P47 Creation of longer-lasting (substantive) oral care flavours

Mainstream oral care flavours are primarily designed to provide hedonic (taste) benefits and to promote breath freshness. In particular, a key criterion for a commercially successful toothpaste flavour is a long lasting reduction in the perception of mouth odour. Various additives can help deliver this benefit, in addition to flavours formulated according to patented guidelines. The residence time (substantivity) in the mouth of flavours and additives is clearly critical with respect to the longevity of the breath-freshening benefit, and little data are available in the literature to guide the selection of substantive components. The aim of this project was to investigate the dynamics of flavour loss from the buccal cavity following brushing using a mass spectrometer equipped with an atmospheric pressure headspace sampler which enabled real-time determination of flavour components in mouth air. A number of flavour ingredients found in peppermint- and spearmint-based oral care flavours were studied. The in vivo decay kinetics of flavour ingredient loss were quantified and found to be strongly related to the physicochemical properties of ingredients, except in the case of esters where a more complex dependence was observed arising from chemical transformation occurring in addition to physical transportation away from the mouth. Surprisingly, some materials were discovered to undergo rapid degradation with a half-life of minutes. Confirmatory studies of the decay kinetics of such materials were carried out in vitro, and structural features were identified which were associated with the observed hydrolytic vulnerability. This work has allowed the development of new guidelines to enable the creation of longer-lasting oral care flavours.     

体外培养脂肪组织来源干细胞与胶原/壳聚糖复合支架的亲和性

目的：制备适合脂肪组织来源的干细胞生长的支架,观察复合支架各组成的体积比率与细胞培养的亲和性. 方法：实验于2006-09/2007-01在大连理工大学干细胞与组织工程研发中心完成.①实验方法：将3.55 g/L Ⅰ型胶原和20 g/L壳聚糖分别以9∶1,7∶3,5∶5,3∶7,1∶9的体积比混合冻干,碳化二亚胺/N-羟基琥珀酰亚胺交联后再次冻干并进行分析.②实验评估：扫描电镜观察不同材料交联前后的微观结构;IPP软件分析计算支架的平均孔径;测量支架的吸水性和孔隙率;通过胶原酶检测支架的体外生物可降解性;扫描电镜和苏木精-伊红染色观察脂肪组织来源的干细胞在复合支架上的生长情况. 结果：①交联前后的微观结构：冻干后的各种支架材料呈白色,表面粗糙,材料内部呈海绵状多孔隙结构,其中以胶原/壳聚糖体积比为9∶1的复合支架最为疏松,1∶9的支架最致密.扫描电镜下支架的胶原含量越高,支架内的胶原丝越多,支架的孔与孔之间相互连通构成了通孔.交联前后支架的形态结构无明显改变.②支架的平均孔径∶交联后体积比为9∶1,7∶3和5∶5的复合支架孔径50～200 μm,可用于细胞的三维培养.③支架的吸水性和孔隙率∶体积比为5∶5的复合支架的吸水性和含水量最高,而7∶3次之;多孔支架在水中未发生明显的溶胀现象;支架的孔隙率均在90%以上.④支架的体外生物可降解性：未交联的支架随着胶原含量的减少,支架的降解速率增加.而交联后随着胶原含量的减少,降解速率减慢,交联后的复合支架降解速度较未交联慢.⑤脂肪组织来源的干细胞在复合支架上的生长情况：脂肪组织来源的干细胞在支架上培养5 d后扫描电镜观察细胞在7∶3的支架上爬行生长并融合成片,苏木精-伊红染色观察支架孔内及表面出现大量的细胞团,并融合成片状,而5∶5支架上黏附生长的细胞较少. 结论：结合支架的孔径、吸水性、孔隙率、体外生物可降解性和细胞与支架的生物相容性,可知体积比为7∶3的复合支架对脂肪组织来源的干细胞的亲和性较好,适于脂肪组织来源的干细胞的三维培养.     

Shunting normal pressure hydrocephalus: the predictive value of combined clinical and CT data.

The value of an ordinal global scale derived from combined clinical and CT data (clin/CT scale) to predict the clinical outcome in 112 patients shunted for presumed normal pressure hydrocephalus (NPH) was analysed. The clinical data were retrospectively collected, all CT scans were re-evaluated, and the clin/CT scale was determined blind to the results of further ancillary tests and to the post-surgical outcome. The scale ranked three classes of prediction: on the basis of clinical and CT characteristics, improvement after shunting was probable, possible, or improbable. The predictive value of the clin/CT scale for the subgroup of communicating NPH was established for two different strategies, depending on the strictness of selection criteria for shunting. In the subgroup of patients with presumed communicating NPH, the prevalence of shunt responsiveness was 29%; the best strategy was to shunt only patients with probable shunt-responsive NPH: the sensitivity was 0.54, the specificity 0.84, and the predictive accuracy 0.75, with a limited number of ineffective shunts (11%) and missed improvements (13%). The study illustrates its need to assess the pre-test probability of NPH based on combined clinical and CT data, before establishing the clinical usefulness of an ancillary test.     

Duodenal mucosal histology and histochemistry in active, treated and healed duodenal ulcer: Correlation with duodenal prostaglandin E2 production

We investigated whether impaired duodenal mucosal prostaglandin E₂ (PGE₂) production previously observed in duodenal ulcer (DU) was a primary pathophysiological abnormality or secondary to mucosal architectural changes that accompany ulceration. One hundred patients were studied: at endoscopy, paired duodenal biopsies were taken in patients with normal endoscopies and from the ulcer edge or scar and background mucosa in active or healed DU. One of the pair of biopsies was used to estimate PGE₂ synthesis ability, the other was processed for histology and histochemistry. The following features graded: goblet cell numbers and staining with Periodic acid-Schiff reagent (PAS), epithelial staining with PAS, villous atrophy, columnar cell height, inflammatory cell infiltrate and micro-erosions and gastric metaplasia taken as a whole. Patients were found to have normal endoscopy (n= 31), active untreated DU (n= 20), active DU on treatment with either cimetidine or ranitidine (n= 13), healed DU on maintenance treatment (n= 27) and healed DU off treatment (n= 9). Active duodenal ulceration was found to be associated with decreased numbers of goblet cells, loss and blunting of villi, increased columnar cell height, increased epithelial cell PAS staining and with gastric metaplasia. After healing, only villous blunting remained. These changes were present, but less marked, at sites removed from the ulcer and were not apparent in the patient groups with healed ulcers. A strong correlation between overall gastric metaplasia and epithelial cell PAS staining and the reduced ability to synthesize PGE₂ (P < 0.001) was only apparent when biopsies from all patients were grouped together, but not within individual patient subgroups. There was no consistent correlation between PGE₂ generation and individual parameters of pathological change in the duodenum. We conclude that, although inflammatory and mucosal changes may contribute, the evidence suggests that the impaired PGE₂ generation in DU disease is, to a large extent, independent of histological and histochemical features.