Cardiac hypertrophy can be induced in isolated human atrial and left ventricular intact myocardium by Ang II and diastolic overstretch but not by isometric afterload. The fact that the induction of cardiac growth is inhibited by the blockade of Ang II subtype 1 receptors is of scientific and clinical importance.

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Bone tissue engineering approaches increasingly focus on the use of mesenchymal stem cells (MSC). In most animal transplantation models MSC are isolated and expanded before auto cell transplantation which might be critical for clinical application in the future. Hence this study compares the potential of directly auto-transplanted versus in vitro expanded MSC with or without bone morphogenetic protein-2 (BMP-2) to induce bone formation in a large volume ceramic bone substitute in the sheep model. MSC were isolated from bone marrow aspirates and directly auto-transplanted or expanded in vitro and characterized using fluorescence activated cell sorting (FACS) and RT-PCR analysis before subcutaneous implantation in combination with BMP-2 and β-tricalcium phosphate/hydroxyapatite (β-TCP/HA) granules. Constructs were explanted after 1 to 12 weeks followed by histological and RT-PCR evaluation. Sheep MSC were CD29+, CD44+ and CD166+ after selection by Ficoll gradient centrifugation, while directly auto-transplanted MSC-populations expressed CD29 and CD166 at lower levels. Both, directly auto-transplanted and expanded MSC, were constantly proliferating and had a decreasing apoptosis over time in vivo. Directly auto-transplanted MSC led to de novo bone formation in a heterotopic sheep model using a β-TCP/HA matrix comparable to the application of 60 μg/ml BMP-2 only or implantation of expanded MSC. Bone matrix proteins were up-regulated in constructs following direct auto-transplantation and in expanded MSC as well as in BMP-2 constructs. Up-regulation was detected using immunohistology methods and RT-PCR. Dense vascularization was demonstrated by CD31 immunohistology staining in all three groups. Ectopic bone could be generated using directly auto-transplanted or expanded MSC with β-TCP/HA granules alone. Hence BMP-2 stimulation might become dispensable in the future, thus providing an attractive, clinically feasible approach to bone tissue engineering.

Since the implementation and use of silicone implants in breast surgery the risks are published and discussed. Especially, the incidence of late silicone implant rupture and its potential risk to induce local siliconomas are still under discussion and not sufficiently evaluated. So far literature data offer no information of intrapulmonal or peripheral located cutaneous siliconomas because of systemic migration of silicone after breast augmentation. In light of silicones checkered history, and given the large and growing number of women who choose to undergo breast augmentation surgery each year, the presented clinical findings in our study are likely to be of interest to medical professionals, producers, and consumers alike. We present six female patients with an average age of 55 (+/-5) years with bilateral rupture of silicone implants after breast augmentation for aesthetic reasons. The average time after operation was 18 (+/-6) years. In five patients, we identified peripheral located cutaneous siliconomas and one patient suffered from an intrapulmonal siliconoma. The diagnosis of bilateral rupture of the silicone implants was performed preoperatively by MRI-scans. All five peripheral cutaneous siliconomas and the intrapulmonal siliconoma were validated by histopathologic analysis. Six female patients suffered from bilateral rupture of silicone implants after breast augmentation. In five patients, we identified peripheral located cutaneous siliconomas which were surgically excised. One patient suffered from an intrapulmonal siliconoma. In this unique case a lobectomy with resection of the pulmonal segment 10 had to be performed. Clinical findings of peripheral cutaneous and even intrapulmonary siliconomas after bilateral rupture of silicone breast implants indicate a systemic hematogen or lymphatic pathway of silicone. These findings suggest that it is mandatory to inform the patient about the potential risk of local siliconomas, but also about the potential risk of peripheral cutaneous or even intrapulmonary siliconomas caused by systemic hematogen or lymphatic pathways of silicone after silent implant failure.