Fig 2: eQDTI-mediated improvements in the resolution of cytoskeletal structures at the Leica STELLARIS 8. (A) Region of interest showing a fixed U2OS cell, immunolabeled for microtubules with QD655 quantum dots, and imaged subsequently by utilizing the Confocal MX (magenta) and Confocal TX (cyan) emission channel. The LIGHTNING MX (yellow) and LIGHTNING TX image (green) was processed from the Confocal MX and TX emission channel respectively. Insets, taken from original images showing the detailed distribution of filamentous structures in the respective channels. Scale bar, 5 µm; insets, 1 µm. (B) Color-coded intensity profiles taken from a cross section (see LIGHTNING MX image in a. Opposed are the and the LIGHTNING MX in yellow and LIGHTNING TX in green channels.

Fig 3: AZE-induced IBA1 and phospho-IRE1Ser724 (pIRE1) expression is prevented by L-proline co-administration in primary microglial cells. (A) Representative photomicrographs showing pIRE1 and IBA1 co-immunofluorescence (co-IF) and (B,C) related quantifications of untreated primary microglia (control) or following exposure to AZE (1000 µM), L-proline (50 µM) or their combination after 24 h. Images were taken on a Leica Stellaris 8 confocal fluorescence microscope (Leica Microsystems) using the 63.5× oil-immersed objective. Scale bar = 20 µm. (B) IBA1 and (C) pIRE1 IF intensities were determined using NIH ImageJ software, ver. 1.52. At least five independent images from independent experiments were quantified for each experimental condition (n = 5). Results shown are the mean ± SEM. ** p < 0.01 or **** p < 0.0001 vs. control; ## p < 0.01 or #### p < 0.0001 vs. AZE, as determined using a one-way ANOVA, followed by Tukey post hoc test. Aze = L-azetidine-2-carboxylic acid; IBA1 = ionized calcium binding adaptor molecule 1; pIRE1 = phospho-inositol-requiring transmembrane kinase/endoribonuclease 1aSer724; DAPI = 4',6-diamidino-2-phenylindole (nuclear dye).