1.A Case of Ophthalmoplegia Caused by Herpes Zoster Ophthalmicus.
Chun Gang BAK ; Dong Chul JUN ; Ju Han KIM ; Hee Tae KIM ; Seung Hyun KIM ; Myung Ho KIM
Journal of the Korean Neurological Association 2002;20(3):295-297
Ophthalmoplegia may accompany herpes zoster ophthalmicus(HZO). A 60-year-old woman with rheumatoid arthritis suffered from HZO in the right side consecutively developed a mydriasis and abduction deficit in the right eye. CSF examination revealed pleocytosis and increased protein, while magnetic resonance imaging of the brain was normal. She was treated with intravenous acyclovir for 7 days. Ophthalmoplegia was completely resolved over the following 8 weeks, but mydriasis persisted.
Acyclovir
;
Arthritis, Rheumatoid
;
Brain
;
Female
;
Herpes Zoster Ophthalmicus*
;
Herpes Zoster*
;
Humans
;
Leukocytosis
;
Magnetic Resonance Imaging
;
Middle Aged
;
Mydriasis
;
Ophthalmoplegia*
2.A Boy with Adrenocortical Tumor Who Progressed to Central Precocious Puberty after Surgery.
Hee Won CHUEH ; Nu Ri BAK ; Myo Jing KIM ; Jae Ho YOO ; Mi Sook RHO ; Won Yeol CHO
Annals of Pediatric Endocrinology & Metabolism 2012;17(1):57-61
Adrenocortical tumors in children are rare and show various clinical symptoms. We present an 8-year-old boy with peripheral precocious puberty caused by adrenocortical tumor. He showed elevated serum DHEA-S and 17-hydroxyprogesterone, and computed tomography revealed an abdominal mass. After surgical resection, he developed central precocious puberty. We report a rare case that showed progression from peripheral precocious puberty to central precocious puberty.
17-alpha-Hydroxyprogesterone
;
Adrenal Cortex Neoplasms
;
Child
;
Humans
;
Puberty, Precocious
3.Omega-3 Polyunsaturated Fatty Acids May Attenuate Streptozotocin-Induced Pancreatic beta-Cell Death via Autophagy Activation in Fat1 Transgenic Mice.
Won Min HWANG ; Dong Ho BAK ; Dong Ho KIM ; Ju Young HONG ; Seung Yun HAN ; Keun Young PARK ; Kyu LIM ; Dong Mee LIM ; Jae Gu KANG
Endocrinology and Metabolism 2015;30(4):569-575
BACKGROUND: Inflammatory factors and beta-cell dysfunction due to high-fat diets aggravate chronic diseases and their complications. However, omega-3 dietary fats have anti-inflammatory effects, and the involvement of autophagy in the etiology of diabetes has been reported. Therefore, we examined the protective effects of autophagy on diabetes using fat-1 transgenic mice with omega-3 self-synthesis capability. METHODS: Streptozotocin (STZ) administration induced beta-cell dysfunction in mice; blood glucose levels and water consumption were subsequently measured. Using hematoxylin and eosin (H&E) and Masson's trichrome staining, we quantitatively assessed STZ-induced changes in the number, mass, and fibrosis of pancreatic islets in fat-1 and control mice. We identified the microtubule-associated protein 1A/1B light chain 3-immunoreactive puncta in beta-cells and quantified p62 levels in the pancreas of fat-1 and control mice. RESULTS: STZ-induced diabetic phenotypes, including hyperglycemia and polydipsia, were attenuated in fat-1 mice. Histological determination using H&E and Masson's trichrome staining revealed the protective effects of the fat-1 expression on cell death and the scarring of pancreatic islets after STZ injection. In the beta-cells of control mice, autophagy was abruptly activated after STZ treatment. Basal autophagy levels were elevated in fat-1 mice beta-cells, and this persisted after STZ treatment. Together with autophagosome detection, these results revealed that n-3 polyunsaturated fatty acid (PUFA) enrichment might partly prevent the STZ-related pancreatic islet damage by upregulating the basal activity of autophagy and improving autophagic flux disturbance. CONCLUSION: Fat-1 transgenic mice with a n-3 PUFA self-synthesis capability exert protective effects against STZ-induced beta-cell death by activating autophagy in beta-cells.
