http://chineseinput.net/에서 pinyin(병음)방식으로 중국어를 변환할 수 있습니다.
변환된 중국어를 복사하여 사용하시면 됩니다.
S-555 A case of vincristine-induced unilateral ptosis in the diffuse large B cell lymphoma
( Byung Chan Ahn ),( Myeong Soon Park ),( Eun Hee Jung ),( Jin Young Kim ),( Keon Uk Park ),( Hong Suk Song ),( Ki Young Kwon ),( Young Rok Do ) 대한내과학회 2016 대한내과학회 추계학술대회 Vol.2016 No.1
Aim Vincristine is commonly used in the treatment of leukemia and lymphoma. This drug is associated with dose-limiting neurotoxicity, which can be manifest as peripheral, autonomic and cranial neuropathy. Cranial nerve neuropathies are reported less frequently and emerge as mostly bilateral pattern. We introduce the recovery of a vincristine-induced unilateral ptosis after treatment with pyridoxine and pyridostigmine. Patient and method A 55-year-old man was diagnosed with diffuse large B cell lymphoma (DLBCL) and had received 5 cycles of R-CHOP chemotherapy. 17 days after the 5th cycle of R-CHOP, he presented unilateral ptosis at left eye with eyeball deviation to lateral side. He received 10mg of cumulative dose of vincristine before development of the symptom. Neurologic exam revealed no hypotonia in both limbs. Ophthalmologic exam, Laboratory tests, CSF study showed normal results. Result Our initial impression was intracranial or intraorbital involvement of DLBCL. However, brain MRI exhibited no abnormal finding. We assumed that the development of ptosis and ophthalmoplegia in the patient receiving a chemotherapy including R-CHOP regimen, and focused on vincristine-induced neurotoxicity. There were some available case reports that pyridoxine and pyridostigmine may be helpful in patients with vincristine-induced neuropathy. The patient received pyridoxine (3 mg/kg twice daily, PO), pyridostigmine (150 mg/m2 twice daily, PO). After 4 weeks of treatment, his symptoms markedly improved. He completed the 6th cycle of R-CHOP chemotherapy without vincristine then received autologous hematopoietic stem cell transplantation. At this time, he is in the recovery phase of transplantation and his neurologic symptoms are completely recovered. Conclusion The neurotoxicity of vincristine is dose-related and cumulative with repeated dosage. Most of the symptoms of neurotoxicity are reversible after adjusting the dosage or elimination of vincristine. In our patient we treated vincristine-induced neurotoxicity with pyridoxine and pyridostigmine treatment. This report shows that vincristine-induced neurotoxicity should be considered as a cause of cranial neuropathy that develops during the treatment of the DLBCL. Aim: Vincristine is commonly used in the treatment of leukemia and lymphoma. This drug is associated with dose-limiting neurotoxicity, which can be manifest as peripheral, autonomic and cranial neuropathy. Cranial nerve neuropathies are reported less frequently and emerge as mostly bilateral pattern. We introduce the recovery of a vincristine-induced unilateral ptosis after treatment with pyridoxine and pyridostigmine. Patient and method: A 55-year-old man was diagnosed with diffuse large B cell lymphoma (DLBCL) and had received 5 cycles of R-CHOP therapy. 17 days after the 5th cycle of R-CHOP, he presented unilateral ptosis at left eye with eyeball deviation to lateral side. He received 10mg of cumulative dose of vincristine before development of the symptom. Neurologic exam revealed no hypotonia in both limbs. Ophthalmologic exam, Laboratory tests, CSF study showed normal results. Results: Our initial impression was intracranial or intraorbital involvement of DLBCL. However, brain MRI exhibited no abnormal finding. We assumed that the development of ptosis and ophthalmoplegia in the patient receiving a chemotherapy including R-CHOP regimen, and focused on vincristine-induced neurotoxicity. There were some available case reports that pyridoxine and pyridostigmine may be helpful in patients with vincristine-induced neuropathy. The patient received pyridoxine (3 mg/kg twice daily, PO), pyridostigmine (150mg/m2 twice daily, PO). After 4 weeks of treatment, his symptoms markedly improved. He completed the sixth cycle of R-CHOP chemotherapy without vincristine then received autologous hematopoietic stem cell transplantation. At this time, he is in the recovery phase of transplantation and his neurologic symptoms are completely recovered. Conclusions: The neurotoxicity of vincristine is dose-related and cumulative with repeated dosage. Most of the symptoms of neurotoxicity are reversible after adjusting the dosage or elimination of vincristine. In our patient we treated vincristine-induced neurotoxicity with pyridoxine and pyridostigmine treatment. This report shows that vincristine-induced neurotoxicity should be considered as a cause of cranial neuropathy that develops during the treatment of the DLBCL.
