• The Korean Journal of Mycology
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• v.27 no.1 s.88
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• pp.32-38
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• 1999

A Saprolegnia sp. was isolated from cultured snakehead, Channa argus, and its physiological characteristics were investigated. The optimum temperature, pH and NaCl concentration for mycelial growth of Saprolegnia sp. were $25^{\circ}C$, 6.0 and 0%, respectively. The mycelial growth was increased with the addition of 10 mM phosphate and 10mg/L casamino acid. The essential oils extracted from three plants, Artemisia princeps var. orientalis, Thuja orientalis and Chamaecyparis obtusa have been tested to know whether they inhibit the growth of Saprolegnia sp. at six different oil concentrations(10, 100, 500, 1,000, 1,500 and 2,000 ppm). Essential oil from A. princeps var. orientalis began to inhibite the mycelial growth of Saprolegnia sp. at the concentration more than 10ppm. Using other essential oils from T. orientalis and C. obtusa, those initially inhibited the mycelial growth of Saprolegnia sp. at the concentration over 10 ppm and complate inhibition of mycelial growth was observed at over 500 ppm. The histopathological features of Snakehead infected by Saprolegnia sp. were studied. A club shape of gill lamella epithelial cells was observed in the gill. The mycelial cells were penetrated into muscular tissue, and the accumulation of the ceroid was observed in the liver, spleen and kideny tissue in common. The necrosis of tubular epithelial cells was seen in the liver tissue, parenchymal tissue in the spleen and tubular epithelial cells in the kidney.

• Proceedings of the Korean Nutrition Society Conference
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• 2004.05a
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• pp.93-93
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• 2004

• Clinical and Experimental Pediatrics
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• v.45 no.5
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• pp.560-567
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• 2002

주산기 뇌손상은 주로 급격한 저산소-허혈 손상에 의하는데 급격한 산소 공급의 차단은 oxidative phosphorylation을 정지 시켜서 뇌대사를 위한 에너지 공급이 차단되게 된다. 에너지 공급이 차단된 뇌세포는 뇌세포막에서 세포 내외의 이온 농도 차를 유지시키던 ATP-dependent $Na^{+}-K^{+}$ pump의 기능이 정지 되고, 세포 내외의 농도 차에 따라 $Na^{+}$, $Cl^{+}$, $Ca^{{+}{+}}$의 대규모 세포 내로 이동이 일어난다. 세포 내로 calcium 이온의 이동은 glutamate 수용체의 활성화에 의해서도 일나는데, 세포 내 calcium 이온의 증가는 protease, lipase, nuclease 등을 활성화 시켜 세포를 사망에 이르게 하는 연속적이고 다양한 생화학적 반응을 일으키게 된다. Glutamate는 대표적인 신경 전달 물질인데 저산소-허혈 손상 시 glutamate 수용체의 지나친 흥분은 미성숙 뇌에 뇌손상을 유발하는데, NMDA 또는 non-NMDA 수용체와 복합체를 형성하고 있는 calcium 이동 통로를 활성화 시켜 세포 내 calcium 이온을 증가시키고, 그 외에 metabotropic recetor는 G-protein의 활성화 등을 통해 뇌손상을 유발하는 다양한 생화학적 반응을 매개한다. 저산소-허혈 손상 후 재산소화와 재관류가 일어나면서 뇌세포의 지연성 사망(secondary neuronal death)이 일어나는데 이는 초기 손상 후 뒤이어 일어나는 다양한 생화학적 반응에 의하는데 다량의 산소 자유기 발생, nitric oxide의 생성, 염증 반응과 싸이토카인, 신경전도 물질의 과흥분 등이 관여하며, 신경 세포 사망은 세포괴사(necrosis)뿐 아니라 일부는 세포 사멸(apoptosis)로 알려진 의도된 세포 사망(programmed cell death)에 의한 것으로 생각되고 있다(Fig. 2).

