1.Report of Benign and Malignant Adenomyoepithelioma of the Breast.
Kwang Jo KIM ; Jin Woo RYU ; Na Hye MYONG
Journal of Korean Breast Cancer Society 2003;6(2):124-126
Adenomyoepithelioma is a rare benign tumor which occurs mainly in the skin, salivary gland and very rarely in the breast, in case of malignant adenomyoepithelioma of the breast is a rare lesion characterized by malignant proliferation of epithelial and myoepithelial cells that show characteristic histology and immunohistochemical features. We report two cases of adenomyoepithelioma, one was benign occuring in the outer upper quadrant of the right breast (48-year-old female), and the other was malignant adenomyoepithelioma occuring in the peri-areolar of the left breast (46-years-old female). We confirmed with both H&E stain and immunohistochemistry. We report benign and malignant adenomyoepithelioma of the breast occurred in middle aged women.
Adenomyoepithelioma*
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Breast*
;
Female
;
Humans
;
Immunohistochemistry
;
Middle Aged
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Salivary Glands
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Skin
2.Acetylcholinesterase Inhibitors from Angelica polymorpha Stem.
Yongsoo KWON ; Hyun Pyo KIM ; Myong Jo KIM ; Wanjoo CHUN
Natural Product Sciences 2017;23(2):97-102
Fourteen compounds were isolated from the stem of Angelica polymorpha. On the basis of spectral data, these compounds were identified as isoimperatorin (1), phellopterin (2), bergapten (3), xanthyletin (4), cnidilin (5), geijerine (6), (−)-3'-acetyl hamaudol (7), 7-demethylsuberosine (8), dehydrogeijerin (9), (−)-hamaudol (10), (+)-visamminol (11), divaricatol (12), scopoletin (13), and decursidate (14), respectively. Among them, compounds 4 - 6, 8, 9, 13, and 14 were isolated for the first time from A. polymorpha. Dehydrogeijerin (6) and geijerin (9) were isolated for the first time from genus Angelica. All isolates tested for inhibitory activity against acetylcholinesterae. Compounds 1 to 13 showed acetylcholinesterase inhibitory activity with IC₅₀ values ranging from 1.4 to 37.5 µM.
Acetylcholinesterase*
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Angelica*
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Cholinesterase Inhibitors*
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Chromones
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Coumarins
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Scopoletin
3.Subsequent Reproductive Experiences after Treatments for Gestational Trophoblastic Disease.
Cheon Ok SEO ; Jae Hoon KIM ; Eun A CHOI ; Hee Young SONG ; Myong Jae PARK ; Seog Nyeon BAE ; Seung Jo KIM ; Sung Eun NAMKOONG
Korean Journal of Obstetrics and Gynecology 1997;40(8):1690-1695
For evaluating the reproductive performances of GTD patients, we found 115 cases of GTD patients, 77 HM and 38 GTT, who became pregnant after the completion of treatments and follow-up period. The results of this study suggest subsequent pregnancies after the completion of treatments may promise normal reproductive outcomes regardless of the chemotherapy.
Drug Therapy
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Follow-Up Studies
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Gestational Trophoblastic Disease*
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Humans
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Pregnancy
4.A New Stereoisomeric Monoterpene Glycoside from Clematis heracleifolia leaves.
Mi Ae KIM ; Heejung YANG ; Myong Jo KIM ; Wanjoo CHUN ; Yongsoo KWON
Natural Product Sciences 2016;22(2):107-110
A new stereoisomeric monoterpene glycoside and five already-known compounds were isolated from the n-BuOH soluble fraction of Clematis heracleifolia leaves. On the basis of spectral data, the structures of the isolated compounds were identified as protocatechuic acid (1), ferulic acid (2), caffeic acid (3), aesculin (4), (6Z)-9-hydroxylinaloyl glucoside (5), and 9-hydroxylinaloyl glucoside (6) and these were isolated for the first time from this plant. Among these compounds, (6Z)-9-hydroxylinaloyl glucoside (5) is a newly isolated from plant source.
