Value-added effects of using aromatic plants in foods and human therapy

Consumers' demands for low-processed and healthier food products led to a search for alternatives to replace or reduce synthetic food additives with natural ones. Aromatic plant derivatives which have GRAS status, have been examined for being natural food preservatives and antioxidants to prolong the shelf-life of foods. They contribute to food safety, owing to their anti-quorum sensing, and anti-biofilm properties. These potential food safety attributes and increasing demand for natural food additive options have led to an interest in the use of them, especially in traditional meat, dairy, and bakery products, which would provide them an added value, and increase the market competitiveness. Therefore, the overall perspective of the value-added effects of using aromatic plants and their derivatives in food production and of their incorporated use into packaging materials for active packaging are discussed in this review. In addition, it provides information on their antimicrobial and antioxidant actions. The review also aims to give detailed information on benefits of vegetal bioactive compounds in health and disease by giving their nutraceutical and health-promoting properties. The current knowledge on their application in the treatment of health disorders is presented, their ability to prevent diseases is discussed, and the areas for future research are proposed

A canine model of Cohen syndrome: Trapped Neutrophil Syndrome

<p>Abstract</p> <p>Background</p> <p>Trapped Neutrophil Syndrome (TNS) is a common autosomal recessive neutropenia in Border collie dogs.</p> <p>Results</p> <p>We used a candidate gene approach and linkage analysis to show that the causative gene for TNS is <it>VPS13B</it>. We chose <it>VPS13B </it>as a candidate because of similarities in clinical signs between TNS and Cohen syndrome, in human, such as neutropenia and a typical facial dysmorphism. Linkage analysis using microsatellites close to <it>VPS13B </it>showed positive linkage of the region to TNS. We sequenced each of the 63 exons of <it>VPS13B </it>in affected and control dogs and found that the causative mutation in Border collies is a 4 bp deletion in exon 19 of the largest transcript that results in premature truncation of the protein. Cohen syndrome patients present with mental retardation in 99% of cases, but learning disabilities featured in less than half of TNS affected dogs. It has been implied that loss of the alternate transcript of <it>VPS13B </it>in the human brain utilising an alternate exon, 28, may cause mental retardation. Mice cannot be used to test this hypothesis as they do not express the alternate exon. We show that dogs do express alternate transcripts in the brain utilising an alternate exon homologous to human exon 28.</p> <p>Conclusion</p> <p>Dogs can be used as a model organism to explore the function of the alternately spliced transcript of VPS13B in the brain. TNS in Border collies is the first animal model for Cohen syndrome and can be used to study the disease aetiology.</p