• Journal of the Korean Association of Oral and Maxillofacial Surgeons
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• v.30 no.6
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• pp.509-515
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• 2004

Photodynamic therapy(PDT) has advanced to clinical trials for the treatment of a variety of solid tumors and presents an alternative treatment option for tumors resistant to chemo-and/or radio-therapy. PDT is based on the combination of laser light of appropriate wavelength and energy to activate a systemically or locally applied photosensitizer that concentrates preferentially in malignant tissues. In this study, phototoxicity of laser EIT 21 was analysed in human osteosarcoma cell(HOS) and the second objective of this study was to determine the ability of laser EIT 21 to induce apoptosis. This study demonstrated that laser EIT 21 had a phototoxicity to HOS cells. In order to examinate whether cell death was induced by necrosis or apoptosis, variety of techniques which assess apoptosis were used. TUNEL assay showed only a few the positive reaction on condensed nuclei. It is hard to find condensed or fragmented nuclei on HOS cells irradiated with laser EIT 21 in Hemastat and AO/EB stain. By DNA electrophoresis, cells also did not show DNA degradation characteristic of apoptosis with a ladder pattern of DNA fragments. Apoptosis-related factors were analyzed by western blotting. The expression of p53 was constant and cells irradiated with laser did not show the caspase-3 and PARP degradation, therefore we suggest that p53 and caspase-3 are not involved in laserinduced cell death.

• Parasites, Hosts and Diseases
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• v.33 no.2
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• pp.131-134
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• 1995

When tachyzoites (RH strain) of Toxoplasmo gondii are injected intramuscularly, experimental mice survive up to 7 days, 1-2 days longer than those infected intraperitoneally. We observed sequential histopathological changes in inguinal Iymph nodes after intramuscular injection of tachyzoites to thighs of specific pathogen free (SPF) mice. Initial findings on 1 or 3 days after the injection were reactive germinal centers, distended sinuses and epithelioid cell clusters in cortical and paracortical regions. Later on 5 days after the injection, however, effacement of nodal structure with depletion of cells and focal necrosis were observed . Necrotizing Iymphadenitis in the experimental murine toxoplasmosis suggests the causal relation between T. gondii infection and the human disease.

• Korean Journal of Veterinary Research
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• v.16 no.1
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• pp.27-34
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• 1976

악상남도(惡尙南道) 김해군(金海郡) S 양돈장(養豚場)에서 1975년 4월 하순부터 5월 하순 사이에 사육돈(飼育豚) 1,200두중 약 350두에서 출혈성하리(出血性下痢)를 주증(主症)으로 하는 전염성(傳染性)이 강한 소화기질환(消化器疾患)이 발생하였다. 환돈(患豚)은 7주령(週齡)에서부터 14주령(週齡)까지에서 가장 많이 발생하고 급성(急性) 또는 아급성(亞急性)으로 경과하였으며 다량의 황백색(黃白色), 수양하리(水樣下痢)를 발하다가 황갈색(黃褐色), 포말성하리(泡沫性下痢) 또는 암적갈색(暗赤褐色) 점액성하리(粘液性下痢)를 나타내었다. 육안적(肉眼的) 병변(病變)은 대장(大腸)에 한하였으며 카타아르성(性), 출혈성(出血性) 내지 괴사성장염(壞死性腸炎)을 시현(示顯)하였으며 괴사(壞死)는 광범(廣凡)하나 표재성(表在性)이고 어떤 예에서는 결장점막(結腸粘膜) 속에 대소(大小)의 미세결절(微細結節)이 밀발(密發)한 것이 특징이었다. 조직학적검사(組織學的檢査)에서는 대장점막(大腸粘膜)에 현저한 배세포증식(杯細胞增殖), 울혈(鬱血) 및 원형세포침윤(圓形細胞浸潤)과 더불어 표재성괴사(表在性壞死)가 관찰되었고 상기(上記) 결절(結節)은 장선(腸腺) 속에 점액(粘液), 섬유소(纖維素) 및 붕괴세포(崩壞細胞)가 축적되어 선와(腺窩)가 확장되고 피복상피(被覆上皮)의 이형성(異形成)(dysplasia)을 일으키고 있음이 판명되었다. 병변부(病變部)의 세균염색(細菌染色)에 의하여 대형(大型) Spirocheta와 Vibrio 고균(孤菌)이 무수(無數)히 발견되었고 Spirocheta가 병변형성(病變形成)에 더 밀접하게 관련되어 있음이 밝혀졌다.

• Korean Journal of Veterinary Research
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• v.29 no.1
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• pp.75-79
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• 1989

The etiologic agents of mucormycosis are several nonpathogenic fungi of the order Mucorales and are ubiquitous. A total of 82 chickens were infected with the disease and developed anorexia, diarrhea, malnutrition, dyspnea, and paralysis in a chicken farm, Sokcho, Kwangwon. At necropsy there were multiple nodular lesions and hemorrhages in livers, spleens, kidneys, gastrointestinal track, and respiratory system. On histopathological examination it was found that the nodular lesions were consisted of granoulomatous inflammation accompanying characteristic hyphae ($4{\sim}24{\mu}$ wide) of the fungi.