Animals
;
Autophagy*
;
Blood Glucose
;
Cell Death
;
Chronic Disease
;
Cicatrix
;
Diet, High-Fat
;
Dietary Fats
;
Drinking
;
Eosine Yellowish-(YS)
;
Fatty Acids, Omega-3
;
Fatty Acids, Unsaturated*
;
Fibrosis
;
Hematoxylin
;
Hyperglycemia
;
Islets of Langerhans
;
Mice
;
Mice, Transgenic*
;
Pancreas
;
Phenotype
;
Polydipsia
;
Streptozocin
4.Two Difficultly Diagnosed Cases with Pseudoaneurysm in Chronic Pancreatitis Pseudoaneurysms Identified Inadvertently during Percutaneous Drainage and Hemosuccus Pancreaticus.
Ji Hoon KIM ; Hwi KONG ; Nam Young JO ; Dong Wook KOH ; Yeon Ho PARK ; Hyo Jung KIM ; Gil Man JUNG ; Jae Seon KIM ; Young Tae BAK ; Chang Hong LEE
Korean Journal of Gastrointestinal Endoscopy 2001;23(4):263-268
Pseudoaneurysm is a rare life-threatening complication of chronic pancreatitis. It can be diagnosed by various imaging modalities including computerized tomography (CT), ultrasound, and angiography. Early diagnosis and radiologic or surgical treatment can promise better outcomes. However, pseudoaneurysm is not easily diagnosed. It can be misdiagnosed as a pseudocyst with secondary infection. Rarely, the correct diagnosis is made by an inadvertent trial with percutaneous drainage. The endoscopically identified hemosuccus pancreaticus is also a rare finding. Recently, we experienced two cases of pseudoaneurysm in patients with chronic pancreatitis. They did not have any evidence of bleeding in the initial endoscopy or evidence of pseudoaneurysms in the initial ultrasound and CT scan. In one case, the pseudoaneurysm was identified during a percutaneous drainage procedure, performed to diagnose and manage a cystic lesion which appeared to be an infected cyst. In the other case, the pseudoaneurysm was suspected after the hemosuccus pancreaticus was found during endoscopy performed due to recurrent hematemesis. Both cases were successfully treated with arterial embolization of the pseudoaneurysms.
Aneurysm, False*
;
Angiography
;
Coinfection
;
Diagnosis
;
Drainage*
;
Early Diagnosis
;
Endoscopy
;
Hematemesis
;
Hemorrhage
;
Humans
;
Pancreatitis, Chronic*
;
Tomography, X-Ray Computed
;
Ultrasonography
5.Inhibition of melanogenesis by sodium 2-mercaptoethanesulfonate
Jeong Hwan KIM ; Chang Taek OH ; Tae Rin KWON ; Jong Hwan KIM ; Dong Ho BAK ; Hyuk KIM ; Won Seok PARK ; Beom Joon KIM
The Korean Journal of Physiology and Pharmacology 2020;24(2):149-156
Sodium 2-mercaptoethanesulfonate (mesna) is a protective agent that is widely used in medicine because of its antioxidant effects. Recently, reactive oxygen species (ROS) were shown to increase pigmentation. Thus, ROS scavengers and inhibitors of ROS production may suppress melanogenesis. Forkhead box-O3a (FoxO3a) is an antimelanogenic factor that mediates ROS-induced skin pigmentation. In this study, we aimed to investigate the whitening effect of mesna and the signaling mechanism mediating this effect. Human melanoma (MNT-1) cells were used in this study. mRNA and protein expression were measured by real-time quantitative PCR and Western blotting analysis to track changes in FoxO3a-related signals induced by mesna. An immunofluorescence assay was performed to determine the nuclear translocation of FoxO3a. When MNT-1 melanoma cells were treated with mesna, melanin production and secretion decreased. These effects were accompanied by increases in FoxO3a activation and nuclear translocation, resulting in downregulation of four master genes of melanogenesis: MITF, TYR, TRP1, and TRP2. We found that mesna, an antioxidant and radical scavenger, suppresses melanin production and may therefore be a useful agent for the clinical treatment of hyperpigmentation disorders.
