in 68 subjects with ulcerative colitis (UC), 50 subjects with Crohn's disease (CD) and 45 healthy volunteers, and related to disease phenotype, clinical and biochemical activity, and therapeutic strategy. Diagnostic utility of rAOPP was evaluated by ROC analysis. Results: In comparison with controls (1.367 ,mol/g), rAOPP were increased in inactive (1.778 ,mol/g, P = 0.053) and active (1.895 ,mol/g, P = 0.013) UC and in active (1.847 ,mol/g, P = 0.003) CD. In CD, but not UC, rAOPP correlated with disease activity (r = 0.42, P = 0.013). Significant correlations with the inflammatory/malnutrition indices-erythrocyte sedimentation rate (ESR) (r = 0.53), leukocytes (r = 0.33), platelets (r = 0.38), IL-6 (r = 0.36), and transferrin (r = ,0.35) were demonstrated in CD. In UC, rAOPP correlated only with ESR (r = 0.35) and IL-6 (r = 0.30). Instead, associations with antioxidant dismutase (r = 0.29) and catalase (r = 0.22) were observed. The diagnostic power of rAOPP in discriminating diseased from non-diseased subjects was less than that of C-reactive protein (CRP). Simultaneous determination of rAOPP and CRP did not significantly improve the power of single CRP determination. Conclusions: IBD was associated with enhanced formation of AOPP, which differed between C and UC with respect to the relationship between rAOPP and disease activity, inflammatory and antioxidant response. These differences may reflect divergent ways that oxidative stress develops in CD and UC. The diagnostic power of rAOPP was insufficient for its clinical application. (Inflamm Bowel Dis 2008) [source] Thermostability of Lyocell Dopes Modified with Surface-Active AdditivesMACROMOLECULAR MATERIALS & ENGINEERING, Issue 8 2005Frank Wendler Abstract Summary: Cellulose/N -methylmorpholine- N -oxide monohydrate (NMMO) spinning solutions were modified with surface-active additives to yield Lyocell fibers with functional properties. Based on cellulose fibers, a new class of materials with tailored adsorption characteristics are produced. Activated charcoal and carbon black used as additives significantly affect the thermostability of the spinning solutions. Considering the degree of filling three general tendencies become evident. It is most obvious that the onset temperature of dope decomposition is shifted towards lower values accompanied by viscosity reduction after annealing at elevated temperatures and an enhanced formation of degradations products. Morpholine, N -methylmorpholine and formaldehyde as the main degradation products were detected in aqueous distillates by means of HPLC. To study the rate of by-product formation during preparation of the solution kinetic measurements were carried out. Thermal instabilities are not only initiated by heavy metal ions, especially Fe(II), but also by the particle size and porosity of the charcoal. The nano-scaled carbon black used causes autocatalytic reactions as revealed by calorimetric measurements. Relationships between amount of Acc versus onset temperature (Ton) and concentration of N -methylmorpholine. [source] Disengaging the IL-2 Receptor with Daclizumab Enhances IL-7,Mediated Proliferation of CD4+ and CD8+ T CellsAMERICAN JOURNAL OF TRANSPLANTATION, Issue 12 2009P. Monti Allograft rejection is mainly driven by the production of IL-2, which expands T cells by linking the IL-2 receptor (IL-2R) composed of three subunits: CD25, CD122 and CD132. Daclizumab, widely used in immunosuppression, is a humanized anti-CD25 antibody that disrupts IL-2 signaling by binding to CD25 and preventing the assembly of the high-affinity IL-2R. Here we show that Daclizumab, while blocking the T-cell response to IL-2, increases CD4+ and CD8+ T-cell proliferative response to the homeostatic cytokine IL-7. The IL-7R shares CD132 with the IL-2R and blocking of CD25 by Daclizumab results in the enhanced formation of the IL-7R that in turn allows IL-7 to bind more efficiently on the cell surface. The consequently increased IL-7R signaling boosts intracellular phosphorylated STAT5 and T-cell proliferation. In addition, treatment with Daclizumab delays the internalization of CD127 upon IL-7 treatment, retaining T-cell sensitivity to IL-7 for a prolonged time. This