Autoimmunity and parasites.

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Biological Effect of Licochalcone C on the Regulation of PI3K/Akt/eNOS and NF-κB/iNOS/NO Signaling Pathways in H9c2 Cells in Response to LPS Stimulation

Polyphenols compounds are a group molecules present in many plants. They have antioxidant properties and can also be helpful in the management of sepsis. Licochalcone C (LicoC), a constituent of Glycyrrhiza glabra, has various biological and pharmacological properties. In saying this, the effect of LicoC on the inflammatory response that characterizes septic myocardial dysfunction is poorly understood. The aim of this study was to determine whether LicoC exhibits anti-inflammatory properties on H9c2 cells that are stimulated with lipopolysaccharide. Our results have shown that LicoC treatment represses nuclear factor-κB (NF-κB) translocation and several downstream molecules, such as inducible nitric oxide synthase (iNOS), intercellular adhesion molecule-1 (ICAM-1) and vascular cell adhesion molecule-1 (VCAM-1). Moreover, LicoC has upregulated the phosphatidylinositol 3-kinase (PI3K)/protein kinase B (Akt)/endothelial nitric oxide synthase (eNOS) signaling pathway. Finally, 2-(4-Morpholinyl)-8-phenyl-1(4H)-benzopyran-4-one hydrochloride (LY294002), a specific PI3K inhibitor, blocked the protective effects of LicoC. These findings indicate that LicoC plays a pivotal role in cardiac dysfunction in sepsis-induced inflammation.The Italian Ministry for University and Research is acknowledged for financial support

Astaxanthin Treatment Reduced Oxidative Induced Pro-Inflammatory Cytokines Secretion in U937: SHP-1 as a Novel Biological Target

It has been suggested that oxidative stress activates various intracellular signaling pathways leading to secretion of a variety of pro-inflammatory cytokines and chemokines. SHP-1 is a protein tyrosine phosphatase (PTP) which acts as a negative regulator of immune cytokine signaling. However, intracellular hydrogen peroxide (H2O2), generated endogenously upon stimulation and exogenously from environmental oxidants, has been known to be involved in the process of intracellular signaling through inhibiting various PTPs, including SHP-1. In this study, we investigated the potential role of astaxanthin, an antioxidant marine carotenoid, in re-establishing SHP-1 negative regulation on pro-inflammatory cytokines secretion in U-937 cell line stimulated with oxidative stimulus. ELISA measurement suggested that ASTA treatment (10 µM) reduced pro-inflammatory cytokines secretion (IL-1β, IL-6 and TNF-α) induced through H2O2, (100 µM). Furthermore, this property is elicited by restoration of basal SHP-1 protein expression level and reduced NF-κB (p65) nuclear expression, as showed by western blotting experiments

Dysregulation of chemo-cytokine production in schizophrenic patients versus healthy controls

<p>Abstract</p> <p>Background</p> <p>The exact cause of schizophrenia is not known, although several aetiological theories have been proposed for the disease, including developmental or neurodegenerative processes, neurotransmitter abnormalities, viral infection and immune dysfunction or autoimmune mechanisms. Growing evidence suggests that specific cytokines and chemokines play a role in signalling the brain to produce neurochemical, neuroendocrine, neuroimmune and behavioural changes. A relationship between inflammation and schizophrenia was supported by abnormal cytokines production, abnormal concentrations of cytokines and cytokine receptors in the blood and cerebrospinal fluid in schizophrenia. Since the neuropathology of schizophrenia has recently been reported to be closely associated with microglial activation we aimed to determined whether spontaneous or LPS-induced peripheral blood mononuclear cell chemokines and cytokines production is dysregulated in schizophrenic patients compared to healthy subjects. We enrolled 51 untreated first-episode schizophrenics (SC) and 40 healthy subjects (HC) and the levels of MCP-1, MIP-1α, IL-8, IL-18, IFN-γ and RANTES were determined by Elisa method in cell-free supernatants of PBMC cultures.</p> <p>Results</p> <p>In the simultaneous quantification we found significantly higher levels of constitutively and LPS-induced MCP-1, MIP-1α, IL-8 and IL-18, and lower RANTES and IFNγ levels released by PBMC of SC patients compared with HC. In ten SC patients receiving therapy with risperidone, olanzapine or clozapine basal and LPS-induced production of RANTES and IL-18 was increased, while both basal and LPS-induced MCP-1 production was decreased. No statistically significant differences were detected in serum levels after therapy.</p> <p>Conclusion</p> <p>The observation that in schizophrenic patients the PBMC production of selected chemo-cytokines is dysregulated reinforces the hypothesis that the peripheral cyto-chemokine network is involved in the pathophysiology of schizophrenia. These preliminary, but promising data are supportive of the application of wider profiling approaches to the identification of biomarker as diagnostic tools for the analysis of psychiatric diseases.</p

