Taste hyposensitivity in Japanese schoolchildren

BACKGROUND: There is some research on taste disorder/hyposensitivity in special groups such as the elderly or patients presenting with specific taste problems, however few studies have been conducted among young populations. The objectives of this study were to estimate the prevalence of taste hyposensitivity and to investigate the relationship between taste hyposensitivity and oral health status in Japanese schoolchildren. METHODS: Subjects were 237 primary and 112 junior high school students in Saitama Prefecture, Japan. In total, 349 (boys: 181, girls: 168) students aged 6–15 years participated in the study. Oral examinations and whole-mouth taste tests using four tastes (sweet, salt, sour and bitter) solutions were conducted on the subjects. A subject who could not recognize the taste of the solution was defined as demonstrating hyposensitivity. RESULTS: Hyposensitivity was observed in 6.3% of all subjects for sweet-taste, 14.3% for salt-taste, 20.9% for sour-taste and 6.0% for bitter-taste. The prevalence of sweet, sour and bitter-taste hyposensitivity decreased as the subjects’ grade advanced. In contrast, the prevalence of salt-taste hyposensitivity increased in 7(th)-9(th) grade subjects. Furthermore, the prevalence of bitter-taste hyposensitivity was significantly higher in males than females among 1(st)-3(rd) graders. Taste hyposensitivity had little association with oral health status, such as decayed teeth, filled teeth, dental plaque, gingival status and tongue coating. CONCLUSIONS: In this study, taste hyposensitivity was observed in 6.0%-20.9% of the students. There was little association between taste hyposensitivity and oral health status. The current study implies that the factors affecting the taste hyposensitivity in children may different from those in the elderly. Therefore it is necessary to further investigate the causes of taste hyposensitivity among younger generation

Social anxiety disorder in genuine halitosis patients

<p>Abstract</p> <p>Background</p> <p>There is a possibility that genuine halitosis patients' anxiety do not recover after oral malodor treatment due to their social anxiety disorder. The objective of this study was to investigate the influence of social anxiety disorder on the level of anxiety in genuine halitosis patients before and after treatment for oral malodor.</p> <p>Methods</p> <p>The subjects were 262 genuine halitosis patients who visited the Fresh Breath Clinic from March, 2008 to October, 2009. The subjects who had score 2 or higher by the organoleptic test were diagnosed as genuine halitosis patients. Gas chromatography (GC) was conducted before and after oral malodor treatment for the oral malodor measurement. Based on their risk of social anxiety disorder, subjects were divided into low- and high-risk groups using the Liebowitz Social Anxiety Scale (LSAS). The questions related to oral malodor and the clinical oral examination were both conducted before oral malodor treatment. The level of anxiety before and after oral malodor treatment was evaluated using the Visual Analogue Scale of Anxiety (VAAS).</p> <p>Results</p> <p>More than 20% of subjects had a score of 60 or more on the LSAS (high LSAS group). The mean age and the percentage of females were significantly higher in the high LSAS group compared to the low LSAS group. The high LSAS group was more likely to have problems associated with oral malodor and to adopt measures against oral malodor compared to the low LSAS group. The mean concentrations of H₂S and CH₃SH by GC significantly decreased after the oral malodor treatment in both LSAS groups. VAAS scores also significantly decreased after treatment in both LSAS groups. The logistic regression analysis indicated that the high LSAS group had a 2.28 times higher risk of having a post-VAAS score of 50 or more compared to the low LSAS group.</p> <p>Conclusions</p> <p>This study revealed that genuine halitosis patients with a strong trait of social anxiety disorder have difficulty overcoming their anxiety about oral malodor. Oral malodor treatment of genuine halitosis patients requires not only regular oral malodor treatment but also attention to social anxiety disorder.</p

The integrin-binding defective FGF2 mutants potently suppress FGF2 signalling and angiogenesis.

We recently found that integrin αvβ3 binds to fibroblast growth factor (FGF)-αvβ31 (FGF1), and that the integrin-binding defective FGF1 mutant (Arg-50 to glutamic acid, R50E) is defective in signalling and antagonistic to FGF1 signalling. R50E suppressed angiogenesis and tumour growth, suggesting that R50E has potential as a therapeutic. However, FGF1 is unstable, and we had to express R50E in cancer cells for xenograft study, since injected R50E may rapidly disappear from circulation. We studied if we can develop antagonist of more stable FGF2. FGF2 is widely involved in important biological processes such as stem cell proliferation and angiogenesis. Previous studies found that FGF2 bound to αvβ3 and antagonists to αvβ3 suppressed FGF2-induced angiogenesis. However, it is unclear how FGF2 interacts with integrins. Here, we describe that substituting Lys-119/Arg-120 and Lys-125 residues in the predicted integrin-binding interface of FGF2 to glutamic acid (the K119E/R120E and K125E mutations) effectively reduced integrin binding to FGF2. These FGF2 mutants were defective in signalling functions (ERK1/2 activation and DNA synthesis) in NIH3T3 cells. Notably they suppressed, FGF2 signalling induced by WT FGF2 in endothelial cells, suggesting that the FGF2 mutants are antagonists. The FGF2 mutants effectively suppressed tube formation in vitro, sprouting in aorta ring assays ex vivo and angiogenesis in vivo The positions of amino acids critical for integrin binding are different between FGF1 and FGF2, suggesting that they do not interact with integrins in the same manner. The newly developed FGF2 mutants have potential as anti-angiogenic agents and useful tools for studying the role of integrins in FGF2 signalling

A dominant-negative FGF1 mutant (the R50E mutant) suppresses tumorigenesis and angiogenesis.

