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This involvement was manifested as a disruption of the inner segment/outer segment (IS/OS) junction and minimal subretinal fluid.
Activation of the intrinsic pathway of apoptosis by a number of stimuli and stresses, triggers the binding and activation of pro-apoptotic proteins BAX or BAK to the MOM leading to the MOM permeabilization (MOMP) without disruption of the inner membrane and the subsequent release of proteins from the mitochondrial intermembrane space (IMS), such as cytochrome c [49, 50].
Infrared imaging showing the presence of a figure of eight or dumb-bell-shaped lesion with disruption of the inner segment-outer segment (IS-OS) junction and hyperreflective debris at the apical side of the retinal pigment epithelium on the corresponding spectral domain ocular coherence tomography (SD-OCT) (B).
In contrast, functional preservation was found if neurodegeneration spared the photoreceptors, but caused quite extensive disruption of the inner retina.
Selective removal is thought to be due to the disruption of the inner membrane by pores which occurs upon depolarization, a signal which may be similar to pore formation due to cytolysin expression [49].
We also observed disruption of the inner and outer segments.
Similar(42)
The incidence of epiretinal membranes, subretinal fluid, discontinued external limiting membrane (ELM), and disruptions of the inner segment/outer segment junction and ELM were evaluated with Fisher's exact test.
SD-OCT showed increased nodularity at the level of and above the RPE, a separation of Bruch membrane from the RPE, partial damage of the RPE, disruption of the photoreceptor inner segment/outer segment (IS/OS) junction, multiple hyperreflective signals in the inner retina, foveal thinning, and parafoveal thickening.
Spectral-domain optical coherence tomography (SD-OCT) demonstrated increased retinal pigment epithelium granularity and disruption of the photoreceptor inner segment outer segment junction subfoveally.
Spectral domain optical coherence tomography (OCT, Spectralis, Heidelberg Engineering, Heidelberg, Germany) demonstrates a steep fovea contour, a thickening of the macular edges, intraretinal cysts, disruption of the photoreceptor inner segment/outer segment layer and macular pseudohole formation.
These compounds, after the disruption of the cell inner membranes, interact with the polyphenol-oxidase enzyme (PPO) released from the chloroplast [[ 37]].
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