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    Mini-Circuits shp
    Shp, supplied by Mini-Circuits, used in various techniques. Bioz Stars score: 94/100, based on 55 PubMed citations. ZERO BIAS - scores, article reviews, protocol conditions and more
    https://www.bioz.com/product/c-900/SHP-Series+Coaxial+Lumped+L-C+High+Pass+Filters/arxiv__2602__14870-136-20-9
    Average 94 stars, based on 55 article reviews
    shp - by Bioz Stars, 2026-10
    94/100 stars

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    Article Title: [2602.14870] Application of RFSoC Technology for Beam Position Monitors at the SuperKEKB Storage Rings Injection Points
    Article Snippet: A survey based on the S-parameter data published by Mini-Circuits showed that a SBP-150+ bandpass or a combination of a SHP-200+ (highpass) and SLP-200+ (lowpass) filters may provide suitable signal conditioning.

    Article Title: Continuous Automatic Polarization Channel Stabilization from Heterodyne Detection of Coexisting Dim Reference Signals
    Article Snippet: For example, in our demonstration, we choose ν<125 MHz, l = 10 kHz, B = 500 MHz, Y = 70 MHz, X = 200 MHz, Detector 1 and Detector 2a band-pass filter (FB1 and FB2a) passband = 10-200 MHz (Mini-circuits SLP-200+ and ZKL-1R5+), Detector 1 and Detector 2a low-pass filter (FL1 and FL2a) passband = 0-200 MHz (Mini-circuits SLP-200+), Detector 2b high-pass filter (FH2b) passband > 200 MHz (Mini-circuits SHP-250+), and Detector 2b band-pass filter (FB2b) passband = 200-400 MHz (Mini-circuits SHP-250+ and SLP-550+).

    Article Title: Investigating the Applicability of Modern Widely Tunable Lasers to Laser Heterodyne Radiometry for Atmospheric Composition Monitoring
    Article Snippet: Subsequently, two filters are employed, a high-pass filter SHP-20+ (Mini-Circuits) and a low-pass filter SLP300+ (Mini-Circuits).

    Article Title: Smart Monitoring of Partial Discharges in Power Apparatus Using UHF Sensor
    Article Snippet: Partial Discharge (PD) activity is a pre-cursor for insulation degradation which may eventually lead to catastrophic failure of power apparatus with severe social and economic consequences.. Electromagnetic emissions gathered over ultra-high frequency (UHF) range (0.5 to 3 GHz) during PD events is widely investigated for health monitoring of high voltage (HV) apparatus.. However, large bandwidth of PD induced UHF signals requires high speed digitizer and large storage space which have restricted field deployment of UHF technique for online PD detection.



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    Semaglutide exerts limited neuroprotective effects in Day 80 forebrain organoids. A–B, Morphological evaluation of late‐stage forebrain organoids. Organoids were treated for 15 days (from Day 65 to Day 80) and analyzed on Day 80. A, Representative bright‐field images. Scale bar, 1 mm. B, Quantification of organoid area on Day 80. n = 11 organoids per group. C–E, Western blot analysis of AD‐associated pathological proteins. Representative bands show the expression of APP (≈ 110 kDa), p‐tau217 (≈ 55 kDa), and total tau (≈ 55 kDa), with β‐actin (42 kDa) as a loading control. D–E, Quantitative analysis of (D) relative APP levels and (E) p‐tau217/tau ratio. n = 4 independent experiments. F–H, Representative immunofluorescence images of MAP2 (green) and DAPI (blue) in Day 80 organoids. Middle panels show the MAP2 channel only, and lower panels show high‐magnification views of the boxed regions. Scale bar, 50 µm. G, Quantification of the ratio of MAP2‐positive area to DAPI‐positive area. n = 6 independent experiments. H, Quantification of MAP2 + fragmented branch density, calculated as the number of MAP2 + fragmented branches normalized to MAP2 + area. n = 6 independent experiments. I–M, Calcium imaging analysis of neuronal network activity in Day 80 organoids. I, Schematic of calcium imaging workflow and representative Fluo‐4 AM raw data. Scale bar, 50 µm. J, Representative heatmaps showing calcium transients (ΔF/F 0 ) in individual ROIs ( n = 40 cells per organoid) over a 5‐minute recording period. K–M, Quantitative analysis of (K) spontaneous calcium firing frequency (events/cell), (L) synchronization <t>index</t> quantified by the mean Pearson correlation coefficient of Δ F / F 0 traces across all cell pairs within each organoid, and (M) percentage of active versus inactive cells. n = 120 ROIs from n = 3 organoids across three independent differentiations. Statistical comparisons were performed based on the biological replicates ( n = 3) rather than technical ROIs. All data are presented as mean ± standard error of the mean. Statistical significance was determined using one‐way analysis of variance. ns, not significant. * P < 0.05, ** P < 0.01, *** P < 0.001, **** P < 0.0001. AD, Alzheimer's disease; APP, amyloid precursor protein; CHOL, cholesterol treatment; CHOL+SEMA, cholesterol + semaglutide treatment; CTR, control group; DAPI, 4′,6‐diamidino‐2‐phenylindole; MAP2, microtubule associated protein 2; p‐tau, phosphorylated tau; ROI, region of interest.
