1.Neural toxicity induced by accidental intrathecal vincristine administration.
Eun Kyung KWACK ; Dong Ja KIM ; Tae In PARK ; Kab Rae CHO ; Il Hoon KWON ; Yoon Kyung SOHN
Journal of Korean Medical Science 1999;14(6):688-692
Described here is a case of accidental intrathecal administration of vincristine with pathologic findings in the central nervous system. A 3-year-old boy with acute lymphoblastic leukemia, was given his ninth course chemotherapy. Vincristine was accidentally injected intrathecally. The clinical course was rapidly progressive (6-day course) and resulted in death. An autopsy was done. The brain and spinal cord was grossly edematous and congested without any specific feature. Histologically, profound loss of neuron was noted in the spinal cord. Remaining neurons in the spinal cord, particularly anterior horn cells were markedly swollen. The spinal nerves show diffuse axonal degeneration and myelin loss. The upstream portion of the spinal cord (brain stem, cerebellum, cerebrum) showed patchy loss of neurons, especially Purkinje cells and granular cells of the cerebellar cortex. Many neurons showed axonal reaction (chromatolysis) with swelling. Several neurons show intracytoplasmic eosinophilic inclusion body. Myelin loss, axonal swelling and enlargement of perivascular spaces were seen throughout the white matter of central nervous system.
Antineoplastic Agents/therapeutic use*
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Brain/pathology
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Brain/drug effects
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Case Report
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Central Nervous System/pathology
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Central Nervous System/drug effects*
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Child, Preschool
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Fatal Outcome
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Histocytochemistry
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Human
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Injections, Spinal
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Leukemia, Lymphocytic, Acute/drug therapy*
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Male
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Medication Errors*
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Spinal Cord/pathology
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Spinal Cord/drug effects
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Spinal Nerves/pathology
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Spinal Nerves/drug effects
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Vincristine/therapeutic use*
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Vincristine/administration & dosage
2.A Case of Megaureter-Megacystis Association.
Tae Il KWACK ; Eun Yong CHOI ; Myung Soo JUNG ; Dong Sun KIM ; Duck Ki YOON
Korean Journal of Urology 1999;40(1):122-125
Megaureter-megacystis association describes the radiographic appearance of the large capacity, thin-walled bladder and massive primary vesicoureteral reflux. The pathophysiology of these massively dilated ureters and the bladder with large capacity bases on the constant recycling of large volumes of a refluxed urine. We report a case of megaureter-megacystis in 5-year-old girl who had large residual urine(750 ml) with massive ureteral reflux. After removal of left non-functional kidney and dilated ureter, she has gained normal bladder capacity.
Child, Preschool
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Female
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Humans
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Kidney
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Recycling
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Ureter
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Urinary Bladder
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Vesico-Ureteral Reflux
3.Regulation of paclitaxel-induced programmed cell death by autophagic induction: A model for cervical cancer.
Eun Young CHI ; Boonlert VIRIYAPAK ; Hyun Sung KWACK ; Yoon Kyung LEE ; Sang Il KIM ; Keun Ho LEE ; Tae Churl PARK
Obstetrics & Gynecology Science 2013;56(2):84-92
OBJECTIVE: Autophagy plays a vital role in homeostasis by combining organelles and cellular proteins with lysosome under starvation conditions. In addition, autophagy provides tumor cells with a source of energy. Continued autophagy will induce cells death. Here we aim to see if autophagic induction has an effect on conventional chemotherapeutic agents. METHODS: Rapamycin, or mammalian target of rapamycin and paclitaxel, apoptosis-inducing agents were used autophagy in HeLa cervical cancer cells. RESULTS: Growth inhibition of cells was not observed after the application of 0, 10, 20 nM of paclitaxel with or without rapamycin. Using a 5 nM concentration of paclitaxel, rapamycin administration inhibited cell growth significantly compared to no treatment. This implies the synergic antitumor effect of paclitaxel and rapamycin. Paclitaxel itself did not show any autophagic effect on cells but did show cell apoptosis by flow cytometry. Light chain 3, a microtubule-associated protein, which reflect autophagy, was increased with 5 nM of paclitaxel after pretreatment with 10 nM of rapamycin. CONCLUSION: These findings suggest that the autophagic inducer, rapamycin, can potentiate autophagic cell death when added as an apoptosis-inducing chemotherapeutic agent. In conclusion, the control of autophagy may be a future target for chemotherapy.
Apoptosis
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Autophagy
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Cell Death
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Flow Cytometry
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Homeostasis
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Light
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Lysosomes
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Organelles
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Paclitaxel
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Proteins
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Sirolimus
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Starvation
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TOR Serine-Threonine Kinases
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Uterine Cervical Neoplasms