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RISS 인기검색어
- 검색키워드
- 저자 : Hana Jin (검색결과 171 건)
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Hana Kwon(Hana Kwon),Hyemin Oh(Hyemin Oh),Hyunjee Chae(Hyunjee Chae),Pattaraporn Thiangthae(Pattaraporn Thiangthae ),Kyoung-Jin Kang(Kyoung-Jin Kang) 대한미용의학회 2022 대한미용의학회지 Vol.6 No.2
Background: Filler injections are commonly used to soften deep nasolabial folds (NLF) by restoring volume in the depressed parts of fold. Recently, a combination technique using hyaluronic acid filler and polydioxanone (PDO) thread significantly improves deep NLF and induced changes in smile. Objective: This study retrospectively confirmed the effects of this combination therapy, focusing on smile changes. Methods: The NLF was divided into 3 parts: the lateral folded part (LFP), medial depressed part (MDP), and central creased part (CCP). Between November and December 2021, 14 patients underwent the combination treatment; of these, 11 were enrolled, excluding 3 who were not properly followed up. On average, 5.82±0.87 (right) and 5.73±0.47 (left) PDO mesh threads (6.0 cm length) were sequentially inserted into the LFP, MDP, and under the CCP of each NLF. Following this, an average of 1.82±0.71 ml (right) and 1.92±0.75 ml (left) of the filler was also sequentially injected into each NLF in a similar manner. They were mainly placed in the superficial and deep fat layers in the entire NLF and sub-malar areas. Smile index was measured during the fully expanded smile stage. The follow-up period was 3 months. The results were estimated using pre- and post-operative photographs. Results: Three months after the combination treatment, patients were pleased with the softening of their NLF. As indicated by the increased smile index (inter-commissural width/inter-labial gap), the old and expanded smile changed to younger and less expanded smile. The original smile type (eight and three patients with the commissure and cuspid types, respectively) remained unchanged. The contour changes in each smile varied according to the smile type. This could be explained by combination treatment’s NLF correction, which restricts facial expression muscle movement. Conclusion: These results demonstrate definite evidence of softening of the NLF, a youthful smile, and an increased smile index.
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Jin, Hana,Lee, Won Sup,Eun, So Young,Jung, Ji Hyun,Park, Hyeon-Soo,Kim, Gonsup,Choi, Yung Hyun,Ryu, Chung Ho,Jung, Jin Myung,Hong, Soon Chan,Shin, Sung Chul,Kim, Hye Jung Lychnia 2014 International journal of oncology Vol.45 No.4
<P>Morin, a flavonoid found in figs and other Moraceae, displays a variety of biological actions, such as anti-oxidant, anti-inflammatory and anti-carcinogenic. However, the anticancer effects of morin and in particular its anti-metastatic effects are not well known. Therefore, in the present study, we investigated the anticancer effects of morin on highly metastatic human breast cancer cells. Our results showed that morin significantly inhibited the colony forming ability of highly metastatic MDA-MB-231 breast cancer cells from low doses (50 mu M) without cytotoxicity. In addition, morin changed MDA-MB-231 cell morphology from mesenchymal shape to epithelial shape and inhibited the invasion of MDA-MB-231 cells in a dose-dependent manner. Morin decreased matrix metalloproteinase-9 (MMP-9) secretion and expression of the mesenchymal marker N-cadherin of MDA-MB-231 cells, suggesting that morin might suppress the EMT process. Furthermore, morin significantly decreased the phosphorylation of Akt, and inhibition of the Akt pathway significantly reduced MDA-MB-231 invasion. In an in vivo xenograft mouse model, morin suppressed MDA-MB-231 cancer cell progression. Taken together, our findings suggest that morin exhibits an inhibitory effect on the cancer progression and EMT process of highly metastatic breast cancer cells at least in part through inhibiting Akt activation. This study provides evidence that morin may have anticancer effects against metastatic breast cancer.</P>
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Jin, Hana,Ham, Sun Ah,Kim, Min Young,Woo, Im Sun,Kang, Eun Sil,Hwang, Jung Seok,Lee, Ko‐,Woon,Kim, Hye Jung,Roh, Gu Seob,Lim, Dae‐,Seog,Kang, Dawon,Seo, Han Geuk Wiley Subscription Services, Inc., A Wiley Company 2012 JOURNAL OF NEUROSCIENCE RESEARCH - Vol.90 No.8
