Hydatid disease (HD) is an endemic illness in many countries, and it poses an important public health problem that's influenced by peoples' socioeconomic status and migration that spreads this disease. Although rare, it may occur in any organ or tissue. The most common site is the liver (59-75%), followed in frequency by lung (27%), kidney (3%), bone (1-4%) and brain (1-2%). Other sites such as the heart, spleen, pancreas and muscles are very rarely affected. Unusual sites for this disease can cause diagnostic problems. This pictorial essay illustrates various radiological findings of HD in the liver, spleen, kidney, pancreas, peritoneal cavity, omentum, adrenal, ovary, lung, mediastinum and retroperitoneum. Familiarity with the imaging findings of HD may be helpful in making an accurate diagnosis and preventing potential complications.

Ulcerative colitis is a chronic recurrent inflammatory bowel disease in which oxidative stress has been implicated. The aim of the present study was to evaluate possible protective effects of N-acetylcysteine against acetic acid-induced colitis in a rat model. Rats were administered intrarectal saline (control group) or acetic acid (colitis model group). Rats with acetic acid-induced colitis were treated by intraperitoneal or intrarectal administration of N-acetylcysteine (500 mg/ kg) (treated group). Another series of rats were pre-treated by intraperitoneal or intrarectal administration of N-acetylcysteine, then administered intrarectal acetic acid (pre-treated group). The degree of tissue injuries was assessed by macroscopical and histopathological scores of the colonic mucosa. Malondialdehyde, myeloperoxidase, reduced glutathione, superoxide dismutase, and catalase levels were measured in tissue extracts of the dissected colon. Administration of N-acetylcysteine intraperitoneally or intrarectally ameliorated macroscopic score alterations produced by acetic acid in treated groups. In addition, microscopical improvement was observed in all N-acetylcysteine-treated rats compared to untreated animals with colitis. In the colonic tissues of the acetic acid-induced colitis, myeloperoxidase activity and malondialdehyde levels were elevated, while the reduced glutathione levels and superoxide dismutase and catalase activities were decreased. However, intraperitoneal or intrarectal treatment with N-acetylcysteine reversed these parameters, compared to the untreated colitis group. Notably, intrarectal administration of N-acetylcysteine elevated the reduced glutathione levels more markedly compared to the other treatment groups. Superoxide dismutase levels were increased in intraperitoneally or intrarectally N-acetylcysteine-treated groups significantly compared to the control, colitis and pre-treated groups. But there was no significant increase in catalase activity. In conclusion, N-acetylcysteine could be beneficial as a complementary agent in treatment of ulcerative colitis.N-acetylcysteine; colitis; reactive oxygen species; acetic acid; GSH

Preoperative diagnosis of thyroid tuberculosis is important because of the availability of medical treatment and the limited role of surgery. This condition should be kept in mind in evaluating patients with a thyroid nodule, in communities where the prevalence of tuberculosis is high.

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Recently, the role of oxidative stress in the pathogenesis of ulcerative colitis has been investigated. This study was designed to evaluate the possible beneficial effects of L-carnitine on tissue injury and oxidative stress in acetic acid-induced colitis in rats. Acetic acid administration induced severe damage macroscopically and histopathologically in colon and significantly increased the levels of malondialdehyde and myeloperoxidase in colonic tissue. Supplementation of L-carnitine to acetic acid-treated rats did not prove to induce any improvements in macroscopic scores, while L-carnitine administration improved histopathologic scores and significantly decreased malondialdehyde and myeloperoxidase levels in treatment groups. Acetic acid administration significantly decreased reduced glutathione, superoxide dismutase, and catalase levels in colonic homogenate. Supplementation of L-carnitine prevented the depletion of reduced glutathione levels but significantly increased superoxide dismutase levels. On the other hand, no significant change in catalase activity was observed. In conclusion, these results may reflect that L-carnitine could be beneficial as a complementary agent in treatment of ulcerative colitis.