330 research outputs found
Nazım Hikmet'in vatan hainliği
Taha Toros Arşivi, Dosya Adı: Nazım Hikmet.
Not: Gazetenin "Tersi Yüzü" köşesinde yayımlanmıştır.İstanbul Kalkınma Ajansı (TR10/14/YEN/0033) İstanbul Development Agency (TR10/14/YEN/0033
IMI - Defining and Classifying Myopia: A Proposed Set of Standards for Clinical and Epidemiologic Studies
PURPOSE. We provide a standardized set of terminology, definitions, and thresholds of myopia
and its main ocular complications.
METHODS. Critical review of current terminology and choice of myopia thresholds was done to
ensure that the proposed standards are appropriate for clinical research purposes, relevant to
the underlying biology of myopia, acceptable to researchers in the field, and useful for
developing health policy.
RESULTS. We recommend that the many descriptive terms of myopia be consolidated into the
following descriptive categories: myopia, secondary myopia, axial myopia, and refractive
myopia. To provide a framework for research into myopia prevention, the condition of ‘‘premyopia’’ is defined. As a quantitative trait, we recommend that myopia be divided into myopia
(i.e., all myopia), low myopia, and high myopia. The current consensus threshold value for
myopia is a spherical equivalent refractive error 0.50 diopters (D), but this carries
significant risks of classification bias. The current consensus threshold value for high myopia
is a spherical equivalent refractive error 6.00 D. ‘‘Pathologic myopia’’ is proposed as the
categorical term for the adverse, structural complications of myopia. A clinical classification is
proposed to encompass the scope of such structural complications.
CONCLUSIONS. Standardized definitions and consistent choice of thresholds are essential
elements of evidence-based medicine. It is hoped that these proposals, or derivations from
them, will facilitate rigorous, evidence-based approaches to the study and management of
myopia
IMI-Management and Investigation of High Myopia in Infants and Young Children
The purpose of this study was to evaluate the epidemiology, etiology, clinical assessment, investigation, management, and visual consequences of high myopia (≤−6 diopters [D]) in infants and young children
Mechanisms Underlying Insulin Deficiency-Induced Acceleration of β-Amyloidosis in a Mouse Model of Alzheimer's Disease
Although evidence is accumulating that diabetes mellitus is an important risk factor for sporadic Alzheimer's disease (AD), the mechanisms by which defects in insulin signaling may lead to the acceleration of AD progression remain unclear. In this study, we applied streptozotocin (STZ) to induce experimental diabetes in AD transgenic mice (5XFAD model) and investigated how insulin deficiency affects the β-amyloidogenic processing of amyloid precursor protein (APP). Two and half months after 5XFAD mice were treated with STZ (90 mg/kg, i.p., once daily for two consecutive days), they showed significant reductions in brain insulin levels without changes in insulin receptor expression. Concentrations of cerebral amyloid-β peptides (Aβ40 and Aβ42) were significantly increased in STZ-treated 5XFAD mice as compared with vehicle-treated 5XFAD controls. Importantly, STZ-induced insulin deficiency upregulated levels of both β-site APP cleaving enzyme 1 (BACE1) and full-length APP in 5XFAD mouse brains, which was accompanied by dramatic elevations in the β-cleaved C-terminal fragment (C99). Interestingly, BACE1 mRNA levels were not affected, whereas phosphorylation of the translation initiation factor eIF2α, a mechanism proposed to mediate the post-transcriptional upregulation of BACE1, was significantly elevated in STZ-treated 5XFAD mice. Meanwhile, levels of GGA3, an adapter protein responsible for sorting BACE1 to lysosomal degradation, are indistinguishable between STZ- and vehicle-treated 5XFAD mice. Moreover, STZ treatments did not affect levels of Aβ-degrading enzymes such as neprilysin and insulin-degrading enzyme (IDE) in 5XFAD brains. Taken together, our findings provide a mechanistic foundation for a link between diabetes and AD by demonstrating that insulin deficiency may change APP processing to favor β-amyloidogenesis via the translational upregulation of BACE1 in combination with elevations in its substrate, APP
Central serous chorioretinopathy: An evidence-based treatment guideline.