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    Semaglutide exerts limited neuroprotective effects in Day 80 forebrain organoids. A–B, Morphological evaluation of late‐stage forebrain organoids. Organoids were treated for 15 days (from Day 65 to Day 80) and analyzed on Day 80. A, Representative bright‐field images. Scale bar, 1 mm. B, Quantification of organoid area on Day 80. n = 11 organoids per group. C–E, Western blot analysis of AD‐associated pathological proteins. Representative bands show the expression of APP (≈ 110 kDa), p‐tau217 (≈ 55 kDa), and total tau (≈ 55 kDa), with β‐actin (42 kDa) as a loading control. D–E, Quantitative analysis of (D) relative APP levels and (E) p‐tau217/tau ratio. n = 4 independent experiments. F–H, Representative immunofluorescence images of MAP2 (green) and DAPI (blue) in Day 80 organoids. Middle panels show the MAP2 channel only, and lower panels show high‐magnification views of the boxed regions. Scale bar, 50 µm. G, Quantification of the ratio of MAP2‐positive area to DAPI‐positive area. n = 6 independent experiments. H, Quantification of MAP2 + fragmented branch density, calculated as the number of MAP2 + fragmented branches normalized to MAP2 + area. n = 6 independent experiments. I–M, Calcium imaging analysis of neuronal network activity in Day 80 organoids. I, Schematic of calcium imaging workflow and representative Fluo‐4 AM raw data. Scale bar, 50 µm. J, Representative heatmaps showing calcium transients (ΔF/F 0 ) in individual ROIs ( n = 40 cells per organoid) over a 5‐minute recording period. K–M, Quantitative analysis of (K) spontaneous calcium firing frequency (events/cell), (L) synchronization <t>index</t> quantified by the mean Pearson correlation coefficient of Δ F / F 0 traces across all cell pairs within each organoid, and (M) percentage of active versus inactive cells. n = 120 ROIs from n = 3 organoids across three independent differentiations. Statistical comparisons were performed based on the biological replicates ( n = 3) rather than technical ROIs. All data are presented as mean ± standard error of the mean. Statistical significance was determined using one‐way analysis of variance. ns, not significant. * P < 0.05, ** P < 0.01, *** P < 0.001, **** P < 0.0001. AD, Alzheimer's disease; APP, amyloid precursor protein; CHOL, cholesterol treatment; CHOL+SEMA, cholesterol + semaglutide treatment; CTR, control group; DAPI, 4′,6‐diamidino‐2‐phenylindole; MAP2, microtubule associated protein 2; p‐tau, phosphorylated tau; ROI, region of interest.
