4 results match your criteria: "a Institute of Food Research[Affiliation]"

We previously identified and characterized an intramolecular trans-sialidase (IT-sialidase) in the gut symbiont Ruminococcus gnavus ATCC 29149, which is associated to the ability of the strain to grow on mucins. In this work we have obtained and analyzed the draft genome sequence of another R. gnavus mucin-degrader, ATCC 35913, isolated from a healthy individual.

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Understanding the association between diet and nutrition in upper gastrointestinal cancer.

Expert Rev Gastroenterol Hepatol

August 2016

a Institute of Food Research, Norwich Research Park, Colney, NR4 7UA, Norwich, UK.

Human vulnerability to cancers of the upper gastrointestinal tract is strongly influenced by environmental factors. The esophagus, in particular, is highly vulnerable to the combined effects of exposure to environmental carcinogens and malnutrition, particularly in certain extreme environments of the developing world. Even in high-income countries, dietary carcinogens and nutrition play a major role in the etiology of oropharyngeal, esophageal and, to a lesser extent, gastric cancers, but the mechanisms are poorly understood.

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Sodium dodecyl sulphate (SDS) and sodium tripolyphosphate (STP) act to remove stained pellicle from dentition and loosen deposits on tooth surfaces that may become cariogenic over time. This study investigated how SDS and STP impact the salivary pellicle adsorbed onto hydroxyapatite and silica sensors using a dual polarisation interferometer and a quartz-crystal microbalance with dissipation. After the pellicle was exposed to SDS and STP the remaining pellicle, although weaker, due to the loss of material, became less dense but with a higher elastic component; suggesting that the viscous component of the pellicle was being removed.

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Procyanidins are polymeric flavanols found in fruits and vegetables and have shown anticarcinogenic/chemopreventive properties. We previously showed that oligomeric procyanidin extracted from apples induced cell cycle arrest and apoptosis in esophageal adenocarcinoma (OA) cells. To understand the mechanism of action, we determined transcriptomic changes induced by procyanidin in OA cells.

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