2 cm(2) vs 15.7 +/- 5.0 cm(2); P = .32), and stroke volume (72 +/- 29 mL vs 65 +/- 19 mL; P = .15); they had a slight decrease in left ventricular end-systolic area (7.9 +/- 4.4 cm(2) vs 6.9 +/- 3.2 cm(2); P = .03).

Conclusions: Early after correction of mitral regurgitation, left ventricular fractional area change decreases significantly, selleck products primarily as the result of a larger end-systolic dimension. This may be a compensatory

mechanism to prevent augmentation of forward stroke volume after mitral valve repair. (J Thorac Cardiovasc Surg 2010;140:1300-5)”
“Epileptiform discharges recorded in the 4-aminopyridine (4-AP) in vitro epilepsy model are mediated by glutamatergic and GABAergic signaling. Using a 60-channel perforated multi-electrode array (pMEA) on corticohippocampal slices from 2 to 3 week old mice we recorded interictal- and ictal-like events. When glutamatergic transmission was blocked, interictal-like events no longer initiated in the hilus or CA3/CA1 pyramidal layers but originated from the dentate gyrus granule and

molecular layers. Furthermore, frequencies of interictal-like events were reduced and durations were increased in these regions while cortical discharges were completely blocked. Following selleck GABA(A) receptor blockade interictal-like events no longer propagated to the dentate gyrus while their frequency in CA3 increased; in addition, ictal-like cortical events became shorter while increasing in frequency. Lastly, drugs that affect tonic and synaptic GABAergic conductance modulated the frequency, duration, initiation and propagation of interictal-like events. These findings confirm and expand on previous studies indicating that multiple synaptic mechanisms contribute to synchronize neuronal network activity in forebrain structures.

This article is part of

a Special Issue entitled ‘Trends in Neuropharmacology: In Memory of Erminio Costa’. (C) 2010 Elsevier Ltd. All rights reserved.”
“Objective: Some arterial grafts have progressive narrowing or occlusion during the first postoperative year despite angiographic patency in the immediate postoperative period. This study analyzed the incidence and predictors of arterial graft deterioration.

Methods: We reviewed 778 distal anastomoses of arterial grafts in 243 patients who underwent off-pump coronary SB431542 artery bypass grafting. All patients underwent both early and 1-year follow-up coronary angiography, with all arterial grafts patent on the early angiograms. Arterial graft deterioration was defined as diffuse graft stenosis or occlusion newly found at 1-year follow-up angiography.

Results: Graft deterioration was present in 13.8% (string sign, 6.9%; occlusion, 6.8%) of distal anastomoses. The incidence of graft deterioration was higher among cases of non-internal thoracic arterial graft (27.7% vs 6.0%, P < .001), non-left anterior descending coronary arterial anastomosis (19.1% vs 2.0%, P < .001), mild (<= 75%) stenosis of the target coronary artery (26.0% vs 7.