Are there any differences in the expression of hormonal receptors and proliferation markers between uterine and extrauterine leiomyomas?

The aim of this study is to determine the immunohistochemical expressions of estrogen receptor, progesterone receptor, and Ki-67 proliferation marker in 8 extrauterine leiomyomas and to compare these values with their uterine counterparts. In all, 8 patients with extrauterine leiomyomas and 20 patients with uterine leiomyomas as a control group were studied. Sections were immunohistochemically stained with estrogen receptor, progesterone receptor, and Ki-67 antibodies. Labeling indices for estrogen receptor, progesterone receptor, and Ki-67 were found to be 33.05 % ± 31.70%, 14.18 % ± 18.80%, and 0.52 % ± 1.32% for extrauterine leiomyomas and 65.09% ± 26.65%, 32.53% ± 32.80%, and 0.37% ± 0.71% for uterine leiomyomas, respectively. The difference of labeling indices for progesterone receptor between uterine leiomyomas and extrauterine leiomyomas was statistically significant (P =.002). This study shows that increased expression of progesterone receptor is observed only in uterine leiomyomas during the reproductive period. However, it seems that additional factors to hormone receptors contribute to the development of extrauterine leiomyomas. © 2008 Sage Publications

Effects of Tempol, a Membrane-Permeable Radical Scavenger, on Local and Remote Organ Injuries Caused by Intestinal Ischemia/Reperfusion in Rats

Background: Tempol is a stable piperidine nitroxide of low molecular weight that permeates biological membranes and scavenges superoxide anions in vitro. In a variety of animal models, deleterious effects of reperfusion injury on both local and remote organs have been demonstrated. In this study, we aimed to investigate the effects of a membrane-permeable radical scavenger, Tempol, on local and remote organ injuries caused by intestinal ischemia/reperfusion (I/R) in rats. Materials and methods: Male Wistar-albino rats were randomized into three groups: (I) Sham-operated control group, laparotomy without I/R injury (n = 12); (II) Intestinal I/R group, 60 min of ischemia by superior mesenteric artery occlusion followed by 2-h of reperfusion (n = 12); and (III) I/R + Tempol-treated group, identical to I/R group except for Tempol administration, 30 mg/kg bolus injection 5 min before reperfusion, followed by an infusion of 30 mg/kg/h intravenously (n = 12). Histopathologically, intestinal mucosal lesions were assessed by Chiu's classification, and pulmonary parenchymal damage was appraised by pulmonary neutrophil infiltration and acute lung injury scaling. Biochemically, myeloperoxidase activity, malondialdehyde, glutathione, and nitrite/nitrate (NOx) levels were determined in both intestinal mucosa and lung parenchyma. Evans blue dye concentration and organ wet/dry weight ratios were used as a marker of organ edema. Animal survival was observed up to 1 week. Results: Intestinal mucosal lesions and pulmonary parenchymal damage were significantly attenuated with Tempol treatment, histopathologically (P < 0.05). Tempol administration significantly reduced myeloperoxidase activity and malondialdehyde levels, and also significantly increased glutathione and NOx levels of both intestinal and lung tissues, biochemically (P < 0.05). Evans blue dye extravasation and wet/dry weight ratios of organs were significantly reduced with Tempol injection (P < 0.05). The survival rates of rats in Tempol-treated group were significantly higher than that of I/R-treated group (P < 0.05). Conclusions: The present study suggests that Tempol administration significantly reduces both local and remote organ injuries caused by intestinal I/R before and throughout the reperfusion period. Further clinical studies are needed to clarify whether Tempol may be a useful therapeutic agent to use in particular operations where the reperfusion injury occurs. © 2008 Elsevier Inc. All rights reserved

A Meta-analysis of Gene Expression Signatures of Blood Pressure and Hypertension

10.1371/journal.pgen.1005035PLoS Genetics113e100503