• Toxicological Research
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• v.25 no.3
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• pp.113-118
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• 2009

Cell death induced by menadione (vitamin K-3,2-methyl-1,4-naphthoquinone) has been investigated in human promyelocytic leukemia HL-60 cells. Menadione was found to induce both apoptosis and necrosis in HL-60 cells. Low concentration ($1{\sim}$50 ${\mu}$M) of menadione induced apoptotic cell death, which was demonstrated by typical DNA ladder patterns on agarose gel electrophoresis and flow cytometry analysis. In contrast, a high concentration of menadione (100 ${\mu}$M) induced necrotic cell death, which was demonstrated by DNA smear pattern in agarose gel electrophoresis. Necrotic cell death was accompanied with a great reduction of cell viability. Menadione activated caspase-3, as evidenced by both increased protease activity and proteolytic cleavage of 116 kDa poly(ADP-ribose) polymerase (PARP) into 85 kDa cleavage product. Caspase-3 activity was maximum at 50 ${\mu}$M of menadione, and very low at 100 ${\mu}$M of menadione. Taken together, our results showed that menadione induced mixed types of cell death, apoptosis at low concentrations and necrosis at high concentrations in HL-60 cells.

• Korean Journal of Clinical Laboratory Science
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• v.39 no.3
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• pp.190-195
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• 2007

In the present study, the author investigated to the cytotoxocity in cultured rat hepatocytes of Viscum album lectin. The cytotoxcity effect in Viscum album lectin on the activity of LDH was also investigated. Viscum album lectin significantly increased LDH leakage into medium of hepatocytes treated or untreated with $CCl_4$ (p<0.001). However, Viscum album lectin significantly increased LDH leakage from $CCl_4$-induced hepatocyte (p<0.001). There was a significant increase in LDH levels relative to the control group. Histological observation basically supported the result obtained from LDH assay. The livers of rats challenged with $CCl_4$ produced a marked increased cytoplasmic vacuoles and inflammatory cells in number, while the number of necrotic cells and swollen hepatocytes did not change significnatly. Rats administered DMSO alone did not alter the normal hepatic architecture. Histological observation of liver section in rat treated 72 hrs with either Viscum album lectin $CCl_4$-induced liver damage showed number of cytoplasmic vaculoe and necrotic cell. The number of inflammatory cell increased markedly. This results suggest to the conclusion that Viscum album lectin has a effect of hepatotoxicity activator.

• Archives of Reconstructive Microsurgery
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• v.9 no.1
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• pp.49-55
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• 2000

Nonunion and avascular necrosis are well-recognized complications of severe ankle injury especially aftrer talar neck fracture. The treatment of avascular necrosis is controversial and methods of treatment are limited. Many modalities have been introduced for the treatment of avascular necrosis of talus. The prolonged non-weight bearing for 2~3 years is not practical but also is occasionally complicated by late segmental collapse. Operative treatment includes tibiotalar arthrodesis and talectomy with tibiocalcaneal arthrodesis, but arthrodesis in patients with talar avascular necrosis is technically demanding and cause stiff, immobile foot and relatively high failure rate was reported. It is desirable to preserve their original joint if possible. Vascularized fibular grafting has been reported as a joint preserving treatment option for osteonecrosis of the hip but has not been described for the ankle. The authors applied free vascularized fibular grafts for 3 cases of avascular necrosis of talus. We observed evidences of revascularization of necrotic talar body and progression of fracture healing and obtained satisfactory results at mean 8 months of follow-up. Vascularized fibular grafting is one of the better alternatives for treating avascular necrosis of talus. It is expected that vascularized fibular grafting can prevent the necrotic talar dome from progressing to collapse and promote directly restored vascularization and new bone formation.

• The Plant Pathology Journal
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• v.15 no.3
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• pp.168-171
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• 1999

Crude extracts of pathogenic Streptomyces turgidiscabies isolates produced necrotic reaction on potato slices. Necrosis was first visible 24 hr after application and increased in severity over several days. However, necrosis was not observed when crude extracts of nonpathogenic strains were applied onto tuber slices. Presence of thaxtomin A from crude extracts of pathogenic S. turgidiscabies was identified by thin layer chromatography and high performance liquid chromatography. Nonpathgenic strains did not produce thaxtomin A in oatmeal broth. Inoculation of potato tuber slices with thaxtomin A partially purified from crude extract of a pathogenic S. turgidiscabies ST5 reproduce necrotic reaction suggesting that thaxtomin A is a pathogenicity determinant in S. turgidiscabies.

• The Plant Pathology Journal
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• v.16 no.5
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• pp.264-268
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• 2000

A fluorescent material was accumulated in inoculated leaves showing necrotic local lesions of tobacco plants with N gene, Nicotiana tabacum cvs. Xanthi-nc NN, Samsun NN, Burley 21 and KF 114, and N. glutinosa, and Datura stramonium at the early growth stages by the inoculation of Tobacco mosaic virus (TMV). It was identified as a coumarin phytoalexin, scopoletin. Although the material was most prominently produced in TMV-inoculated tobacco leaves with local necrotic lesions, its accumulation was also noted in uninoculated leaves of TMV-inoculated plants. Its accumulation was somewhat greater in high resistance-induced leaves than low resistance-induced and intact leaves. Scopoletin treatment induced the expression of a pathogenesis-related protein, PR-1, prominently at the concentration of 500 or 1000 ${\mu}$g/ml. This suggests that scopoletin is a phytoalexin abundantly accumulating in N gene-containing resistant plants in response to TMV infection, and may be related to hypersensitive responses (HR) and systemic acquired resistance (SAR) in the resistant tobacco plants.

