• The Journal of Korean Obstetrics and Gynecology
• /
• v.20 no.3
• /
• pp.1-12
• /
• 2007

Purpose: Uterine leiomyomas (fibroids) are common estrogen-dependent uterine tumors. Houttuynia cordata thunberg has cancer-preventing properties and often used in Chinese medicine. In the present study we used Houttuynia cordata thunberg to determine its effect on cell proliferation and apoptosis in human uterine leiomyoma cells. Methods: Primary cultured human uterine leiomyoma cells were treated with Houttuynia cordata thunberg. Cell viability analysis was analyzed by 3-(4,5-dimethylthiazol-2-yl)-2,5-diphenyltetrazolium bromide (MTS) assay and Flow cytometry was performed to ascertain the effects Houttuynia cordata thunberg. Expression of cell cycle related proteins and apoptosis related proteins were evaluated by Western blot analysis. Results: Cell viability was significantly influenced by Houttuynia cordata thunberg treatment in a dose-dependent manner in leiomyoma cells compare to normal myometrial cells. Flow cytometric analysis showed that Houttuynia cordata thunberg induced Sub G1 arrest. DNA fragmentation assay was carried out and apoptosis was detected. Activation of caspase-3, down-regulation of Bcl-2, with concomitant increase in p21 was observed. Houttuynia cordata thunberg treatment of uterine leiomyoma cellsresulted in a concentration-dependent cell death induced via the caspase dependent mechanism. Conclusion: These results suggest that Houttuynia cordata thunberg treatment in uterine leiomyoma cells leads to growth inhibition and induced apoptosis. These results suggest that Houttuynia cordata thunberg will be a promising agent for use in therapeutics agents against human uterine endometrial cancer.

• Journal of Korean Neurosurgical Society
• /
• v.29 no.7
• /
• pp.918-922
• /
• 2000

Objective : The authors analyzed the results of management outcomes for basilar bifurcation aneurysms treated with transcranial surgery and endovascular surgery. Methods : At the authors' institution between May 1989 and December 1998, 47 aneurysms with 45 patients were treated with transcranial surgery including surgical clipping/wrapping and endovascular surgery for basilar bifurcation aneurysms. The medical records and neuroimaging studies of the patients were reviewed retrospectively. Results : Of the 45 patients, 87 percent of the aneurysms were ruptured and 13% unruptured. Forty six percent of the patients had multiple aneurysms including basilar bifurcation aneurysm. Of the 39 patients with subarachnoid hemorrahge, 77% were in good neurological status(Hunt Hess grade I-III), 23% were in poor grade(H-H grade IV-V). Thirty two patients were treated with transcranial surgery and 15 patients were treated with endovascular surgery. Two patients who had treated with wrapping surgery later bled during follow-up period and treated with endovascular surgery. The management outcome of the transcranial surgery was : Glasgow outcome scale(GOS) I 66%, GOS II 12.5%, GOS III 6.3%, GOS IV 6.3% and GOS V(death) 9.4%. The major causes of morbidity related to transcranial surgery were perforator occlusion, vasospasm and retraction injury. The management outcome of the endovascular surgery was : GOS I 66.7%, GOS II 6.7%, and GOS V 26.7%. The major causes of mortality related to endovascular surgery were related to intraoperative aneurysmal bleeding. Conclusion : This report documents that more than 75% of patients undergoing treatment either transcranial or endovascular surgery can expect good clinical outcomes. Treatment modality in management of basilar bifurcation aneurysm must be carefully selected based on various considering factors.

• Tuberculosis and Respiratory Diseases
• /
• v.83 no.4
• /
• pp.312-320
• /
• 2020

Background: Systemic sclerosis (SSc) involves multiple organ systems and has the highest mortality among connective tissue diseases. Interstitial lung disease is the most common cause of death among SSc patients and requires closer studies and follow-ups. This study aimed to identify lung function changes and predictors of progressive disease in systemic sclerosis-related interstitial lung disease (SSc-ILD). Methods: A retrospective study extracted SSc patients from an electronic database January 2002-July 2019. Eligible cases were SSc patients >age 15 diagnosed with SSc-ILD. Factors associated with progressive disease were analyzed by univariate and multivariate logistic regression analyses. Results: Seventy-eight SSc-ILD cases were enrolled. Sixty-five patients (83.3%) were female, with mean age of 44.7±14.4, and 50 (64.1%) were diffuse type SSc-ILD. Most SSc-ILD patients had crackles (75.6%) and dyspnea on exertion (71.8%), and 19.2% of the SSc-ILD patients had no abnormal respiratory symptoms but had abnormal chest radiographic findings. The most common diagnosis of SSc-ILD patients was non-specific interstitial pneumonia (43.6%). The lung function values of diffusing capacity of the lung for carbon monoxide (DLCO) and DLCO per unit alveolar volume declined in progressive SSc-ILD during a 12-month follow-up. Male and no previous aspirin treatment were the two significant predictive factors of progressive SSc-ILD with adjusted odds ratios of 5.72 and 4.99, respectively. Conclusion: This present study showed that short-term lung function had declined during the 12-month follow-up in progressive SSc-ILD. The predictive factors in progressive SSc-ILD were male sex and no previous aspirin treatment. Close follow-up of the pulmonary function tests is necessary for early detection of progressive disease.