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    Semaglutide exerts limited neuroprotective effects in Day 80 forebrain organoids. A–B, Morphological evaluation of late‐stage forebrain organoids. Organoids were treated for 15 days (from Day 65 to Day 80) and analyzed on Day 80. A, Representative bright‐field images. Scale bar, 1 mm. B, Quantification of organoid area on Day 80. n = 11 organoids per group. C–E, Western blot analysis of AD‐associated pathological proteins. Representative bands show the expression of APP (≈ 110 kDa), p‐tau217 (≈ 55 kDa), and total tau (≈ 55 kDa), with β‐actin (42 kDa) as a loading control. D–E, Quantitative analysis of (D) relative APP levels and (E) p‐tau217/tau ratio. n = 4 independent experiments. F–H, Representative immunofluorescence images of MAP2 (green) and DAPI (blue) in Day 80 organoids. Middle panels show the MAP2 channel only, and lower panels show high‐magnification views of the boxed regions. Scale bar, 50 µm. G, Quantification of the ratio of MAP2‐positive area to DAPI‐positive area. n = 6 independent experiments. H, Quantification of MAP2 + fragmented branch density, calculated as the number of MAP2 + fragmented branches normalized to MAP2 + area. n = 6 independent experiments. I–M, Calcium imaging analysis of neuronal network activity in Day 80 organoids. I, Schematic of calcium imaging workflow and representative Fluo‐4 AM raw data. Scale bar, 50 µm. J, Representative heatmaps showing calcium transients (ΔF/F 0 ) in individual ROIs ( n = 40 cells per organoid) over a 5‐minute recording period. K–M, Quantitative analysis of (K) spontaneous calcium firing frequency (events/cell), (L) synchronization <t>index</t> quantified by the mean Pearson correlation coefficient of Δ F / F 0 traces across all cell pairs within each organoid, and (M) percentage of active versus inactive cells. n = 120 ROIs from n = 3 organoids across three independent differentiations. Statistical comparisons were performed based on the biological replicates ( n = 3) rather than technical ROIs. All data are presented as mean ± standard error of the mean. Statistical significance was determined using one‐way analysis of variance. ns, not significant. * P < 0.05, ** P < 0.01, *** P < 0.001, **** P < 0.0001. AD, Alzheimer's disease; APP, amyloid precursor protein; CHOL, cholesterol treatment; CHOL+SEMA, cholesterol + semaglutide treatment; CTR, control group; DAPI, 4′,6‐diamidino‐2‐phenylindole; MAP2, microtubule associated protein 2; p‐tau, phosphorylated tau; ROI, region of interest.
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    Semaglutide exerts limited neuroprotective effects in Day 80 forebrain organoids. A–B, Morphological evaluation of late‐stage forebrain organoids. Organoids were treated for 15 days (from Day 65 to Day 80) and analyzed on Day 80. A, Representative bright‐field images. Scale bar, 1 mm. B, Quantification of organoid area on Day 80. n = 11 organoids per group. C–E, Western blot analysis of AD‐associated pathological proteins. Representative bands show the expression of APP (≈ 110 kDa), p‐tau217 (≈ 55 kDa), and total tau (≈ 55 kDa), with β‐actin (42 kDa) as a loading control. D–E, Quantitative analysis of (D) relative APP levels and (E) p‐tau217/tau ratio. n = 4 independent experiments. F–H, Representative immunofluorescence images of MAP2 (green) and DAPI (blue) in Day 80 organoids. Middle panels show the MAP2 channel only, and lower panels show high‐magnification views of the boxed regions. Scale bar, 50 µm. G, Quantification of the ratio of MAP2‐positive area to DAPI‐positive area. n = 6 independent experiments. H, Quantification of MAP2 + fragmented branch density, calculated as the number of MAP2 + fragmented branches normalized to MAP2 + area. n = 6 independent experiments. I–M, Calcium imaging analysis of neuronal network activity in Day 80 organoids. I, Schematic of calcium imaging workflow and representative Fluo‐4 AM raw data. Scale bar, 50 µm. J, Representative heatmaps showing calcium transients (ΔF/F 0 ) in individual ROIs ( n = 40 cells per organoid) over a 5‐minute recording period. K–M, Quantitative analysis of (K) spontaneous calcium firing frequency (events/cell), (L) synchronization <t>index</t> quantified by the mean Pearson correlation coefficient of Δ F / F 0 traces across all cell pairs within each organoid, and (M) percentage of active versus inactive cells. n = 120 ROIs from n = 3 organoids across three independent differentiations. Statistical comparisons were performed based on the biological replicates ( n = 3) rather than technical ROIs. All data are presented as mean ± standard error of the mean. Statistical significance was determined using one‐way analysis of variance. ns, not significant. * P < 0.05, ** P < 0.01, *** P < 0.001, **** P < 0.0001. AD, Alzheimer's disease; APP, amyloid precursor protein; CHOL, cholesterol treatment; CHOL+SEMA, cholesterol + semaglutide treatment; CTR, control group; DAPI, 4′,6‐diamidino‐2‐phenylindole; MAP2, microtubule associated protein 2; p‐tau, phosphorylated tau; ROI, region of interest.
