Journal: iScience

Article Title: A quantitative metabolic signature of host response during SARS-CoV-2 infection and recovery

doi: 10.1016/j.isci.2026.115390

Figure Lengend Snippet: Metabo-time confidently represented individualized normalization of host systemic oxidative stress and immune response during COVID-19 recovery, better than physical days since hospitalization (A) The normalization of serum reactive oxygen species levels during recovery was better captured by metabo-time than physical days since hospitalization, as evidenced by the higher R 2 statistic correlating ROS levels with metabo-time than days since hospitalization. This was quantitatively tested by joint linear modeling of ROS on both physical time and metabo-time. (B) Quantification and statistical analysis; ( n = 34), where the conditional regression coefficient (i.e., association) of physical time with ROS was null. Still, the effect of metabo-time remained highly significant, suggesting that metabo-time can fully replace physical time to characterize the individualized recovery of ROS levels. (C) Longitudinal correlation of host serum cytokine levels versus metabo-time and physical time yielded consistent findings across cytokines. (D) Cytokines identified as statistically significantly correlated with metabo-time (i.e., “normalizing” during COVID-19 recovery) were consistent with previous observations ( n = 36). , ,

Article Snippet: Correlation between Metabo-time and log-transformed CRP values was assessed using Spearman’s rank correlation coefficient.

Techniques:

Journal: bioRxiv

Article Title: Discovery and Preclinical Validation of a Clinically Optimized Mitochondrial Complex I Modulator for Alzheimer’s Disease

doi: 10.64898/2026.04.10.717554

Figure Lengend Snippet: a C273 increases resistance to oxidative stress induced by H 2 O 2 in MC65 Tet-Off cells expressing Aβ. Cells were pretreated with C273 prior to H 2 O 2 exposure, and cell viability was assessed to determine LD 50 values. LD 50 values were calculated by nonlinear regression using GraphPad Prism. b, c C273 restores intracellular NADPH ( b ) and GSH ( c ) levels in MC65 Tet-Off cells. d C273 suppresses IL-1β-induced NF-κB activation. NF-κB reporter HEK293 cells were pretreated for 24 h with C273 (50 nM, 500 nM, or 5 μM), AICAR (0.5 mM), or metformin (0.5 mM), followed by stimulation with IL-1β (1 ng/ml) for 6 h. NF-κB luciferase activity was measured using the Luciferase Assay System (Promega, E1501). n = 4 independent experiments. e C273 restores mitochondrial biogenesis, expression of ETC complexes, autophagy markers, and antioxidant proteins in MC65 Tet-Off cells. MC65 cells were cultured under Tet-On (Aβ-) or Tet-Off (Aβ+) conditions and treated with vehicle or C273 (5 nM, 50 nM, or 500 nM) for 24 h. Protein levels were analyzed by Western blot. Statistical analysis was performed via one-way ANOVA to compare the vehicle-, metformin-, AICAR- and C273-treated groups. Data are presented as mean ± SD. * P < 0.05; ** P < 0.01.

Article Snippet: NF-κB Reporter (Luc) HEK293 cell line and the antioxidant response element (ARE) Luciferase Reporter HepG2 hepatic cell line were purchased from BPS Bioscience (CA, USA) and were cultured in accordance of manufacturer instructions.

Techniques: Expressing, Activation Assay, Luciferase, Activity Assay, Cell Culture, Western Blot

Journal: Bone Research

Article Title: Spatially resolved osteoblast-traced transcriptomics uncovers TGF-β as a combination target with sclerostin in osteoporosis

doi: 10.1038/s41413-026-00521-9

Figure Lengend Snippet: Dual inhibition of TGF-β and sclerostin increases bone mass in a hindlimb unloading model. a Experimental timeline of hindlimb unloading using C57B1/6 J mice and treatment with TGFβ-Ab, Scl-Ab, or both. Mice euthanized at week 12. b Representative μCT images of femoral diaphysis. c Representative confocal images of trabecular bone showing calcein (green), alizarin (red) signals, and DAPI (blue). Scale bar = 100 μm. d Representative images of TRAP-stained femur sections; violet = TRAP-positive, green = counterstain. Scale bar = 200 μm. e – h Bar plot of trabecular bone volume/total volume (Tra. BV/TV, e ), trabecular thickness (Tb. Th, f ), trabecular separation (Tb. Sp, g ), and trabecular number (Tb. N, h ) from μCT. Data = mean ± standard deviation. i , j Bar plot of mineral apposition rate (Tra. MAR, i ) and trabecular bone formation rate per bone surface (Tra. BFR/BS, j ) from labeling images. Data = mean ± standard deviation k Box plot of TRAP+ osteoclasts per bone surface (OC.N/BS), measured through ImageJ from TRAP-stained slides. l – n Box plot of serum P1NP ( l ) and TRAP ( m ) levels, and RANKL/OPG ratio ( n ). Group sizes: Control ( n = 5), Un_con ( n = 5), Scl-Ab ( n = 6), TGFβ-Ab ( n = 6), and Scl-Ab+TGFβ-Ab ( n = 7). Each point represents an individual mouse. ANOVA was used for statistics; * P < 0.05; ** P < 0.01; *** P < 0.001; **** P < 0.000 1; ns not significant

Article Snippet: Serum levels of P1NP, CTx1, TRAcP, OPG, RANKL, and TGF-β1 were measured via an enzyme-linked immunosorbent assay (ELISA) performed using ELISA kit for mouse P1NP (AC-33F1, Immunodiagnostic Systems, UK), mouse CTx1 (AC-06F1, Immunodiagnostic Systems, UK), mouse TRAcP 5b (SB-TR103, Immunodiagnostic Systems, UK), mouse OPG (MOP00, R&D systems, USA), mouse RANKL (MTR00, R&D systems, USA), and mouse TGF-β1 (DY1679-05 and DY007B, R&D systems, USA) according to the manufacturer’s instruction.

Techniques: Inhibition, Staining, Standard Deviation, Labeling, Control