Clematis*
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Esculin
;
Plants
;
Stereoisomerism*
5.A New Phenolic Compound from Lespedeza tomentosa
Hyeon Seok JANG ; Seong Yeon CHOI ; Heejung YANG ; Myong Jo KIM ; Wanjoo CHUN ; Yongsoo KWON
Natural Product Sciences 2021;27(3):169-171
A new phenolic compound and three known flavonoids isolated from the MeOH extracts of Lespedeza tomentosa. Based on spectral data, the isolated compounds were identified as methyl 4,5-dihydroxy-3-methoxy-2-(3-methylbut-2-en-1-yl)benzoate (1), 1-methoxylespeflorin G11 (2), farrerol (3) and 1-methoxylespeflorin I2 (4). Methyl 4,5- dihydroxy-3-methoxy-2-(3-methylbut-2-en-1-yl)benzoate (1) is newly isolated from plant source.
6.A New Phenolic Compound from Lespedeza tomentosa
Hyeon Seok JANG ; Seong Yeon CHOI ; Heejung YANG ; Myong Jo KIM ; Wanjoo CHUN ; Yongsoo KWON
Natural Product Sciences 2021;27(3):169-171
A new phenolic compound and three known flavonoids isolated from the MeOH extracts of Lespedeza tomentosa. Based on spectral data, the isolated compounds were identified as methyl 4,5-dihydroxy-3-methoxy-2-(3-methylbut-2-en-1-yl)benzoate (1), 1-methoxylespeflorin G11 (2), farrerol (3) and 1-methoxylespeflorin I2 (4). Methyl 4,5- dihydroxy-3-methoxy-2-(3-methylbut-2-en-1-yl)benzoate (1) is newly isolated from plant source.
7.In vitro Antibacterial and Morphological Effects of the Urushiol Component of the Sap of the Korean lacquer tree (Rhus vernicifera Stokes) on Helicobacter pylori.
Ki Tae SUK ; Hyun Soo KIM ; Moon Young KIM ; Jae Woo KIM ; Young UH ; In Ho JANG ; Soo Ki KIM ; Eung Ho CHOI ; Myong Jo KIM ; Jung Soo JOO ; Soon Koo BAIK
Journal of Korean Medical Science 2010;25(3):399-404
Eradication regimens for Helicobacter pylori infection have some side effects, compliance problems, relapses, and antibiotic resistance. Therefore, alternative anti-H. pylori or supportive antimicrobial agents with fewer disadvantages are necessary for the treatment of H. pylori. We investigated the pH-(5.0, 6.0, 7.0, 8.0, 9.0, and 10.0) and concentration (0.032, 0.064, 0.128, 0.256, 0.514, and 1.024 mg/mL)-dependent antibacterial activity of crude urushiol extract from the sap of the Korean lacquer tree (Rhus vernicifera Stokes) against 3 strains (NCTC11637, 69, and 219) of H. pylori by the agar dilution method. In addition, the serial (before incubation, 3, 6, and 10 min after incubation) morphological effects of urushiol on H. pylori were examined by electron microscopy. All strains survived only within pH 6.0-9.0. The minimal inhibitory concentrations of the extract against strains ranged from 0.064 mg/mL to 0.256 mg/mL. Urushiol caused mainly separation of the membrane, vacuolization, and lysis of H. pylori. Interestingly, these changes were observed within 10 min following incubation with the 1 x minimal inhibitory concentrations of urushiol. The results of this work suggest that urushiol has potential as a rapid therapeutic against H. pylori infection by disrupting the bacterial cell membrane.
Anti-Bacterial Agents/chemistry/*pharmacology/therapeutic use
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Catechols/chemistry/*pharmacology/therapeutic use
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Cell Membrane/drug effects/ultrastructure
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Helicobacter Infections/drug therapy
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Helicobacter pylori/*drug effects/ultrastructure
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Humans
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Microbial Sensitivity Tests
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Microbial Viability/drug effects
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Molecular Structure
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Rhus/*chemistry
8.Celecoxib Attenuates Kainic Acid-induced Neuronal Cell Death Through Suppression of Microglial c-Jun N-terminal Kinase Phosphorylation.