• Journal of Korean Society of Health-System Pharmacists
• /
• v.35 no.4
• /
• pp.430-440
• /
• 2018

Background : Hyponatremia is the most common electrolyte disturbance in hospitalized patients and has been associated with increased morbidity and mortality. Tolvaptan, a vasopressin receptor antagonist, is increasingly used for the treatment of euvolemic and hypervolemic hyponatremia. The aim of this study was to evaluate the effectiveness and safety of tolvaptan for the management of hyponatremia. Methods : This study was a retrospective evaluation of 106 patients who received at least one dose of tolvaptan for hyponatremia at a single tertiary academic hospital between January 2014 and June 2015. The primary endpoint was the change in serum sodium concentration after tolvaptan administration within 24 hours, with secondary endpoints of overcorrection and adverse effects. Results : The mean initial dose of tolvaptan was $20.2{\pm}7.2mg$ and the median duration of treatment was 15 days (range, 1-261 days). The maximal changes in sodium levels at 24 and 48 hours were $8.2{\pm}4.7mmol/L$ and $10.5{\pm}15.3mmol/L$, respectively. Of 99 patients in whom sodium concentrations were followed up, sodium overcorrection was observed in 26 (26.3%) patients, which was associated with concomitant use of an enzyme inhibitor (odds ratio [OR] = 4.80, 95% Cl: 1.27-18.15). However, sex, body mass index (BMI), serum albumin, a daily dose of tolvaptan, and concomitant use of hypertonic saline did not show any significant difference in overcorrection. The most commonly reported adverse effects were mild and related to aquaresis, such as polyuria, thirst, and constipation. However, severe adverse effects such as hyperkalemia, hypotension, and one death related to osmotic demyelination were also reported. Conclusions : Tolvaptan is effective for treating hyponatremia. Nevertheless, the drug should be used cautiously due to serious adverse effects related to sodium overcorrection.

• Biomolecules & Therapeutics
• /
• v.30 no.6
• /
• pp.616-624
• /
• 2022

Mebendazole (MBZ), a microtubule depolymerizing drug commonly used for the treatment of helminthic infections, has been suggested as a repositioning candidate for the treatment of brain tumors. However, the efficacy of MBZ needs further study to improve the beneficial effect on the survival of those patients. In this study, we explored a novel strategy to improve MBZ efficacy using a drug combination. When glioblastoma cells were treated with MBZ, cell proliferation was dose-dependently inhibited with an IC₅₀ of less than 1 µM. MBZ treatment also inhibited glioblastoma cell migration with an IC₅₀ of less than 3 µM in the Boyden chamber migration assay. MBZ induced G2-M cell cycle arrest in U87 and U373 cells within 24 h. Then, at 72 h of treatment, it mainly caused cell death in U87 cells with an increased sub-G1 fraction, whereas polyploidy was seen in U373 cells. However, MBZ treatment did not affect ERK1/2 activation stimulated by growth factors. The marked induction of autophagy by MBZ was observed, without any increased expression of autophagy-related genes ATG5/7 and Beclin 1. Co-treatment with MBZ and the autophagy inhibitor chloroquine (CQ) markedly enhanced the anti-proliferative effects of MBZ in the cells. Triple combination treatment with temozolomide (TMZ) (another autophagy inducer) further enhanced the anti-proliferative effect of MBZ and CQ. The combination of MBZ and CQ also showed an enhanced effect in TMZ-resistant glioblastoma cells. Therefore, we suggest that the modulation of protective autophagy could be an efficient strategy for enhancing the anti-tumor efficacy of MBZ in glioblastoma cells.