Concise Synthesis of Biologically Interesting Mollugin and Its Analogues
Lee, Yong-Rok,Wang, Xue,Kim, Yun-Mi,Shim, Jae-Jin,Kim, Byung-Nam,Han, Do-Hung Korean Chemical Society 2007 Bulletin of the Korean Chemical Society Vol.28 No.10
The synthesis of naturally occurring mollugin and its analogues, 3,4-dihydromollugin, cis-3,4-dihydroxy-3,4- dihydromollugin, and trans-3,4-dihydroxy-3,4-dihydromollugin was achieved starting from 1,4-dihydroxynaphthalene- 2-carboxylic acid. The key reaction is an electrocyclization for pyranyl ring formation in the presence of PhB(OH)2/AcOH.
( In-a Cho ),( Kyeong-rok Kang ),( Su-gwan Kim ),( Do Kyung Kim ),( Chun Sung Kim ),( Sook-young Lee ),( Seung Sik Cho ),( Goo Yoon ),( Byung Soo Park ),( Jae-sung Kim ) 조선대학교 구강생물학연구소 2017 Oral Biology Research (Oral Biol Res) Vol.41 No.4
This study investigates the anti-cancer effects of licochalcone-E (Lico-E), a phenolic chalconoid derived from the genus Glycyrrhiza, in the human KB squamous cancer cell. Concentration-dependent cytotoxicity in KB cells increased following 24 hours of treatment with 12.5, 25, or 50 μg/ml Lico-E, with an estimated IC<sub>50</sub> value of approximately 25 μg/ml. Chromatin condensation, a typical apoptotic phenomenon, was observed in KB cells treated with Lico-E. Consistent with this finding, Lico-E increased caspase-3 activity in KB cells. FasL, a death ligand associated with extrinsic apoptotic signaling pathways, was significantly up-regulated by Lico-E treatment. Subsequently, the pro-apoptotic factor caspase-8, a part of the extrinsic apoptotic signaling pathway, was activated in a concentrationdependent manner by Lico-E treatments. Expression of anti-apoptotic factors such as Bcl-2 and Bcl-xL, components of the mitochondriadependent apoptotic signaling pathway, significantly decreased following Lico-E treatment. Conversely, expression of pro-apoptotic factors such as Bax, Bad, Apaf-1, and caspase-9 increased with Lico-E concentrations. Finally, Lico-E activated caspase-3 and Poly (ADP-ribose) polymerase (PARP) to induce cell death. Z-VAD-fmk significantly inhibited cell death through suppression of caspase-3 expression in KB cells treated with Lico-E. Taken together, Lico-E induces KB cell death through death receptor and mitochondriadependent apoptotic signaling pathways.
Role of Ras/ERK-dependent pathway in the erythroid differentiation of K562 cells
Kang, Chi-Dug,Do, In-Rok,Kim, Kwang-Woon,Ahn, Byung-Kwon,Kim, Sun-Hee,Chung, Byung-Seon,Jhun, Byung-Hak,Yoo, Mi-Ae 부산대학교 유전공학연구소 1999 분자생물학 연구보 Vol.15 No.-
The chronic myelogenous leukemic K562 cell line carrying Bcr-Abl tyrosine kinase is considered as pluripotent hematopoietic progenitor cells expressing markers for erythroid, granulocytic, monocytic, and megakaryocytid lineages. Here we investigated the signaling modulations required for induction of erythroid differentiation of K562 cells. When the K562 cells were treated with herbimycin A(an inhibitor of protein tyrosine kinase), ras antisense oligonucleotide, and PD98059 (a specific inhibitor of MEK), inhibition of ERK/MAPK activity and cell growth, and induction of erythroid differentiation were observed. The ras mutant, pZIPRas^61leu -transfected cells, K562-Ras^61leu have shown a markedly decreased cell proliferation rate with approximately 2-fold doubling time, compared with 2-fold doubling time, compared with the parental K562 cells, and about 60% of these cells have shown the phenotype of erythroid differentiation. In addition, herbimycin A inhibited the growth rate and increased the erythroid differentiation, but did not affect the elevated activity of ERK/MAPK in the K562-Ras^61leu cells. On the other hand, effects of PD98059 on the growth and differentiation of K562-Ras^61leu cells were biphasic. At low concentration of PD98059, which inhibited the elevated activity of ERK/MAPK to the level of parental cells, the growth rate increased and the erythroid differentiation decreased slightly, and at high concentration of PD98059, which inhibited the elevated activity of ERK/MAPK below that of the parental cells, the growth rate turned down and the erythroid differentiation was restored to the untreated control level. Taken together, these results suggest that an appropriate activity of ERK/MAPK is required to maintain the rapid growth and transformed phenotype of K562 cells.