Identification and Capture of Phenolic Compounds from a Rapeseed Meal Protein Isolate Production Process By-Product by Macroporous Resin and Valorization Their Antioxidant Properties.

In this study, phenolic compounds from an aqueous protein by-product from rapeseed meal (RSM) were identified by HPLC-DAD and HPLC-ESI-MS, including sinapine, sinapic acid, sinapoyl glucose, and 1,2-di-sinapoyl gentibiose. The main phenolic compound in this by-product was sinapine. We also performed acid hydrolysis to convert sinapine, and sinapic acid derivatives present in the permeate, to sinapic acid.

Multicriteria Optimization of Phenolic Compounds Capture from a Sunflower Protein Isolate Production Process by-Product by Adsorption Column and Assessment of Their Antioxidant and Anti-Inflammatory Effects.

The aim of this study was to valorize liquid effluent from the sunflower protein isolate process by extracting phenolic compounds it contains. To do so, XAD7 resin was used. A multicriteria optimization methodology based on design of experiments showed the optimal conditions were adsorption flow rate of 15 BV/h at pH 2.

Phenolamides: Plant specialized metabolites with a wide range of promising pharmacological and health-promoting interests.

Phenolamides constitute a family of metabolites, widely represented in the plant kingdom, that can be found in all plant organs with a predominance in flowers and pollen grains. They represent a large and structurally diverse family, resulting from the association of phenolic acids with aliphatic or aromatic amines. Initially revealed as active compounds in several medicinal plant extracts, phenolamides have been extensively studied for their health-promoting and pharmacological properties.

Repeated corticosterone injections in adult mice alter stress hormonal receptor expression in the cerebellum and motor coordination without affecting spatial learning.

Receptors for glucocorticoid (GR) and corticotropin-releasing hormone (CRH) are largely found in brain sensorimotor structures, particularly in cerebellum, underlining a potential role of stress hormones in the regulation of motor function. Since CRH is involved in neuroplasticity, known for its trophic effect on synapses, we investigated how manipulations in corticosterone serum levels can modulate the CRH system in the cerebellum and affect motor coordination. Corticosterone at doses of either 15 or 30mg/kg was injected in mice and the status of hormonal expression evaluated in cerebellum, hippocampus, and hypothalamus in undisturbed housing conditions or after different behavioral tests.

Aldosterone up-regulates MMP-9 and MMP-9/NGAL expression in human neutrophils through p38, ERK1/2 and PI3K pathways.

Aldosterone and mineralocorticoid receptors are important regulators of inflammation. During this process, chemokines and extracellular matrix degradation by matrix metalloproteases, such as MMP-9, help leukocytes reaching swiftly and infiltrating the injured tissue, two processes essential for tissue repair. Leukocytes, such as neutrophils, are a rich source of MMP-9 and possess mineralocorticoid receptors (MR).

Aldosterone increases VEGF-A production in human neutrophils through PI3K, ERK1/2 and p38 pathways.

Aldosterone is now recognised as an important actor in inflammation processes. Neoangiogenesis plays a crucial role in this complex process and immune cells, such as neutrophils, appear to be able to secrete different forms of (pro)angiogenic molecules, especially VEGF-A. The present work was undertaken to investigate whether aldosterone was able to regulate VEGF-A production in human neutrophils.

The role of Product Development Partnerships in research and development for neglected diseases.

Product Development Partnerships (PDPs) are playing an increasingly important role in the development of new medicines for neglected diseases of the developing world; however, there has been limited information on their funding and expenditure patterns. This paper analyses funding for the 14 PDPs working on neglected disease research and development (R&D) by using unpublished data from the Global Funding of Innovation for Neglected Diseases (G-FINDER) project, which surveyed 2007 global investments into R&D of products for neglected diseases. PDPs captured US$469 million or 23% of 'external' R&D funding for neglected diseases, i.

Neglected disease research and development: how much are we really spending?

Mary Moran and colleagues survey global investment into research and development of new pharmaceutical products to prevent, manage, or cure diseases of the developing world.

C-reactive protein induces pro- and anti-inflammatory effects, including activation of the liver X receptor alpha, on human monocytes.

Non-specific markers of inflammation such as C-reactive protein (CRP) are associated statistically with an increased risk of atherosclerosis through mechanisms that have not yet been fully elucidated. We investigated the effects of CRP on several aspects of human monocyte biology, a cell type involved in the initiation and progression of atherosclerosis. Blood monocytes isolated from healthy men and premenopausal women (n = 9/group) were exposed to purified CRP (25 microg/ml) for 12 hours.

C-reactive protein (CRP) increases VEGF-A expression in monocytic cells via a PI3-kinase and ERK 1/2 signaling dependent pathway.

C-reactive protein (CRP) is an independent predictor of atherosclerosis and its complications. Monocytes/macrophages are implicated in this complex disease which is, among other mechanisms, characterised by angiogenesis. The aim of this study was to analyse whether CRP plays a role in VEGF-A regulation by monocytic cells.

Sequencing and expression of the CD3 gamma/delta mRNA in Pleurodeles waltl (urodele amphibian).

The CD3 complex is an essential component of the T-cell receptor (TCR) implicated in T-cell maturation and activation. This TCR has been identified in both cartilaginous and bony vertebrates. In different studies where the CD3 chains were cloned and sequenced, it appeared that the CD3 complex is composed of several chains, all susceptible to phosphorylation and able to transduce signals.