• Tuberculosis and Respiratory Diseases
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• v.63 no.1
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• pp.52-58
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• 2007

Background: Photodynamic therapy is a viable option for lung cancer treatment, and many studies have shown that it is capable of inducing cell death in lung cancer cells. However, the precise mechanism of this cell death has not been fully elucidated. To investigate the early changes in cancer cell transcription, we treated A549 cells with the photosensitizer DH-I-180-3 and then we illuminated the cells. Methods: We investigated the gene expression profiles of the the A549 lung cancer cell line, using a DEG kit, following photodynamic therapy and we evaluated the cell viability by performing flow cytometry. We identified the genes that were significantly changed following photodynamic therapy by performing DNA sequencing. Results: The FACS data showed that the cell death of the lung cancer cells was mainly caused by necrosis. We found nine genes that were significantly changed and we identified eight of these genes. We evaluated the expression of two genes, 3-phosphoglycerate dehydrogenase and ribosomal protein S29. The expressed level of carbonic anhydrase XII, clusterin, MRP3s1 protein, complement 3, membrane cofactor protein and integrin beta 1 were decreased. Conclusion: Many of the gene products are membrane-associated proteins. The main mechanism of photodynamic therapy with using the photosensitizing agent DH-I-180-3 appears to be necrosis and this may be associated with the altered production of membrane proteins.

• Journal of Yeungnam Medical Science
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• v.9 no.2
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• pp.224-238
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• 1992

Hepatic fibrosis was induced in Sprague-Dawley rats to evaluate the ultrastructural changes of fat-storing cells(Ito cells). For experimental induction of liver fibrosis, the rats were administered intraperitoneally with 0.5ml of 50% $Ccl_4$ solution per Kg body weight, twice weekly for 12 weeks. The rats were sacrified every week. The liver tissues were examined under light and eletron microscopes. And the immunohistochemical study of desmin was also performed. The results were summarized as follows : Light microscopic findings : The cellular infiltrations with inflammatory cells and Kupffer cells developed from 1 week after $Ccl_4$ injection, and were the most severe in 4 weeks. The strong immunoreactivity for desmin was also evident in 4 weeks. The centrilobular necrosis and fibrosis developed from 2 weeks after injection, and the necrosis persisted until 8 weeks. The progress of fibrosis was accompanied by decreases in cellular infiltration and reactivity for desmin, and increased gradual nodular formation was also observed. The cirrhosis was developed after 10 weeks. Electron microscopic findings : An increase in number of fat-storing cells was observed from 1 week after injection. Transitional cells characterized by a depletion of lipid droplets and a hypertrophy of the rER appeared after 2 weeks. The number of transitional cells with abundant collagen fibers in the extracellular spaces increased in 4 weeks. With progression of fibrosis the number of fat-storing cells decreased and proliferating fibroblasts with dilated rER were observed. According to these results it was revealed that there was an apparent transition from fat-storing cells to transitional cells and to fibroblasts. These cells had a few similar characteristics and may belong to the same cell population. Thus it was suggested that fat-storing cells might play an important role in hepatic fibrosis.

• Journal of Life Science
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• v.30 no.4
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• pp.402-409
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• 2020

Nervous necrosis virus (NNV) contains a bi-segmented viral genome, RNA1 (3.4 kb, RdRp), and RNA2 (1.4 kb, capsid protein) in a small particle (25 nm). Despite its extremely compact size, NNV has caused serious damage by infecting approximately 120 fish species worldwide since it was first reported in the late 1980s. In order to minimize the damage caused by NNV infection and develop effective vaccines, it is necessary to understand the intra cellular signaling system according to NNV infection. NNV infection induces cell cycle arrest at the G1 phase via the p53-dependent pathway to use the cellular system for its replication. Otherwise, host cells recognize NNV infection through the RIG-1-like receptor (RLR) signaling pathway to control the virus and infected cells, and then ISGs required for antiviral action are activated via the IFN signaling pathway. Moreover, apoptosis of infected cells is triggered by the unfolded protein response (UPR) through ER stress and mitochondria-mediated cell death. Cell signaling studies on the NNV infection mechanisms are still at an early stage and many pathways have yet to be identified. Understanding the various disease-specific cellular signaling systems associated with NNV infection is essential for rapid and accurate diagnosis and vaccine development.