Nose reconstruction by chondrocutaneous preauricular free flaps: anatomical basis and clinical results

Full-thickness defects of the nose result in considerable and distressing disfigurements. Ideally, reconstruction of such defects must be achieved in as few stages as possible and secondary, disfigurement kept to a minimum. In this study, the authors aimed to learn whether nose reconstruction could benefit from chondrocutaneous free flaps taken from the auricular tragus. In 72 ears, the vascular blood supply of the tragus was studied following injection of colored latex. Color-coded Duplex sonography served as a noninvasive method for demonstrating the blood supply of the target area. The procedure of nose reconstruction using the free chondrocutaneous tragus flap and the cosmetic results of this procedure in six patients are presented. Except for 2.8 percent of the anatomical specimens, the superficial temporal artery gave rise to the tragus and its overlying skin. The diameter of these branches ranged from 0.65 to 0.82 mm. Using the tragus composite free flap, the anatomical shape of the nose could be reconstructed successfully, and 6 months after surgery, the color and texture of the flap were very similar to those of the remaining nose. Using deeper parts of the tragus cartilage resulted in minimal scars and maintenance of the tragus anatomical shape. Free tragus flaps could be an alternative approach for nose reconstruction.     

DIGE proteome analysis reveals suitability of ischemic cardiac in vitro model for studying cellular response to acute ischemia and regeneration

Proteomic analysis of myocardial tissue from patient population is suited to yield insights into cellular and molecular mechanisms taking place in cardiovascular diseases. However, it has been limited by small sized biopsies and complicated by high variances between patients. Therefore, there is a high demand for suitable model systems with the capability to simulate ischemic and cardiotoxic effects in vitro, under defined conditions. In this context, we established an in vitro ischemia/reperfusion cardiac disease model based on the contractile HL-1 cell line. To identify pathways involved in the cellular alterations induced by ischemia and thereby defining disease-specific biomarkers and potential target structures for new drug candidates we used fluorescence 2D-difference gel electrophoresis. By comparing spot density changes in ischemic and reperfusion samples we detected several protein spots that were differentially abundant. Using MALDI-TOF/TOF-MS and ESI-MS the proteins were identified and subsequently grouped by functionality. Most prominent were changes in apoptosis signalling, cell structure and energy-metabolism. Alterations were confirmed by analysis of human biopsies from patients with ischemic cardiomyopathy.With the establishment of our in vitro disease model for ischemia injury target identification via proteomic research becomes independent from rare human material and will create new possibilities in cardiac research.     

MicroRNAs; easy and potent targets in optimizing therapeutic methods in reparative angiogenesis

The age‐related senescence of adult tissues is associated with the decreased level of angiogenic capability and with the development of a degenerative disease such as atherosclerosis which thereafter result in the deteriorating function of multiple systems. Findings indicate that tissue senescence not only diminishes repair processes but also promotes atherogenesis, serving as a double‐edged sword in the development and prognosis of ischaemia‐associated diseases. Evidence evokes microRNAs (miRNAs) as molecular switchers that underlie cellular events in different tissues. Here, miRNAs would promote new potential targets for optimizing therapeutic methods in blood flow recovery to the ischaemic area. Effectively beginning an ischaemia therapy, a more characteristic of miRNA changes in adult tissues is prerequisite and in the forefront. It may also be a preliminary phase in treatment strategies by stem cell‐based therapy.