<P><B>Abstract</B></P><P>Glutamate‐induced neurotoxicity has been implicated in the pathogenesis of neurodegenerative disorders; however, little is known about the cellular events that underlie neurotoxicity or how to impede these events. This study demonstrates that peroxisome proliferator‐activated receptor (PPAR)‐δ regulates glutamate‐induced neurotoxicity in HT22 mouse hippocampal cells. Activation of PPARδ by GW501516, a specific ligand, significantly inhibited glutamate‐induced cell death and reactive oxygen species (ROS) production in HT22 cells. The siRNA‐mediated knockdown of PPARδ abrogated the effects of GW501516 in neuronal toxicity and ROS production induced by glutamate. In addition, ligand‐activated PPARδ reduced the glutamate‐induced level of intracellular calcium ions (Ca<SUP>2+</SUP>) by modulating the influx of Ca<SUP>2+</SUP> from the extracellular space. Similarly, glutamate‐induced cell death and intracellular Ca<SUP>2+</SUP> levels were attenuated in the presence of LY83583, an inhibitor of soluble guanylyl cyclase. Taken together, these results suggest that PPARδ plays an important role in glutamate‐induced neurotoxicity by modulating oxidative stress and Ca<SUP>2+</SUP> influx. © 2012 Wiley Periodicals, Inc.</P>
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Jin, Hana,Ko, Young Shin,Kim, Hye Jung D.A. Spandidos 2018 International journal of oncology Vol.53 No.5
<P>In the tumor microenvironment, extracellular nucleotides are released and accumulate, and can activate the P2Y<SUB>2</SUB> receptor (P2Y<SUB>2</SUB>R), which regulates various responses in tumor cells, resulting in tumor progression and metastasis. Moreover, the inflammasome has recently been reported to be associated with tumor progression. However, the role of P2Y<SUB>2</SUB>R in inflammasome activation in breast cancer cells is not yet well defined. Therefore, in this study, we investigated the role of P2Y<SUB>2</SUB>R in inflammasome-mediated tumor progression in breast cancer using breast cancer cells and radiotherapy-resistant (RT-R) breast cancer cells. We established RT-R-breast cancer cells (RT-R-MDA-MB-231, RT-R-MCF-7, and RT-R-T47D cells) by repeated irradiation (2 Gy each, 25 times) in a previous study. In this study, we found that the RT-R breast cancer cells exhibited an increased release of adenosine triphosphate (ATP) and P2Y<SUB>2</SUB>R activity. In particular, the RT-R-MDA-MB-231 cells derived from highly metastatic MDA-MB-231 cells, exhibited a markedly increased ATP release, which was potentiated by tumor necrosis factor (TNF)-α. The MDA-MB-231 cells exhibited inflammasome activation, as measured by caspase-1 activity and interleukin (IL)-1β secretion following treatment with TNF-α and ATP; these effects were enhanced in the RT-R-MDA-MB-231 cells. However, the increased caspase-1 activities and IL-1β secretion levels induced in response to treatment with TNF-α or ATP were significantly reduced by P2Y<SUB>2</SUB>R knockdown or the presence of apyrase in both the MDA-MB-231 and RT-R-MDA-MB-231 cells, suggesting the involvement of ATP-activated P2Y<SUB>2</SUB>R in inflammasome activation. In addition, TNF-α and ATP increased the invasive and colony-forming ability of the MDA-MB-231 and RT-R-MDA-MB-231 cells, and these effects were caspase-1-dependent. Moreover, matrix metalloproteinase (MMP)-9 activity was modulated by caspase-1, in a P2Y<SUB>2</SUB>R-dependent manner in the MDA-MB-231 and RT-R-MDA-MB-231 cells. Finally, nude mice injected with the RT-R-MDA-MB-231-EV cells (transfected with the empty vector) exhibited increased tumor growth, and higher levels of MMP-9 in their tumors and IL-1β levels in their serum compared with the mice injected with the RT-R-MDA-MB-231- P2Y<SUB>2</SUB>R shRNA cells (transfected with P2Y<SUB>2</SUB>R shRNA). On the whole, the findings of this study suggest that extracellular ATP promotes tumor progression in RT-R-breast cancer cells and breast cancer cells by modulating invasion and associated molecules through the P2Y<SUB>2</SUB>R-inflammasome activation pathway.</P>
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Jin Hana,김향경 대한외과초음파학회 2021 대한외과초음파학회지 Vol.8 No.2
Critical limb ischemia is a clinical syndrome of ischemic pain at rest or tissue loss resulting from non-healing ulcers or gangrene related to peripheral artery disease. The primary therapeutic goal is to preserve limb function. The most important factor for determining the healing potential of a wound is the degree of perfusion to the affected segment. Several tests objectively measure the degree of tissue perfusion: for example, ankle-brachial index, toe pressure, ultrasound, transcutaneous oxygen pressure, two-dimensional perfusion angiography, indocyanine green angiography, diagnostic nuclear medicine imaging, and laser doppler skin perfusion pressure. In this study, we investigated tests that can measure tissue perfusion and discussed the advantages and limitations of each test.
