Journal: Bioactive Materials

Article Title: A cell motility-based selective hydrogel enables rapid generation of nerve-repairing blood clots

doi: 10.1016/j.bioactmat.2026.05.015

Figure Lengend Snippet: Effect and mechanism of the nano-gelatin on NSCs . (A) A diagram of the layered composite structure of the nano-gelatin after hemostasis. (B) Representative SEM images showing the platelet-derived extracellular vesicles in the nano-gelatin after hemostasis. (C) ALB contents in the cryogels following hemostasis (N = 4). (D) NGF contents in the cryogels (N = 3). (E) SDF-1 contents in the cryogels (N = 3). (F) Representative images showing NSCs migrating through the Transwell membrane into the plate with cryogels. (G) Quantification of the NSC numbers that migrated through the Transwell membrane into the plate (N = 4). (H) Representative images of the live/dead staining showing the survival and morphology of NSCs on the cryogels. (I) Cytotoxicity of the cryogels on NSCs by CCK-8 assay. (J) Representative images of immunostaining against F-actin, paxillin, and vinculin for cells encapsulated in the nano-gelatin and the GelMA hydrogel. (K) Representative images of immunostaining against Tuj-1 and GFAP. (L) Volcano plot analyzing DEGs between the nano-gelatin group and the control group. (M) The enriched GO pathways. (N) The enriched KEGG pathways. (O) The heatmaps of DEGs associated with Focal adhesion. (P) Schematic diagram of the potential mechanism by which the nano-gelatin regulates NSC migration and differentiation to promote nerve repair. Statistical analysis was performed using one-way ANOVA followed by Tukey's multiple comparisons test.

Article Snippet: Then, the samples were fixed and stained with astrocyte marker GFAP (1:500, CST, Rabbit mAb #80788) and neuron marker Tuj-1 (1:200, HUABIO, SP06-00) to assess differentiation.

Techniques: Derivative Assay, Membrane, Staining, CCK-8 Assay, Immunostaining, Control, Migration

Journal: Neuron

Article Title: A hypothalamic neuronal population coordinates metabolic adaptations to cold

doi: 10.1016/j.neuron.2026.08.024

Figure Lengend Snippet: A. Cold exposure and c-Fos staining scheme. B-C. Representative c-Fos staining and Allen Brain Atlas reference (B) and dPVp c-Fos quantification (C) in male WT mice at 23°C or 6°C for 1 h (n=5/group). D-F. RNAscope for Slc32a1 and Fos after cold exposure (6°C, 40 min) (D) and quantification of Slc32a1 + / Fos + (E) and Fos + / Slc32a1 + cells (F) (n=3). G. GCaMP6m expression in GABAergic dPVp neurons of Vgat-Flp mice and representative fiber placement. H-I. Cold-evoked (6°C, 5 s) Ca 2+ signals (H) and individual responses (I) in GABA dPVp neurons (n=8). J-K. GABA dPVp Ca 2+ responses to 22–6°C (J) and AUC quantification (K) (n=4). Data are expressed as mean ± SEM. *p < 0.05, ****p < 0.0001.

Article Snippet: To study the role of Kcnk2 in mediating the adaptive response of dPVp neurons to cold, TRAP2 mice received synapsin-driven Cre-dependent AAV9 carrying GFP (Addgene, #100043, titer: 2×10 11 GC/ml, 0.2 μl/injection) or Kcnk2 (Baylor IDDRC Neuroconnectivity Core, titer: x10 11 GC/ml, 0.2 μl/injection) or Kcnk2-E306A (Baylor IDDRC Neuroconnectivity Core, titer: 2×10 11 GC/ml, 0.2 μl/injection) into the dPVp.

Techniques: Staining, RNAscope, Expressing

Journal: Neuron

Article Title: A hypothalamic neuronal population coordinates metabolic adaptations to cold

