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The Effects of Cyclophosphamide on Apoptosis in Murine Lymphoma
Yang, Jehoon,Bae, Hyung Joon,Seo, Deuk Rok,Koh, Phil Ok,Kwak, Soo Dong 대한의생명과학회 2001 Biomedical Science Letters Vol.7 No.4
Whereas apoptosis is a critical mode of cell deletion in normal organism development, apoptotic cells are also obserced in tumor therapy. We therefore investigated the expression of apoptotic cells induced as a function of time and dose in murine A-20 lymphoma treated with cyclophosphamide in vivo, by H&E and TUNEL method. The percent of apoptotic cells were scored from tumor section using TUNEL method. The expression of apoptotic positive cell was determined over a 10-day period following treatment of the mice with 200 mg/kg. Apotosis increased further with time, reaching a peak value between 12∼24 hr (scored 6.7±1.0%∼6.1±0.7%), and then slowly declined to backgroud levels by 10 days after treatment. The dependence of induction of apoptosis on the dose of cyclophoshamide was determined by treatment with 50, 100, or 200 mg/kg at 12 hr after treatment. Apoptosis was dose dependent in that as the dose was increased the percentage of apoptosis increased. However, the increase in apoptosis at the lower dose used (50 mg/kg was higher on a per unit dose basis than that at the higher dose used (200 mg/kg). This result show that the alkylating agent cyclophoshamide strongly induces apoptosis in murine lymphoma.
Amyloid Polymorphism of α-Synuclein Induced by Active Firefly Luciferase
Yang, Jee Eun,Hong, Je Won,Kim, Jehoon,Paik, Seung R. Korean Chemical Society 2014 Bulletin of the Korean Chemical Society Vol.35 No.2
Amyloidogenic proteins often exhibit fibrillar polymorphism through alternative assembly processes, which has been considered to have possible pathological implications. Here, firefly luciferase (LUC) is shown to induce amyloid polymorphism of ${\alpha}$-synuclein, the major constituent of Lewy bodies found in Parkinson's disease, by acting as a novel template. The drastically accelerated fibrillation kinetics of ${\alpha}$-synuclein with LUC required the nucleation center produced by the active enzyme of LUC. Fluorescent dye binding, transmission electron microscopy, and Fourier transformed infrared spectroscopy revealed the morphologically distinctive amyloid fibrils of ${\alpha}$-synuclein prepared in the absence or presence of LUC. As the altered morphological characteristics became inherent to the mature fibrils, those properties were inherited to next-generations via nucleation-dependent fibrillation process. The seed control, therefore, would be an effective means to modify amyloid fibrils with different biochemical characteristics. In addition, the LUC-directed amyloid fibrillar polymorphism also suggests that other cellular biomolecules including enzymes in general are able to diversify amyloid fibrils, which could be self-propagated with diversified biological activities, if any, inside cells.
Amyloid Polymorphism of α-Synuclein Induced by Active Firefly Luciferase
Jee Eun Yang,Je Won Hong,Jehoon Kim,Seung R. Paik 대한화학회 2014 Bulletin of the Korean Chemical Society Vol.35 No.2
Amyloidogenic proteins often exhibit fibrillar polymorphism through alternative assembly processes, which has been considered to have possible pathological implications. Here, firefly luciferase (LUC) is shown to induce amyloid polymorphism of α-synuclein, the major constituent of Lewy bodies found in Parkinson’s disease, by acting as a novel template. The drastically accelerated fibrillation kinetics of α-synuclein with LUC required the nucleation center produced by the active enzyme of LUC. Fluorescent dye binding, transmission electron microscopy, and Fourier transformed infrared spectroscopy revealed the morphologically distinctive amyloid fibrils of α-synuclein prepared in the absence or presence of LUC. As the altered morphological characteristics became inherent to the mature fibrils, those properties were inherited to next-generations via nucleation-dependent fibrillation process. The seed control, therefore, would be an effective means to modify amyloid fibrils with different biochemical characteristics. In addition, the LUC-directed amyloid fibrillar polymorphism also suggests that other cellular biomolecules including enzymes in general are able to diversify amyloid fibrils, which could be self-propagated with diversified biological activities, if any, inside cells.
