Evaluation of wiping edible sesame oils in the oral cavities of hospitalised older patients who resist oral hygiene management.

Context: One of the causes of aspiration pneumonia is poor oral hygiene. We need care methods that caregivers can quickly, safely and inexpensively implement for convalescents with inadequate self-care. Edible sesame oil containing sesamin or sesaminol has already been shown to inhibit bacterial and fungal growth and have a vasodilating effect. Aims: The aim of this study is to evaluate the usefulness of using edible sesame oils for oral hygiene management. Settings and Design: This study evaluates an oral hygiene management method using two types of sesame oils in elderly hospitalised patients resistant to oral hygiene management. Methods and Material: The inpatients received oral care for 90 days. In the intervention groups, nurses brushed and wiped the oral cavity with roasted sesame oil (RSO) or sesame salad oil, while in the control group, care with tap water alone and brushing were done. Bacteria and Candida counts from tongue swabs, water content from the tongue's surface and cheek mucosa, oral health assessment tool (OHAT) and cytology of the cheek mucosa were assessed every 30 days before and after the intervention. Results: RSO showed a tendency to reduce the number of bacteria and Candida. There was an improvement in the OHAT scores with both oils. The water content or cytology was not changing. Conclusions: Sesame oils may improve oral hygiene and maintain health in older patients.

Effect of edible sesame oil on growth of clinical isolates of Candida albicans.

Elderly individuals are at increased risk of oral thrush (oral candidiasis) due to decreased saliva secretion. Due to their antimicrobial properties, edible oils can be effective natural agents for oral care. The objective of the present study was to compare the effects of sesame oil, which is widely used for cooking in Asian countries, and two other edible oils on the growth of both mycelial and yeast forms of five clinical isolates of Candida albicans, a causative microorganism of oral thrush. We assessed the effect of each oil in concentrations of 0.078%, 0.156%, and 0.313% on growth of the mycelial forms of the clinical isolates over 24 hr using the crystal violet method. We also evaluated the effect of each oil on growth of the yeast forms by counting the number of viable yeast cells after culturing in the oils for 24 hr. Sesame oil inhibited the growth of both mycelial and yeast forms. Safflower and olive oil also inhibited the growth of both forms of C. albicans but to a lesser extent than sesame oil. The ability to inhibit the growth of the mycelial form correlated with sesame oil concentration. Roasting influenced growth inhibition ability and high-roasted sesame oil most effectively inhibited the yeast form. The growth inhibitory effect differed among the five isolates. We hypothesize that the sesamin and fatty acid components of sesame oil are involved in its antifungal activity.

Two genomic regions of chromosomes 1 and 18 explain most of the stroke susceptibility under salt loading in stroke-prone spontaneously hypertensive rat/Izm.

To clarify the genetic mechanisms of stroke susceptibility in the stroke-prone spontaneously hypertensive rat (SHRSP), a quantitative trait locus (QTL) analysis was performed. Using 295 F2 rats of a cross between SHRSP/Izm and SHR/Izm, 2 major QTLs for stroke latency under salt loading were identified on chromosomes (chr) 1 and 18. Evaluation of 6 reciprocal single and double congenic rats for these QTLs showed that substitution of the SHRSP for the SHR fragment at the chr 1 and 18 QTLs increased the relative risk for stroke by 8.4 and 5.0, respectively. The combined effect of the 2 QTLs was 10× greater than that of the background genome (by Cox hazard model). Blood pressure monitoring by radio telemetry indicated that the combination of the 2 QTLs had a clear effect on the salt-dependent blood pressure increase, suggesting an important role for the salt-sensitive blood pressure increase in the susceptibility of SHRSP to stroke. A haplotype analysis of 11 substrains of SHRSP and SHR using 340 simple sequence repeat markers in the chr 1 QTL suggested that the 7-Mbp fragment between D1Rat260 and D1Rat178 was most likely to harbor the responsible gene(s), which was confirmed by a study of additional subcongenic strains. This study indicated a major role for 2 QTLs on chr 1 and 18 in stroke susceptibility in SHRSP under salt loading. The salt-sensitive blood pressure increase was implied to play a key role in the stroke susceptibility.

Chronic allergy to dietary ovalbumin induces lymphocyte migration to rat small intestinal mucosa that is inhibited by MAdCAM-1.