doi: 10.1016/j.neuron.2026.08.024

Figure Lengend Snippet: A. Scheme for cold-induced tdTomato TRAP labeling. B. Cold-TRAPed tdTomato, cold-induced c-Fos, and their colocalization in dPVp of male TRAP2/tdTomato mice. C-D. Percentage of c-Fos + tdTomato + cells among tdTomato + (C) or c-Fos + (D) cells (n=3). E. Scheme for cold-induced hM3Dq expression in TRAP2 mice. F-G. Food intake (F) and rectal temperature (G) after saline or CNO in hM3Dq-expressing WT (n=10) and TRAP2 (n=8) mice. H-K. Energy expenditure (H), XY (I) and Z (J) activity, and food intake (K) after saline or CNO in WT (n=8) and TRAP2 (n=5) mice. L. BAT temperature after CNO (n=7/group). M-N. BAT Ucp1 (M) and serum NE (N) 2 h after CNO (WT, n=9; TRAP2, n=8). O-Q. Thermal gradient scheme (O), zone occupancy (P), and preferred temperature (Q) after CNO (n=7/group). R-T. Two-chamber temperature preference scheme (R), distance traveled (S), and warm-chamber occupancy (T) after CNO (n=8/group). U-V. 2-h refeeding after saline (U) or CNO (V) in fasted WT (n=10) and TRAP2 (n=8) mice. W-X. Core (W) and BAT surface (X) temperatures after saline or CNO in TRAP2 mice (n=7). Y-Z. Changes in core and BAT temperatures after saline (Y) or CNO (Z) (n=7). Data are expressed as mean ± SEM. *p < 0.05, **p < 0.01, ***p < 0.001, ****p < 0.0001.

Article Snippet: To study the role of Kcnk2 in mediating the adaptive response of dPVp neurons to cold, TRAP2 mice received synapsin-driven Cre-dependent AAV9 carrying GFP (Addgene, #100043, titer: 2×10 11 GC/ml, 0.2 μl/injection) or Kcnk2 (Baylor IDDRC Neuroconnectivity Core, titer: x10 11 GC/ml, 0.2 μl/injection) or Kcnk2-E306A (Baylor IDDRC Neuroconnectivity Core, titer: 2×10 11 GC/ml, 0.2 μl/injection) into the dPVp.

Techniques: Activation Assay, Labeling, Expressing, Saline, Activity Assay

Journal: Neuron

Article Title: A hypothalamic neuronal population coordinates metabolic adaptations to cold

doi: 10.1016/j.neuron.2026.08.024

Figure Lengend Snippet: A. Scheme for cold-induced hM4Di expression in TRAP2 mice. B. Representative dPVp hM4Di-mCherry expression. C-E. Action potentials (C), firing frequency (D), and resting membrane potential (E) of hM4Di + cold-activated dPVp neurons before and after CNO (10 μM; n=7). F-I. Food intake (F, H) and rectal temperature (G, I) at RT or cold after saline (F-G) or CNO (H-I) in hM4Di-expressing WT (n=8) and TRAP2 (n=7) mice. J-L. Two-chamber temperature preference scheme (J), distance traveled (K), and warm-chamber occupancy (L) after CNO (WT, n=8; TRAP2, n=7). M-N. Food intake in fasted WT (n=8) and TRAP2 (n=7) mice after saline (M) or CNO (N). O. Scheme for chronic hM3Dq activation in HFD-fed WT and TRAP2 mice. P-R. Cumulative food intake (P), rectal temperature (Q), and body weight (R) during daily CNO treatment (n=8/group). S-V. GTT and AUC after 12 days (S-T) and ITT and AUC after 16 days (U-V) of CNO (n=8/group). Data are expressed as mean ± SEM. *p < 0.05, **p < 0.01, ***p < 0.001.

Article Snippet: To study the role of Kcnk2 in mediating the adaptive response of dPVp neurons to cold, TRAP2 mice received synapsin-driven Cre-dependent AAV9 carrying GFP (Addgene, #100043, titer: 2×10 11 GC/ml, 0.2 μl/injection) or Kcnk2 (Baylor IDDRC Neuroconnectivity Core, titer: x10 11 GC/ml, 0.2 μl/injection) or Kcnk2-E306A (Baylor IDDRC Neuroconnectivity Core, titer: 2×10 11 GC/ml, 0.2 μl/injection) into the dPVp.

