Refractive outcomes of small lenticule extraction (SMILE) Pro® with a 2 MHz femtosecond laser.

PURPOSE: To evaluate the initial visual outcomes of Small Incision Lenticule Extraction (SMILE) Pro® using a 2 MHz femtosecond laser (VisuMax 800, Carl Zeiss Meditec) and to assess the efficacy, safety, predictability, accuracy, and complication rate. METHODS: This retrospective analysis included eyes which underwent the SMILE Pro® procedure using VisuMax 800 femtosecond laser to correct myopia. All surgeries were performed by one surgeon (DB). Follow-up was conducted 3 months postoperatively to evaluate visual outcomes after neuroadaptation, corrected visual acuity (CDVA) and intra- and postoperative complications. RESULTS: One hundred and fifty-two eyes of 82 patients (mean age 31 ± 6 years) results at 3 months are presented. The mean spherical equivalent (SE) was - 4.44 ± 1.86 D preoperatively while -0.24 ± 0.32 D postoperatively. 99% of eyes achieved SE within ± 1.0 D of attempted correction and 91% were within ± 0.5 D. Efficacy index was 0.93 while the safety index was 1. No complications occurred intra- or postoperatively. No eyes lost more than 1 line of their preoperative CDVA. All highly myopic eyes (- 6.25 to - 10.00 D; n = 18) achieved 20/20 at 3 months postoperatively and were within 0.5 D from the attempted SE and no eyes lost more than 1 line of CDVA. CONCLUSION: The SMILE Pro® is a safe, efficient, and predictable procedure for the treatment of myopia and myopic astigmatism, with comparable results of conventional SMILE surgery. High myopic eyes achieve better results than low and moderate myopia. No complications were recorded in our patients.

Mitochondrial and Contractile Function of Human Right Atrial Tissue in Response to Remote Ischemic Conditioning.

Background Remote ischemic preconditioning ( RIPC ) by repeated brief cycles of limb ischemia/reperfusion attenuates myocardial ischemia/reperfusion injury. We aimed to identify a functional parameter reflecting the RIPC -induced protection in human. Therefore, we measured mitochondrial function in right atrial tissue and contractile function of isolated right atrial trabeculae before and during hypoxia/reoxygenation from patients undergoing coronary artery bypass grafting with RIPC or placebo, respectively. Methods and Results One hundred thirty-seven patients under isoflurane anesthesia underwent RIPC (3×5 minutes blood pressure cuff inflation on the left upper arm/5 minutes deflation, n=67) or placebo (cuff uninflated, n=70), and right atrial appendages were harvested before ischemic cardioplegic arrest. Myocardial protection by RIPC was assessed from serum troponin I/T concentrations over 72 hours after surgery. Atrial tissue was obtained for isolation of mitochondria ( RIPC /placebo: n=10/10). Trabeculae were dissected for contractile function measurements at baseline and after hypoxia/reoxygenation (60 min/30 min) and for western blot analysis after hypoxia/reoxygenation ( RIPC /placebo, n=57/60). Associated with cardioprotection by RIPC (26% decrease in the area under the curve of troponin I/T), mitochondrial adenosine diphosphate-stimulated complex I respiration (+10%), adenosine triphosphate production (+46%), and calcium retention capacity (+37%) were greater, whereas reactive oxygen species production (-24%) was less with RIPC than placebo. Contractile function was improved by RIPC (baseline, +7%; reoxygenation, +24%). Expression and phosphorylation of proteins, which have previously been associated with cardioprotection, were not different between RIPC and placebo. Conclusions Cardioprotection by RIPC goes along with improved mitochondrial and contractile function of human right atrial tissue. Clinical Trial Registration URL: https://www.clinicaltrials.gov . Unique identifier: NCT 01406678.

Interaction between connexin 43 and nitric oxide synthase in mice heart mitochondria.

Connexin 43 (Cx43), which is highly expressed in the heart and especially in cardiomyocytes, interferes with the expression of nitric oxide synthase (NOS) isoforms. Conversely, Cx43 gene expression is down-regulated by nitric oxide derived from the inducible NOS. Thus, a complex interplay between Cx43 and NOS expression appears to exist. As cardiac mitochondria are supposed to contain a NOS, we now investigated the expression of NOS isoforms and the nitric oxide production rate in isolated mitochondria of wild-type and Cx43-deficient (Cx43(Cre-ER(T)/fl) ) mice hearts. Mitochondria were isolated from hearts using differential centrifugation and purified via Percoll gradient ultracentrifugation. Isolated mitochondria were stained with an antibody against the mitochondrial marker protein adenine-nucleotide-translocator (ANT) in combination with either a neuronal NOS (nNOS) or an inducible NOS (iNOS) antibody and analysed using confocal laser scanning microscopy. The nitric oxide formation was quantified in purified mitochondria using the oxyhaemoglobin assay. Co-localization of predominantly nNOS (nNOS: 93 ± 4.1%; iNOS: 24.6 ± 7.5%) with ANT was detected in isolated mitochondria of wild-type mice. In contrast, iNOS expression was increased in Cx43(Cre-ER(T)/fl) mitochondria (iNOS: 90.7 ± 3.2%; nNOS: 53.8 ± 17.5%). The mitochondrial nitric oxide formation was reduced in Cx43(Cre-ER(T)/fl) mitochondria (0.14 ± 0.02 nmol/min./mg protein) in comparison to wild-type mitochondria (0.24 ± 0.02 nmol/min./mg). These are the first data demonstrating, that a reduced mitochondrial Cx43 content is associated with a switch of the mitochondrial NOS isoform and the respective mitochondrial rate of nitric oxide formation.