• Asian Pacific Journal of Cancer Prevention
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• v.16 no.2
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• pp.831-836
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• 2015

Tumor fluid accumulation occurs in both human cancer and experimental tumor models. Solid tumors show a tendency to tumor fluid accumulation because of their anatomical and physiological features and this may be influenced by molecular factors. Fluid accumulation in the peri-tumor area also occurs in the Dunning model of rat prostate cancer as the tumor grows. In this study, the effects of tumor fluids that were obtained from Dunning prostate tumor-bearing Copenhagen rats on the strongly metastatic MAT-LyLu cell line were investigatedby examining the cell's migration and tumor fluid's toxicity and the kinetic parameters such as cell proliferation, mitotic index, and labelling index. In this research, tumor fluids were obtained from rats injected with $2{\times}10^5$ MAT-LyLu cells and treated with saline solution, and 200 nM tetrodotoxin (TTX), highly specific sodium channel blocker was used. Sterilized tumor fluids were added to medium of MAT-LyLu cells with the proportion of 20% in vitro. Consequently, it was demonstrated that Dunning rat prostate tumor fluid significantly inhibited proliferation (up to 50%), mitotic index, and labeling index of MAT-LyLu cells (up to 75%) (p<0.05) but stimulated the motility of the cells in vitro.

• Tuberculosis and Respiratory Diseases
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• v.48 no.4
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• pp.513-521
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• 2000

Background : TNF may play an important role(central mediator) in the development of an acute respiratory distress syndrome. Since TNF induced lung injury in the acute respiratory distress syndrome and abnormalities in surfactant function have been described in acute respiratory distress syndrome, the authors investigated the effects of TNF on the regulation of surfactant protein A, B and C mRNA accumulation. Methods : The effects of TNF on gene expression of surfactant protein A, B, and C were analyzed using filter hybridization, 12 and 24 hours after intravenous injection of TNF in rats. Results : 1. The accumulation of SP-A mRNA in the TNF treated group (12 and 24 hours after TNF injection) was significantly decreased by 22.9% and 27.4%, respectively, compared to the control group (P<.025, P<.025). 2. The accumulation of SP-B mRNA in 24 hours after TNF treated group was significantly decreased by 20.5% compared to that of the control group(P<.01). 3. The accumulation of SP-C mRNA in 12 hours after TNF treated group was significantly decreased by 31% the compared to that of the control group(P<.01). Conclusions : These findings indicate the marked inhibitory effects of tumor necrosis factor on surfactant proteins expression in vivo. This finding. in turn, supports the idea of inhibitory effects of tumor necrosis factor on surfactant proteins expression as it relates to pathogenesis of acute respiratory distress syndrome.

• BMB Reports
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• v.48 no.8
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• pp.454-460
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• 2015

Naturally occurring reoviruses are live replication-proficient viruses that specifically infect human cancer cells while sparing their normal counterpart. Since the discovery of reoviruses in 1950s, they have shown various degrees of safety and efficacy in pre-clinical or clinical applications for human anti-cancer therapeutics. I have recently discovered that cellular tumor suppressor genes are also important in determining reoviral tropism. Carcinogenesis is a multi-step process involving the accumulation of both oncogene and tumor suppressor gene abnormalities. Reoviruses can exploit abnormal cellular tumor suppressor signaling for their oncolytic specificity and efficacy. Many tumor suppressor genes such as p53, ataxia telangiectasia mutated (ATM), and retinoblastoma associated (RB) are known to play important roles in genomic fidelity/maintenance. Thus, a tumor suppressor gene abnormality could affect host genomic integrity and likely disrupt intact antiviral networks due to the accumulation of genetic defects which in turn could result in oncolytic reovirus susceptibility. This review outlines the discovery of oncolytic reovirus strains, recent progresses in elucidating the molecular connection between oncogene/tumor suppressor gene abnormalities and reoviral oncotropism, and their clinical implications. Future directions in the utility of reovirus virotherapy is also proposed in this review. [BMB Reports 2015; 48(8): 454-460]

• Journal of Korean Medical classics
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• v.32 no.4
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• pp.109-118
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• 2019

Objectives : In this study, the relationship between Tingling disease(痺證) and Accumulation (積) was examined focusing on the occurrence of Tingling disease and its development into tangible lesion. Methods : Based on related contents in the "Huangdineijing", the process of creation and development of Tingling and its transformation to Accumulation was mainly examined. Results : While Tingling disease is usually caused by the three Qis of Wind-Cold-Dampness, due to its Yin nature there is high tendency of Qi and blood to be blocked and Blood and Fluid-Humor agglomerating into Accumulation. Symptoms of dysaesthesia are merely expressions manifesting in this process. Development into colic accumulation [疝瘕], Gu(蠱), or convulsion[瘛] after Tingling has traveled to the five zang is also related to its transformation into Accumulation. In the case of Tingling disease of the five zang in the "Huangdineijing", it is not a diagnostic category for treatment but actual lesions in the five zang six fu. In other words, in the beginning stages of Tingling disease, some sort of solidification that causes abnormal senses among other symptoms happens, and this solidification starts taking up space within the flesh. If it is not eliminated and persists, it enters into the inner organs and develops Tingling disease of the zangfu. Conclusions : Understanding Tingling disease(痺證) as a presymptom to developing Accumulation, rather than abnormality of sense will enable people to have higher chances in treating tumor.

