Acne Scars

Ultrasound Obstet Gynecol. 2009 Jun 29; 34(1): 85-89Wang CB, Chiu WW, Lee CY, Sun YL, Lin YH, Tseng CJOBJECTIVES: To determine the prevalence of clinical symptoms associated with Cesarean scar defects, and to determine the association between the size of these defects, clinical complaints, uterine position, and a history of multiple Cesarean sections. METHODS: In this cross-sectional study, Cesarean scar defects in women with a history of transverse lower-segment Cesarean section were measured by transvaginal ultrasound while being assessed for other gynecological conditions. The relationships between the size of the Cesarean scar defect and the clinical symptoms, uterine position and number of previous Cesarean sections were evaluated. Patients with other uterine pathologies, including endometrial hyperplasia, polyps, malignancy and submucosal myomas, were excluded from the study. RESULTS: During a 3-year period, 4250 women were assessed by transvaginal sonography, of whom 293 (6.9%) were diagnosed with Cesarean scar defects. Eighty-six patients were excluded due to other uterine pathologies. Altogether, 207 patients with Cesarean scar defects were included in this study. Women who had undergone multiple Cesarean sections tended to have larger scar defects (in width and depth) than did those who had undergone a single Cesarean section. Women with retroflexed uteri also tended to have wider defects than those with anteflexed uteri. Defect width was significantly greater in women with postmenstrual spotting, dysmenorrhea and chronic pelvic pain. CONCLUSIONS: Multiple Cesarean sections and retroflexed uteri are risk factors for larger Cesarean scar defects. The size of the Cesarean scar defect is associated with clinical symptoms such as postmenstrual spotting, dysmenorrhea and chronic pelvic pain. Copyright (c) 2009 ISUOG. Published by John Wiley & Sons, Ltd.

J Cell Physiol. 2009 Jun 29; Liesmaa I, Leskinen HK, Kokkonen JO, Ruskoaho H, Kovanen PT, Lindstedt KABradykinin receptors are differentially expressed in the coronary vascular endothelium of rat and human hearts during the pathogenesis of heart failure, but the mechanisms responsible for this regulation have remained vague. Here we show by quantitative real-time PCR, Western blot analysis, and immunohistochemistry, that hypoxia triggers the expression of bradykinin type-2 receptors (BK-2Rs) in cultured human coronary artery endothelial cells (HCAECs), in isolated rat cardiac microvascular endothelial cells (RCMECs), and in rat hearts subjected to ligation of the left anterior descending coronary artery. Mild hypoxia (5% O(2)) induced a fourfold temporal increase in BK-2R mRNA expression in HCAECs, which was also observed at the protein level, whereas severe hypoxia (1% O(2)) slightly inhibited the mRNA expression of BK-2Rs. In addition, HOE-140, a BK-2R antagonist, inhibited mRNA and protein expression of BK-2Rs. The BK-2Rs induced by mild hypoxia were biologically active, that is, capable of inducing intracellular production of nitric oxide (NO) upon activation of HCAECs with bradykinin (BK), a response attenuated by HOE-140. In rat hearts recovering from myocardial infarction, BK-2Rs were upregulated in the endothelium of vessels forming at the border zone between fibrotic scar tissue and healthy myocardium. Furthermore, in an in vitro wound-healing assay, RCMEC migration was increased under mild hypoxic culture conditions in the presence of BK and was attenuated with HOE-140. Our present results show that mild hypoxia triggers a temporal expression of functional BK-2Rs in human and rat endothelial cells and support a role for BK-2Rs in hypoxia-induced angiogenesis. J. Cell. Physiol. (c) 2009 Wiley-Liss, Inc.

Gastrointest Endosc. 2009 Jul; 70(1): 159-65Raju GS, Malhotra A, Ahmed IBACKGROUND: Colonoscopic full-thickness resection (CFTR) of the colon may obviate the need for surgical resection of benign lesions. OBJECTIVE: To develop an animal model for CFTR of the colon followed by endoscopic suture closure with through-the-endoscope devices. DESIGN: Pilot study. SETTING: University medical center. ANIMALS: Twenty pigs. INTERVENTIONS: A 2-cm circular area was resected on the antimesenteric side of the colon (phase 1, n = 10) and on the mesenteric side (phase 2, n = 10) by using an insulated tip knife cut followed by the use of a grasping forceps and a snare to resect and retrieve the specimen. The tissue apposition system was used to close the defect. MAIN OUTCOME MEASUREMENTS: Resection and closure times were recorded. The animals were euthanized at 2 weeks and examined for peritonitis, adhesions, wound healing, and T-tag injury to adjacent viscera. RESULTS: The CFTR was successful in all 20 attempts. The median resection time was 6 minutes (range 2.5-35 minutes). Suture closure was successful in 19 animals. It took a median time of 41 minutes (range 21-125 minutes) and 4 sutures to close the defect. Eighteen animals survived without clinical signs of distress; there was a well-healed scar without peritonitis or distant adhesions on necropsy at 2 weeks. One animal failed to thrive, and necropsy revealed mild peritonitis, small abscesses, distant adhesions, and a 2-mm hole at the suture site. Two of the 132 T-tags were inserted in the adjacent viscera. LIMITATIONS: Colon resection in the proximal colon was not studied. CONCLUSIONS: In this animal model, CFTR of the colon followed by suture closure can be accomplished successfully by using through-the-endoscope devices.