Central serous chorioretinopathy (CSC) is a relatively common disease that causes vision loss due to macular subretinal fluid leakage and it is often associated with reduced vision-related quality of life. In CSC, the leakage of subretinal fluid through defects in the retinal pigment epithelial layer's outer blood-retina barrier appears to occur secondary to choroidal abnormalities and dysfunction. The treatment of CSC is currently the subject of controversy, although recent data obtained from several large randomized controlled trials provide a wealth of new information that can be used to establish a treatment algorithm. Here, we provide a comprehensive overview of our current understanding regarding the pathogenesis of CSC, current therapeutic strategies, and an evidence-based treatment guideline for CSC. In acute CSC, treatment can often be deferred for up to 3-4 months after diagnosis; however, early treatment with either half-dose or half-fluence photodynamic therapy (PDT) with the photosensitive dye verteporfin may be beneficial in selected cases. In chronic CSC, half-dose or half-fluence PDT, which targets the abnormal choroid, should be considered the preferred treatment. If PDT is unavailable, chronic CSC with focal, non-central leakage on angiography may be treated using conventional laser photocoagulation. CSC with concurrent macular neovascularization should be treated with half-dose/half-fluence PDT and/or intravitreal injections of an anti-vascular endothelial growth factor compound. Given the current shortage of verteporfin and the paucity of evidence supporting the efficacy of other treatment options, future studies-ideally, well-designed randomized controlled trials-are needed in order to evaluate new treatment options for CSC
Transport Properties of the Quark-Gluon Plasma -- A Lattice QCD Perspective
Transport properties of a thermal medium determine how its conserved charge
densities (for instance the electric charge, energy or momentum) evolve as a
function of time and eventually relax back to their equilibrium values. Here
the transport properties of the quark-gluon plasma are reviewed from a
theoretical perspective. The latter play a key role in the description of
heavy-ion collisions, and are an important ingredient in constraining particle
production processes in the early universe. We place particular emphasis on
lattice QCD calculations of conserved current correlators. These Euclidean
correlators are related by an integral transform to spectral functions, whose
small-frequency form determines the transport properties via Kubo formulae. The
universal hydrodynamic predictions for the small-frequency pole structure of
spectral functions are summarized. The viability of a quasiparticle description
implies the presence of additional characteristic features in the spectral
functions. These features are in stark contrast with the functional form that
is found in strongly coupled plasmas via the gauge/gravity duality. A central
goal is therefore to determine which of these dynamical regimes the quark-gluon
plasma is qualitatively closer to as a function of temperature. We review the
analysis of lattice correlators in relation to transport properties, and
tentatively estimate what computational effort is required to make decisive
progress in this field.Comment: 54 pages, 37 figures, review written for EPJA and APPN; one parag.
added end of section 3.4, and one at the end of section 3.2.2; some Refs.
added, and some other minor change
Cigarette Smoke-Related Hydroquinone Dysregulates MCP-1, VEGF and PEDF Expression in Retinal Pigment Epithelium in Vitro and in Vivo
Age-related macular degeneration (AMD) is the leading cause of legal blindness in the elderly population. Debris (termed drusen) below the retinal pigment epithelium (RPE) have been recognized as a risk factor for dry AMD and its progression to wet AMD, which is characterized by choroidal neovascularization (CNV). The underlying mechanism of how drusen might elicit CNV remains undefined. Cigarette smoking, oxidative damage to the RPE and inflammation are postulated to be involved in the pathophysiology of the disease. To better understand the cellular mechanism(s) linking oxidative stress and inflammation to AMD, we examined the expression of pro-inflammatory monocyte chemoattractant protein-1 (MCP-1), pro-angiogenic vascular endothelial growth factor (VEGF) and anti-angiogenic pigment epithelial derived factor (PEDF) in RPE from smoker patients with AMD. We also evaluated the effects of hydroquinone (HQ), a major pro-oxidant in cigarette smoke on MCP-1, VEGF and PEDF expression in cultured ARPE-19 cells and RPE/choroids from C57BL/6 mice.MCP-1, VEGF and PEDF expression was examined by real-time PCR, Western blot, and ELISA. Low levels of MCP-1 protein were detected in RPE from AMD smoker patients relative to controls. Both MCP-1 mRNA and protein were downregulated in ARPE-19 cells and RPE/choroids from C57BL/6 mice after 5 days and 3 weeks of exposure to HQ-induced oxidative injury. VEGF protein expression was increased and PEDF protein expression was decreased in RPE from smoker patients with AMD versus controls resulting in increased VEGF/PEDF ratio. Treatment with HQ for 5 days and 3 weeks increased the VEGF/PEDF ratio in vitro and in vivo.We propose that impaired RPE-derived MCP-1-mediated scavenging macrophages recruitment and phagocytosis might lead to incomplete clearance of proinflammatory debris and infiltration of proangiogenic macrophages which along with increased VEGF/PEDF ratio favoring angiogenesis might promote drusen accumulation and progression to CNV in smoker patients with dry AMD
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