mesenchymal stem cell (MSC) transplantation on adverse electrophysiological remodelling in the heart following myocardial infarction (MI).METHODS: Three weeks after coronary ligation to induce MI in Lewis rats, 3ϫ10 6 MSCs or culture medium were directly injected into each infarct.One to two weeks later, hearts were excised, Langendorff-perfused, and optically mapped using a potentiometric fluorescent dye (di-4-ANEPPS), high-speed CMOS cameras (100ϫ100 pixels, 1 kHz sample/s, 0.4 mm/ pixel) and custom software designed to measure various cardiac electrical parameters.Hearts were then fixed in formalin and sectioned for morphometric and histological analyses.Vascular density was determined by counting alpha smooth muscle actin (␣SMA)-immunopositive structures observed in histological sections.Male donor cell survival in female hearts was evaluated by quantitative PCR for the Y-chromosomal gene Sry.Quantitative RT-PCR was performed to assess the changes in expression levels of various rat cardiac ion channels in the infarct region.The ion channel expression was normalized to -actin expression levels.RESULTS: Optical mapping showed that MSC transplantation attenuated the reduction in conduction velocity (CV) and the prolongation of effective refractory period (ERP) in the infarcted hearts.Morphometric and histological analyses showed better-preserved ventricular wall thickness and higher vascular density in the infarcted hearts transplanted with MSCs.A number of ion channel genes showed changes in expression following infarction.In particular, the expression of Kir2.1, an ion channel which mediates the inward rectifier potassium current I K1 , was reduced in MI and partially restored with MSC transplantation.CONCLUSION: MSC transplantation improves conduction and reduces refractoriness, as well as increases vascularization and limits structural remodelling in infarcted hearts.MSCs also partially restore Kir2.1 expression, which would enhance I K1 currents and contribute to a more negative resting membrane potential.This in turn may increase CV by allowing for more sodium channels to open during depolarization.Since I K1 contributes to the late phase of repolarization, MSC-induced restoration of Kir2.1 would also lead to the shortening of ERP
Objectives To report complications, clinical outcomes and CT‐imaging outcomes of a surgical system designed for the management of humeral intracondylar fissures and humeral condylar fractures. Materials and Methods Retrospective review of fracture healing from medical records, direct owner contact and an online data‐submission service. Follow‐up included CT scans and a calculated “bone‐opacity continuity index” to quantify bone healing. Results There was one major surgical complication and one major medical complication out of 34 fissure cases, and two major surgical and one major medical complication out of 14 fractures. Follow‐up times ranged from 29 to 1268 days. All cases with CT follow‐up had some continuity of bone opacity across the condyle. Clinical Significance In the cases included in this study, this repair system was associated with low complication rates and favourable healing rates, particularly for humeral intracondylar fissure.