• Journal of Life Science
• /
• v.18 no.1
• /
• pp.120-128
• /
• 2008

The death ligand tumor necrosis factor-related apoptosis-inducing ligand (TRAIL)/ Apo1L is a cytokine that activates apoptosis through cell surface death receptors. TRAIL has sparked growing interest in oncology due to its reported ability to selectively trigger cancer cell death. Euphorbiae humifusae Wind has been used in traditional Oriental medicine as a folk remedy used for the treatment of cancer. However, the mechanism responsible for the anticancer effects of E. humifusae not clearly understood. Here, we show that treatment with subtoxic doses of water extract of E. humifusae (WEEH) in combination with TRAIL induces apoptosis in TRAIL-resistant human gastric carcinoma AGS cells. Combined treatment with WEEH and TRAIL induced chromatin condensation and sub-G1 phase DNA content. These indicators of apoptosis were correlated with the induction of caspase activity that resulted in the cleavage of poly (ADP-ribose) polymerase. Combined treatment also triggered the loss of mitochondrial membrane potential. Furthermore, co-treatment with WEEH and TRAIL down-regulated the protein levels of the anti-apoptotic proteins such as Bcl-2, Bcl-xL, XIAP and cIAP-1. Although more study will be needed to examine the detailed mechanisms, this combined treatment may offer an attractive strategy for safely treating gastric adenocarcinomas and the results provide important new insights into the possible molecular mechanisms of the anticancer activity of E. humifusae.

• Biomolecules & Therapeutics
• /
• v.29 no.3
• /
• pp.321-330
• /
• 2021

Oxidative stress plays a crucial role in the development of neuronal disorders including brain ischemic injury. Thioredoxin 1 (Trx1), a 12 kDa oxidoreductase, has anti-oxidant and anti-apoptotic functions in various cells. It has been highly implicated in brain ischemic injury. However, the protective mechanism of Trx1 against hippocampal neuronal cell death is not identified yet. Using a cell permeable Tat-Trx1 protein, protective mechanism of Trx1 against hydrogen peroxide-induced cell death was examined using HT-22 cells and an ischemic animal model. Transduced Tat-Trx1 markedly inhibited intracellular ROS levels, DNA fragmentation, and cell death in H2O2-treatment HT-22 cells. Tat-Trx1 also significantly inhibited phosphorylation of ASK1 and MAPKs in signaling pathways of HT-22 cells. In addition, Tat-Trx1 regulated expression levels of Akt, NF-κB, and apoptosis related proteins. In an ischemia animal model, Tat-Trx1 markedly protected hippocampal neuronal cell death and reduced astrocytes and microglia activation. These findings indicate that transduced Tat-Trx1 might be a potential therapeutic agent for treating ischemic injury.

• Journal of Microbiology
• /
• v.44 no.1
• /
• pp.98-105
• /
• 2006

Yersinia enterocolitica induces a broad range of gastrointestinal syndromes, including acute enteritis. We previously reported that the clinical isolate, Y. enterocolitica KU14, which lacks pYV, was still capable of causing clinical infection. The present study demonstrated that KU14 did not trigger the death of macrophages in vitro, unlike WA-314 (ATCC51871, which harbors the pYV virulence plasmid). However, the intracellular growth of KU14 in the macrophages was greater than that of WA-C (ATCC51872, a non-plasmid harboring the derivative pYV plasmid). Treatment with a cholesterol-binding drug $(\beta-cyclodextrin)$ that affected lipid rafts resulted in a dramatic reduction in the inracellular growth of KU14. These data clearly indicate that the enhanced inracellular growth of KU14 is related to lipid raft-mediated infection.

• Clinical and Experimental Pediatrics
• /
• v.53 no.5
• /
• pp.629-633
• /
• 2010

Pertussis is a highly contagious respiratory tract disease caused by $Bordetella$ $pertussis$ infection. The clinical manifestation of this infection can be severe enough to cause death. Although pertussis has been supposed to be a vaccine-preventable disease ever since the widespread vaccination of children against pertussis was started, since the 1990s, cases of pertussis and related fatalities are on the rise, especially in countries with high vaccination coverage. In Korea, there have been no deaths due to pertussis since 1990, and the vaccination rate continues to be approximately 94%. However, the number of pertussis cases reported to the Korea Center for Disease Control and Prevention has tended to increase in the 2000s, and in 2009, there was an obvious increase in the number of pertussis cases reported. This review aims to present the latest information about the pathogenesis, diagnosis, treatment, and prevention of pertussis.

• Asian Pacific Journal of Cancer Prevention
• /
• v.15 no.5
• /
• pp.1905-1907
• /
• 2014

Increasingly it is being realized that despite considerable advancements in therapeutic interventions related to treatment of cancer, satisfactory results are still difficult to achieve. Rapidly accumulating evidence has started to shed light on the fact that cancer cells escape from death via constitutive activation of pro-survival signaling cascades. Cell biology and genetics have extensively enhanced our current understanding of the molecular mechanisms that underlie loss of apoptosis in cancer cells. This review is focused on ionizing radiation mediated restoration of TRAIL mediated apoptosis as evidenced by cell culture and animal model studies. Moreover, we also bring to the limelight radiation induced expression of miRNAs and how miRNAs further control response of cancer cells to radiation.