Fibroblast growth factor-1 (FGF1) and FGF2 play a critical role in angiogenesis, a formation of new blood vessels from existing blood vessels. Integrins are critically involved in FGF signaling through crosstalk. We previously reported that FGF1 directly binds to integrin αvβ3 and induces FGF receptor-1 (FGFR1)-FGF1-integrin αvβ3 ternary complex. We previously generated an integrin binding defective FGF1 mutant (Arg-50 to Glu, R50E). R50E is defective in inducing ternary complex formation, cell proliferation, and cell migration, and suppresses FGF signaling induced by WT FGF1 (a dominant-negative effect) in vitro. These findings suggest that FGFR and αvβ3 crosstalk through direct integrin binding to FGF, and that R50E acts as an antagonist to FGFR. We studied if R50E suppresses tumorigenesis and angiogenesis. Here we describe that R50E suppressed tumor growth in vivo while WT FGF1 enhanced it using cancer cells that stably express WT FGF1 or R50E. Since R50E did not affect proliferation of cancer cells in vitro, we hypothesized that R50E suppressed tumorigenesis indirectly through suppressing angiogenesis. We thus studied the effect of R50E on angiogenesis in several angiogenesis models. We found that excess R50E suppressed FGF1-induced migration and tube formation of endothelial cells, FGF1-induced angiogenesis in matrigel plug assays, and the outgrowth of cells in aorta ring assays. Excess R50E suppressed FGF1-induced angiogenesis in chick embryo chorioallantoic membrane (CAM) assays. Interestingly, excess R50E suppressed FGF2-induced angiogenesis in CAM assays as well, suggesting that R50E may uniquely suppress signaling from other members of the FGF family. Taken together, our results suggest that R50E suppresses angiogenesis induced by FGF1 or FGF2, and thereby indirectly suppresses tumorigenesis, in addition to its possible direct effect on tumor cell proliferation in vivo. We propose that R50E has potential as an anti-cancer and anti-angiogenesis therapeutic agent ("FGF1 decoy")

Feeding the outer bran fraction of rice alters hepatic carbohydrate metabolism in rats

Dietary intake of fiber-rich food has been reported to contribute to multiple health benefits. The aim of the current study is to investigate the effects of a diet containing the outer bran fraction of rice (OBFR), which is rich in insoluble fiber, on the intestinal environment and metabolite profiles of rats. Fourteen 8-week-old male Sprague–Dawley rats were divided into a control group and an OBFR group. For a period of 21 days, the control group was fed a control diet, while the OBFR group was fed a diet containing 5% OBFR. Metabolomics analysis revealed drastic changes in the cecal metabolites of the rats fed the OBFR diet. Furthermore, in the plasma and liver tissue, the concentrations of metabolites involved in pyruvate metabolism, the pentose phosphate pathway, gluconeogenesis, or valine, leucine, isoleucine degradation were changed. Concordantly, the OBFR diet increased the expression of genes encoding enzymes involved in these metabolic pathways in the livers of the rats. Collectively, these results suggest that the OBFR diet altered the concentrations of metabolites in the cecal contents, plasma, and liver, and the hepatic gene expressions of rats, and that this may have mainly contributed to carbohydrate metabolism in the liver

Cultivated Grapevines Represent a Symptomless Reservoir for the Transmission of Hop Stunt Viroid to Hop Crops: 15 Years of Evolutionary Analysis

Hop stunt was a mysterious disorder that first emerged in the 1940s in commercial hops in Japan. To investigate the origin of this disorder, we infected hops with natural Hop stunt viroid (HpSVd) isolates derived from four host species (hop, grapevine, plum and citrus), which except for hop represent possible sources of the ancestral viroid. These plants were maintained for 15 years, then analyzed the HpSVd variants present. Here we show that the variant originally found in cultivated grapevines gave rise to various combinations of mutations at positions 25, 26, 54, 193, and 281. However, upon prolonged infection, these variants underwent convergent evolution resulting in a limited number of adapted mutants. Some of them showed nucleotide sequences identical to those currently responsible for hop stunt epidemics in commercial hops in Japan, China, and the United States. Therefore, these results indicate that we have successfully reproduced the original process by which a natural HpSVd variant naturally introduced into cultivated hops was able to mutate into the HpSVd variants that are currently present in commercial hops. Furthermore, and importantly, we have identified cultivated grapevines as a symptomless reservoir in which HSVd can evolve and be transmitted to hop crops to cause epidemics