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Journal: The Journal of Physiological Sciences : JPS
Article Title: Genetic inactivation of TRPM4 does not alter the temperature-dependent movement of mouse microglia
doi: 10.1016/j.jphyss.2026.100067
Figure Lengend Snippet: Generation of Trpm4 -knockout mouse line. A. Map of the mouse Trpm4 locus showing exons 15 and 16 targeted for deletion by sgRNAs. Top, WT allele. Bottom, KO allele. The sgRNAs were designed to target introns 14 and 16 flanking exons 15 and 16. Specific primers for amplifying the WT(Fw2/Rv) or KO (Fw1/Rv) allele were used. B. A representative result of genotyping PCR using a mixture of the Fw1, Fw2, and Rv primers. Two fragments were amplified from heterozygote mouse samples, each indicating the WT or KO fragment. The bottom fragment (695 bp) was amplified using the WT primer pair. The top fragment (928 bp) was amplified using the KO primer pair, indicating successful deletion of exons 15 and 16, which was confirmed by direct sequencing. (C and D). The expression patterns of Trpm4 gene in mouse brain (C) or primary microglia (D) using Gapdh as a control. In (C), “M4-plasmid” indicates an amplified fragment using mouse TRPM4 plasmid as a template. E. Western blot analysis of Trpm4 in mouse TRPM4-expressing HEK293T cells (M4-HEK) and mouse colon samples from WT or TRPM4KO mice. The expected molecular weight of Trpm4 is 134 kDa.
Article Snippet: After transferring the proteins to a nitrocellulose membrane, the membrane was blocked for 1 h at room temperature and then incubated with
Techniques: Knock-Out, Amplification, Sequencing, Expressing, Control, Plasmid Preparation, Western Blot, Molecular Weight
Journal: The Journal of Physiological Sciences : JPS
Article Title: Genetic inactivation of TRPM4 does not alter the temperature-dependent movement of mouse microglia
doi: 10.1016/j.jphyss.2026.100067
Figure Lengend Snippet: Genetic elimination of Trpm4 does not alter the temperature-dependent microglia movement. A. Trajectories of primary microglia from a representative preparation of WT and TRPM4KO mice recorded for 2 h at 33 °C, 37 °C, and 40 °C. Paths are arranged to show origins at x (horizontal axis) = y (vertical axis) = 0. Each line indicates the trajectory of a single cell. n indicates the number of cells analyzed per preparation. B. The average distances of migrating microglia isolated from WT or TRPM4KO mice exposed to 33 °C (WT, n = 117; TRPM4KO, n = 151), 37 °C (WT, n = 235; TRPM4KO, n = 240), or 40 °C (WT, n = 150; TRPM4KO, n = 175) were measured. Open circles indicate the migration distance of each microglia over 2 h. Horizontal lines indicate means ± SEM. At 33 °C, 37 °C, and 40 °C, WT microglia moved 112.94 ± 6.1 μm, 175.28 ± 5.24 μm, and 204.31 ± 7.27 μm, respectively, whereas TRPM4KO microglia moved 113.46 ± 5.1 μm, 175.28 ± 4.13 μm, and 201.35 ± 5.61 μm, respectively. **P < 0.01 (two-way ANOVA followed by post hoc Bonferroni test for multiple comparisons).
Article Snippet: After transferring the proteins to a nitrocellulose membrane, the membrane was blocked for 1 h at room temperature and then incubated with
Techniques: Single Cell, Isolation, Migration
Journal: Veterinary and Animal Science
Article Title: Aerococcus viridans, Staphylococcus haemolyticus and Corynebacterium bovis : sub-inhibitory exposure of lactic acid and cross-resistance to β-lactams antibiotics
doi: 10.1016/j.vas.2026.100620
Figure Lengend Snippet: Trend of LA MIC changes for S. haemolyticus during sub-inhibitory treatment.
Article Snippet: Fig 5 dummy alt text While
Techniques:
Journal: Veterinary and Animal Science
Article Title: Aerococcus viridans, Staphylococcus haemolyticus and Corynebacterium bovis : sub-inhibitory exposure of lactic acid and cross-resistance to β-lactams antibiotics
doi: 10.1016/j.vas.2026.100620
Figure Lengend Snippet: Correlation of LA and ꞵ-lactam antibiotic* tolerance between pre- and post-exposure in S. haemolyticus . Tolerance compared in measured MIC steps (+1). ▼ = 1 step decrease from the initial MIC. One MIC-step equals to a 2-fold change in antibiotic MICs and a 1.3-fold change in LA MICs. *Cefquinome, penicillin + novobiocin, and amoxicillin + clavulanic acid showed no changes at all.
Article Snippet: Fig 5 dummy alt text While
Techniques:
Journal: Biomaterials Research
Article Title: Injectable Poloxamer and Hyaluronic Acid Hydrogel for Sustained Co-Delivery of Dexamethasone and Lidocaine Ameliorates Neuropathic Pain
doi: 10.34133/bmr.0373
Figure Lengend Snippet: TRPV1-mediated nociceptive sensitization in the DRG and spinal cord dorsal horn (SC) following CCI and treatment. (A) Schematic illustration of the proposed mechanism: Injury-induced TRPV1 ion channel activation triggers calcium influx and downstream CGRP release, which activates adenylate cyclase/PKA signaling to amplify neuropathic pain sensitization. (B) Representative immunofluorescence images of the DRG stained for TRPV1 (red), NeuN (green), and DAPI (blue). The Injury group shows marked up-regulation of TRPV1 in sensory neurons. Dex/Lid@PLX/HA treatment substantially reduces TRPV1 expression, restoring it to near-Naive levels. Scale bars, 200 μm (overview) and 50 μm (inset). (C) Immunofluorescence staining for TRPV1 (red) and NeuN (green) in the spinal dorsal horn. The dashed line indicates the dorsal horn boundary. Dex/Lid@PLX/HA significantly suppresses injury-induced central TRPV1 up-regulation. Scale bar, 200 μm. (D to F) Quantitative analysis of the relative TRPV1 + area in the DRG (top) and spinal cord (middle), and the SGC/neuron ratio. Dex/Lid@PLX/HA shows marked suppression of TRPV1 overexpression relative to the injury group. Data are presented as mean ± SEM. **** P < 0.0001, ** P < 0.01, * P < 0.05, ns: not significant.
Article Snippet: The sections were then incubated overnight at 4 °C with the following primary antibodies:
Techniques: Activation Assay, Immunofluorescence, Staining, Expressing, Over Expression