• The Plant Pathology Journal
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• v.17 no.6
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• pp.315-324
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• 2001

Tobacco (Nicotiana tabacum cvs.Xanthi-nc and NC 82) plants infected with Tobacco mosaic virus (TMV) were examined ultrastructurally. Local lesions produced by TMV were sunken and withered. The plants were subjected to temperature shift (TS), a method to produce programmed cell death (PCD), by placing the infected plants initially at high temperature (35$^{\circ}C$) for 2 days and then shifting them to greenhouse temperature (22-27$^{\circ}C$). As a result, expanded lesions around the original necrotic lesions were produced. The expanded area initially had no symptoms, but it withered and became necrotic 15 h after TS. No ultrastructural changes related to PCD were noted at 0 h after TS in Xanthi-nc tobacco tissues as well as in healthy and susceptible tobacco tissues infected with TMV, At 6 h after TS, chloroplasts were convoluted and cytoplasm began to be depleted; however no necrotic cells were found. At 17 h after TS, ground cytoplasm of affected cells was completely depleted and chloroplasts were stacked together with bent cell wall or dispersed in the intracellular space. Necrotic cells were also observed, containing virus particles in the necrotic cytoplasm. There were initially two types of symptoms in the expanded lesions: chlorosis and non-chlorosis (green). Abundant TMV particles and X-bodies were only found in the chlorotic tissue areas. These results suggest that PCD by TMV infection may start with the wilting of cells and tissues before necrotic lesion formation.

• The Plant Pathology Journal
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• v.19 no.2
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• pp.123-127
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• 2003

A severe disease of muskmelon (Cucumis melo cv. Alsnight) grown on rockwool in a plastic house was characterized by leaf and stem necrosis followed by death of the plants. In 2001, an isolate of Melon necrotic spot virus-MN (MNSV-MN) of the genus Camovirus was identified as the causal agent of the disease on the basis of biological reactions and nucleotide sequence analyses of coat protein (CP) gene. MNSV-MN induced necrotic local lesions on mechanically inoculated leaves and systemic necrotic spots on the upper leaves of melon cvs. Alsnight, Rui III, Party, Imperial, and Seolhang. However, the inoculated leaves of watermelon and cucumber showed only necrotic lesions. DsRNAs extracted from the melon infected with MNSV-MN were separated into three components. Molecular sizes of the dsRNAs were estimated at approximately 4.5, 1.8, and 1.6 kbp. The amplified cDNA products of CP gene for MNSV-MN by RT-PCR showed approximately 1.2 kbp. The amplified DNA was digested to three fragments by MspI treatment. The cDNA of the genomic RNA of MNSV-MN was cloned and the region deduced to encode the CP was sequenced. The CP coding region, located near 3' end of the genome, consisted of 1,170 nucleotides and had the potential to encode a 390 amino acid protein. The nucleotide and amino acid sequences of MNSV-MN CP gene were 84.0-94.6% and 90.8-94.9% identical with other MNSV isolates found in the GeneBank database, respectively. This is the first report on the occurrence of MNSV in Korea.

• Korean Journal of Veterinary Research
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• v.45 no.4
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• pp.593-599
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• 2005

An abattoir study on the abdominal fat necrosis in adult cattle was performed pathologically. Grossly, masses of fat necrosis were leekgreen in colour, lobulated on the cut surface, and saponificated in the texture. These necrotic adipose tissues infiltrated usually into neighboring parenchymal organs including intestines and pancreas, leading to fibrosis or atrophy of them. Histopathologically, necrotic fat cells contained acidophilic, opaque, amorphous substance or basophilic fibrillar or granular minerals in their cytoplasms. The lesions of fat necrosis were divided by fibroconnective tissue. With increase of the severity, necrotic fat cells fused each other and then formed fat cysts. In this severe lesion, necrotic fat cells were partialy or completely replaced by macrophages. Multinucleated giant cells were scattered in this lesion. Interestingly, small artery in the lesion of fat necrosis revealed severe thickening of internal elastic membrane. Severe fibrosis was observed in or between the outer longitudinal and inner circular muscular externas causing segregation, degeneration and necrosis of muscle fibers. The nerve cells of Auerbach's and Meissner's plexuses surrounded by fibrosis were degenerated or necrotic. In addition, necrotic fat cells infiltrated into the pancreas, resulting in pancreas atrophy. From these results, it is speculated that fat necrosis might compromise intestinal movement due to necrosis of muscular externa and ganglion cells of Auerbach's and Meissner's plexuses.