effect of Daclizumab highlights the redundancy of the cytokine system, which may influence T-cell proliferation in transplanted patients, and provides information to improve future immunosuppressive strategies. [source] A new amyloid , variant favoring oligomerization in Alzheimer's-type dementiaANNALS OF NEUROLOGY, Issue 3 2008Takami Tomiyama PhD Objective Soluble oligomers of amyloid , (A,), rather than amyloid fibrils, have been proposed to initiate synaptic and cognitive dysfunction in Alzheimer's disease (AD). However, there is no direct evidence in humans that this mechanism can cause AD. Here, we report a novel amyloid precursor protein (APP) mutation that may provide evidence to address this question. Methods A Japanese pedigree showing Alzheimer's-type dementia was examined for mutations in APP, PSEN1, and PSEN2. In addition, 5,310 Japanese people, including 2,121 patients with AD, were screened for the novel APP mutation. The pathogenic effects of this mutation on A, production, degradation, aggregation, and synaptotoxicity were also investigated. Results We identified a novel APP mutation (E693,) producing variant A, lacking gulutamate-22 (E22,) in Japanese pedigrees showing Alzheimer's-type dementia and AD. Although the secretion of total A, was markedly reduced by this mutation, the variant A, was more resistant to proteolytic degradation. The mutant peptides showed the unique aggregation property of enhanced oligomerization but no fibrillization, and inhibited hippocampal long-term potentiation more potently than wild-type peptide in rats in vivo. Consistent with the nonfibrillogenic property of the variant A,, a very low amyloid signal was observed in the patient's brain on positron emission tomography using Pittsburgh compound-B. Interpretation The E693, mutation has been suggested as a cause of dementia because of enhanced formation of synaptotoxic A, oligomers. Our findings may provide genetic validation in humans for the emerging hypothesis that the synaptic and cognitive impairment in AD is primarily caused by soluble A, oligomers. Ann Neurol 2008 [source] Photosensitized Oxidation of Sulfides: Discriminating between the Singlet-Oxygen Mechanism and Electron Transfer Involving Superoxide Anion or Molecular OxygenCHEMISTRY - A EUROPEAN JOURNAL, Issue 18 2006Sergio M. Bonesi Dr. Abstract The oxidation of diethyl and diphenyl sulfide photosensitized by dicyanoanthracene (DCA), N -methylquinolinium tetrafluoroborate (NMQ+), and triphenylpyrylium tetrafluoroborate (TPP+) has been explored by steady-state and laser flash photolysis studies in acetonitrile, methanol, and 1,2-dichloroethane. In the Et2S/DCA system sulfide-enhanced intersystem crossing leads to generation of 1O2, which eventually gives the sulfoxide via a persulfoxide; this mechanism plays no role with Ph2S, though enhanced formation of 3DCA has been demonstrated. In all other cases an electron-transfer (ET) mechanism is involved. Electron-transfer sulfoxidation occurs with efficiency essentially independent of the sulfide structure, is subject to quenching by benzoquinone, and does not lead to Ph2SO cooxidation. Formation of the radical cations R2S.+ has been assessed by flash photolysis (medium-dependent yield, dichloroethane,CH3CN>CH3OH) and confirmed by quenching with 1,4-dimethoxybenzene. Electron-transfer oxidations occur both when the superoxide anion is generated by the reduced sensitizer (DCA.,, NMQ.) and when this is not the case (TPP.). Although it is possible that different mechanisms operate with different ET sensitizers, a plausible unitary mechanism can be proposed. This considers that reaction between R2S.+ and O2., mainly involves back electron transfer, whereas sulfoxidation results primarily from the reaction of the sulfide radical cation with molecular oxygen. Calculations indeed show that the initially formed fleeting complex RS2+,,,OO. adds to a sulfide molecule and gives strongly stabilized R2SO.+OSR2 via an accessible transition state. This intermediate gives the sulfoxide, probably via a radical cation chain path. This mechanism explains the larger scope of ET sulfoxidation with respect to the singlet-oxygen process. [source] | ||||||||||