Publications by authors named "Rozina Noristani"

Article Synopsis
  • Hypoxia disrupts mitochondrial and endoplasmic reticulum (ER) homeostasis, leading to an accumulation of misfolded proteins and the activation of the Unfolded Protein Response (UPR).
  • Mitochondrial chaperone TRAP1 helps protect cells from stress by maintaining mitochondrial function and reducing reactive oxygen species (ROS) production.
  • Metformin has shown potential in mitigating hypoxic damage in flies lacking TRAP1 by reducing ROS levels and affecting UPR activation, suggesting a crucial link among Metformin, TRAP1, and cellular stress responses.
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Transforming growth factor-β-activated kinase 1 (TAK1) is upregulated after cerebral ischemia and contributes to an aggravation of brain injury. TAK1 acts as a key regulator of NF-ΚB and the MAP kinases JNK and p38 and modulates post-ischemic neuroinflammation and apoptosis. Microglia are the main TAK1-expressing immunocompetent cells of the brain.

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Background And Purpose: Transmembrane BAX Inhibitor-1 Motif-containing (TMBIM) family members exert inhibitory activities in apoptosis and necroptosis. FAIM2 (TMBIM-2) is neuroprotective against murine focal ischemia and is regulated by erythropoietin (EPO). Similar to FAIM2, GRINA (TMBIM-3) is predominantly expressed in the brain.

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Purpose: To evaluate the effect of adapted capsulotomy laser settings on the cutting quality in femtosecond laser-assisted cataract surgery.

Setting: Ruhr-University Eye Clinic, Bochum, Germany.

Design: Prospective randomized case series.

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Purpose: To report a patient who developed a white cataract after Nd:YAG laser vitreolysis with a posterior capsule defect.

Methods: Femtosecond laser-assisted capsulotomy was performed for optic capture fixation in a patient with a cataract due to a posterior capsule defect after Nd:YAG laser-vitreolysis.

Results: A 55-year-old, highly myopic woman presented with visual impairment 4 days after Nd:YAG laser vitreolysis due to preexisting floaters.

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Glaucoma is a multifactorial disease and especially mechanisms occurring independently from an elevated intraocular pressure (IOP) are still unknown. Likely, the immune system contributes to the glaucoma pathogenesis. Previously, IgG antibody depositions and retinal ganglion cell (RGC) loss were found in an IOP-independent autoimmune glaucoma model.

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Purpose: To determine the efficacy of femtosecond laser-assisted cataract surgery in eyes with radial keratometry.

Methods: Femtosecond laser-assisted cataract surgery was performed in 3 patients (6 eyes) who had six to eight radial keratotomy incisions.

Results: In all cases, the anterior segment of the eye was visualized with integrated three-dimensional optical coherence tomography and it was possible to position the laser corneal incisions between the radial keratotomy incisions.

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The immunization with optic nerve homogenate antigen (ONA) or S100 induced retinal degeneration. Since many neurological diseases are reinforced or initiated by immune cells, leucocytes were analyzed. CD3(+) T-cells in the retina increased slightly in ONA rats, but not in S100 treated retinas.

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It is well established that the immunization with ocular antigens causes a retinal ganglion cell (RGC) decline, which is accompanied by glia alterations. In this study, the degenerative effects of the immunization with an optic nerve homogenate (ONA) and its purified compound S100 were analyzed on retinas and optic nerves. Since a participation of glia cells in cell death mechanisms is currently discussed, rats were immunized with S100 or ONA.

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Purpose: To evaluate a single-piece hydrophobic acrylic intraocular lens (IOL) with ultraviolet-ozone (UV-O3) treatment on the posterior surface and compare it with an identical untreated IOL in a rabbit model.

Setting: John A. Moran Eye Center, University of Utah, Salt Lake City, Utah, USA.

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Purpose: To evaluate long-term uveal and capsular biocompatibility of a new accommodating intraocular lens (IOL).

Setting: John A. Moran Eye Center, University of Utah, Salt Lake City, Utah, USA.

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