No abstract

Objective To examine whether women with gestational diabetes (GDM) and their offspring have reduced endothelial progenitor cell (EPC) subsets and vascular reactivity. Study Design Women with GDM, healthy controls, and their infants participated. Maternal blood and cord blood were assessed for colony forming unit-endothelial cells (CFU-ECs) and EPC subsets using polychromatic flow cytometry. Cord blood endothelial colony forming cells (ECFCs) were enumerated. Vascular reactivity was tested by laser Doppler imaging. Results Women with GDM had fewer CD34+CD133+CD45+CD31+ cells (circulating progenitor cells, CPCs) at 24–32 weeks gestation and 1–2 days post-partum compared to controls. No differences were detected in CFU-ECs or ECFCs. In controls, CPCs were higher in the third trimester compared to post-partum. Cord blood from GDM pregnancies had reduced CPCs. Vascular reactivity was not different between GDM and control subjects. Conclusion The normal physiologic increase in CPCs during pregnancy is impaired in women with GDM, which may contribute to endothelial dysfunction and GDM-associated morbidities.

Background Children born to mothers with gestational diabetes mellitus (GDM) experience increased risk of developing hypertension, type 2 diabetes mellitus, and obesity. Disrupted function of endothelial colony forming cells (ECFCs) may contribute to this enhanced risk. The goal of this study was to determine if cord blood ECFCs from GDM pregnancies exhibit altered functionality. Methods ECFCs isolated from the cord blood of control and GDM pregnancies were assessed for proliferation, senescence, and Matrigel network formation. The requirement for p38MAPK in hyperglycemia-induced senescence was determined using inhibitor and overexpression studies. Results GDM ECFCs were more proliferative than control ECFCs. However, GDM ECFCs exhibited decreased network forming ability in Matrigel. Aging of ECFCs by serial passaging led to increased senescence and reduced proliferation of GDM ECFCs. ECFCs from GDM pregnancies were resistant to hyperglycemia-induced senescence compared to controls. In response to hyperglycemia, control ECFCs activated p38MAPK, which was required for hyperglycemia-induced senescence. In contrast, GDM ECFCs had no change in p38MAPK activation under equivalent conditions. Conclusion Intrauterine exposure of ECFCs to GDM induces unique phenotypic alterations. The resistance of GDM ECFCs to hyperglycemia-induced senescence and decreased p38MAPK suggest that these progenitor cells have undergone changes to induce tolerance to a hyperglycemic environment.

IntroductionAlthough rare, the atrioesophageal fistula is one of the most feared complications in radiofrequency catheter ablation of atrial fibrillation due to the high risk of mortality.ObjectiveThis is a prospective controlled study, performed during regular radiofrequency catheter ablation of atrial fibrillation, to test whether esophageal displacement by handling the transesophageal echocardiography transducer could be used for esophageal protection.MethodsSeven hundred and four patients (158 F/546M [22.4%/77.6%]; 52.8±14 [17-84] years old), with mean EF of 0.66±0.8 and drug-refractory atrial fibrillation were submitted to hybrid radiofrequency catheter ablation (conventional pulmonary vein isolation plus AF-Nests and background tachycardia ablation) with displacement of the esophagus as far as possible from the radiofrequency target by transesophageal echocardiography transducer handling. The esophageal luminal temperature was monitored without and with displacement in 25 patients.ResultsThe mean esophageal displacement was 4 to 9.1cm (5.9±0.8 cm). In 680 of the 704 patients (96.6%), it was enough to allow complete and safe radiofrequency delivery (30W/40ºC/irrigated catheter or 50W/60ºC/8 mm catheter) without esophagus overlapping. The mean esophageal luminal temperature changes with versus without esophageal displacement were 0.11±0.13ºC versus 1.1±0.4ºC respectively, P<0.01. The radiofrequency had to be halted in 68% of the patients without esophageal displacement because of esophageal luminal temperature increase. There was no incidence of atrioesophageal fistula suspected or confirmed. Only two superficial bleeding caused by transesophageal echocardiography transducer insertion were observed.ConclusionMechanical esophageal displacement by transesophageal echocardiography transducer during radiofrequency catheter ablation was able to prevent a rise in esophageal luminal temperature, helping to avoid esophageal thermal lesion. In most cases, the esophageal displacement was sufficient to allow safe radiofrequency application without esophagus overlapping, being a convenient alternative in reducing the risk of atrioesophageal fistula.

Abstract. The purpose of this study was to determine by immunohistochemistry the expression of estrogen and progesterone receptors in ovarian follicular structures from cows with cystic ovarian disease (COD) and to compare these with normal ovarian structures. Secondary, tertiary, atretic, and cystic follicles were evaluated. The follicular cysts of animals with COD presented a significantly higher expression of estrogen receptor a in all follicular layers than secondary, tertiary, and atretic follicles in both groups (P , .05). The intensity of estrogen receptor b in the granulosa cell layer was stronger in tertiary than in secondary and atretic follicles in normal animals (P , .05) and in growing and cystic follicles in animals with COD (P , .05). Theca cells were scarcely stained in the 2 groups. Growing follicles and cysts from COD animals were less stained than tertiary follicles from normal animals (P , .05). Differences did not exist between the 2 groups with regard to the progesterone receptor. Ovaries of animals with COD exhibited altered estrogen receptors expression compared with that in normal animals.