• The Korean Journal of Nuclear Medicine
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• v.22 no.1
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• pp.77-81
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• 1988

Tumor localizing properties of $^{67}Ga$ citrate and $^{169}Yb$ citrate were studies with sarcoma 180 bearing mice. To compare precisely the accumulation of $^{67}Ga$ citrate and $^{169}Yb$ citrate in tumor tissue itself, $^{67}Ga$ and l63yb were administered simultaneously as a mixture of same chemical form of citrate. The yield of $^{169}Yb$ labeled citrated and the of radiopharmaceuticals purity was identified more than 90% by chromatography on silica gel plates. $^{67}Ga$ and $^{169}Yb$ were injected into mice and the mice were killed at 3, 24, and 48 hours following intraperitoneal injection of the radiopharmaceuticals. The retention value of $^{67}Ga$ and $^{169}Yb$ in tumor was similar but they differ from each other markedly in normal tissue distribution. $^{169}Yb$ citrate is cleared up from blood more rapidly than $^{67}Ga$ citrate, and a high tumor to blood ratio is achieved shortly after injection.

• Molecules and Cells
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• v.45 no.4
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• pp.193-201
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• 2022

Excessive production of reactive oxygen species (ROS) is a key phenomenon in tumor necrosis factor (TNF)-α-induced cell death. However, the role of ROS in necroptosis remains mostly elusive. In this study, we show that TNF-α induces the mitochondrial accumulation of superoxide anions, not H₂O₂, in cancer cells undergoing necroptosis. TNF-α-induced mitochondrial superoxide anions production is strictly RIP3 expression-dependent. Unexpectedly, TNF-α stimulates NADPH oxidase (NOX), not mitochondrial energy metabolism, to activate superoxide production in the RIP3-positive cancer cells. In parallel, mitochondrial superoxide-metabolizing enzymes, such as manganese-superoxide dismutase (SOD2) and peroxiredoxin III, are not involved in the superoxide accumulation. Mitochondrial-targeted superoxide scavengers and a NOX inhibitor eliminate the accumulated superoxide without affecting TNF-α-induced necroptosis. Therefore, our study provides the first evidence that mitochondrial superoxide accumulation is a consequence of necroptosis.

• Korean Journal of Veterinary Research
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• v.45 no.4
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• pp.517-525
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• 2005

This study was performed to evaluate using wild-type (WT) and $C{\times}32$ knockout (KO) mice if lack of cell to cell communication by connexin 32 gap junction enhances the benzene-induced hematotoxicity and hemopoietic tumor development. The WT and $C{\times}32$ KO mice were exposed to 300 ppm of benzene for 6 hours/day, 5 days/week for a total of 26 weeks by inhalation, and then sacrificed to evaluate the toxicities of hemopoietic organs or allowed to live out their life span to evaluate the hemopoietic tumor incidence. The significant increase and decrease of organ weight were respectively noted in spleen and thymus of both WT and $C{\times}32$ KO mice without significant difference between the genotypes. Histopathologically, benzene exposure for 26 weeks induced the morphological changes in hemopoietic organs, characterized by fat cell accumulation in the bone marrow and extramedullary hemopoiesis in the spleen. The fat cell accumulation was, compared with that of WT mice, considerably exacerbated in the $C{\times}32$ KO mice. However, no significant difference was observed in the changes of hematological values and bone marrow cellularity as well as in the onset and incidence of hemopoietic tumors between WT and $C{\times}32$ KO mice. In conclusion, this study indicated little significant role of the cellular communication by $C{\times}32$ gap junction in the action mechanism of benzene hematotoxicity and leukemogenicity.

• The Korean Journal of Nuclear Medicine
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• v.33 no.3
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• pp.337-340
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• 1999

Thallium-201 brain SPECT is utilized in the diagnosis of brain tumor especially in cases where CT or MRI findings alone cannot differentiate malignant lesion from benign. Recently we came across two cases of positive T1-201 brain SPECT in clinically suspected brain tumor patients that turned out to be hemorrhagic cerebral infarction instead on biopsy. The findings in these cases demonstrate that thallium-201 accumulation may occur by the breakdown of the blood-brain barrier and phagocytic cell infiltration in the liquefaction stage of infarction.

• Proceedings of the Korean Institute of Information and Commucation Sciences Conference
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• 2016.05a
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• pp.715-717
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• 2016

Conventional drug carriers such as liposomes, nanoparticles, polymer micelles, polymeric conjugate and lipid microemulsion for cancer chemotherapy shield normal tissues from toxic drugs to treat cancer cells in tumors. However, inaccurate tumor targeting uncontrolled drug release from the carriers and unwanted accumulation in healthy sites can limit treatment efficacy with current conventional drug carriers with insufficient concentrations of drugs in the tumors and unexpected side effects as a result. In this research, we examined the use of sickle red blood cells as a new drug carrier with novel tumor targeting and controlled release properties. Sickle red blood cells show natural tumor preferential accumulation without any manipulation and controlled drug release is possible using a hemolysis method with photosensitizers.

• The KIPS Transactions:PartB
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• v.13B no.6 s.109
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• pp.601-606
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• 2006

The image data amount that used in medical institution with great development of medical technology is increasing rapidly. Therefore, people need automation method that use image processing description than macrography of doctors for analysis many medical image. In this paper. we propose that acquire texture information to using GLCM about liver area of abdomen CT image, and automatically detects liver tumor using PCA from this data. Method by one feature as intensity of existent liver humor detection was most but we changed into 4 principal component accumulation images using GLCM's texture information 8 feature. Experiment result, 4 principal component accumulation image's variance percentage is 89.9%. It was seen this compare with liver tumor detecting that use only intensity about 92%. This means that can detect liver tumor even if reduce from dimension of image data to 4 dimensions that is the half in 8 dimensions.