Techniques: Expressing, Membrane, Saline, Activation Assay

Journal: Neuron

Article Title: A hypothalamic neuronal population coordinates metabolic adaptations to cold

doi: 10.1016/j.neuron.2026.08.024

Figure Lengend Snippet: A. Scheme for cold-induced Kir2.1 expression in TRAP2 mice. B. Representative dPVp Kir2.1-tdTomato expression. C. Action potentials, firing frequency, and resting membrane potential of mCherry control (n=7) or Kir2.1 + (n=9) cold-activated dPVp neurons. D. Body weight of Kir2.1-expressing WT (n=7) and TRAP2 (n=6) mice. E-H. Food intake (E, G) and BAT temperature (F, H) at room temperature (E-F) or cold (G-H). I-J. Core (I) and BAT surface (J) temperatures during cold exposure (n=7/group). K. Energy expenditure and body-mass regression, with predicted values at 26 g. L-N. XY (L) and Z (M) activity and food intake (N). O-P. BAT Ucp1 (O) and serum NE (P). Q-S. Two-chamber temperature preference scheme (Q), distance traveled (R), and warm-chamber occupancy (S). T-U. Thermal gradient zone occupancy (T) and preferred temperature (U). V. Food intake after overnight fasting. W-Z. GTT and AUC (W-X) and ITT and AUC (Y-Z). Unless indicated, WT n=7 and TRAP2 n=6. Data are expressed as mean ± SEM. *p < 0.05, **p < 0.01, ***p < 0.001, ****p < 0.0001.

Article Snippet: To study the role of Kcnk2 in mediating the adaptive response of dPVp neurons to cold, TRAP2 mice received synapsin-driven Cre-dependent AAV9 carrying GFP (Addgene, #100043, titer: 2×10 11 GC/ml, 0.2 μl/injection) or Kcnk2 (Baylor IDDRC Neuroconnectivity Core, titer: x10 11 GC/ml, 0.2 μl/injection) or Kcnk2-E306A (Baylor IDDRC Neuroconnectivity Core, titer: 2×10 11 GC/ml, 0.2 μl/injection) into the dPVp.

Techniques: Inhibition, Expressing, Membrane, Control, Activity Assay

Journal: Neuron

Article Title: A hypothalamic neuronal population coordinates metabolic adaptations to cold

doi: 10.1016/j.neuron.2026.08.024

Figure Lengend Snippet: A. snRNA-seq gene expression in the caudal hypothalamus of cold-exposed male WT mice. B-D. Representative Lef1/c-Fos staining at 23°C or 6°C for 1 h (B) and Lef1 + /c-Fos + colocalization (C-D; n=3). E-F. Food intake (E) and rectal temperature (F) after CNO in WT and Lef1-Dq mice (n=6/group). G-H. Thermal zone occupancy (G) and preferred temperature (H) in control and Lef1-Dq mice (n=6/group). I-L. Food intake (I, K) and body temperature (J, L) in control and Lef1-Kir2.1 mice at room temperature (I-J) or cold (K-L; n=6/group). M-O. Rectal temperature (M), BAT Ucp1 (N), and serum NE (O) in control and Lef1-KD mice. P-Q. Thermal zone occupancy (P) and preferred temperature (Q). R. Cold-induced body temperature change. S-V. GTT/AUC (S-T) and ITT/AUC (U-V). For Lef1-KD studies, control n=7 and Lef1-KD n=8 unless indicated; N, n=5/group; O, n=6/group. Data are expressed as mean ± SEM. *p < 0.05, **p < 0.01, ***p < 0.001.

Article Snippet: To study the role of Kcnk2 in mediating the adaptive response of dPVp neurons to cold, TRAP2 mice received synapsin-driven Cre-dependent AAV9 carrying GFP (Addgene, #100043, titer: 2×10 11 GC/ml, 0.2 μl/injection) or Kcnk2 (Baylor IDDRC Neuroconnectivity Core, titer: x10 11 GC/ml, 0.2 μl/injection) or Kcnk2-E306A (Baylor IDDRC Neuroconnectivity Core, titer: 2×10 11 GC/ml, 0.2 μl/injection) into the dPVp.

Techniques: Gene Expression, Staining, Control

Journal: Neuron

Article Title: A hypothalamic neuronal population coordinates metabolic adaptations to cold