Jong Seon BYUN ; So Young CHO ; Song In KIM ; Yong Soo KWON ; Seong Ho JEON ; Myong Jo KIM ; Hee Jae LEE ; Sung Soo KIM ; Wanjoo CHUN
Experimental Neurobiology 2009;18(1):13-18
In the present study, neuroprotective property of celecoxib, a selective cyclooxygenase-2 (COX-2) inhibitor, and its underlying mechanism were examined in the animal model of kainic acid (KA)-induced excitotoxicity. KA, administered intracerebroventricularly (i.c.v.), induced marked neuronal cell death with concurrent microglial activation and subsequent induction of inducible nitric oxide synthase (iNOS) in the hippocampus. Histopathological analysis demonstrated that celecoxib (100 mg/kg), pre-treated 1 hr before or post-treated 2 hr after KA i.c.v. injection, significantly attenuated KA-induced death of pyramidal neurons in CA3 region. Celecoxib obviously suppressed KA-induced microglial activation and subsequent iNOS expression. KA- induced phosphorylation of c-Jun N-terminal kinases (JNK) was attenuated with celecoxib treatments. The results of the present study demonstrate that suppression of JNK phosphorylation by celecoxib contributes to its neuroprotective action against KA-induced excitotoxicity suggesting that celecoxib may be a potentially valuable in the treatment of acute brain pathologies associated with excitotoxic neuronal damage such as epilepsy, stroke, and traumatic brain injury.
Brain
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Brain Injuries
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Cell Death
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Cyclooxygenase 2
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Epilepsy
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Hippocampus
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JNK Mitogen-Activated Protein Kinases
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Kainic Acid
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Microglia
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Models, Animal
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Neurons
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Nitric Oxide Synthase Type II
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Phosphorylation
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Phosphotransferases
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Pyrazoles
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Stroke
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Sulfonamides
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Celecoxib
9.A Case of Endobronchial Aspergillosis Completely Obstructing Lobar Bronchus.
Byong Jo PARK ; Young Ki KIM ; Hansoo KIM ; Yee Hyung KIM ; Hyang Ie LEE ; Hong Mo KANG ; Cheon Woong CHOI ; Jee Hong YOO ; Myong Jae PARK
Tuberculosis and Respiratory Diseases 2005;59(3):311-314
Pulmonary aspergillosis may present with three different features, according to the immune status of the host. These forms are invasive aspergillosis, allergic bronchopulmonary aspergillosis (ABPA) or aspergilloma. Bronchial involvement is an uncommon type of invasive pulmonary aspergillosis. We encountered an unusual case of an endobronchial aspergillosis that completely obstructed the left upper lobe, which was initially thought to be lung cancer. We report this case along with a review of the relevant literature.
Aspergillosis*
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Aspergillosis, Allergic Bronchopulmonary
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Bronchi*
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Invasive Pulmonary Aspergillosis
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Lung Neoplasms
;
Pulmonary Aspergillosis
10.Kainic Acid-induced Neuronal Death is Attenuated by Aminoguanidine but Aggravated by L-NAME in Mouse Hippocampus.
Jong Seon BYUN ; Sang Hyun LEE ; Seong Ho JEON ; Yong Soo KWON ; Hee Jae LEE ; Sung Soo KIM ; Young Myeong KIM ; Myong Jo KIM ; Wanjoo CHUN
The Korean Journal of Physiology and Pharmacology 2009;13(4):265-271
Nitric oxide (NO) has both neuroprotective and neurotoxic effects depending on its concentration and the experimental model. We tested the effects of NG-nitro-L-arginine methyl ester (L-NAME), a nonselective nitric oxide synthase (NOS) inhibitor, and aminoguanidine, a selective inducible NOS (iNOS) inhibitor, on kainic acid (KA)-induced seizures and hippocampal CA3 neuronal death. L-NAME (50 mg/kg, i.p.) and/or aminoguanidine (200 mg/kg, i.p.) were administered 1 h prior to the intracerebroventricular (i.c.v.) injection of KA. Pretreatment with L-NAME significantly increased KA-induced CA3 neuronal death, iNOS expression, and activation of microglia. However, pretreatment with aminoguanidine significantly suppressed both the KA-induced and L-NAME-aggravated hippocampal CA3 neuronal death with concomitant decreases in iNOS expression and microglial activation. The protective effect of aminoguanidine was maintained for up to 2 weeks. Furthermore, iNOS knockout mice (iNOS-/-) were resistant to KA-induced neuronal death. The present study demonstrates that aminoguanidine attenuates KA-induced neuronal death, whereas L-NAME aggravates neuronal death, in the CA3 region of the hippocampus, suggesting that NOS isoforms play different roles in KA-induced excitotoxicity.
Animals
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Guanidines
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Hippocampus
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Kainic Acid
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Mice
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Mice, Knockout
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Microglia
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Models, Theoretical
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Neurons
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NG-Nitroarginine Methyl Ester
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Nitric Oxide
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Nitric Oxide Synthase
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Protein Isoforms
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Seizures