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    Semaglutide exerts limited neuroprotective effects in Day 80 forebrain organoids. A–B, Morphological evaluation of late‐stage forebrain organoids. Organoids were treated for 15 days (from Day 65 to Day 80) and analyzed on Day 80. A, Representative bright‐field images. Scale bar, 1 mm. B, Quantification of organoid area on Day 80. n = 11 organoids per group. C–E, Western blot analysis of AD‐associated pathological proteins. Representative bands show the expression of APP (≈ 110 kDa), p‐tau217 (≈ 55 kDa), and total tau (≈ 55 kDa), with β‐actin (42 kDa) as a loading control. D–E, Quantitative analysis of (D) relative APP levels and (E) p‐tau217/tau ratio. n = 4 independent experiments. F–H, Representative immunofluorescence images of MAP2 (green) and DAPI (blue) in Day 80 organoids. Middle panels show the MAP2 channel only, and lower panels show high‐magnification views of the boxed regions. Scale bar, 50 µm. G, Quantification of the ratio of MAP2‐positive area to DAPI‐positive area. n = 6 independent experiments. H, Quantification of MAP2 + fragmented branch density, calculated as the number of MAP2 + fragmented branches normalized to MAP2 + area. n = 6 independent experiments. I–M, Calcium imaging analysis of neuronal network activity in Day 80 organoids. I, Schematic of calcium imaging workflow and representative Fluo‐4 AM raw data. Scale bar, 50 µm. J, Representative heatmaps showing calcium transients (ΔF/F 0 ) in individual ROIs ( n = 40 cells per organoid) over a 5‐minute recording period. K–M, Quantitative analysis of (K) spontaneous calcium firing frequency (events/cell), (L) synchronization <t>index</t> quantified by the mean Pearson correlation coefficient of Δ F / F 0 traces across all cell pairs within each organoid, and (M) percentage of active versus inactive cells. n = 120 ROIs from n = 3 organoids across three independent differentiations. Statistical comparisons were performed based on the biological replicates ( n = 3) rather than technical ROIs. All data are presented as mean ± standard error of the mean. Statistical significance was determined using one‐way analysis of variance. ns, not significant. * P < 0.05, ** P < 0.01, *** P < 0.001, **** P < 0.0001. AD, Alzheimer's disease; APP, amyloid precursor protein; CHOL, cholesterol treatment; CHOL+SEMA, cholesterol + semaglutide treatment; CTR, control group; DAPI, 4′,6‐diamidino‐2‐phenylindole; MAP2, microtubule associated protein 2; p‐tau, phosphorylated tau; ROI, region of interest.
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    Semaglutide exerts limited neuroprotective effects in Day 80 forebrain organoids. A–B, Morphological evaluation of late‐stage forebrain organoids. Organoids were treated for 15 days (from Day 65 to Day 80) and analyzed on Day 80. A, Representative bright‐field images. Scale bar, 1 mm. B, Quantification of organoid area on Day 80. n = 11 organoids per group. C–E, Western blot analysis of AD‐associated pathological proteins. Representative bands show the expression of APP (≈ 110 kDa), p‐tau217 (≈ 55 kDa), and total tau (≈ 55 kDa), with β‐actin (42 kDa) as a loading control. D–E, Quantitative analysis of (D) relative APP levels and (E) p‐tau217/tau ratio. n = 4 independent experiments. F–H, Representative immunofluorescence images of MAP2 (green) and DAPI (blue) in Day 80 organoids. Middle panels show the MAP2 channel only, and lower panels show high‐magnification views of the boxed regions. Scale bar, 50 µm. G, Quantification of the ratio of MAP2‐positive area to DAPI‐positive area. n = 6 independent experiments. H, Quantification of MAP2 + fragmented branch density, calculated as the number of MAP2 + fragmented branches normalized to MAP2 + area. n = 6 independent experiments. I–M, Calcium imaging analysis of neuronal network activity in Day 80 organoids. I, Schematic of calcium imaging workflow and representative Fluo‐4 AM raw data. Scale bar, 50 µm. J, Representative heatmaps showing calcium transients (ΔF/F 0 ) in individual ROIs ( n = 40 cells per organoid) over a 5‐minute recording period. K–M, Quantitative analysis of (K) spontaneous calcium firing frequency (events/cell), (L) synchronization <t>index</t> quantified by the mean Pearson correlation coefficient of Δ F / F 0 traces across all cell pairs within each organoid, and (M) percentage of active versus inactive cells. n = 120 ROIs from n = 3 organoids across three independent differentiations. Statistical comparisons were performed based on the biological replicates ( n = 3) rather than technical ROIs. All data are presented as mean ± standard error of the mean. Statistical significance was determined using one‐way analysis of variance. ns, not significant. * P < 0.05, ** P < 0.01, *** P < 0.001, **** P < 0.0001. AD, Alzheimer's disease; APP, amyloid precursor protein; CHOL, cholesterol treatment; CHOL+SEMA, cholesterol + semaglutide treatment; CTR, control group; DAPI, 4′,6‐diamidino‐2‐phenylindole; MAP2, microtubule associated protein 2; p‐tau, phosphorylated tau; ROI, region of interest.