6.Delphinidin enhances radio-therapeutic effects via autophagyinduction and JNK/MAPK pathway activation in non-small celllung cancer
Seong Hee KANG ; Dong-Ho BAK ; Byung Yeoup CHUNG ; Hyoung-Woo BAI ; Bo Sun KANG
The Korean Journal of Physiology and Pharmacology 2020;24(5):413-422
Delphinidin is a major anthocyanidin compound found in various vegetablesand fruits. It has anti-oxidant, anti-inflammatory, and various other biologicalactivities. In this study we demonstrated the anti-cancer activity of delphinidin,which was related to autophagy, in radiation-exposed non-small cell lung cancer(NSCLC). Radiosensitising effects were assessed in vitro by treating cells with a subcytotoxicdose of delphinidin (5 M) before exposure to -ionising radiation (IR). Wefound that treatment with delphinidin or IR induced NSCLC cell death in vitro; howeverthe combination of delphinidin pre-treatment and IR was more effective thaneither agent alone, yielding a radiation enhancement ratio of 1.54 at the 50% lethaldose. Moreover, combined treatment with delphinidin and IR, enhanced apoptoticcell death, suppressed the mTOR pathway, and activated the JNK/MAPK pathway.Delphinidin inhibited the phosphorylation of PI3K, AKT, and mTOR, and increasedthe expression of autophagy-induced cell death associated-protein in radiation-exposedNSCLC cells. In addition, JNK phosphorylation was upregulated by delphinidinpre-treatment in radiation-exposed NSCLC cells. Collectively, these results show thatdelphinidin acts as a radiation-sensitizing agent through autophagy induction andJNK/MAPK pathway activation, thus enhancing apoptotic cell death in NSCLC cells.
7.Inhibition of melanogenesis by sodium 2-mercaptoethanesulfonate
Jeong Hwan KIM ; Chang Taek OH ; Tae Rin KWON ; Jong Hwan KIM ; Dong Ho BAK ; Hyuk KIM ; Won Seok PARK ; Beom Joon KIM
The Korean Journal of Physiology and Pharmacology 2020;24(2):149-156
Sodium 2-mercaptoethanesulfonate (mesna) is a protective agent that is widely used in medicine because of its antioxidant effects. Recently, reactive oxygen species (ROS) were shown to increase pigmentation. Thus, ROS scavengers and inhibitors of ROS production may suppress melanogenesis. Forkhead box-O3a (FoxO3a) is an antimelanogenic factor that mediates ROS-induced skin pigmentation. In this study, we aimed to investigate the whitening effect of mesna and the signaling mechanism mediating this effect. Human melanoma (MNT-1) cells were used in this study. mRNA and protein expression were measured by real-time quantitative PCR and Western blotting analysis to track changes in FoxO3a-related signals induced by mesna. An immunofluorescence assay was performed to determine the nuclear translocation of FoxO3a. When MNT-1 melanoma cells were treated with mesna, melanin production and secretion decreased. These effects were accompanied by increases in FoxO3a activation and nuclear translocation, resulting in downregulation of four master genes of melanogenesis: MITF, TYR, TRP1, and TRP2. We found that mesna, an antioxidant and radical scavenger, suppresses melanin production and may therefore be a useful agent for the clinical treatment of hyperpigmentation disorders.
8.Delphinidin enhances radio-therapeutic effects via autophagyinduction and JNK/MAPK pathway activation in non-small celllung cancer
Seong Hee KANG ; Dong-Ho BAK ; Byung Yeoup CHUNG ; Hyoung-Woo BAI ; Bo Sun KANG
The Korean Journal of Physiology and Pharmacology 2020;24(5):413-422
Delphinidin is a major anthocyanidin compound found in various vegetablesand fruits. It has anti-oxidant, anti-inflammatory, and various other biologicalactivities. In this study we demonstrated the anti-cancer activity of delphinidin,which was related to autophagy, in radiation-exposed non-small cell lung cancer(NSCLC). Radiosensitising effects were assessed in vitro by treating cells with a subcytotoxicdose of delphinidin (5 M) before exposure to -ionising radiation (IR). Wefound that treatment with delphinidin or IR induced NSCLC cell death in vitro; howeverthe combination of delphinidin pre-treatment and IR was more effective thaneither agent alone, yielding a radiation enhancement ratio of 1.54 at the 50% lethaldose. Moreover, combined treatment with delphinidin and IR, enhanced apoptoticcell death, suppressed the mTOR pathway, and activated the JNK/MAPK pathway.Delphinidin inhibited the phosphorylation of PI3K, AKT, and mTOR, and increasedthe expression of autophagy-induced cell death associated-protein in radiation-exposedNSCLC cells. In addition, JNK phosphorylation was upregulated by delphinidinpre-treatment in radiation-exposed NSCLC cells. Collectively, these results show thatdelphinidin acts as a radiation-sensitizing agent through autophagy induction andJNK/MAPK pathway activation, thus enhancing apoptotic cell death in NSCLC cells.
9.Obstructive Jaundice due to Biliary Cast Syndrome Followed by Orthotopic Liver Transplantation.
