• Journal of Oral Medicine and Pain
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• v.21 no.2
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• pp.351-367
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• 1996

In the field Of individual identification in forensic Science, if the body is charred, it is sometimes impossible to identify the morphologic changes and charred tissue such as blood, muscle and bone can not be identified by forensic microbiologic method such as DNA typing. So the author used the characteristics of teeth which is relatively firm compare to other organs and stable to external environment such as heat and also possess cells needed for the DNA typing. The author conducted the experiment on teeth to detect DNA related to individual identification regarding to temperature in which other charredorgans can not be detected. The experiment was done on 64 extracted third molars consisted of unheated ones, and heated teeth to $100^{\circ}C$, $150^{\circ}C$, $200^{\circ}C$ for 45 min, 90 min, and 120 min respectively and to $250^{\circ}C$ for 45 min. DNA was extracted from each tooth and amplified fragment length polymorphism procedure(AMP-FLPs) using polymerase chain reaction(PCR) was applied and observed for the matching DNA in HumTH01 and HumCD4 locus and the followings Are the results : 1. It was able to detect matching DNA in HumTH01 and HumCD4 locus in every teeth which no heating has been done. 2. It was able to detect matching DNA in HumTH01 and HumCD4 locus in every teeth heated to $100^{\circ}C$ for 45, 90 and 120 min. 3. It was able to detect matching DNA in HumTH01 and HumCD4 locus in teeth heated to $l00^{\circ}C$, $200^{\circ}C$ for 45, 90, 120 min. 4. It was impossible to detect matching DNA in HumTH01 and HumCD4 locus in teeth heated to $250^{\circ}C$. So, it is possible to extract DNA from teeth that otherwise can not be extracted from other organs in the charred body and it can be concluded that teeth are highly reliable and applicatable as forensic odontology for individual identification.

• Journal of Microbiology and Biotechnology
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• v.28 no.1
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• pp.65-76
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• 2018

Although there has been a steady increase in the prevalence of food allergies worldwide in recent decades, no effective therapeutic strategies have been developed. Modulation of the gut microbiota composition and/or function through probiotics has been highlighted as a promising target for protection against food allergies. In this study, we aimed to investigate the allergy-reducing effects of a probiotic mixture (P5: Lactococcus lactis KF140, Pediococcus pentosaceus KF159, Lactobacillus pentosus KF340, Lactobacillus paracasei 698, and Bacillus amyloliquefaciens 26N) in mice with ovalbumin (OVA)-induced food allergy. Administration of P5 significantly suppressed the oral OVA challenge-induced anaphylactic response and rectal temperature decline, and reduced diarrhea symptoms. Moreover, P5 also significantly inhibited the secretion of IgE, Th2 cytokines (interleukin (IL)-4, IL-5, IL-10, and IL-13), and Th17 cytokines (IL-17), which were increased in mice with OVA-induced food allergy, and induced generation of CD4+Foxp3+ regulatory T cells. These results revealed that P5 may have applications as a preventive agent against food allergy.

• BMB Reports
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• v.46 no.12
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• pp.594-599
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• 2013

The anti-inflammatory activity of eriodictyol and its mode of action were investigated. Eriodictyol suppressed tumor necrosis factor (mTNF)-${\alpha}$, inducible nitric oxide synthase (miNOS), interleukin (mIL)-6, macrophage inflammatory protein (mMIP)-1, and mMIP-2 cytokine release in LPS-stimulated macrophages. We found that the anti-inflammatory cascade of eriodictyol is mediated through the Toll-like Receptor (TLR)4/CD14, p38 mitogen-activated protein kinases (MAPK), extracellular-signal-regulated kinase (ERK), Jun-N terminal kinase (JNK), and cyclooxygenase (COX)-2 pathway. Fluorescence quenching and saturation-transfer difference (STD) NMR experiments showed that eriodictyol exhibits good binding affinity to JNK, $8.79{\times}10^5M^{-1}$. Based on a docking study, we propose a model of eriodictyol and JNK binding, in which eriodictyol forms 3 hydrogen bonds with the side chains of Lys55, Met111, and Asp169 in JNK, and in which the hydroxyl groups of the B ring play key roles in binding interactions with JNK. Therefore, eriodictyol may be a potent anti-inflammatory inhibitor of JNK.