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    Semaglutide exerts limited neuroprotective effects in Day 80 forebrain organoids. A–B, Morphological evaluation of late‐stage forebrain organoids. Organoids were treated for 15 days (from Day 65 to Day 80) and analyzed on Day 80. A, Representative bright‐field images. Scale bar, 1 mm. B, Quantification of organoid area on Day 80. n = 11 organoids per group. C–E, Western blot analysis of AD‐associated pathological proteins. Representative bands show the expression of APP (≈ 110 kDa), p‐tau217 (≈ 55 kDa), and total tau (≈ 55 kDa), with β‐actin (42 kDa) as a loading control. D–E, Quantitative analysis of (D) relative APP levels and (E) p‐tau217/tau ratio. n = 4 independent experiments. F–H, Representative immunofluorescence images of MAP2 (green) and DAPI (blue) in Day 80 organoids. Middle panels show the MAP2 channel only, and lower panels show high‐magnification views of the boxed regions. Scale bar, 50 µm. G, Quantification of the ratio of MAP2‐positive area to DAPI‐positive area. n = 6 independent experiments. H, Quantification of MAP2 + fragmented branch density, calculated as the number of MAP2 + fragmented branches normalized to MAP2 + area. n = 6 independent experiments. I–M, Calcium imaging analysis of neuronal network activity in Day 80 organoids. I, Schematic of calcium imaging workflow and representative Fluo‐4 AM raw data. Scale bar, 50 µm. J, Representative heatmaps showing calcium transients (ΔF/F 0 ) in individual ROIs ( n = 40 cells per organoid) over a 5‐minute recording period. K–M, Quantitative analysis of (K) spontaneous calcium firing frequency (events/cell), (L) synchronization <t>index</t> quantified by the mean Pearson correlation coefficient of Δ F / F 0 traces across all cell pairs within each organoid, and (M) percentage of active versus inactive cells. n = 120 ROIs from n = 3 organoids across three independent differentiations. Statistical comparisons were performed based on the biological replicates ( n = 3) rather than technical ROIs. All data are presented as mean ± standard error of the mean. Statistical significance was determined using one‐way analysis of variance. ns, not significant. * P < 0.05, ** P < 0.01, *** P < 0.001, **** P < 0.0001. AD, Alzheimer's disease; APP, amyloid precursor protein; CHOL, cholesterol treatment; CHOL+SEMA, cholesterol + semaglutide treatment; CTR, control group; DAPI, 4′,6‐diamidino‐2‐phenylindole; MAP2, microtubule associated protein 2; p‐tau, phosphorylated tau; ROI, region of interest.
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    Semaglutide exerts limited neuroprotective effects in Day 80 forebrain organoids. A–B, Morphological evaluation of late‐stage forebrain organoids. Organoids were treated for 15 days (from Day 65 to Day 80) and analyzed on Day 80. A, Representative bright‐field images. Scale bar, 1 mm. B, Quantification of organoid area on Day 80. n = 11 organoids per group. C–E, Western blot analysis of AD‐associated pathological proteins. Representative bands show the expression of APP (≈ 110 kDa), p‐tau217 (≈ 55 kDa), and total tau (≈ 55 kDa), with β‐actin (42 kDa) as a loading control. D–E, Quantitative analysis of (D) relative APP levels and (E) p‐tau217/tau ratio. n = 4 independent experiments. F–H, Representative immunofluorescence images of MAP2 (green) and DAPI (blue) in Day 80 organoids. Middle panels show the MAP2 channel only, and lower panels show high‐magnification views of the boxed regions. Scale bar, 50 µm. G, Quantification of the ratio of MAP2‐positive area to DAPI‐positive area. n = 6 independent experiments. H, Quantification of MAP2 + fragmented branch density, calculated as the number of MAP2 + fragmented branches normalized to MAP2 + area. n = 6 independent experiments. I–M, Calcium imaging analysis of neuronal network activity in Day 80 organoids. I, Schematic of calcium imaging workflow and representative Fluo‐4 AM raw data. Scale bar, 50 µm. J, Representative heatmaps showing calcium transients (ΔF/F 0 ) in individual ROIs ( n = 40 cells per organoid) over a 5‐minute recording period. K–M, Quantitative analysis of (K) spontaneous calcium firing frequency (events/cell), (L) synchronization <t>index</t> quantified by the mean Pearson correlation coefficient of Δ F / F 0 traces across all cell pairs within each organoid, and (M) percentage of active versus inactive cells. n = 120 ROIs from n = 3 organoids across three independent differentiations. Statistical comparisons were performed based on the biological replicates ( n = 3) rather than technical ROIs. All data are presented as mean ± standard error of the mean. Statistical significance was determined using one‐way analysis of variance. ns, not significant. * P < 0.05, ** P < 0.01, *** P < 0.001, **** P < 0.0001. AD, Alzheimer's disease; APP, amyloid precursor protein; CHOL, cholesterol treatment; CHOL+SEMA, cholesterol + semaglutide treatment; CTR, control group; DAPI, 4′,6‐diamidino‐2‐phenylindole; MAP2, microtubule associated protein 2; p‐tau, phosphorylated tau; ROI, region of interest.