Dizionario gramsciano / Gramscian Dictionary: Philology

This is a translation into English of the Dizionario gramsciano entry “Philology” by Ludovico De Lutiis. Philology, the “methodological expression of the importance of particular facts”, underlies Gramsci’s writings in the Notebooks and lies at the centre of various reflections; it is indispensable for reconstructing an author’s thought and, indeed, the past. Gramsci drew inspiration for his own anti-positivist approach, con-trasted to that of Bukharin, in part from Ernst Bernheim’s outline of historical method . Reading a text or situation, and knowing how not to read too much into it (a refusal to “importune” [sollecitare] the text), is essential to objective, dispassionate understanding. In these terms the interpretation of the present is “living philology”, where “human nature is the totality of historically determined social relations”. This “philology of history and politics” form part of Gramsci’s critique of determinist Marxism. Through the interpretation of a situation by a “collective organism”, i.e. through “living philology”, the essential link is formed “between great mass, party and leading group” in order to “move together as ‘collective-man’”

Artificial reproduction and larval ontogeny of Squalius lucumonis (Pisces, Cyprinidae), a critically endangered species in the IUCN Red List

This study refers on the first exhaustive description of sensory organs and digestive apparatus during Squalius lucumonis ontogeny. No data are available in literature, at our knowledge, on larvae, juvenile and adult stages of this species. The observations were carried out on live and fixed (Scanning Electron Microscopy and histological examination) larvae and juveniles obtained from the first attempt of artificial reproduction, and on one wild adult. The obtained results could be of some interest for restocking aquaculture, particularly when the optimization of the larval rearing phase is concerned

Chronic treatment with rosuvastatin modulates nitric oxide synthase expression and reduces ischemia-reperfusion injury in rat hearts

Objective: Due to reported modulatory effects of statins on nitric oxide synthase (NOS) expression, we tested the hypothesis of protective effects of in vivo chronic treatment with rosuvastatin, a novel 3-hydroxy-3-methyl-glutaryl coenzyme A-reductase inhibitor, on ischemia– reperfusion injury, and investigated mechanisms involved. Methods: After 3 weeks of in vivo treatment with rosuvastatin (0.2–20 mg/kg/day) or placebo, excised hearts from Wistar rats were subjected to 15 min global ischemia and 22–180 min reperfusion. We evaluated creatine-phosphokinase and nitrite levels in the coronary effluent, heart weight changes, microvascular permeability (extravasation of fluoresceine-labeled albumin), ultrastructural alterations, and the expression of endothelial (e) and inducible (i) nitric oxide synthase (NOS) (by reverse-transcription polymerase chain reaction and Western blotting). Results: Rosuvastatin 0.2 and 2 mg/kg/day significantly reduced myocardial damage and vascular hyperpermeability, concomitant with a reduction in endothelial and cardiomyocyte lesions. At 2 mg/kg/day, rosuvastatin significantly increased eNOS mRNA and protein compared with untreated hearts, and conversely decreased iNOS mRNA and protein, as well as nitrite production after ischemia–reperfusion. The addition of the NOS inhibitor NE-nitro-l-arginine methylester (l-NAME, 30 Amol/L) significantly reduced cardioprotection against ischemia–reperfusion. Conclusions: Chronic treatment with rosuvastatin before ischemia reduces ischemia–reperfusion injury and prevents coronary endothelial cell and cardiomyocyte damage by NO-dependent mechanism

