However, gene C4H-1 was down regulated in susceptible genotypes after 24 and 48 h.a.i. while up regulated
in resistant genotypes. Phenol profiling using HPTLC showed the presence of three phenolic acids i.e. caffeic acid, ferulic acid and salicylic acid in non-infected and infected castor genotypes. Higher content of caffeic and ferulic acid was detected in infected and non-infected resistant genotypes at 0, 24 and 48 h.a.i, whereas caffeic acid was not detected in susceptible genotypes at 0 h.a.i. These results suggest the critical role of phenols in castor disease resistance. (C) 2013 Elsevier B.V. All rights reserved.”
“Probiotic bacteria were previously encapsulated in sub-100 mu m Ca2+ alginate microcapsules for enhanced survival in human gastrointestinal tract. The aim of this study is to evaluate the altered mucoadhesive property of the probiotic https://www.selleckchem.com/products/pexidartinib-plx3397.html delivery system by coating it with mucoadhesive chitosan or thiolated chitosan, for prolonged retention in human colon. The results confirmed that cross-linking with calcium ions reduced the mucoadhesive property of alginate hydrogel, thus questioning the intrinsic mucoadhesiveness of uncoated systems. In contrast, chitosan and thiolated chitosan were found to be adsorbed on sub100 mu m Ca2+ alginate microcapsules, and substantially improved the mucoadhesion performance of the system. The
adhesion performance was correlated Captisol to the amount of mucoadhesive coating polymer adsorbed on the see more surface of the system. The coated system was demonstrated on HT29-MTX colonic epithelial monolayer to deliver markedly higher amount of probiotic bacteria to the in vitro model of colonic mucosa. Additionally, the coatings were also found to exert significantly stronger mucoadhesion to colonic mucosa tissue at slight acid neutral pH with less ambient water, which conforms to the physiological environment of the colon, thus supporting prolonged retention in this region.”
“Purpose of review
Recent identification of over 60 loci contributing
to the susceptibility of developing type 1 diabetes (T1D) provides a timely opportunity to assess what is currently known of the genetics of T1D, and what these discoveries may tell us about the disease itself.
The major findings will be discussed under five main themes: T1D risk gene identification, molecular mechanisms of susceptibility, shared genetic cause with other diseases, development of novel analytical methods, and understanding disease heterogeneity.
The plethora of T1D risk genes that have been identified risk overwhelming clinicians with lists of gene names and symbols that have little bearing on management, and provide a challenge for researchers to place the genetics of T1D in a more amenable clinical context.