• Research in Plant Disease
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• v.12 no.3
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• pp.185-188
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• 2006

In September and October 2005, melons(Cucumis melo L.) from the commercial greenhouses in Naju and Gwangju exhibited severe foliar necrosis and fruit rot. Leaf symptoms initially appeared as V-shaped, necrotic lesions and extending to the midrib. Symptoms on the fruit were occurred randomly as necrotic and sunken spots. Two isolates from diseased leaves and fruits were identified as Acidovorax avenae subsp. citrulli on the basis of bacteriological and genetic characteristics. Pathogenicity of the isolates was confirmed by inoculating on 3-week-old melon and cucumber seedlings. This is the first report of bacterial fruit blotch of melon in Korea.

• BMB Reports
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• v.31 no.2
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• pp.183-188
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• 1998

2-chloroethylethyl sulfide (CEES) is an alkylating agent that readily reacts with a wide variety of biological molecules causing metabolic abnormality. The mechanism of cell death during CEES injury is poorly understood. We have examined the effect of exposure of thymocytes with various concentrations of CEES to determine the pattern of cell death in thymocytes injury induced by CEES. In the present study, we show that two patterns of cell death occurred by either one of two mechanisms: apoptosis and necrosis. Exposure to low level of CEES (100 ${\mu}M$) for 5 h caused an induction of apoptosis on thymocytes, as identified by the following criteria: DNA fragmentation visualized by the characteristic "ladder" pattern was observed upon agarose gel electrophoresis and morphological features were revealed by microscopical observations. In contrast, exposure to high levels of CEES (500 ${\mu}M$) induce necrotic features such as cell lysis. Thus, depending on the concentrations, CEES can result in either apoptotic or necrotic cell damage. Our findings suggest that thymocytes which are not killed directly, but merely injured by low levels of CEES, are able to activate an internally-programmed cell death mechanism, whereas thymocytes receiving severe damages apparently can not.

• Korean Journal of Veterinary Pathology
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• v.1 no.2
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• pp.125-134
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• 1997

Porcine Reproductive and Respiratory Syndrome Virus infection (PRRSV) was confirmed by serology histopathology immunohistochemistry and bacteriologic examination in young pigs. Four suckling and six weaned piglets submitted from three different farms showed coughing sneezing labored rapid abdominal respiration lethargy and anorexia. Grossly apical and cardiac lung lobes appeared mottled with pale to dark tan discoloration. Submandibular and bronchial lymph nodes were tan and enlarged. All piglets were seropositive for PRRSV antibodies by the indirect immunofluorescent antibody(IFA) test. Microscopically lung lesions were characterized by hyperplasia and hypertrophy of type 2 pneumocytes infiltration of mononuclear cells in alveolar intersitium accumulation of necrotic debris in alveolar spaces accompanied by proliferation of alveolar multinucleated syncytial cells. Using immunohistochemical technique PRRSV antigens were demonstrated in alveolar macrophages and type 2 pneumocytes in histologic lung tissue sections. Also PRRSV antigens were detected in brain lymph nodes spleen and heart. Additionally piglets showed nonsuppurative meningoencephalitis mandibular necrotic lymphadenopathy splenic atrophy and myocardial necrosis.

• Korean Journal of Veterinary Service
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• v.22 no.2
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• pp.113-119
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• 1999

The most common cause of death is ostrich chick fading syndrome(OCFS), which is due to bacterial infection during artificial incubation and hatching. Six farmed ostrich chicks aged 3 and 10 days in Chonbuk province, were submitted to Chonbuk Livestock Development and Research Institute for necropsy, Clinically, birds showed hair loss, ocular exudate, lethargy, diarrhea, and subsequently died 3-5 days after onset of clinical signs. Grossly, umbilicus was enlarged. White-yellowish purulent nodules were scattered on the lung and the membrane of air-sac was thickened and had inflamed exudate on the surface in two chicks that died 3 days after hatching. In 10 days-old chick, intestine was shown rodding segmentally. Yolk sac was still retarded and its surface was partially hemorrahgic. The synovial fluid of the leg was yellowish. Microscopically, multifocal purulent exudates were scattered on the lung. Capillary microthrombi in the glomerulus were prominent and tubular epithelia were necrotic. Necrotic hepatocytes were scattered and intestine were congested. Microbiologically, Pseudomonas sp and/or E coli were isolated from air-sac, lung and/or liver. This case suggests that poor hygiene during artificial incubation, hatching or in the first week after hatching may cause high mortality of the ostrich chicks.

• The Plant Pathology Journal
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• v.20 no.2
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• pp.147-154
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• 2004

A simple and reliable procedure for RT-PCR detection of Apple stem pitting virus (ASPV), Cherry rasp leaf virus (CRLV), and Cherry necrotic rusty mottle virus (CNRMV) was developed. Two virus specific primer sets for each virus were found to specifically detect each virus among fourteen sets of designed oligonucleotide primers. Total RNAs extracted from healthy and from ASPV-,CRLV- and CNRMV-infected plant tissues were used to synthesize cDNA using oligo dT primer and then amplified by virus-specific primers for each virus. Each primer specifically amplified DNA fragments of 578 bp and 306 bp products for ASPV (prAS CP-C and prAS CP-N primers, respectively); 697 bp and 429 bp products for CRLV (prCR4 and prCR5-JQ3D3 primers, respectively); and 370 bp and 257 bp products for CNRMV (prCN4 and prCN6-NEG 1 primers, respec-tively) by RT-PCR. DNA sequencing of amplified DNA fragments confirmed the nature of each amplified DNA. Altogether, these results suggest that these virus specific primer sets can specifically amplify viral sequences in infected tissues and thus indicate that they can be used for specific detection of each virus.