Ready-to-Eat Innovative Legumes Snack: The Influence of Nutritional Ingredients and Labelling Claims in Italian Consumers' Choice and Willingness-to-Pay.

The global offer of legume-based snacks has sharply increased in recent years. However, to date, few studies have focused on the relationship between product supply and demand concerning the importance of attributes of such innovative foods. In this research, we identified the key internal and external determinants that affect legumes snack (LS) price and choice by Italian industries and consumers, respectively.

Seafood Choice and Consumption Behavior: Assessing the Willingness to Pay for an Edible Sea Urchin.

Consumers' behavior towards sea urchin and preferences towards their origin certification and place of consumption may condition their market. In this context, the aim of this research was to elicit the preferences and perceptions of Italian sea urchin dishes using a discrete choice experiment (DCE) approach. A field survey of 453 respondents in Apulia (southern Italy) was conducted for this purpose.

Health-Nutrients and Origin Awareness: Implications for Regional Wine Market-Segmentation Strategies Using a Latent Analysis.

A healthy-nutrient wine has been recently developed by Apulian wineries (southern Italy), using autochthonous wine grapes cultivars, selected strains and specific processes of production. As such, this research elicits Italian wine consumers' preferences towards this innovative Apulian wine with regard to additional labelling information associated with health-nutrients and the origin of grapes on the bottle of wine. For this purpose, a social survey based on the choice experiment approach is considered.

Re.Ger.O.P.: An Integrated Project for the Recovery of Ancient and Rare Olive Germplasm.

The olive tree is one of the most important economic, cultural, and environmental resources for Italy, in particular for the Apulian region, where it shows a wide diversity. The increasing attention to the continuous loss of plant genetic diversity due to social, economic and climatic changes, has favored a renewed interest in strategies aimed at the recovery and conservation of these genetic resources. In the frame of a project for the valorization of the olive Apulian biodiversity (Re.

Structural insights into the multi-determinant aggregation of TDP-43 in motor neuron-like cells.

TDP-43 is aggregated in patients with ALS and FLTD through mechanisms still incompletely understood. Since aggregation in the cytosol is most probably responsible for the delocalization and loss of proper RNA-binding function of TDP-43 in the nucleus, interception of the formation of aggregates may represent a useful therapeutic option. In this study, we investigated the relative importance of the N-terminal and C-terminal moieties of TDP-43 in the aggregation process and the weight of each of the six cysteine residues in determining unfolding and aggregation of the different domains.

Oxidative stress and mitochondrial damage in the pathogenesis of ALS: New perspectives.

This review attempts to reconcile the present dual view of the mechanisms operating in Amyotrophic Lateral Sclerosis (ALS). On one side, oxidative stress, mitochondrial damage and protein aggregation are considered as causative of the disease, as strongly supported by evidence obtained in models based on the expression of ALS-typical mutant SOD1. On the other hand, evidence from models expressing ALS-typical mutations in RNA-binding proteins such as FUS and TDP43 indicate that mRNA (dys)metabolism is a major pathway in this disease.

c-MYC inhibition impairs hypoxia response in glioblastoma multiforme.

The c-MYC oncoprotein is a DNA binding transcription factor that enhances the expression of many active genes. c-MYC transcriptional signatures vary according to the transcriptional program defined in each cell type during differentiation. Little is known on the involvement of c-MYC in regulation of gene expression programs that are induced by extracellular cues such as a changing microenvironment.

Nuclear accumulation of mRNAs underlies G4C2-repeat-induced translational repression in a cellular model of C9orf72 ALS.

A common feature of non-coding repeat expansion disorders is the accumulation of RNA repeats as RNA foci in the nucleus and/or cytoplasm of affected cells. These RNA foci can be toxic because they sequester RNA-binding proteins, thus affecting various steps of post-transcriptional gene regulation. However, the precise step that is affected by C9orf72 GGGGCC (G4C2) repeat expansion, the major genetic cause of amyotrophic lateral sclerosis (ALS), is still poorly defined.

