• 한국수산과학회지
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• 제43권5호
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• pp.415-420
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• 2010

In Korea, oysters are used as an ingredient of Kimchi (Korean pickled cabbage) in early winter. Although viral contamination of oysters, including contamination by norovirus, can provoke gastroenteric illness, little is known of the epidemiological relationship to outbreaks. We postulated that Kimchi ripening can reduce the infectivity of norovirus, in order to test this hypothesis, we carried out a model experiment. Since norovirus is currently regarded as non-culturable, feline calicivirus (FCV) was used as a surrogate to examine the activation of norovirus with Kimchi ripening. In commercial well-prepared Kimchi, the infectivity ($TCID_{50}$) of FCV decreased by 2 log every 12 hours and reached the limit of detection after 48 hours during over-aging at $25^{\circ}C$. During storage at $4^{\circ}C$, the infectivity ($TCID_{50}$) of FCV decreased slowly and reached 5.00 $TCID_{50}$ after 48 hours. The low pH appears to affect the infectivity of FCV directly via organic acids produced by ripening during over-aging and storage. In neutralized lab-prepared Kimchi (pH 7.0), the infectivity ($TCID_{50}$) of FCV also decreased and reached the limit of detection after 72 hours at $4^{\circ}C$. This indicates that there are substances beside organic acids in Kimchi that originate from the raw materials and are produced during ripening. Among the raw materials, salt-fermented anchovies and garlic showed high direct antiviral activity. The main factor decreasing the infectivity of FCV in Kimchi was the high acidity caused by organic acids, regardless of the type, produced by ripening. Furthermore, unknown secondary products of microorganisms associated with Kimchi ripening and antiviral materials originating from raw material might contribute to the decreased infectivity of FCV, the surrogate of norovirus.

• Archives of Pharmacal Research
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• 제22권5호
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• pp.437-447
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• 1999

Type I diabetes, also known as insulin-dependent diabetes mellitus (IDDM) results from the destruction of insulin-producing pancreatic $\beta$ cells by a progressive $\beta$ cell-specific autoimmune process. The pathogenesis of autoimmune IDDM has been extensively studied for the past two decades using animal models such as the non-obese diabetic (NOD) mouse and the Bio-Breeding (BB) rat. However, the initial events that trigger the immune responses leading to the selective destruction of the $\beta$ cells are poorly understood. It is thought that $\beta$ cell auto-antigens are involved in the triggering of $\beta$ cell-specific autoimmunity. Among a dozen putative $\beta$ cell autoantigens, glutamic acid decarboxylase (GAD) has bee proposed as perhaps the strongest candidate in both humans and the NOD mouse. In the NOD mouse, GAD, as compared with other $\beta$ cell autoantigens, provokes the earliest T cell proliferative response. The suppression of GAD expression in the $\beta$ cells results in the prevention of autoimmune diabetes in NOD mice. In addition, the major populations of cells infiltrating the iselts during the early stage of insulitis in BB rats and NOD mice are macrophages and dendritic cells. The inactivation of macrophages in NOD mice results in the prevention of T cell mediated autoimmune diabetes. Macrophages are primary contributors to the creation of the immune environment conducive to the development and activation of $\beta$cell-specific Th1-type CD4+ T cells and CD8+ cytotoxic T cells that cause autoimmune diabetes in NOD mice. CD4+ and CD8+ T cells are both believed to be important for the destruction of $\beta$ cells. These cells, as final effectors, can kill the insulin-producing $\beta$ cells by the induction of apoptosis. In addition, CD8+ cytotoxic T cells release granzyme and cytolysin (perforin), which are also toxic to $\beta$ cells. In this way, macrophages, CD4+ T cells and CD8+ T cells act synergistically to kill the $\beta$ cells in conjunction with $\beta$ cell autoantigens and MHC class I and II antigens, resulting in the onset of autoimmune type I diabetes.

• 한국동물위생학회지
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• 제45권2호
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• pp.117-124
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• 2022

In the event of an outbreak of a livestock epidemic, it has been considered that the existing burial-centered carcass disposal method should be improved ecofriendly for prevention of leachate and odors from burial basically in regard of pathogen inactivation. Therefore, the aim of this study is whether it was possible to treat the carcass of cattle and chickens using the chemical carcass treatment method. It was conducted to establish detailed treatment standards for the chemical treatment method of cattle and chicken carcasses based on the results of the proof of the absence of infectious diseases in cattle chickens. After inoculating cattle carcass with 10 pathogens (foot and mouth disease virus, bovine viral diarrhea virus, Mycobacterium bovis, Mycobacterium avium subsp. Paratuberculosis, Brucella abortus, Bacillus anthracis, Clostridium chauvoei, Clostridium perfringens, Escherichia coli, and Salmonella Typhimurium) and chicken carcasses with low pathogenic avian influenza virus, Clostridium perfringens type C, E. coli and Salmonella Typhimurium, these were treated at 90℃ for 5 hours in a potassium hydroxide liquid solution corresponding to 15% of the body weight. This method liquefies all cadaveric components and inactivates all inoculated pathogens by PCR and culture. Based on these results, it was possible to prove that chemical treatment of cattle and chicken carcasses is effective in killing pathogens and is a safe method without the risk of disease transmission. The chemical treatment method of livestock carcasses can be suggested as an alternative to the current domestic burial-centered livestock carcass treatment method, preventing environmental pollution, and contributing to public health.