Sang Hyun BAK ; Ho Soon CHOI ; Sun Young YANG ; Dae Won JUN ; Sung Hee HAN ; Hang Lak LEE ; Oh Young LEE ; Byung Chul YOON ; Jun Soo HAHM ; Min Ho LEE ; Dong Hoo LEE ; Choon Suhk KEE
The Korean Journal of Gastroenterology 2006;48(2):119-123
Biliary complication occurs in 6-34% of all liver transplant patients. Although bile leaks and strictures are relatively common, other biliary complications such as T-tube leak, choledocholithiasis, and biliary cast syndrome can also be observed. The biliary cast syndrome describes the presence of casts causing obstruction with its resultant sequelae of biliary infection, hepatocyte damage secondary to bile stasis and ductal damage, all contributing to cholangiopathy. Because the exact timing of cast formation after orthotopic liver transplantation is not consistent, it is difficult to define the true incidence of biliary cast syndrome without long-term follow-up data. Proposed etiological mechanisms include acute cellular rejection, prolongation of cold ischemic time, infection, biliary drainage tubes, and biliary obstruction. The diagnosis of biliary cast syndrome is usually confirmed by endoscopic retrograde cholangiopancreatography. There have been few published articles about biliary casts in Korea. Herein, we report a case of biliary cast syndrome followed by orthotopic liver transplantation.
Adult
;
Bile Duct Diseases/*complications/diagnosis/etiology
;
Female
;
Humans
;
Jaundice, Obstructive/*etiology
;
Liver Transplantation/*adverse effects
;
Male
;
Middle Aged
;
Retrospective Studies
;
Syndrome
10.Analysis of the Causes of Subfrontal Recurrence in Medulloblastoma and Its Salvage Treatment.
Jae Ho CHO ; Woong Sub KOOM ; Chang Geol LEE ; Kyoung Ju KIM ; Su Jung SHIM ; Jino BAK ; Kyoungkeun JEONG ; Tae Gon KIM ; Dong Seok KIM ; Joong Uhn CHOI ; Chang Ok SUH
The Journal of the Korean Society for Therapeutic Radiology and Oncology 2004;22(3):165-176
PURPOSE: Firstly, to analyze factors in terms of radiation treatment that might potentially cause subfrontal relapse in two patients who had been treated by craniospinal irradiation (CSI) for medulloblastoma. Secondly, to explore an effective salvage treatment for these relapses. MATERIALS AND METHODS: Two patients who had high-risk disease (T3bM1, T3bM3) were treated with combined chemoradiotherapy. CT-simulation based radiation-treatment planning (RTP) was performed. One patient who experienced relapse at 16 months after CSI was treated with salvage surgery followed by a 30.6 Gy IMRT (intensity modulated radiotherapy). The other patient whose tumor relapsed at 12 months after CSI was treated by surgery alone for the recurrence. To investigate factors that might potentially cause subfrontal relapse, we evaluated thoroughly the charts and treatment planning process including portal films, and tried to find out a method to give help for placing blocks appropriately between subfrotal-cribrifrom plate region and both eyes. To salvage subfrontal relapse in a patient, re-irradiation was planned after subtotal tumor removal. We have decided to treat this patient with IMRT because of the proximity of critical normal tissues and large burden of re-irradiation. With seven beam directions, the prescribed mean dose to PTV was 30.6 Gy (1.8 Gy fraction) and the doses to the optic nerves and eyes were limited to 25 Gy and 10 Gy, respectively. RESULTS: Review of radiotherapy portals clearly indicated that the subfrontal-cribriform plate region was excluded from the therapy beam by eye blocks in both cases, resulting in cold spot within the target volume. When the whole brain was rendered in 3-D after organ drawing in each slice, it was easier to judge appropriateness of the blocks in port film. IMRT planning showed excellent dose distributions (Mean doses to PTV, right and left optic nerves, right and left eyes: 31.1 Gy, 14.7 Gy, 13.9 Gy, 6.9 Gy, and 5.5 Gy, respectively. Maximum dose to PTV: 36 Gy). The patient who received IMRT is still alive with no evidence of recurrence and any neurologic complications for 1 year. CONCLUSION: To prevent recurrence of medulloblastoma in subfrontal-cribriform plate region, we need to pay close attention to the placement of eye blocks during the treatment. Once subfrontal recurrence has happened, IMRT may be a good choice for re-irradiation as a salvage treatment to maximize the differences of dose distributions between the normal tissues and target volume.
Brain
;
Chemoradiotherapy
;
Craniospinal Irradiation
;
Humans
;
Medulloblastoma*
;
Optic Nerve
;
Radiotherapy
;
Recurrence*