• 한국생물공학회:학술대회논문집
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• 2000.04a
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• pp.583-583
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• 2000

• Research in Plant Disease
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• v.16 no.3
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• pp.254-258
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• 2010

Melon necrotic spot virus (MNSV) is a very destructive disease to melon (Cucumis melo) plants. A MNSV was isolated from melon leaf showing necrotic spot symptoms at the plastic house in Naju, Korea in 2009. The isolate, designated as MNSV-Me, was identified and characterized by biological responses on several host plants, immuno captured RT-PCR and partial nucleotide sequencings of the genome. To evaluate MNSV-Me resistance in melon, thirty-five melon cultivars were mechanically inoculated on the cotyledon of the seedlings with the virus. MNSV-Me produced necrotic spots on the inoculated leaves of the all melon cultivars tested. Twenty-five cultivars were susceptible to the virus and they showed systemic necrotic spots on the leaves and/or necrosis longer than 3 cm in length on the stems within about forty days after inoculation. Five cultivars gave moderate resistance, no symptoms on the upper leaves but necrosis on the stem shorter than 3 cm in length. In an evaluation of MNSV-Me resistance in melon cultivars, 'Elstitan', 'Elsluxery', 'Betalichihage', 'Betalichi' and 'Womderfulhagae 1st' were found to have resistance by showing only faint necrosis on their stems.

• IMMUNE NETWORK
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• v.3 no.3
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• pp.188-200
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• 2003

Background: Immunization of dendritic cells (DCs) pulsed with tumor antigen can activate tumor-specific cytotoxic T lymphocytes (CTL) that are responsible for protection and regression. In this study, we examined whether the uptake of necrotic tumor cells could modulate DC phenotypes and whether the immunization of necrotic tumor cell-loaded DCs could elicit efficient tumor specific immune responses followed by a regression of established tumor burdens. Methods: We prepared necrotic tumor cell-pulsed DCs for the therapeutic vaccination and investigated their phenotypic characteristics, the immune responses induced by these DCs, and therapeutic vaccine efficacy against colon carcinoma in vivo. Several parameters including phagocytosis of tumor cells, surface antigen expression, chemokine receptor expression, IL-12 production, and NK as well as CTL activation were assessed to characterize the immune response. Results: DCs derived from mouse bone marrow efficiently phagocytosed necrotic tumor cells and after the uptake, they produced remarkably increased levels of IL-12. A decreased CCR1 and increased CCR7 expression on DCs was also observed after the tumor uptake, suggesting that antigen uptake could induce DC maturation. Furthermore, co-culturing of DCs with NK cells in vitro enhanced IL-12 production in DCs and IFN-${\gamma}$ production in NK cells, which was significantly dependent on IL-12 production and cell-to-cell contact. Immunization of necrotic tumor cell-loaded DCs induced cytotoxic T lymphocytes as well as NK activation, and protected mice against subsequent tumor challenge. In addition, intratumoral or contra-lateral immunization of these DCs not only inhibited the growth of established tumors, but also eradicated tumors in more than 60% of tumor-bearing mice. Conclusion: Our data indicate that production of IL-12, chemokine receptor expression and NK as well as CTL activation may serve as major parameters in assessing the effect of tumor cell-pulsed DC vaccine. Therefore, DCs loaded with necrotic tumor cells offer a rational strategy to treat tumors and eventually lead to prolonged survival.

• The Korean Journal of Cytopathology
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• v.10 no.2
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• pp.169-174
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• 1999

Spontaneous infarction of fibroadenoma of the breast is very uncommon and may lead to difficulties in clinical and pathological diagnosis. Most reported cases occured in young women during pregnancy or lactation. This report describes imprint cytologic features of an infarcted fibroadenoma in a 19-year-old young woman without evidence of pregnancy. The smears revealed many individually scattered degenerated or necrotic epithelial or spindle stromai cells and naked nuclei on dirty necrotic background. A few sheets of cohesive uniform epithelial cells and a few fragments of stromal cells were also present. Most of the epithelial cells had pyknotic and hyperchromatic nuclei, however, cellular atypism such as pleomorphism, prominent nucleoli or mitosis were not present. Though the necrotic ductular and glandular outline of this case may bear a superficial resemblance to adenocarcinoma, obvious cytologic atypia or mitosis, even in the necrotic areas were not present.

