protein content  (Bio-Rad)

Journal: medRxiv

Article Title: Glutamate Carboxypeptidase II (GCPII)-Targeted PET to Identify Muscle Denervation in Peripheral Nervous System Injuries

doi: 10.64898/2026.03.18.26348533

Figure Lengend Snippet: Composite images of α-bungarotoxin (red) targeting postsynaptic neuromuscular junctions (i.e., motor endplates), anti-neurofilament H (purple) targeting the axonal cytoskeletons, and anti-GCPII (green) demonstrating muscle innervation after nerve transection with or without repair; arrowheads emphasize axons. (A) Healthy muscle after sham surgery demonstrating a normal innervated neuromuscular junction with surrounding GCPII expression. Contrast this with the appearance of neuromuscular junctions at (B) 4 weeks, (C) 8 weeks, and (D) 16 weeks after sciatic nerve transection with repair; note progressive flattening and fragmentation of endplates consistent with chronic denervation, the absence of axons, and lack of GCPII expression. Nerve transection with immediate repair demonstrates infiltration of axons and neuromuscular junction reinnervation between (E) 4 weeks and (F) 8 weeks. Also note recovery of GCPII expression near the reinnervated neuromuscular junction, which persists at (G) 16 weeks after nerve repair. Panels are 20× magnification, scale bar: 20 μm.

Article Snippet: For GCPII content, primary antibody was rabbit anti-GCPII polyclonal antibody (Proteintech, 13163-1-AP, 1:50), secondary antibody was anti-rabbit CoraLite488-conjugated IgG (H+L) (Proteintech, SA00013-2, 1:200).

Techniques: Expressing

Journal: medRxiv

Article Title: Glutamate Carboxypeptidase II (GCPII)-Targeted PET to Identify Muscle Denervation in Peripheral Nervous System Injuries

doi: 10.64898/2026.03.18.26348533

Figure Lengend Snippet: Images of anti-GCPII (green), anti-cytochrome C (red) targeting mitochondria, and DAPI (blue) targeting nuclei at 12 weeks after nerve transection with or without repair. White boxes around key area of each image. Panel D (sham surgery) is a composite of Panels A-C; Panel H (sciatic nerve transection without repair) is a composite of Panels E-G; Panel L (nerve transection with repair) is a composite of Panels I-K. Note localization of GCPII staining near clusters of subsarcolemmal mitochondria overlying myocyte nuclei, irrespective of denervation. A similar staining pattern was present at all tested timepoints between two and 16 weeks after nerve transection with or without repair. Panels are 63× magnification, scale bar: 10 μm.

Article Snippet: For GCPII content, primary antibody was rabbit anti-GCPII polyclonal antibody (Proteintech, 13163-1-AP, 1:50), secondary antibody was anti-rabbit CoraLite488-conjugated IgG (H+L) (Proteintech, SA00013-2, 1:200).

Techniques: Staining

Journal: Journal of Neurochemistry

Article Title: Neuroprotective Effects of Strength Training on Behavioral Deficit, Oxidative Damage, Astrogliosis, and Neuronal Death in a Bipolar Disorder Model

doi: 10.1111/jnc.70392

Figure Lengend Snippet: Effect of previous strength training on oxidative stress‐related biochemical parameters in cerebral cortex of a model of BD. Box plots represent Superoxide Dismutase (SOD; A), Catalase (CAT; B), Glutathione Peroxidase (GPx; C), Glutathione S‐Transferase (GST; D) activity, Dichlorodihydrofluorescein (DCFH) oxidation (E), Non‐Protein Thiols (NPSH) levels (F), 3‐Nitrotyrosine (3‐NT; G), 4‐hydroxynonenal (4‐HNE; H), and Phosphorylated Nuclear Factor Kappa B (p‐NFκB)/Nuclear Factor Kappa B (NFκB) total ratio (I) in the cerebral cortex. Data were analyzed by two‐way analysis of variance (ANOVA) followed by Tukey's post hoc test (A–G, I) or by Scheirer–Ray–Hare test (H) and are presented in box and whisker plots, where the bottom border represents the 25th percentile, the line bisecting the box represents the median, the upper border the 75th percentile, and whiskers represent extreme values ( n = 5–6). Immunoblot images of 3‐NT, 4‐HNE, and p‐NFκB/NFκB total ratio are shown below. * indicates difference from sedentary + artificial cerebrospinal fluid (aCSF) group. # indicates difference from sedentary + ouabain (OUA) group.

Article Snippet: The evaluation of non‐protein thiol (NPSH) content was performed as previously described in the literature (Ellman ).

Techniques: Activity Assay, Whisker Assay, Western Blot

Journal: Journal of Neurochemistry

Article Title: Neuroprotective Effects of Strength Training on Behavioral Deficit, Oxidative Damage, Astrogliosis, and Neuronal Death in a Bipolar Disorder Model

doi: 10.1111/jnc.70392

Figure Lengend Snippet: Effect of previous strength training on oxidative stress‐related biochemical parameters in hippocampus of a model of bipolar disorder (BD). Box plots represent Superoxide Dismutase (SOD; A), Catalase (CAT; B), Glutathione Peroxidase (GPx; C), Glutathione S‐Transferase (GST; D) activity, Dichlorodihydrofluorescein (DCFH) oxidation (E), Non‐Protein Thiols (NPSH) levels (F), 3‐Nitrotyrosine (3‐NT; G), 4‐hydroxynonenal (4‐HNE; H), and Phosphorylated Nuclear Factor Kappa B (p‐NFκB)/Nuclear Factor Kappa B (NFκB) total ratio (I) in the hippocampus. Data were analyzed by two‐way ANOVA followed by Tukey's post hoc test and are presented in box and whisker plots, where the bottom border represents the 25th percentile, the line bisecting the box represents the median, the upper border the 75th percentile, and whiskers represent extreme values ( n = 5–6). Immunoblot images of 3‐NT, 4‐HNE, and p‐NFκB/NFκB total ratio are shown below. * indicates difference from sedentary + artificial cerebrospinal fluid (aCSF) group. # indicates difference from sedentary + ouabain (OUA) group. a indicates main effect of OUA.

Article Snippet: The evaluation of non‐protein thiol (NPSH) content was performed as previously described in the literature (Ellman ).

Techniques: Activity Assay, Whisker Assay, Western Blot