doi: 10.1016/j.neuron.2026.08.024

Figure Lengend Snippet: A. Scheme for GCaMP6m and GFP/Kcnk2/Kcnk2-E306A expression in dPVp of TRAP2 mice. B-D. Cold-evoked (6°C, 15 s) Ca 2+ signals in GFP (B), Kcnk2 (C), and Kcnk2-E306A (D) mice (n=11/group). E. AUC for B-D. F-L. Food intake and BAT temperature at room temperature (F-G) or cold (H), BAT Ucp1 and serum NE (I), thermal preference (J), fasting-induced feeding (K), and GTT/ITT (L) in control (n=6), Kcnk2 (n=7), and E306A (n=6) mice. M. Scheme for dPVp Kcnk2-E306A expression and cannulation. N-Q. Food intake (N), rectal temperature (O), and thermal preference (P-Q) after dPVp ACSF or Spadin in WT and TRAP2 mice (n=7/group). R. Scheme for dPVp Cas9/sgKcnk2 injection and representative GFP expression. S-Z. Food intake (S), rectal/BAT temperature (T), BAT Ucp1 (U), serum NE (V), thermal preference (W), body weight (X), GTT (Y), and ITT (Z) in control and sgKcnk2 mice (n=8/group). Data are expressed as mean ± SEM. *p < 0.05, **p < 0.01, ***p < 0.001.

Article Snippet: To study the role of Kcnk2 in mediating the adaptive response of dPVp neurons to cold, TRAP2 mice received synapsin-driven Cre-dependent AAV9 carrying GFP (Addgene, #100043, titer: 2×10 11 GC/ml, 0.2 μl/injection) or Kcnk2 (Baylor IDDRC Neuroconnectivity Core, titer: x10 11 GC/ml, 0.2 μl/injection) or Kcnk2-E306A (Baylor IDDRC Neuroconnectivity Core, titer: 2×10 11 GC/ml, 0.2 μl/injection) into the dPVp.

Techniques: Expressing, Control, Injection

Journal: Neuron

Article Title: A hypothalamic neuronal population coordinates metabolic adaptations to cold

doi: 10.1016/j.neuron.2026.08.024

Figure Lengend Snippet: A-C. Action potentials (A), firing frequency (B), and resting membrane potential (C) of tdTomato + dPVp neurons during 34→30°C or 30→34°C shifts (n=11). D-E. Action potentials (D) and resting membrane potential (E) during temperature shifts with TTX and synaptic blockers (n=11). F. Thermal coefficient during 34→30°C cooling (n=11). G-I. Action potentials (G), firing frequency (H), and resting membrane potential (I) during temperature shifts with spadin (n=11). J-K. Action potentials (J) and resting membrane potential (K) during temperature shifts in Kcnk2-E306A-expressing neurons (n=11). L-N. K + currents during temperature shifts in control (L), spadin-treated (M), or Kcnk2-E306A-expressing (N) neurons. Data are expressed as mean ± SEM and individual data points. *p < 0.05, **p < 0.01, ***p < 0.001.

Article Snippet: To study the role of Kcnk2 in mediating the adaptive response of dPVp neurons to cold, TRAP2 mice received synapsin-driven Cre-dependent AAV9 carrying GFP (Addgene, #100043, titer: 2×10 11 GC/ml, 0.2 μl/injection) or Kcnk2 (Baylor IDDRC Neuroconnectivity Core, titer: x10 11 GC/ml, 0.2 μl/injection) or Kcnk2-E306A (Baylor IDDRC Neuroconnectivity Core, titer: 2×10 11 GC/ml, 0.2 μl/injection) into the dPVp.

Techniques: Membrane, Expressing, Control

Journal: Neuron

Article Title: A hypothalamic neuronal population coordinates metabolic adaptations to cold

doi: 10.1016/j.neuron.2026.08.024

Figure Lengend Snippet: A. Scheme for Cre-dependent ChR2 injection into the dPVp and representative fluorescence images showing ChR2-GFP expression in the dPVp and fibers in the LS, DBB, POA, LH, DMH, PVT, LPAG, DRN, periLC, LPBN, NTS, and RPa of TRAP2 mice. B. Scheme for retrograde Rabies tracing from cold-activated dPVp neurons. C. Rabies-GFP expression in the dPVp, POA and DMH.

Article Snippet: To study the role of Kcnk2 in mediating the adaptive response of dPVp neurons to cold, TRAP2 mice received synapsin-driven Cre-dependent AAV9 carrying GFP (Addgene, #100043, titer: 2×10 11 GC/ml, 0.2 μl/injection) or Kcnk2 (Baylor IDDRC Neuroconnectivity Core, titer: x10 11 GC/ml, 0.2 μl/injection) or Kcnk2-E306A (Baylor IDDRC Neuroconnectivity Core, titer: 2×10 11 GC/ml, 0.2 μl/injection) into the dPVp.