The recombination-activating gene 1 of Pleurodeles waltl (urodele amphibian) is transcribed in lymphoid tissues and in the central nervous system.

The recombination-activating gene 1 (RAG1) product is required for the somatic rearrangement of immunoglobulin and T-cell receptor genes. We cloned and sequenced the large continuous open reading frame coding for the salamander Pleurodeles waltl RAG1 protein. Semi-quantitative RT-PCR experiments were performed to quantify the expression of RAG1 in different tissues.

Phenothiazine-induced increase in thyroid autoantigens and costimulatory molecules on thyroid cells: a pathophysiological mechanism for drug-induced autoimmunity?

We have previously demonstrated (J Immunol 1995; 154:3593) that MHC class II antigens can be induced on thyroid epithelial cells (TEC) by alimemazine, a member of the phenothiazine group. Although this expression of MHC class II antigens on TEC confers the theoretical ability to behave as antigen-presenting cells (APC), the simultaneous expression of self antigens and co-receptor(s) must also occur for efficient presentation of self antigens. Therefore, we investigated whether alimemazine applied at pharmacologic doses would modify the expression of thyroid antigens, and simultaneously, the expression of intercellular adhesion molecule-1 (ICAM-1), B7, and LFA-1 co-receptors in human TEC in culture.

Grafts of ovaries in males and females of Pleurodeles waltl (urodele amphibia): evidence of a long-term tolerance of allografts; application following a space biology experiment.

Ovary grafts were investigated in the salamander Pleurodeles using juveniles and adults as donors and hosts. Ovaries were provided by standard or histo-compatible strains and by standard females which had been submitted to a space flight. Laparotomy of the hosts was used to control viability of grafts.

Molecular heterogeneity of antigen- or idiotype-induced anti-thyroglobulin monoclonal autoantibodies.

To define the molecular basis of the cognitive interaction in experimental autoimmune thyroiditis (EAT), we sequenced the variable regions of monoclonal autoantibodies to thyroglobulin (Tg), specific or not for the F40D peptide, a Tg peptide capable of inducing EAT in CBA/J mice. Three MoAbs were obtained by immunization with syngeneic Tg of CBA/J (3B8G9, 2F6F2) or C57Bl/6 (4D11F4) mice. 3B8G9 was specific for F40D peptide, whereas 2F6F2 and 4D11F4 were not.

Phenothiazine induces de novo MHC class II antigen expression on thyroid epithelial cells. A new mechanism for drug-induced autoimmunity.

Autoimmune responses are initiated by MHC class II-restricted T cell responses directed against tissue-specific autoantigens. Furthermore, HLA-DR expression in thyroid epithelial cells is a prominent feature of autoimmune thyroid disease. In the present work, we were particularly interested in a phenothiazine, a neuroleptic and anti-depressant drug of pharmacologic importance named alimemazine.

One monoclonal antibody to human thyrotropin (TSH) receptor agonist of TSH hormone stimulates the proliferation of human thyroid cells.

The question of thyroid cell growth induction by monoclonal antibodies (mAbs) to human thyrotropin receptor (hTSH-R), which stimulate increases in cAMP thyroid cells, is under debate and their implication in Graves' disease (GD) is controversial. In order to address this issue, we used characterized reagents, i.e.

Induction of autoimmunity by immunization of mice with human thyrotropin receptor.

The development of autoimmunity was investigated after repeated immunizations with human thyrotropin receptor (hTSH-R) of five congenic strains of female and male mice. After each immunization, free T3 levels and antibodies to hTSH-R and to six peptides of the hTSH-R were assayed. Our results showed that H-2s and H-2q female mice developed features of autoimmunity such as antibody responses to hTSH-R and to hTSH-R peptides, transient variations in the levels of free T3 thyroid hormone, and lymphocytic infiltrations in their thyroid glands.

Antibodies specific for human thyrotropin receptor induce MHC antigen expression in thyroid cells.

Autoantibodies (AAbs) to hormone receptors are found in autoimmune diseases such as Graves' disease (GD) or myasthenia gravis. A structural link between hormone receptor and MHC genes has been documented, suggesting a possible co-regulation of MHC and hormone receptor genes. Thus, in vitro experiments were designed to search for a pathologic role for AAbs.

Production of Ab2 beta, anti-idiotypic monoclonal antibodies, specific for human thyrotropin receptor.

We had previously selected five monoclonal antibodies (mAb1) upon their specific binding to human thyrotropin (hTSH). These mAbs1, which are specific for two distinct epitopes of the hTSH beta-chain, also inhibit the hTSH binding to human thyroid membrane preparations. We then immunized BALB/c mice with the various mAbs1 in attempt to generate anti-idiotypic Abs (Ab2) directed to the hTSH receptor (hTSHR).

Ig VH gene family usage in spleen cells of CBA/J mice immunized with experimental autoimmune thyroiditis (EAT) inducer antigens.

Experimental autoimmune thyroiditis (EAT) is an autoimmune disorder of the thyroid gland induced in susceptible strains of mice by thyroglobulin (Tg). We recently showed that low Mr (< 10 kDa) Tg tryptic fragments and a 40 amino-acid peptide (F40D) from Tg could induce EAT as well as native Tg. Because it has been reported that autoantibodies (A-Abs) express VH families preferentially located in the D-proximal VH gene segment, we investigated whether A-Abs specific for one pathogenic peptide from Tg were also skewed towards D proximal VH gene segment.