Saetbyul Hong,이승은,강인성,Jehoon Yang,Hunnyun Kim,Jeyun Kim,Kyung-Sun Kang 대한수의학회 2021 Journal of Veterinary Science Vol.22 No.1
Background: Niemann-Pick disease type C (NPC) is caused by the mutation of NPC genes, which leads to the abnormal accumulation of unesterified cholesterol and glycolipids in lysosomes. This autosomal recessive disease is characterized by liver dysfunction, hepatosplenomegaly, and progressive neurodegeneration. Recently, the application of induced neural stem cells (iNSCs), converted from fibroblasts using specific transcription factors, to repair degenerated lesions has been considered a novel therapy. Objectives: The therapeutic effects on NPC by human iNSCs generated by our research group have not yet been studied in vivo; in this study, we investigate those effects. Methods: We used an NPC mouse model to efficiently evaluate the therapeutic effect of iNSCs, because neurodegeneration progress is rapid in NPC. In addition, application of human iNSCs from NPC patient-derived fibroblasts in an NPC model in vivo can give insight into the clinical usefulness of iNSC treatment. The iNSCs, generated from NPC patient-derived fibroblasts using the SOX2 and HMGA2 reprogramming factors, were transplanted by intracerebral injection into NPC mice. Results: Transplantation of iNSCs showed positive results in survival and body weight change in vivo. Additionally, iNSC-treated mice showed improved learning and memory in behavior test results. Furthermore, through magnetic resonance imaging and histopathological assessments, we observed delayed neurodegeneration in NPC mouse brains. Conclusions: iNSCs converted from patient-derived fibroblasts can become another choice of treatment for neurodegenerative diseases such as NPC.
수술 전 혈소판 기능 검사를 위한 PFA<sup>®</sup>-100의 임상적 이용
김성만,양승배,이제훈,Kim, Sung-Man,Yang, Seung-Bae,Lee, Jehoon 대한임상검사과학회 2009 대한임상검사과학회지(KJCLS) Vol.41 No.1
The Platelet Function Analyzer (PFA)$^{(R)}$-100 measures the ability of platelets activated in a high-shear environment to occlude an aperture in a membrane treated with collagen and epinephrine (CEPI) or collagen and ADP (CADP). The time taken for the flow across the membrane to stop (closure time, CT) is recorded. The aim of this study was to assess the potential of the PFA$^{(R)}$-100 as a primary clinical screening tool using the wide spectrum of clinical samples assessed for platelet function as well as to perform the optimal algorithm for the use of PFA$^{(R)}$-100. We established the reference interval in 460 hospital inpatients defined as having normal platelet function based on classical laboratory tests. The reference interval by using the range $5^{th}$ and $95^{th}$ percentile was 84~251 seconds for males CEPI-CT and 85~249 seconds for females CEPI-CT. A total of 1,200 inpatients were enrolled to identify impaired hemostasis before surgical interventions. The abnormal group showing prolonged CEPI-CT was 303 cases (18.9%). Only 3 cases had both abnormal CEPI-CT and CADP-CT. Several factors including sample errors, drugs, hematologic abnoralities were contributed to unexpected prolonged CEPI-CT for screening test. The von Willebrand factor (vWF:Ag) assay was performed only in one patient to verify the algorithm for the use of PFA$^{(R)}$-100. The PFA$^{(R)}$-100 was sensitive and rapid method for primary screening test of platelet dysfunction, so we can substitute it for the bleeding time in routine clinical practice.
Kim, Jae‐,Hun,Im, Geun Ho,Yang, Jehoon,Choi, Dongil,Lee, Won Jae,Lee, Jung Hee John Wiley Sons, Ltd 2012 NMR in biomedicine Vol.25 No.4
<P>Dynamic contrast‐enhanced MRI (DCE‐MRI) is widely accepted for the evaluation of cancer. DCE‐MRI, a noninvasive measurement of microvessel permeability, blood volume and blood flow, is extremely useful for understanding disease mechanisms and monitoring therapeutic responses in preclinical research. For the accurate quantification of pharmacokinetic parameters using DCE‐MRI, determination of the arterial input function (AIF) from a large arterial vessel near the tumor is required. However, a manual determination of AIF in mouse MR images is often difficult because of the small spatial dimensions or the location of the tumor. In this study, we propose an algorithm for the automatic detection of AIF from mouse DCE‐MR images using Kendall's coefficient of concordance. The proposed method was tested with computer simulations and then applied to tumor‐bearing mice (<I>n</I> = 8). Results from computer simulations showed that the proposed algorithm is capable of categorizing simulated AIF signals according to their noise levels. We found that the resulting pharmacokinetic parameters computed from our method were comparable with those from the manual determination of AIF, with acceptable differences in <I>K</I><SUP>trans</SUP> (5.14 ± 3.60%), <I>v</I><SUB>e</SUB> (6.02 ± 3.22%), <I>v</I><SUB>p</SUB> (5.10 ± 7.05%) and <I>k</I><SUB>ep</SUB> (5.38 ± 4.72%). The results of the current study suggest the usefulness of an automatically defined AIF using Kendall's coefficient of concordance for quantitative DCE‐MRI in mouse models for cancer evaluation. Copyright © 2011 John Wiley & Sons, Ltd.</P>