Oxidative stress and mitochondrial damage: importance in non-SOD1 ALS.

It is well known that mitochondrial damage (MD) is both the major contributor to oxidative stress (OS) (the condition arising from unbalance between production and removal of reactive oxygen species) and one of the major consequences of OS, because of the high dependance of mitochondrial function on redox-sensitive targets such as intact membranes. Conditions in which neuronal cells are not able to cope with MD and OS seem to lead or contribute to several neurodegenerative diseases including Amyotrophic Lateral Sclerosis (ALS), at least in the most studied superoxide dismutase 1 (SOD1)-linked genetic variant. As summarized in this review, new evidence indicates that MD and OS play a role also in non-SOD1 ALS and thus they may represent a target for therapy despite previous failures in clinical trials.

COX2 inhibitor NS398 reduces HT-29 cell invasiveness by modulating signaling pathways mediated by EGFR and HIF1-α.

Background: Signals from the tumor microenvironment (hypoxia, growth factors) are known to induce an invasive phenotype. Cyclooxygenase-2 (COX2) overexpression, involved in colorectal carcinoma (CRC) progression, is also associated with epidermal growth factor receptor (EGFR) up-regulation. The present study investigated whether inhibition of COX2 may affect, under normoxia and hypoxia, EGF-induced cell proliferation and invasiveness by using immunoblotting, trypan blue assay, Boyden chamber assay and zymography.

Expression of Cox-2 in human breast cancer cells as a critical determinant of epithelial-to-mesenchymal transition and invasiveness.

Introduction: Cyclooxygenase-2 (COX-2) is overexpressed in several malignancies and is implicated in breast cancer progression.

Objectives: We investigated whether changes in COX-2 expression may affect epithelial-to-mesenchymal transition (EMT) and then invasive potential of human breast cancer cells, in relationship with hypoxia. COX-2-null MCF-7 human breast cancer cells, MCF-7 cells transiently expressing COX-2 and COX-2-expressing MDA-MB-231 cells were employed.

OC125, M11 and OV197 epitopes are not uniformly distributed in the tandem-repeat region of CA125 and require the entire SEA domain.

The human cancer antigen 125 (CA125) is over-expressed in epithelial ovarian cancer cells and it plays a role in the pathogenesis of ovarian cancer. This protein presents a repeat region containing up to sixty tandem repeat units. The anti-CA125 monoclonal antibodies have been previously classified into three groups: two major families, the OC125-like antibodies and M11-like antibodies, and a third group, the OV197-like antibodies.

A novel nitro-oxy substituted analogue of rofecoxib reduces human colon cancer cell growth.

Rofecoxib is a specific COX-2 inhibitor able to exert antiproliferative activity against colorectal cancer cells. It was withdrawn from the market after the demonstration of an increased risk of cardiovascular complications after prolonged use. Nevertheless, it remains an interesting compound for laboratory research as an experimental COX-2 inhibitor.

Celecoxib inactivates epithelial-mesenchymal transition stimulated by hypoxia and/or epidermal growth factor in colon cancer cells.

Celecoxib, a selective cyclooxygenase-2 (COX-2) inhibitor, has been reported to exert chemopreventive and antitumor effects on colon cancer, one of the most common solid epithelial malignancy worldwide. The aim of this study was to elucidate whether celecoxib may be able to affect epithelial-mesenchymal transition (EMT), a critical process involved in cancer cell invasiveness and metastasis and then proposed to be relevant for cancer progression. Human HT-29 colon cancer cells were exposed to carefully controlled hypoxic conditions and/or epidermal growth factor (EGF) and then investigated for EMT changes and signal transduction pathways involved by using morphological, molecular, and cell biology techniques.

Antiproliferative effects of COX-2 inhibitor celecoxib on human breast cancer cell lines.

The inducible COX-2 enzyme is over-expressed in human breast cancer and its over-expression generally correlates with angiogenesis, deregulation of apoptosis and worse prognosis. This observation may explain the beneficial effect of nonsteroidal anti-inflammatory drugs and COX-2 inhibitors on breast cancer treatment. Here, we evaluated the antiproliferative activity of celecoxib, a selective COX-2 inhibitor, and its nitro-oxy derivative on human breast cancer cells characterized by low and high COX-2 expression, respectively.