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Jin, Hana,Eun, So Young,Lee, Jong Sil,Park, Sang Won,Lee, Jae Heun,Chang, Ki Churl,Kim, Hye Jung BioMed Central 2014 Breast cancer research Vol.16 No.5
<P><B>Introduction</B></P><P>Extracellular nucleotides are released and detectable in a high concentration within the tumor microenvironment. G protein-coupled P2Y<SUB>2</SUB> nucleotide receptor (P2Y<SUB>2</SUB>R) is activated equipotently by adenosine triphosphate (ATP) and uridine 5′-triphosphate (UTP), which mediate proinflammatory responses such as cell migration and proliferation. However, the role of P2Y<SUB>2</SUB>R in the process of cancer metastasis remains unclear. This study aimed to determine the role of P2Y<SUB>2</SUB>R in the proliferation, migration and invasion of highly metastatic MDA-MB-231 breast cancer cells through crosstalk with endothelial cells (ECs).</P><P><B>Methods</B></P><P>ATP release and P2Y<SUB>2</SUB>R activity between high metastatic breast cancer cell MDA-MB-231 and low metastatic breast cancer cell MCF-7 were compared. Then, the role of P2Y<SUB>2</SUB>R on tumor growth and invasion via crosstalk with ECs was examined in vitro, using MDA-MB-231 cells and ECs transfected with control- or P2Y<SUB>2</SUB>R-siRNA, and in vivo, using an animal model injected with control-shRNA- or P2Y<SUB>2</SUB>R-shRNA-transfected MDA-MB-231 cells.</P><P><B>Results</B></P><P>We found that this highly metastatic breast cancer cell line released higher levels of ATP and showed a higher P2Y<SUB>2</SUB>R activity in comparison to a low metastatic breast cancer cell line, MCF-7. In MDA-MB-231 cells, P2Y<SUB>2</SUB>R activation by ATP or UTP increased proliferation at 24 or 72 hours, which was abolished by P2Y<SUB>2</SUB>R knock-down. In addition, the adhesion of MDA-MB-231 cells to ECs and cell migration were both significantly increased by ATP or UTP through the expression of intercellular adhesion molecule-1 (ICAM-1) and vascular cell adhesion molecule-1 (VCAM-1) in MDA-MB-231 or ECs but not in cells where P2Y<SUB>2</SUB>R was knocked down. Furthermore, ATP- or UTP-mediated activation of P2Y<SUB>2</SUB>R induced MDA-MB-231 invasion through ECs, increased matrix metalloproteinase-9 (MMP-9) activity and vascular endothelial growth factor (VEGF) production in MDA-MB-231 and induced the phosphorylation of vascular endothelial (VE)-cadherin in ECs. Tumor growth and metastasis to other tissues were dramatically reduced, and body weight was increased in mice injected with P2Y<SUB>2</SUB>R-shRNA-transfected MDA-MB-231 cells compared to mice injected with control shRNA-transfected MDA-MB-231 cells.</P><P><B>Conclusion</B></P><P>This study suggests that P2Y<SUB>2</SUB>R may play an important role in cancer metastasis via modulation of the crosstalk between cancer cells and ECs.</P><P><B>Electronic supplementary material</B></P><P>The online version of this article (doi:10.1186/bcr3694) contains supplementary material, which is available to authorized users.</P>
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Park, Jin-Hee,Kim, Hyoung Kyu,Jung, Hana,Kim, Ki Hyang,Kang, Mi Seon,Hong, Jun Hyuk,Yu, Byeng Chul,Park, Sungjae,Seo, Su-Kil,Choi, Il Whan,Kim, Soon Ha,Kim, Nari,Han, Jin,Park, Sae Gwang Spandidos Publications 2017 International journal of oncology Vol.50 No.1
<P>A major goal of breast cancer research is to prevent the molecular events that lead to tumour metastasis. It is well-established that both cytoplasmic and mitochondrial reactive oxygen species (ROS) play important roles in cell migration and metastasis. Accordingly, this study examined the molecular mechanisms of the anti-metastatic effects of NecroX-5, a mitochondrial ROS scavenger. NecroX-5 inhibited lung cancer metastasis by ameliorating migration in a mouse model. In human cancer cells, the inhibition of migration by NecroX-5 is cell type-dependent. We observed that the effect of NecroX-5 correlated with a reduction in mitochondrial ROS, but mitochondrial ROS reduction by MitoQ did not inhibit cell migration. NecroX-5 decreased intracellular calcium concentration by blocking Ca2+ influx, which mediated the inhibition of cell migration, AKT down regulation and the reduction of mitochondrial ROS levels. However, the reduction of mitochondrial ROS was not associated with supressed migration and AKT downregulation. Our study demonstrates the potential of NecroX-5 as an inhibitor of breast cancer metastasis.</P>
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Su Jin Kim,Jin Wook Kim,Young Sam Cho,Kyung Jin Chung,Hana Yoon,Khae Hawn Kim 대한배뇨장애요실금학회 2019 International Neurourology Journal Vol.23 No.4
Shift workers often experience problems associated with circadian disruption associated with artificial light at night and nocturia is commonly noted in night-shift workers. Nocturia associated with circadian disruption is due to increased urine production of the kidney and decreased storage function of the bladder. A recent discovery of peripheral clock genes in the bladder and their role in contractile property of the bladder support that micturition is closely related to the circadian rhythm. Moreover, there are clinical studies showed that shift workers more often experienced nocturia due to circadian disruption. However, comparing with other health problems, concerns on nocturia and voiding dysfunction associated with circadian disruption are insufficient. Therefore, further studies about voiding dysfunction associated with the circadian disruption in shift workers are necessary.
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