Techniques: Injection, Fluorescence, Expressing

Journal: Frontiers in Immunology

Article Title: RBM15 affects mitophagy in intracerebral hemorrhage by promoting E2F1 nuclear translocation via NXF1

doi: 10.3389/fimmu.2026.1892295

Figure Lengend Snippet: NXF1 knockdown attenuates inflammatory response in vitro. (A) Expression level of NXF1 mRNA was assessed by qPCR. (B) Protein expression level of NXF1 was detected by Western blotting. (C) Cytokine levels were measured using ELISA. * P < 0.05; ** P < 0.01; *** P < 0.001.

Article Snippet: The following ELISA kits were used for detection: mouse NSE ELISA kit (Elabscience, E-EL-M0089), mouse IL-10 ELISA kit (Elabscience, E-EL-M0046c), mouse IL-6 ELISA kit (Elabscience, E-EL-M0044c), mouse TNF-α ELISA kit (Elabscience, E-EL-M3063), mouse TGF-β ELISA kit (RnDSystems, DY1679), mouse IL-1 ELISA kit (Elabscience, E-EL-M0037c).

Techniques: Knockdown, In Vitro, Expressing, Western Blot, Enzyme-linked Immunosorbent Assay

Journal: Frontiers in Immunology

Article Title: RBM15 affects mitophagy in intracerebral hemorrhage by promoting E2F1 nuclear translocation via NXF1

doi: 10.3389/fimmu.2026.1892295

Figure Lengend Snippet: NXF1 down-regulation improves the pathological changes in ICH mice. (A) Changes in lesion volume after NXF1 downregulation in ICH mice. (B) Western blotting was used to detect the expression levels of NXF1 in brain tissue. (C) HE staining was used to detect hematomas in ICH mice. Scale bar: 500 μm (40x), 200 μm (100x). (D) Changes in heart rate, blood pressure, blood glucose level, brain water content, and mNSS in ICH mice. (E) TUNEL staining was used to detect cell apoptosis. Scale bar: 100 μm (200x). (F) FJ-C staining was used to detect apoptosis in neuronal cells. Scale bar: 100 μm (200x). (G) ELISA kits were used to detect the content of IL-6, IL-1β, TNF-α, IL-10, TGF-β, and NSE. * P < 0.05; ** P < 0.01; *** P < 0.001.

Article Snippet: The following ELISA kits were used for detection: mouse NSE ELISA kit (Elabscience, E-EL-M0089), mouse IL-10 ELISA kit (Elabscience, E-EL-M0046c), mouse IL-6 ELISA kit (Elabscience, E-EL-M0044c), mouse TNF-α ELISA kit (Elabscience, E-EL-M3063), mouse TGF-β ELISA kit (RnDSystems, DY1679), mouse IL-1 ELISA kit (Elabscience, E-EL-M0037c).

Techniques: Western Blot, Expressing, Tissue, H&E Stain, TUNEL Assay, Staining, Enzyme-linked Immunosorbent Assay

Journal: Stem Cells Translational Medicine

Article Title: Functional characterization of human iPSC–derived sensory neuron processes in microfluidic cultures

doi: 10.1093/stcltm/szag065

Figure Lengend Snippet: Expression of SCN9A and SCN10A mRNA within human-induced pluripotent stem cell (hiPSC)-SN soma in coculture hiPSC-CN. (A-C) mRNA labeling of hiPSC-SN via RNAscope at DIV27 with SCN9A (magenta) and DAPI (cyan) (A), SCN10A (green) and DAPI (B) and overlapped with β3-tubulin expression (C). Clear expression of SCN9A is observed in the sensory neurons, with sparser SCN10A expression throughout the neurons. (D, E) Relative mRNA expression for both SCN9A and SCN10A was measured in the iPSC-derived sensory neurons at 2 different time points in coculture using qPCR. No difference in the expression levels for either mRNA was found between DIV21 and DIV27 ( P- value .6211and .8897, respectively). For each time point, samples were prepared from the hiPSC-SN soma compartments of 4 independent microfluidic cultures plates and analyzed in technical triplicates. Scale bar 50 µm.

Article Snippet: Human iPSC-derived sensory neuron progenitors (ax0055) and human iPSC-derived neural stem cells (ax0015) were purchased from Axol Bioscience Ltd. No additional ethical approval was required for this study.

Techniques: Expressing, Labeling, RNAscope, Derivative Assay