Helicobacter pylori Infection and Halitosis – Evidence, Hypothesis, and Korean Red Ginseng to Mitigate Its Effect

Halitosis is a common and ignored condition, but in some, it is a disease-associated health problem, suggestive of overt disease conditions and hasaffected about 25–30% of world’s population, bothering nonmedical social disturbance in many people. Although two kinds, pseudohalitosis and halitophobia, are also concerned, genuine halitosis originated from the oral cavity, such as gingivitis, caries, and poor oral hygiene, in 80% and the remaining 20% are extraoral sources of halitosis, which should not be ignored because of stigmata suggestive of overt tissue dysfunctions, for instance, poor nutrition and hygiene, alcohol abuse, smoking, and systemic illness such as chronic obstructive pulmonary disease, liver cirrhosis, diabetes mellitus, and chronic renal diseases. In this chapter, Helicobacter pylori (H. pylori)–associated halitosis as one of the extragastric manifestations is introduced. Since diagnostics of halitosis includes subjective methods (examiner’s sense of smell) and objective methods (instrumental analysis), under the hypothesis of a possible relationship between H. pylori infection and objective halitosis, the real levels of volatile sulfur compounds (VSCs) in the breath showed significant correlation between VSC levels and the degree of H. pylori–associated erosive gastritis as well as gastric cancer. These findings are further validated through either measuring H2S level in gastric juices of H. pylori–infected gastritis or checking the expressions of cystathionine-γ-lyase (CSE) and cystathionine-β-synthase (CBS) responsible for H2S generation in biopsied stomach. The eradication of H. pylori significantly ameliorated halitosis, accompanied with significant reductions in gastric H2S levels (p<0.01). Korean red ginseng was very effective in either reducing H. pylori–associated H2S or alleviating halitosis in patients with H. pylori–associated chronic atrophic gastritis. Conclusively, H. pylori infection demonstrates to have an important relationship with the development of halitosis, and its eradication could possibly promote the improvement of this condition

Hydrated copper and gold monovalent cations: Ab initio study

To understand the hydration phenomena of noble transition metals, we investigated the structures, hydration energies, electronic properties, and spectra of the Cu+(H3O)(1-6) and Au+ (H2O)(1-6) clusters using ab initio calculations. The coordination numbers of these clusters are found to be only two, which is highly contrasted to those of Ag+ (H2O)(n) (which have the coordination numbers of 3-4) as well as the hydrated alkali metal ions (which have the coordination numbers of similar to6). For the possible identification of their interesting hydration structures, we predict their IR spectra for the OH stretch modes. (C) 2005 American Institute of Physics.open384

Resistin enhances the expansion of regulatory T cells through modulation of dendritic cells

<p>Abstract</p> <p>Background</p> <p>Resistin, a member of adipokine family, is known to be involved in the modulation of immune responses including inflammatory activity. Interestingly, resistin is secreted by adipocytes in mice and rats whereas it is secreted by leukocytes in humans. However, the mechanism behind the effect of resistin on the expansion of regulatory T cells (Tregs) remains poorly understood. Therefore, we examined regulatory effect of resistin on the induction and cellular modification of Tregs.</p> <p>Results</p> <p>Both protein and mRNA expression of <it>FoxP3</it>, a representative marker of Tregs, increased in a dose-dependent manner when peripheral blood mononuclear cells were treated with resistin. At the same time, resistin had no direct effect on the induction of <it>FoxP3 </it>in CD4⁺T cells, suggesting an indirect role through other cells type(s). Since DCs are an important player in the differentiation of T cells, we focused on the role of DCs in the modulation of Tregs by resistin. Resistin suppressed the expression of interferon regulatory factor (IRF)-1 and its target cytokines, IL-6, IL-23p19 and IL-12p40, in DCs. Furthermore, <it>FoxP3 </it>expression is increased in CD4⁺T cells when co-cultured with DCs and concomitantly treated with resistin.</p> <p>Conclusion</p> <p>Our results suggest that resistin induces expansion of functional Tregs only when co-cultured with DCs.</p

The C-terminal region of Bfl-1 sensitizes non-small cell lung cancer to gemcitabine-induced apoptosis by suppressing NF-κB activity and down-regulating Bfl-1

Gemcitabine is used to treat several cancers including lung cancer. However, tumor cells often escape gemcitabine-induced cell death via various mechanisms, which include modulating bcl-2 family members and NF-κB activation. We previously reported that the C-terminal region of Bfl-1 fused with GFP (BC) is sufficient to induce apoptosis in 293T cells. In the present study, we investigated the anti-tumor effect of combined BC gene therapy and gemcitabine chemotherapy in vitro and in vivo using non-small cell lung cancer cell lines and a xenograft model. Cell lines were resistant to low dose gemcitabine (4-40 ng/ml), which induced NF-κB activation and concomitant up-regulation of Bfl-1 (an NF-κB-regulated anti-apoptotic protein). BC induced the apoptosis of A549 and H157 cells with caspase-3 activation. Furthermore, co-treatment with BC and low dose gemcitabine synergistically and efficiently induced mitochondria-mediated apoptosis in these cells. When administered alone or with low dose gemcitabine, BC suppressed NF-κB activity, inhibited the nuclear translocation of p65/relA, and down-regulated Bfl-1 expression. Furthermore, direct suppression of Bfl-1 by RNA interference sensitized cells to gemcitabine-induced cell death, suggesting that Bfl-1 importantly regulates lung cancer cell sensitivity to gemcitabine. BC and gemcitabine co-treatment also showed a strong anti-tumor effect in a nude mouse/A549 xenograft model. These results suggest that lung cancer cells become resistant to gemcitabine via NF-κB activation and the subsequent overexpression of Bfl-1, and that BC, which has both pro-apoptotic and NF-κB inhibitory effects, could be harnessed as a gene therapy to complement gemcitabine chemotherapy in non-small cell lung cancer

Lung Metastasis from an Immature Teratoma of the Nasal Cavity Masquerading as Small Cell Carcinoma of the Lung

We report a case of small cell lung cancer that turned out to be a metastatic teratoma from the nasal cavity rather than a new primary cancer. A 54-year-old woman was diagnosed with an immature teratoma of the nasal cavity with a predominant neuroblastomatous component. Small cell lung cancer was detected by bronchoscopic biopsy 21 months later, and it was treated with concurrent radiochemotherapy as if it had been a new primary cancer. Since a recurrent tumor containing fat-like density grew slowly on the serial chest CT scans after achieving complete response, we reached the conclusion that the small undifferentiated cells could be metastatic neuroblastomatous components from the immature teratoma of the nasal cavity