Antiproliferative effect of a novel nitro-oxy derivative of celecoxib in human colon cancer cells: role of COX-2 and nitric oxide.

It has been shown previously that a novel nitrooxy derivative of celecoxib exerts antiproliferative and pro-apoptotic effects in human colon cancer cells. The aim of this study was to elucidate whether these biological properties depend on COX-2 inhibition and/or NO release. Therefore, the derivative was decomposed into the parent compound celecoxib and the NO donor benzyl nitrate and the biological role of each was tested in COX-2-positive (HT-29) and -negative (SW-480) colon cancer cells.

COX-2 expression in human breast carcinomas: correlation with clinicopathological features and prognostic molecular markers.

Objective: COX-2 is implicated in carcinogenesis and tumour progression in many cancers, including breast cancer. Recently, it has been reported that human breast carcinomas aberrantly express COX-2, and that raised tissue levels of COX-2 may have prognostic value. Patients expressing high levels of COX-2 can develop local recurrence, and have reduced disease-free and disease-related overall survival.

Characterization of the acute inflammatory response in the hybrid tambacu (Piaractus mesopotamicus male x Colossoma macropomum female) (Osteichthyes).

This work evaluated the acute inflammatory response induced by injections of 0.5 mL saline solution (control), 500 microg carrageenin and 0.5 mL thioglycollate 3% in the swim bladder of juvenile tambacu hybrid.

CLA reduces breast cancer cell growth and invasion through ERalpha and PI3K/Akt pathways.

We previously reported that conjugated linoleic acid (CLA), a naturally occurring fatty acid, inhibits the growth of ERalpha(+) MCF-7 and ERalpha(-) MDA-MB-231 human breast cancer cells by negative modulation of the ERK/MAPK pathway and apoptosis induction. Here we show that in these cell lines CLA also down-regulates the PI3K/Akt cascade. In MCF-7 cells CLA also triggers ERalpha/PP2A complex formation reducing the phosphorylation state and transcriptional activity of Eralpha whereas in MDA-MB-231 cells CLA does not induce PP2A activation.

Novel nitro-oxy derivatives of celecoxib for the regulation of colon cancer cell growth.

Celecoxib is a non-steroidal anti-inflammatory drug (NSAID) developed as a selective inhibitor of cyclooxygenase-2 (COX-2). Despite the associated cardiovascular toxicity risk, celecoxib has been found to be effective in reducing cancer risk in animal and human studies. In the present study the antiproliferative activity of novel nitro-oxy-methyl substituted analogues of celecoxib (NO-cel), potentially less cardiotoxic, has been investigated in vitro on human colon cancer cells and compared with action of the parent drug.

Redox mechanisms switch on hypoxia-dependent epithelial-mesenchymal transition in cancer cells.

Epithelial-mesenchymal transition (EMT) and hypoxia are considered as crucial events favouring invasion and metastasis of many cancer cells. In this study, different human neoplastic cell lines of epithelial origin were exposed to hypoxic conditions in order to investigate whether hypoxia per se may trigger EMT programme as well as to mechanistically elucidate signal transduction mechanisms involved. The following human cancer cell lines were used: HepG2 (from human hepatoblastoma), PANC-1 (from pancreatic carcinoma), HT-29 (from colon carcinoma) and MCF-7 (from breast carcinoma).

Involvement of PPARalpha in the growth inhibitory effect of arachidonic acid on breast cancer cells.

Epidemiological studies suggest that dietary PUFA may influence breast cancer progression. n-3 PUFA are generally known to exert antitumour effects, whereas reports relative to n-6 PUFA anti-carcinogen effects are controversial. Arachidonic acid (AA; 20:4n-6) and its metabolites have been shown to inhibit the growth of human breast cancer cell lines, even if the downstream mechanisms by which AA may influence carcinogenesis remain unresolved.