FT-IR and DSC studies of poly(vinylidene chloride-co-acrylonitrile) complexed with LiBF4.

Poly(vinylidene chloride-co-acrylonitrile) (PVdC-co-AN) based solvent free electrolytes were prepared for different compositions of PVdC-co-AN and LiBF4 using solution casting technique. The ionic conductivity, thermal behavior, complexation and structure of polymer electrolytes have been investigated as a function of LiBF4 content at different weight ratios. DSC studies revealed that the glass transition temperature Tg decreases with the increase of salt concentration up to an optimum level. The change in the glass transition temperature (Tg) with respect to the LiBF4 concentration is reflected in the bulk resistance of the electrolytes and the sample containing 6 wt.% of LiBF4 exhibited minimum bulk resistance compared to other samples. FT-IR studies confirm the interaction of polymer and salt which is mainly between Li-cation and nitrogen atom of C≡N group. The crystalline phase of polymer host is completely changed on the addition of Li salt.

Biliary epithelial trefoil peptide expression is increased in biliary diseases.

AIMS: Maintenance of the cellular integrity of the biliary epithelium may involve the production of mucins and mucin-associated peptides. In the luminal gastrointestinal tract, mucins and the mucin-associated trefoil peptides (TFF) are integral to cytoprotection and cellular repair of the mucosa. METHODS AND RESULTS: Samples of normal and diseased human liver tissue were examined using histological and immunohistochemical techniques, for the expression of TFF and mucins. Bile ducts were classified as small, medium or large depending upon the number of biliary epithelial cells. TFF expression was demonstrated in biliary epithelial cells of both normal and diseased liver tissue. TFF expression was greatest in the large bile ducts. In normal liver tissue, expression of at least one TFF was demonstrated in 2-7% of small bile ducts, 5-31% of medium bile ducts and 31-85% of large bile ducts. Seventy-seven percent of large bile ducts secreted mucins and all three TFF concurrently, compared with 3% of medium bile ducts and no small bile ducts. Biliary disease resulted in an increased expression of TFF1 and TFF3 in the medium bile ducts. CONCLUSIONS: The biliary epithelial cells in normal and diseased human liver tissue express TFF, particularly in the larger bile ducts. TFF expression may be up-regulated or induced in biliary diseases as a response to injury, as is seen in epithelial damage elsewhere in the gastrointestinal tract.

Spatio-temporal expression of trefoil peptide following severe gastric ulceration in the rat implicates it in late-stage repair processes.

BACKGROUND: The trefoil peptide (TFF1) is a member of a family of mucin-associated regulatory peptides that are widely distributed in gastrointestinal tissues and have been implicated in the maintenance of the gastric mucosa. The role of TFF1 in gastric mucosal repair was examined by analysis of the spatio-temporal expression of TFF1 following gastric ulceration in the rat. METHODS: Gastric ulcers were induced in rats by application of glacial acetic acid to the serosa of the fundus. At various time points post injury (0-28 days), macroscopic and microscopic examination of the gastric mucosa was performed. In addition, the spatio-temporal expression of TFF1 protein and proliferating cell nuclear antigen were identified by immunohistochemistry, TFF1 message by in situ hybridization, and acidic/neutral secreting mucins by Alcian blue-periodic acid-Schiff staining. RESULTS: In normal rat gastric tissue, TFF1 peptide and mRNA were expressed in mucosal cells of the superficial epithelium. Trefoil peptide and mRNA were significantly induced between 4 and 28 days post ulceration, with expression extending beyond the superficial epithelium and being localized to acidic mucin-producing cells deep within the repairing mucosa. CONCLUSIONS: Spatio-temporal expression of TFF1 mRNA and peptide following macroscopic repair implicates TFF1 as a potential mediator of late stage-repair processes. Whether this is through direct stimulation of cellular differentiation or the enhancement of mucosal protective properties through an interaction with gastric mucins remains to be elucidated.