Anatomic Success of Scleral Buckling for Rhegmatogenous Retinal Detachment - A Retrospective Study of 524 Cases

Background/Aim: Our purpose was to investigate the anatomic success of scleral buckling surgery for rhegmatogenous retinal detachment. Material and Methods: A total of 524 consecutive patients were retrospectively analysed. Several parameters including the lens status, number of breaks and extent of retinal detachment, preoperative proliferative vitreoretinopathy and refractive errors were examined. The minimum follow-up was 6 months. The primary success rate was defined as anatomic success being stable over a period of at least 6 months after surgery. The secondary success rate was defined as anatomic success after the second intervention if necessary. Besides an analysis over all patients, the patients were grouped according to the severity of the preoperative situation in simple, medium and severe cases. Results: The overall primary anatomic success rate was 84.7% and the secondary success rate 96.4% after 1 initial scleral buckling surgery and 1 additional surgery in case of persisting retinal detachment, and 19.1% of the patients with an initially attached retina after 1 scleral buckling surgery experienced a redetachment in the postoperative course and were successfully treated in 60/85 cases. In phakic patients (n = 359) the primary success rate was 89.7%, whereas in pseudophakic patients (n = 165) a primary success rate of 73.9% was obtained. The primary success was additionally influenced by the extent of the retinal detachment measured in clock hours (p <0.001), undetected holes (p = 0.004), small (p = 0.037) and no gas tamponade (p = 0.021). In simple, medium and severe cases, phakic patients always achieved better anatomic results (89.9, 89.1 and 90.2%) compared to pseudophakic ones (82.5, 70.3 and 36.4%). Conclusion: Scleral buckling is a very good surgical option in phakic patients irrespective of the preoperative severity and simple cases in pseudophakic patients. Scleral buckling represents a surgical technique worth being trained and performed in the light of favourable results especially in phakic eyes. Copyright (C) 2010 S. Karger AG, Base

Different intermittency for longitudinal and transversal turbulent fluctuations

Scaling exponents of the longitudinal and transversal velocity structure functions in numerical Navier-Stokes turbulence simulations with Taylor-Reynolds numbers up to \rel = 110 are determined by the extended self similarity method. We find significant differences in the degree of intermittency: For the sixth moments the scaling corrections to the classical Kolmogorov expectations are $\delta\xi_6^L= -0.21 \pm 0.01$ and \dx_6^T= -0.43 \pm 0.01, respectively, independent of \rel. Also the generalized extended self similarity exponents \rho_{p,q} = \dx_p/\dx_q differ significantly for the longitudinal and transversal structure functions. Within the She-Leveque model this means that longitudinal and transversal fluctuations obey different types of hierarchies of the moments. Moreover, the She-Leveque model hierarchy parameters $\beta^L$ and $\beta^T$ show small but significant dependences on the order of the moment.Comment: 20 pages, 10 eps-figures, to appear in Physics of Fluids, December 199

Subleading contributions to the width of the D_{s0}*(2317)

We construct the effective chiral Lagrangian involving the D--mesons and Goldstone bosons at next-to-leading order taking into account strong as well as electromagnetic interactions. This allows us to disentangle -- to leading order in isospin violation -- the electromagnetic and the strong contribution to the D--meson mass differences. In addition, we also apply the interaction to the decay D_{s0}^*(2317)-> D_s pi0 under the assumption that the D_{s0}^*(2317) is a hadronic molecule. We find (180+-110) keV for the decay width $\Gamma (D_{s0}^*(2317)-> D_s pi0) -- consistent with currently existing experimental constraints as well as previous theoretical investigations. The result provides further evidence that this decay width can serve as a criterion for testing the nature of the D_{s0}^*(2317).Comment: 11 pages, 2 figure

A Mild Impairment of Mitochondrial Electron Transport Has Sex-Specific Effects on Lifespan and Aging in Mice

Impairments of various aspects of mitochondrial function have been associated with increased lifespan in various model organisms ranging from Caenorhabditis elegans to mice. For example, disruption of the function of the ‘Rieske’ iron-sulfur protein (RISP) of complex III of the mitochondrial electron transport chain can result in increased lifespan in the nematode worm C. elegans. However, the mechanisms by which impaired mitochondrial function affects aging remain under investigation, including whether or not they require decreased electron transport. We have generated knock-in mice with a loss-of-function Risp mutation that is homozygous lethal. However, heterozygotes (Risp+/P224S) were viable and had decreased levels of RISP protein and complex III enzymatic activity. This decrease was sufficient to impair mitochondrial respiration and to decrease overall metabolic rate in males, but not females. These defects did not appear to exert an overtly deleterious effect on the health of the mutants, since young Risp+/P224S mice are outwardly normal, with unaffected performance and fertility. Furthermore, biomarkers of oxidative stress were unaffected in both young and aged animals. Despite this, the average lifespan of male Risp+/P224S mice was shortened and aged Risp+/P224S males showed signs of more rapidly deteriorating health. In spite of these differences, analysis of Gompertz mortality parameters showed that Risp heterozygosity decreased the rate of increase of mortality with age and increased the intrinsic vulnerability to death in both sexes. However, the intrinsic vulnerability was increased more dramatically in males, which resulted in their shortened lifespan. For females, the slower acceleration of age-dependent mortality results in significantly increased survival of Risp+/P224S mice in the second half of lifespan. These results demonstrate that even relatively small perturbations of the mitochondrial electron transport chain can have significant physiological effects in mammals, and that the severity of those effects can be sex-dependent

Mclk1+/- mice are not resistant to the development of atherosclerosis

<p>Abstract</p> <p>Background</p> <p>Mice with a single copy of <it>Mclk1 </it>(a.k.a. <it>Coq7</it>), a gene that encodes a mitochondrial enzyme required for the biosynthesis of ubiquinone and other functions, live longer than wild-type mice. The prolonged survival implies a decreased mortality from age-dependent lethal pathologies. Atherosclerosis is one of the main age-dependent pathologies in humans and can be modeled in mice that lack Apolipoprotein E (<it>ApoE</it>^-/-) or mice that lack the Low Density Lipoprotein Receptor (<it>LDLr</it>^-/-) in addition to being fed an atherosclerosis-inducing diet. We sought to determine if <it>Mclk1 </it>heterozygosity protects against atherosclerosis and dyslipidemia in these models.</p> <p>Results</p> <p>We found that <it>Mclk1 </it>heterozygosity did not protect against dyslipidemia, oxidative stress, or atherosclerosis in young (6 or 10 months) or older (18 months) mice. Furthermore, the absence of <it>ApoE </it>suppressed the lifespan-promoting effects of <it>Mclk1 </it>heterozygosity.</p> <p>Conclusion</p> <p>These findings indicate that although <it>Mclk1 </it>heterozygosity can extend lifespan of mice, it does not necessarily protect against atherosclerosis. Moreover, in the presence of hyperlipidemia and chronic inflammation, <it>Mclk1 </it>heterozygosity is incapable of extending lifespan.</p