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Nonlinear Dynamics pfus restored normal nonlinear dynamics
Integrated mechanistic framework of <t>pFUS-mediated</t> seizure suppression. pFUS modulates neural activity through dual cellular pathways: the preferential activation of GABAergic interneurons and astrocytic mechano-transduction, leading to disrupted hypersynchrony <t>and</t> <t>restored</t> excitation–inhibition balance. These cellular effects propagate to network-level modulation, characterized by desynchronization and increased signal complexity. Ultimately, these processes drive system-level outcomes, including acute seizure reduction and long-term benefits mediated by neuroprotection.
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1) Product Images from "Pulsed focused ultrasound for seizure suppression: Mechanisms, models, and clinical translation"

Article Title: Pulsed focused ultrasound for seizure suppression: Mechanisms, models, and clinical translation

Journal: Neurotherapeutics

doi: 10.1016/j.neurot.2026.e00920

Integrated mechanistic framework of pFUS-mediated seizure suppression. pFUS modulates neural activity through dual cellular pathways: the preferential activation of GABAergic interneurons and astrocytic mechano-transduction, leading to disrupted hypersynchrony and restored excitation–inhibition balance. These cellular effects propagate to network-level modulation, characterized by desynchronization and increased signal complexity. Ultimately, these processes drive system-level outcomes, including acute seizure reduction and long-term benefits mediated by neuroprotection.
Figure Legend Snippet: Integrated mechanistic framework of pFUS-mediated seizure suppression. pFUS modulates neural activity through dual cellular pathways: the preferential activation of GABAergic interneurons and astrocytic mechano-transduction, leading to disrupted hypersynchrony and restored excitation–inhibition balance. These cellular effects propagate to network-level modulation, characterized by desynchronization and increased signal complexity. Ultimately, these processes drive system-level outcomes, including acute seizure reduction and long-term benefits mediated by neuroprotection.

Techniques Used: Activity Assay, Activation Assay, Transduction, Inhibition

Related Articles

Injection:

Article Title: Pulsed focused ultrasound for seizure suppression: Mechanisms, models, and clinical translation
Article Snippet: 2 , KA chronic epilepsy C57BL/6 mice (N = 34)/KA injection at CA3 region , MI: 2.2, I SPTA : 1.7 W/cm 2 (free-field output), DC: 5 %, SD: 30 s, one session , pFUS in mTLE models produced: (1) acute-phase: 4-fold SE delay; (2) chronic-period: ∼84% fewer spontaneous recurrent seizures; (3) restored sociability, reduced depression , [ ] . .. 3 , KA chronic epilepsy C57BL/6 mice (N = 14)/KA injection at CA3 region , MI: 0.37, I SPTA : 1.13 W/cm 2 (with skull attenuation), DC: 50 %, SD: 30 s, one session , pFUS-seizure suppression correlated with restoration of neural signal complexity: Approximate entropy increased (delta and theta band); largest lyapunov exponent increased. pFUS restored normal nonlinear dynamics , [ ] . .. 4 , KA chronic epilepsy C57BL/6 mice (N = 37)/KA injection at CA3 region , MI: 0.37, I SPTA : 1.13 W/cm 2 (with skull attenuation), DC: 50 %, SD: 30 s, one session , pFUS produced 42–99% spike reduction, ∼4-fold seizure latency prolongation; pFUS decoupled phase-amplitude coupling between slow and fast oscillations, disrupting pathological cross-frequency synchronization underlying seizures , [ ] .



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Image Search Results


Molecular dynamics–based analyses of DPP4 and SGLT2: (a) root mean square fluctuation (RMSF), (b) dynamic cross-correlation matrix (DCCM), and (c) principal component analysis (PCA).

Journal: Journal of Taibah University Medical Sciences

Article Title: Computational discovery of fenugreek–paitan–turmeric (FPT) bioactive compounds targeting SGLT2 and DPP-4 for glucose homeostasis regulation

doi: 10.1016/j.jtumed.2026.05.008

Figure Lengend Snippet: Molecular dynamics–based analyses of DPP4 and SGLT2: (a) root mean square fluctuation (RMSF), (b) dynamic cross-correlation matrix (DCCM), and (c) principal component analysis (PCA).

Article Snippet: Molecular dynamics–based analyses of DPP4 and SGLT2: (a) root mean square fluctuation (RMSF), (b) dynamic cross-correlation matrix (DCCM), and (c) principal component analysis (PCA).

Techniques:

Spatiotemporally controlled tumor cell ablation in vitro. (A) Design of adenoviral vector for all‐in‐one delivery of PyroRACS. Expression cassettes for RACS and GSDMD NT were incorporated into a single adenoviral vector. ITR, inverted terminal repeat; pCMV, cytomegalovirus promoter; pCBH, CBH promoter; IRES, internal ribosome entry site. (B) Titer determination of the adenovirus encoding PyroRACS. Data are presented as mean ± SD; unpaired t ‐test, n = 3 independent replicates. PFU, plaque‐forming units. (C,D) Pyroptosis induction in bladder cancer cells. Bladder cancer cells 5637 and BIU87 were transduced with adenovirus at specified multiplicity of infection (MOI). Pyroptotic cells were stained with Annexin V‐FITC/PI 24 h post‐illumination (660 nm, 1 mW/cm 2 , 30 s). Cell death was quantified by flow cytometry. Representative fluorescence images of pyroptotic 5637 and BIU87 cells (C), scale bar: 20 µm. Flow cytometry quantification of pyroptotic cells (D); data are presented as mean ± SD, unpaired t ‐test, n = 4 biological replicates. (E,F) DAMPs release kinetics during pyroptosis. ATP (E) and LDH (F) levels in culture supernatants were quantified at indicated time points post‐illumination, with non‐illuminated cells serving as negative controls. Data are presented as mean ± SD (F); unpaired t ‐test, n = 4 biological replicates. RLU, relative luminescence units; LDH, lactate dehydrogenase. (G,H) Assessment of cytotoxicity under non‐induced conditions. Following adenoviral transduction, 5637 or BIU87 cells were cultured in the dark for 48 h. The levels of ATP (G) and LDH (H) in the culture supernatant were quantified, with non‐transduced cells (UT) as negative controls. Data: mean ± SD, n = 3 (5637) or 4 (BIU87) biological replicates. (I) Spatio‐specific pyroptosis induction. 5637 cells transduced with adenovirus at a MOI of 50. At 48 h post‐transduction, cells were illuminated through a custom‐designed striped photomask to induce localized cell death, followed by SYTOX Green staining 24 h post‐illumination (660 nm, 50 µW/cm 2 , 3 min). The upper panel shows the custom‐designed striped photomask used for patterned illumination. Scale bar: 1 mm; n = 2 independent experiments. (J) Light dose‐dependent pyroptosis induction. 5637 cells transduced with adenovirus at a MOI of 100. At 48 h post‐transduction, cells were illuminated (660 nm, 1 mW/cm 2 ) for the indicated durations. Cell death was quantified by flow cytometry 24 h after illumination. Data: mean ± SD; unpaired t ‐test, n = 3 biological replicates; * p < 0.05, ** p < 0.01, **** p < 0.0001.

Journal: Advanced Science

Article Title: Engineering a 660 nm‐Responsive Optogenetic Inducer of Pyroptosis for Precision Cancer Therapy

doi: 10.1002/advs.76768

Figure Lengend Snippet: Spatiotemporally controlled tumor cell ablation in vitro. (A) Design of adenoviral vector for all‐in‐one delivery of PyroRACS. Expression cassettes for RACS and GSDMD NT were incorporated into a single adenoviral vector. ITR, inverted terminal repeat; pCMV, cytomegalovirus promoter; pCBH, CBH promoter; IRES, internal ribosome entry site. (B) Titer determination of the adenovirus encoding PyroRACS. Data are presented as mean ± SD; unpaired t ‐test, n = 3 independent replicates. PFU, plaque‐forming units. (C,D) Pyroptosis induction in bladder cancer cells. Bladder cancer cells 5637 and BIU87 were transduced with adenovirus at specified multiplicity of infection (MOI). Pyroptotic cells were stained with Annexin V‐FITC/PI 24 h post‐illumination (660 nm, 1 mW/cm 2 , 30 s). Cell death was quantified by flow cytometry. Representative fluorescence images of pyroptotic 5637 and BIU87 cells (C), scale bar: 20 µm. Flow cytometry quantification of pyroptotic cells (D); data are presented as mean ± SD, unpaired t ‐test, n = 4 biological replicates. (E,F) DAMPs release kinetics during pyroptosis. ATP (E) and LDH (F) levels in culture supernatants were quantified at indicated time points post‐illumination, with non‐illuminated cells serving as negative controls. Data are presented as mean ± SD (F); unpaired t ‐test, n = 4 biological replicates. RLU, relative luminescence units; LDH, lactate dehydrogenase. (G,H) Assessment of cytotoxicity under non‐induced conditions. Following adenoviral transduction, 5637 or BIU87 cells were cultured in the dark for 48 h. The levels of ATP (G) and LDH (H) in the culture supernatant were quantified, with non‐transduced cells (UT) as negative controls. Data: mean ± SD, n = 3 (5637) or 4 (BIU87) biological replicates. (I) Spatio‐specific pyroptosis induction. 5637 cells transduced with adenovirus at a MOI of 50. At 48 h post‐transduction, cells were illuminated through a custom‐designed striped photomask to induce localized cell death, followed by SYTOX Green staining 24 h post‐illumination (660 nm, 50 µW/cm 2 , 3 min). The upper panel shows the custom‐designed striped photomask used for patterned illumination. Scale bar: 1 mm; n = 2 independent experiments. (J) Light dose‐dependent pyroptosis induction. 5637 cells transduced with adenovirus at a MOI of 100. At 48 h post‐transduction, cells were illuminated (660 nm, 1 mW/cm 2 ) for the indicated durations. Cell death was quantified by flow cytometry 24 h after illumination. Data: mean ± SD; unpaired t ‐test, n = 3 biological replicates; * p < 0.05, ** p < 0.01, **** p < 0.0001.

Article Snippet: Cytotoxic lactate dehydrogenase (LDH) release dynamics were quantified using a commercial LDH assay kit (MCE, Cat. HY‐K1090) according to the manufacturer's instructions.

Techniques: In Vitro, Plasmid Preparation, Expressing, Transduction, Infection, Staining, Flow Cytometry, Fluorescence, Cell Culture