Brook chub, Squalius lucumonis (Pisces, Cyprinidae) conservation aquaculture: First attempt at artificial reproduction and larval rearing

Many recovery programs for endangered species rely on the release of hatchery-reared juveniles to support threatened populations or to re-build new ones. In the framework of a conservation plan for the Italian critically endangered fish (sensu IUCN Red List) Squalius lucumonis, artificial reproduction and larval rearing was carried out for the first time. Wild breeders were collected during reproductive period (May–June) by electrofishing from Fosso Corese, a small tributary of Tiber River (Central Italy). In situ stripping of gametes followed by manual fecundation was carried out. Ex situ incubation of eggs and larval rearing were conducted in the hatchery of LESA (University of Tor Vergata). With the aim of producing fingerlings with “wild-like” behavior, a larval rearing technique in a “green water” large volume tank was applied. For the first time, about 400 fingerlings (87 days old) of brook chub were obtained from about 2300 free embryos (17% survival rate). This result is promising as it demonstrates the technical feasibility of brook chub conservation aquaculture, the first step for an in situ-ex situ recovery plan for this species based on reared fingerlings' restocking

Chronic treatment with rosuvastatin modulates nitric oxide synthase expression and reduces ischemia-reperfusion injury in rat hearts.

Di Napoli P, Taccardi AA, Grilli A, De Lutiis MA, Barsotti A, Felaco M, De Caterina R. Chronic treatment with rosuvastatin modulates nitric oxide synthase expression and reduces ischemia-reperfusion injury in rat hearts. Cardiovasc Res. 2005 Jun 1;66(3):462-71. Epub 2005 Mar 2. Laboratory of Experimental Cardiology, Department of Clinical Sciences and Bioimaging, and Center of Excellence of Aging, G. d'Annunzio University, Chieti, Italy. OBJECTIVE: Due to reported modulatory effects of statins on nitric oxide synthase (NOS) expression, we tested the hypothesis of protective effects of in vivo chronic treatment with rosuvastatin, a novel 3-hydroxy-3-methyl-glutaryl coenzyme A-reductase inhibitor, on ischemia-reperfusion injury, and investigated mechanisms involved. METHODS: After 3 weeks of in vivo treatment with rosuvastatin (0.2-20 mg/kg/day) or placebo, excised hearts from Wistar rats were subjected to 15 min global ischemia and 22-180 min reperfusion. We evaluated creatine-phosphokinase and nitrite levels in the coronary effluent, heart weight changes, microvascular permeability (extravasation of fluoresceine-labeled albumin), ultrastructural alterations, and the expression of endothelial (e) and inducible (i) nitric oxide synthase (NOS) (by reverse-transcription polymerase chain reaction and Western blotting). RESULTS: Rosuvastatin 0.2 and 2 mg/kg/day significantly reduced myocardial damage and vascular hyperpermeability, concomitant with a reduction in endothelial and cardiomyocyte lesions. At 2 mg/kg/day, rosuvastatin significantly increased eNOS mRNA and protein compared with untreated hearts, and conversely decreased iNOS mRNA and protein, as well as nitrite production after ischemia-reperfusion. The addition of the NOS inhibitor N(omega)-nitro-L-arginine methylester (L-NAME, 30 micromol/L) significantly reduced cardioprotection against ischemia-reperfusion. CONCLUSIONS: Chronic treatment with rosuvastatin before ischemia reduces ischemia-reperfusion injury and prevents coronary endothelial cell and cardiomyocyte damage by NO-dependent mechanisms