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

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*

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

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

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.

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.

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.

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.

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

Cholestatic liver cirrhosis (CLC) eventually proceeds to end-stage liver failure by mediating overwhelming deposition of collagen, which is produced by activated interstitial myofibroblasts. Although the beneficial effects of Rhus verniciflua Stokes (RVS) on various diseases are well-known, its therapeutic effect and possible underlying mechanism on interstitial fibrosis associated with CLC are not elucidated. This study was designed to assess the protective effects of RVS and its possible underlying mechanisms in rat models of CLC established by bile duct ligation (BDL). We demonstrated that BDL markedly elevated the serological parameters such as aspartate aminotransferase, alanine transaminase, total bilirubin, and direct bilirubin, all of which were significantly attenuated by the daily uptake of RVS (2 mg/kg/day) for 28 days (14 days before and after operation) via intragastric route. We observed that BDL drastically induced the deterioration of liver histoarchitecture and excessive deposition of extracellular matrix (ECM), both of which were significantly attenuated by RVS. In addition, we revealed that RVS inhibited BDL-induced proliferation and activation of interstitial myofibroblasts, a highly suggestive cell type for ECM production, as shown by immunohistochemical and semi-quantitative detection of α-smooth muscle actin and vimentin. Finally, we demonstrated that the anti-fibrotic effect of RVS was associated with the inactivation of Smad3, the key downstream target of a major fibrogenic cytokine, i.e., transforming growth factor β (TGF-β). Simultaneously, we also found that RVS reciprocally increased the expression of Smad7, a negative regulatory protein of the TGF-β/Smad3 pathway. Taken together, these results suggested that RVS has a therapeutic effect on CLC, and these effects are, at least partly, due to the inhibition of liver fibrosis by the downregulation of Smad3 and upregulation of Smad7.
Actins ; Alanine Transaminase ; Aspartate Aminotransferases ; Bile Ducts ; Bilirubin ; Collagen ; Down-Regulation* ; Extracellular Matrix ; Fibrosis* ; Ligation ; Liver Cirrhosis ; Liver Failure ; Liver* ; Models, Animal ; Myofibroblasts ; Negotiating ; Rhus* ; Transforming Growth Factors ; Up-Regulation* ; Vimentin