Nutritional, textural and quality attributes of white and dark muscles of little tuna (Euthynnus affinis)

205-211The proximate composition, fatty acid profile, texture, colour and freshness of white and dark muscles of little tuna (Euthynnus affinis) were investigated. The moisture content was higher in white muscle (75.52±0.13%) compared to that in dark muscle (74.85±0.10%). Both white and dark muscle had higher levels of protein, 23.12± 0.13% and 23.15± 0.02%, respectively. Analysis of fatty acid profile by gas chromatography showed that the dark muscle had high levels of eicosapentaenoie acid (C20:5) and docosahexaenoic acid (C22:6) compared to white muscle. Texture profile analysis showed that dark muscle had higher values for hardness (3.74±0.15kgF), whereas adhesiveness, cohesiveness, springiness and chewiness values were greater for white muscle. Colour analysis revealed dark muscle had lower L* value than that of white muscle. The total volatile base nitrogen, tri - methyl amine, texture profile analysis and histamine contents were higher in dark muscle. Overall nutritional quality of dark muscle was superior to that of white muscle

Interleukin-17 Stimulates C-Reactive Protein Expression in Hepatocytes and Smooth Muscle Cells via p38 MAPK and ERK1/2-Dependent NF-κB and C/EBPβ Activation

Elevated systemic levels of the acute phase C-reactive protein (CRP) are predictors of future cardiovascular events. There is evidence that CRP may also play a direct role in atherogenesis. Here we determined whether the proinflammatory interleukin (IL)-17 stimulates CRP expression in hepatocytes (Hep3B cell line and primary hepatocytes) and coronary artery smooth muscle cells (CASMC). Our results demonstrate that IL-17 potently induces CRP expression in Hep3B cells independent of IL-1β and IL-6. IL-17 induced CRP promoter-driven reporter gene activity that could be attenuated by dominant negative IκBα or C/EBPβ knockdown and stimulated both NF-κB and C/EBP DNA binding and reporter gene activities. Targeting NF-κB and C/EBPβ activation by pharmacological inhibitors, small interfering RNA interference and adenoviral transduction of dominant negative expression vectors blocked IL-17-mediated CRP induction. Overexpression of wild type p50, p65, and C/EBPβ stimulated CRP transcription. IL-17 stimulated p38 MAPK and ERK1/2 activation, and SB203580 and PD98059 blunted IL-17-mediated NF-κB and C/EBP activation and CRP transcription. These results, confirmed in primary human hepatocytes and CASMC, demonstrate for the first time that IL-17 is a potent inducer of CRP expression via p38 MAPK and ERK1/2-dependent NF-κB and C/EBPβ activation and suggest that IL-17 may mediate chronic inflammation, atherosclerosis, and thrombosis

Critical Comparison of the Strengths and Weaknesses of Positivism and Interpretivism as Two Approaches to the Study of Politics

International audienc

Dipeptidyl peptidase IV inhibitors derived from a mangrove flora Rhizophora mucronata: An in silico approach

Dipeptidyl peptidase IV (DPP IV) is responsible for conversion of glucose tolerance (GLP-1), into inactive form. The inhibition of DPP IV would be beneficial in the treatment of diabetes mellitus. Therefore, the aim of the present study was to isolate and evaluate cystine, phenyl acetic acid, acrylamide, caprylone and oleic acid from Rhizophora mucronata inhibitory action on DPP IV inhibitors using in silico approach. In silico analysis of cystine, phenyl acetic acid, acrylamide, caprylone and oleic acid on human apo DPP IV protein was done by using Autodoc 4.0. Among the five compounds cysteine acts as an inhibitor with binding energy -5.89 kcal/mol, seven hydrogen bond interactions at residues VAL459, VAL 459, GLU408, GLU206, ARG358, GLU205 and SER209 to suppresses the action of DPP IV protein

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Neutralization of Interleukin-18 Ameliorates Ischemia/Reperfusion-induced Myocardial Injury*

Ischemia/reperfusion (I/R) injury is characterized by the induction of oxidative stress and proinflammatory cytokine expression. Recently demonstrating that oxidative stress and TNF-α each stimulate interleukin (IL)-18 expression in cardiomyocytes, we hypothesized that I/R also induces IL-18 expression and thus exacerbates inflammation and tissue damage. Neutralization of IL-18 signaling should therefore diminish tissue injury following I/R. I/R studies were performed using a chronically instrumented closed chest mouse model. Male C57BL/6 mice underwent 30 min of ischemia by LAD coronary artery ligation followed by various periods of reperfusion. Sham-operated or ischemia-only mice served as controls. A subset of animals was treated with IL-18-neutralizing antibodies 1 h prior to LAD ligation. Ischemic LV tissue was used for analysis. Our results demonstrate that, compared with sham operation and ischemia alone, I/R significantly increased (i) oxidative stress (increased MDA/4-HNE levels), (ii) neutrophil infiltration (increased MPO activity), (iii) NF-κB DNA binding activity (p50, p65), and (iv) increased expression of IL-18Rβ, but not IL-18Rα or IL-18BP transcripts. Administration of IL-18-neutralizing antibodies significantly reduced I/R injury measured by reduced infarct size (versus control IgG). In isolated adult mouse cardiomyocytes, simulated ischemia/reperfusion enhanced oxidative stress and biologically active IL-18 expression via IKK-dependent NF-κB activation. These results indicate that IL-18 plays a critical role in I/R injury and thus represents a promising therapeutic target