• Toxicological Research
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• v.13 no.3
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• pp.215-222
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• 1997

The features of seizure-related brain injuries in rats poisoned i.p. with diisopropylfiuorophosphate were investigated. Pyridostigmine bromide (0.1 mg/kg) and atropine methylnitrate (20 mg/kg), which are centrally inactive, were pretreated i.m. 30 min and 10 min, respectively. before diisopropylfluorophosphate (10 mg /kg, $2LD_50$) poisoning to reduce the mortality and eliminate peripheral signs. Diisopropylfluorophosphate induced severe limbic seizures, and early necrotic and delayed apoptotic brain injuries. The necrotic brain injury, which was closely related to seizure intensity, was exerted as early as 1 hr predominently in hippocampus and piriform cortex. showing spongiform change (malacia) of neurophils in severe cases, in contrast to a typical apoptotic (TUNEL-positive)pattern after 12 hr in thalamus, and a mixed type in amygdala. Nitric oxide content in cerebrospinal fiuid significantly increased after 2 hr, reaching a maximal level at 6 hr. Pretreatment with $_L-N^G$-nitroarginine, an inhibitor of nitric oxide synthase, reduced nitric oxide content and attenuated only apoptotic brain injury in all four brain regions examined without affecting seizure intensity and necrotic injury. Taken together, early necrotic and delayed apoptotic brain injuries induced by diisopropylfiuorophosphate poisoning in rats may be related to seizure intensity and nitric oxide production, respectively.

• Journal of fish pathology
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• v.15 no.1
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• pp.1-7
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• 2002

On April of 2000 and February of 2001, a disease characterized by darkening, ascites and enlargement of the spleen occurred in flounder, Paralichthys olivaceus, farmed near northern and eastern coasts of Korea. Various degree of necrosis including liquefactive-type was observed mainly in hemopoietic tissue of spleen and kindney. Certain tissue such as branchial soft tissue including epithelium showed a similar necrotic findings. But some tissues such as intentine had several necrotic clusters of wandering cells, being possibly leukocytes. Necrotic evidences of blood cells were evident in various tissues including hemopoietic tissues. Necrobiotic bodies were frequently encountered in blood smear preparations. Bullet type-virious were detected in the spleenic cells. Each virion was about 500 nm in diameter and 170nm in length. From these results, this disease was thought to be a rhabdoviral disease.

• Korean Journal of Veterinary Research
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• v.37 no.1
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• pp.161-166
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• 1997

From January of 1991 to December of 1992, 42 chickens collected from 21 poultry farms and also diagnosed as necrotic enteritis(NE) was examined clinical signs, gross and histopathological findings. Main clinical signs were characterized by decreased appetite, mild to severe depression, reductance to move, ruffled feathers, greenish to yellow-browinish diarrhea sometimes including blood. As progressed, diseased chickens showed feces mixed with necrotic debris which detached from the intestinal mucosa and mostly resulted in the death. In chronic cases, there were dirty feathers around cloaca due to diarrhea and notably retarded growth. Principle gross lesions were usually confined to the jejunum and ileum, especially toward the lower part of Meckel's diverticulum. The part of small intestine was frequently distended with gas, and also showed mucosal congestion and hemorrhages with varying degrees. Sometimes, the intestinal mucosa was thickened, and also covered with fibronecrotic psuedomembrane. In addition, there were focal necrosis and severely multifocal ulcreation in the mucosa of small intestine. Major histopathological findings included villous necrosis and erosion of the small intestine covering with lots of bacterial colonies, inflammatory cell infiltration in the lamina propria, and dilatation and hyperplasia of crypts. Luminal exudate contained bacterial colonies, fibrin, erythrocytes, and desquamated epithelium. Thirteen(61.9%) out of 21 NE-occurring farms were complicated with intestinal coccidiosis.