• Journal of radiological science and technology
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• v.46 no.5
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• pp.379-394
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• 2023

Targeted Alpha Therapy (TAT) is a new method of cancer treatment that protects normal tissues while selectively killing tumor cells using high cytotoxicity and short range of alpha particles, and target alpha therapy is a highly specific and effective cancer treatment strategy, and its potential has been proven through many clinical and experimental studies. This treatment method accurately delivers alpha particles by selecting specific molecules present in cancer tissue, which has an effective destruction and tumor suppression effect on cancer cells, and one of the main advantages of target alpha treatment is the physical properties of alpha particles. Alpha particles have a very high energy and short effective distance, interacting with target molecules in cancer tissues and having a fatal effect on cancer cells, which is known to cause DNA damage and cell death in cancer cells. TAT has shown positive results in preclinical and clinical studies for various types of cancers, especially those that resist or are unresponsive to existing treatments, but there are several challenges and limitations to overcome for successful clinical transition and application. These include the provision and production of suitable alpha radioisotopes, optimization of target vectors and delivery formulations, understanding and regulation of radiological effects, accurate dosage calculation and toxicity assessment. Future research should focus on developing new or improved isotopes, target vectors, transfer formulations, radiobiological models, combination strategies, imaging techniques, etc. for TAT. In addition, TAT has the potential to improve the quality of life and survival of cancer patients due to the possibility of a new treatment for overcoming cancer, and to this end, prospective research on more carcinomas and more diverse patient groups is needed.

• Progress in Medical Physics
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• v.8 no.1
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• pp.47-52
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• 1997

Simulations were performed using a Monte Carlo technique in order to show physical phenomena occurring when a heavy charged particle such as proton or alpha particle traverses the medium. It was confirmed that the sharp Bragg peak occurred deeper in the water with the increasing proton energy. It is found that the use of such a sharp Bragg peak due to heavy charged particles would be far superior to the case of the photon or electron, since the absorbed dose in the target tissues would be better localized, thereby minimizing the damage to the surrounding tissues.

• The Korean Journal of Nuclear Medicine Technology
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• v.20 no.1
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• pp.28-31
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• 2016

Purpose $^{223}Ra-Dichloride$ is used for the medicine of castration-resistant prostate cancer (CRPC) and which emits ${\alpha}-ray$ of 28 Mev that is used for therapy. However $^{223}Ra-Dichloride$ emits ${\beta}-ray$ of 3.6% and ${\gamma}-ray$ of 1.1%(80,156,270 keV) aside from ${\alpha}-ray$ in decay. Therefore we would like to evaluate external radiation expose dose rate of ${\gamma}-ray$ of $^{223}Ra-Dichloride$. Materials and Methods We calculated external radiation expose dose rate using ${\gamma}-constant$ of $^{223}Ra-Dichloride$, $^{99m}Tc$ based on Health physics(2012). $^{223}Ra-Dichloride$ of 3.5 MBq and $^{99m}Tc-MDP$ of 740 MBq were applied. external radiation expose dose rate 15 times from 1m by survey meter. Results ${\gamma}-contant$ of $^{223}Ra$, $^{99m}Tc-MDP$ from 1m distance based on Health physics(2012) is 0.0469, 0.0215. calculated value of external radiation expose dose rate was $16{\mu}Sy$, $34{\mu}Sy$ which activity is $^{223}Ra-Dichloride$ of 3.5 MBq and $^{99m}Tc-MDP$ of 740 MBq from 1 m and measured mean value of 1 m was $0.7{\mu}Sy/h$, $18{\mu}Sy/h$. Conclusion ${\gamma}-constant$ of $^{223}Ra$ is higher than $^{99m}Tc$ based on Health physics(2012). however calculated maximum external radiation expose dose rate of $^{223}Ra-Dichloride$ is lower than $^{99m}Tc$ due to actually used quantity of activity of $^{223}Ra-Dichloride$ is small. measured value of $^{223}Ra-Dichloride$ is also lower than $^{99m}Tc-MDP$. Therefore external radiation expose dose rate of ${\gamma}-ray$ of $^{223}Ra-Dichloride$ is very low.

• Journal of Life Science
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• v.33 no.3
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• pp.295-303
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• 2023

Immune and metabolic systems are important factors in maintaining homeostasis. Immune response and metabolic regulation are highly associated, so, when the normal metabolism is disturbed, the immune response changed followed the metabolic diseases occur. Likewise, obesity is highly related to immune response. Obesity, which is caused by an imbalance in energy metabolism, is associated with metabolic diseases, such as insulin resistance, type 2 diabetes, fatty liver diseases, atherosclerosis and hypertension. As known, obesity is characterized in chronic low-grade inflammation. In obesity, the microenvironment of immune cells became inflammatory by the unique activation phenotypes of immune cells such as macrophage, natural killer cell, T cell. Also, the immune cells interact each other in cellular or cytokine mechanisms, which intensify the obesity-induced inflammatory response. This phenomenon suggests the possibility of regulating the activation of immune cells as a pharmacological therapeutic strategy for obesity in addition to the common pharmacological treatment of obesity which is aimed at inhibiting enzymes such as pancreatic lipase and α-amylase or inhibiting differentiation of preadipocytes. In this review, we summarize the activation phenotypes of macrophage, natural killer cell and T cell, and their aspects in obesity. We also summarize the pharmacological substances that alleviates obesity by regulating the activation of immune cells.

• Journal of the Korean Society of Radiology
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• v.13 no.1
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• pp.133-140
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• 2019

Triglycerides (TG) are one of the triggers of chronic inflammatory lesions in the blood vessels. In the key factors in the development of inflammatory diseases, Pro-inflammatory cytokines such as tumor necrosis factor-alpha $(TNF-){\alpha}$ and interleukin-1 beta ($IL-1{\beta}$) contribute to the development of inflammatory lesions by recruiting other immune cells in the inflamed area or causing cell necrotic death. In this study, I investigated the effect of Jurkat T lymphocytes and U937 monocytes involved in vascular inflammation development on the expression of $TNF-{\alpha}$ and $IL-1{\beta}$ on exposure to TGs. In Jurkat cells, mRNA expression of $TNF-{\alpha}$ is increased by exposure to TGs. However, the expression levels of $TNF-{\alpha}$ and $IL-1{\beta}$ were increased by TGs in U937 cells. To investigate whether inducible nitric oxide synthase (iNOS) is involved in the increase of expression of $TNF-{\alpha}$ and $IL-1{\beta}$ by TGs, treatment of W1400 (an iNOS inhibitor) resulted in recovery of expression level both $TNF-{\alpha}$ and $IL-1{\beta}$. Based on the present study, it was confirmed that the expression of $TNF-{\alpha}$ and $IL-1{\beta}$ in monocytes and T lymphocytes. This increased cytokines contribute to development of vascular inflammatory lesions. In addition, iNOS is involved in the increase of $TNF-{\alpha}$ and $IL-1{\beta}$ expression by TGs.