Melanosis ilei is a condition that's characterized by gross greyish-black or brownish-black pigmentation of the mucosa of the terminal ileum. There were several substances that produce gastrointestinal tract pigmentation such as lipofuscin, iron sulphide (FeS), Hemosiderin and exogenous material such as silicates and titanium. We report here on a case of a 58-year-old female who ingested charcoal for a long time, and she was diagnosed with melanosis ilei by colonoscopy. Her condition improved after she stopped ingesting the charcoal.
Charcoal ; Colonoscopy ; Female ; Gastrointestinal Tract ; Hemosiderin ; Humans ; Ileum ; Iron ; Lipofuscin ; Melanosis* ; Middle Aged ; Mucous Membrane ; Pigmentation ; Silicates ; Titanium

Most ingested foreign bodies spontaneously pass through the upper and lower intestinal tract. The impaction of an ingested foreign body in the colon is rare. Foreign bodies swallowed inadvertently often cause serious complications, such as perforation, obstruction, abscess formation, enterocolic fistula, or hemorrhage. Physicians should proceed with routine medical care while considering the possibility of the ingestion of a foreign body In cases where abdominal pain of an unknown origin is observed, particularly in elderly patients who wear dentures, alcoholics, mentally disturbed, or rapid eating, and presenting with altered bowel habits. We report a case of a colonoscopically-removed wooden toothpick that impacted the sigmoid colon and was complicated by the formation of a local abscess with a review of the literature.
Abdominal Pain ; Abscess ; Aged ; Alcoholics ; Colon ; Colon, Sigmoid* ; Colonoscopy ; Dentures ; Eating ; Fistula ; Foreign Bodies ; Hemorrhage ; Humans

OBJECTIVE: The purpose of this study was to evaluate retrospective data concerning patients with adnexal masses that were managed surgically during pregnancy and their effect on fetal outcome. METHODS: Data were reviewed concerning pregnant women who required surgery at our hospital from January 1991 to December 2000 for an adnexal mass. RESULTS: In the recent 10 years at our hospital a total of 47 pregnant women aged 27.9+/-3.6 years were diagnosed with adnexal masses that required surgery. The masses were removed at 12.3+/-3.7 weeks of gestation and maximum diameter was 8.4+/-2.3 cm. The pathologic features of the 47 lesions were as follows : 17 mature cystic teratomas, 14 epithelial origins (12 serous cystadenoma, 2 mucinous cystadenoma), 9 functional cysts, 4 endometriotic cysts, 2 paraovarian cysts, 1 malignant neoplasm. Of the 41 patients for whom the outcome of pregnancy was available, 2 (4.2%) gave preterm birth before 37 weeks, while 4 (8.5%) experienced spontaneous abortion. There were not any perinatal death for the 43 infants. CONCLUSION: Although our studies are smaller for confirmation, so larger studies are required, but our results suggest that an adnexal mass may be associated with an adverse fetal outcome. Surgical intervention at<22 weeks of gestation might not have been related to the adverse fetal outcomes.
Abortion, Spontaneous ; Cystadenoma, Serous ; Female ; Humans ; Infant ; Mucins ; Pregnancy* ; Pregnant Women ; Premature Birth ; Retrospective Studies ; Teratoma

Oxidative stress plays a crucial role in the development of neuronal disorders including brain ischemic injury. Thioredoxin 1 (Trx1), a 12 kDa oxidoreductase, has anti-oxidant and anti-apoptotic functions in various cells. It has been highly implicated in brain ischemic injury. However, the protective mechanism of Trx1 against hippocampal neuronal cell death is not identified yet. Using a cell permeable Tat-Trx1 protein, protective mechanism of Trx1 against hydrogen peroxide-induced cell death was examined using HT-22 cells and an ischemic animal model. Transduced Tat-Trx1 markedly inhibited intracellular ROS levels, DNA fragmentation, and cell death in H 2O 2-treatment HT-22 cells. Tat-Trx1 also significantly inhibited phosphorylation of ASK1 and MAPKs in signaling pathways of HT-22 cells. In addition, Tat-Trx1 regulated expression levels of Akt, NF-κB, and apoptosis related proteins. In an ischemia animal model, Tat-Trx1 markedly protected hippocampal neuronal cell death and reduced astrocytes and microglia activation. These findings indicate that transduced Tat-Trx1 might be a potential therapeutic agent for treating ischemic injury.

Aldose reductase (AR) protein, a member of the NADPH-dependent aldo-keto reductase family, reduces a wide range of aldehydes and enhances cell survival by inhibition of oxidative stress. Oxidative stress is known as one of the major pathological factor in ischemia. Since the precise function of AR protein in ischemic injury is fully unclear, we examined the function of AR protein in hippocampal neuronal (HT-22) cells and in an animal model of ischemia in this study. Cell permeable Tat-AR protein was produced by fusion of protein transduction domain in Tat for delivery into the cells. Tat-AR protein transduced into HT-22 cells and significantly inhibited cell death and regulated the mitogen-activate protein kinases (MAPKs), Bcl-2, Bax, and Caspase-3 under oxidative stress condition. In an ischemic animal model, Tat-AR protein transduced into the brain tissues through the blood-brain barrier (BBB) and drastically decreased neuronal cell death in hippocampal CA1 region. These results indicate that transduced Tat-AR protein has protective effects against oxidative stress-induced neuronal cell death in vitro and in vivo, suggesting that Tat-AR protein could be used as potential therapeutic agent in ischemic injury.
Aldehyde Reductase ; Aldehydes ; Blood-Brain Barrier ; Brain ; CA1 Region, Hippocampal ; Caspase 3 ; Cell Death ; Cell Survival ; Humans ; In Vitro Techniques ; Ischemia ; Models, Animal ; Neurons ; Oxidative Stress ; Oxidoreductases ; Protein Kinases

Oxidative stress plays a crucial role in the development of neuronal disorders including brain ischemic injury. Thioredoxin 1 (Trx1), a 12 kDa oxidoreductase, has anti-oxidant and anti-apoptotic functions in various cells. It has been highly implicated in brain ischemic injury. However, the protective mechanism of Trx1 against hippocampal neuronal cell death is not identified yet. Using a cell permeable Tat-Trx1 protein, protective mechanism of Trx1 against hydrogen peroxide-induced cell death was examined using HT-22 cells and an ischemic animal model. Transduced Tat-Trx1 markedly inhibited intracellular ROS levels, DNA fragmentation, and cell death in H 2O 2-treatment HT-22 cells. Tat-Trx1 also significantly inhibited phosphorylation of ASK1 and MAPKs in signaling pathways of HT-22 cells. In addition, Tat-Trx1 regulated expression levels of Akt, NF-κB, and apoptosis related proteins. In an ischemia animal model, Tat-Trx1 markedly protected hippocampal neuronal cell death and reduced astrocytes and microglia activation. These findings indicate that transduced Tat-Trx1 might be a potential therapeutic agent for treating ischemic injury.