Few models have described a chronic food allergy with morphological changes in the intestinal mucosa. Here we established an ovalbumin (OVA)-induced, cell-mediated, allergic rat model and examined lymphocyte migration in the gut. Brown Norway rats were intraperitoneally sensitized to OVA and then given 10 mg OVA/day by gastric intubation for 6 wk. Lymphocyte subsets and adhesion molecules were examined immunohistochemically, and the migration of T lymphocytes to microvessels of Peyer's patches and villus mucosa was observed by using an intravital microscope. Serum OVA-specific IgG and IgE levels were increased in animals repeatedly exposed to OVA. Significant villus atrophy and increased crypt depth was accompanied by increased infiltration of T lymphocytes in the small intestinal mucosa of the group given OVA. Expression of rat mast cell protease II and of mucosal addressin cell adhesion molecule-1 (MAdCAM-1) was also increased in these groups. The administration of anti-MAdCAM-1 antibody significantly attenuated the OVA-induced changes in the mucosal architecture and in CD4 T lymphocyte infiltration. Intravital observation demonstrated that in rats with a chronic allergy, T lymphocytes significantly accumulated in villus microvessels as well as in Peyer's patches via a MAdCAM-1-dependent process. Our model of chronic food allergy revealed that lymphocyte migration was increased with MAdCAM-1 upregulation.

Alteration of intestinal intraepithelial lymphocytes and increased bacterial translocation in a murine model of cirrhosis.

Alterations in immunological defense in the gut may lead to the bacterial infection that is frequently associated with cirrhosis of the liver. The aim of this study was to investigate the changes in distribution and function of intestinal intraepithelial lymphocytes (IELs) in relation to intestinal barrier dysfunction in experimental cirrhosis. Cirrhosis was induced in mice by treatment with carbon tetrachloride (CCl4) intraperitoneally with 5% alcohol in drinking water for 12 weeks. Bacterial translocation was assessed in mesenteric lymph nodes (MLNs) by the transport of fluorescence-labeled latex beads and by bacteriological cultures. The lymphocyte subpopulation was compared in three groups (cirrhosis, alcohol alone and controls). IFN-gamma production from isolated IELs was determined by ELISA after stimulation with anti-CD3 or IL-12/IL-18. The total number of IELs significantly increased in the cirrhosis and alcohol groups. There was a preferential increase in TCRgammadelta+CD8+ population in the alcohol group, but no change in cirrhosis. Bacterial translocation was negative in the control group, and a small number was noted in the alcohol group, whereas it was significantly noted in the cirrhosis group. Although the number of IEL was significantly increased in the cirrhosis group, their proliferative response was decreased, and IFN-gamma production from each IEL was markedly diminished in either stimulation by anti-CD3 or IL-12/IL-18. These changes were more remarkable in the cirrhosis group than in the alcohol group. In conclusion, bacterial translocation due to intestinal barrier dysfunction in cirrhosis may be closely correlated with the alteration of the immune function in IELs.

Significant role of ceramide pathway in experimental gastric ulcer formation in rats.

Ceramides have emerged as key participants in the signaling pathway of cytokines and apoptosis. We previously revealed that phorbol 12-myristate 13-acetate (PMA) induced experimental ulcers in rat gastric mucosa. In this study, we investigated the role of ceramide in ulcer formation and its relation to the activation of transcription factors and apoptosis. PMA was subserosally injected to rat glandular stomach. Fumonisin B1 (FB1), an inhibitor of ceramide synthase, was administered together with the PMA. The time course of ceramide content was quantified using thin layer chromatography and the number of apoptotic cells was determined by immunohistochemistry. The activation of transcription factor nuclear factor-kappaB (NF-kappaB) or activator protein-1 (AP-1) was evaluated using an electrophoretic mobility shift assay. The administration of FB1 attenuated PMA-induced gastric ulcer formation in a dose-dependent manner. Before the ulcers became obvious, the ceramide content (C18 and C24 ceramide) increased significantly in the gastric wall. The activation of NF-kappaB and AP-1 and an increase in the number of apoptotic cells were also observed. Both of these were significantly inhibited by the coadministration of FB1. However, NF-kappaB inhibitors attenuated gastric ulcer formation without affecting the ceramide content or the number of apoptotic cells. Ceramide formation in the stomach significantly contributes to PMA-induced tissue damage, possibly via the activation of transcription factors and an increase in apoptosis in the gastric mucosa. However, after the increase in ceramide levels, the NF-kappaB and apoptosis pathways may be separately involved in ulcer formation.