Our results suggest that application of ozonated water may be useful in reducing the number of C. albicans on denture plates.

The WNT family activates an oncogenic signaling mediated through beta-catenin and is up-regulated in a variety of malignant neoplasms. The signaling translocates beta-catenin into the nucleus and stimulates carcinoma cells in the epithelial-mesenchymal transition (EMT). However, WNT expression and signaling in oral carcinomas have not been examined. The present study focused on unveiling the involvement of WNTs in oral carcinomas, and showed that carcinoma cells express 11 of 19 WNT family members by reverse-transcription/PCR. WNT-expressing carcinoma cells exhibited increased beta-catenin levels in the cytoplasmic pool and translocation to the nucleus. The activation state of signaling correlated with the expression of membrane-type 1 matrix metalloproteinase, which degrades territorial matrices in carcinoma invasion. Immunohistochemistry disclosed that WNT3 expression and nuclear localization of beta-catenin were predominant in carcinoma cells at the invasive front. These results suggest that enhanced WNT expression and signaling accelerate the progression of carcinomas via activating EMTs and local invasiveness.

Over the past few decades, the prevalence of overweight and obesity has increased markedly worldwide, along with the adoption of westernized lifestyles characterized by excessive energy intake and a lack of physical activity. Consequently, obesity and a cluster of obesity-related comorbidities often referred to as the metabolic syndrome have become a serious public health problem and a major risk factor for the development of severe diseases such as cardiovascular disease. 1) Obesity is strongly associated with insulin resistance, in which elevation of circulating fatty acids results in increased fatty acid availability that exceeds the fat disposal capacity of cells, which decreases insulin-stimulated glucose oxidation in muscles and subsequently leads to contractile dysfunction of the heart. 2) The precise mechanisms underlying these "lipotoxic" consequences remain incompletely defined, but it is currently accepted that excessive fatty acid uptake into cells leads to the accumulation of proinflammatory lipid metabolites such as fatty acyl-CoA, diacylglycerol and ceramide. These metabolites stimulate stress-activated kinases, which interfere with insulin signaling. 2,3) It is also becoming clear that fatty acid beta-oxidation is increased in the insulin-resistant heart and oxidative skeletal muscle, and that mitochondrial overload and incomplete oxidation of fatty acids contribute to the impairment of insulin sensitivity. 2,4) Under these conditions, enhanced beta-oxidation, which is not accompanied by appropriate upregulation of the tricarboxylic acid (TCA) cycle or electron transport chain (ETC) activity, fails to oxidize fatty acids completely to CO 2 and deposits incomplete fat catabolites along with diminished levels of TCA cycle intermediates. These stressful environments created within mitochondria are thought to exacerbate cellular insulin resistance by enhanced oxidative stress, for example. 4) However, acyl-CoA thioesterase (ACOT) exists within the mitochondrial matrix of mammalian cells 5) and its expression is expected to be upregulated in response to fatty acid overload, as demonstrated in diabetic and fasted animals. 6,7) ACOT comprises a group of enzymes that are localized in multiple compartments in cells and catalyze the hydrolysis of long-chain acyl-CoA thioesters to free fatty acids and CoA-SH. For example, ACOT1 (formerly known as CTE-I or ACH2) and ACOT7a (CTE-II, BACH or ACT) are localized in the cytosol while ACOT2 (MTE-I or ARTISt) and ACOT7b (MTE-II or LACH1) are present in mitochondria. [8][9][10] These catalytic properties of ACOT mean that it is capable of lowering the increased levels of acyl-CoA imported by carnitine palmitoyltransferase (CPT) across the mitochondrial membranes from the cytosol. Accordingly, ACOT could counteract the enhanced beta-oxidation and reduce the mitochondrial stress caused by the imbalance between beta-oxidation and TCA cycle/ETC activity during fatty acid overload. Moreover, the ACOT isoforms present in the cytosol could scavenge surplus acyl-CoA to prev...

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