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    Complete Genomics Inc hi c
    Semaglutide exerts limited neuroprotective effects in Day 80 forebrain organoids. A–B, Morphological evaluation of late‐stage forebrain organoids. Organoids were treated for 15 days (from Day 65 to Day 80) and analyzed on Day 80. A, Representative bright‐field images. Scale bar, 1 mm. B, Quantification of organoid area on Day 80. n = 11 organoids per group. C–E, Western blot analysis of AD‐associated pathological proteins. Representative bands show the expression of APP (≈ 110 kDa), p‐tau217 (≈ 55 kDa), and total tau (≈ 55 kDa), with β‐actin (42 kDa) as a loading control. D–E, Quantitative analysis of (D) relative APP levels and (E) p‐tau217/tau ratio. n = 4 independent experiments. F–H, Representative immunofluorescence images of MAP2 (green) and DAPI (blue) in Day 80 organoids. Middle panels show the MAP2 channel only, and lower panels show high‐magnification views of the boxed regions. Scale bar, 50 µm. G, Quantification of the ratio of MAP2‐positive area to DAPI‐positive area. n = 6 independent experiments. H, Quantification of MAP2 + fragmented branch density, calculated as the number of MAP2 + fragmented branches normalized to MAP2 + area. n = 6 independent experiments. I–M, Calcium imaging analysis of neuronal network activity in Day 80 organoids. I, Schematic of calcium imaging workflow and representative Fluo‐4 AM raw data. Scale bar, 50 µm. J, Representative heatmaps showing calcium transients (ΔF/F 0 ) in individual ROIs ( n = 40 cells per organoid) over a 5‐minute recording period. K–M, Quantitative analysis of (K) spontaneous calcium firing frequency (events/cell), (L) synchronization <t>index</t> quantified by the mean Pearson correlation coefficient of Δ F / F 0 traces across all cell pairs within each organoid, and (M) percentage of active versus inactive cells. n = 120 ROIs from n = 3 organoids across three independent differentiations. Statistical comparisons were performed based on the biological replicates ( n = 3) rather than technical ROIs. All data are presented as mean ± standard error of the mean. Statistical significance was determined using one‐way analysis of variance. ns, not significant. * P < 0.05, ** P < 0.01, *** P < 0.001, **** P < 0.0001. AD, Alzheimer's disease; APP, amyloid precursor protein; CHOL, cholesterol treatment; CHOL+SEMA, cholesterol + semaglutide treatment; CTR, control group; DAPI, 4′,6‐diamidino‐2‐phenylindole; MAP2, microtubule associated protein 2; p‐tau, phosphorylated tau; ROI, region of interest.
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    Semaglutide exerts limited neuroprotective effects in Day 80 forebrain organoids. A–B, Morphological evaluation of late‐stage forebrain organoids. Organoids were treated for 15 days (from Day 65 to Day 80) and analyzed on Day 80. A, Representative bright‐field images. Scale bar, 1 mm. B, Quantification of organoid area on Day 80. n = 11 organoids per group. C–E, Western blot analysis of AD‐associated pathological proteins. Representative bands show the expression of APP (≈ 110 kDa), p‐tau217 (≈ 55 kDa), and total tau (≈ 55 kDa), with β‐actin (42 kDa) as a loading control. D–E, Quantitative analysis of (D) relative APP levels and (E) p‐tau217/tau ratio. n = 4 independent experiments. F–H, Representative immunofluorescence images of MAP2 (green) and DAPI (blue) in Day 80 organoids. Middle panels show the MAP2 channel only, and lower panels show high‐magnification views of the boxed regions. Scale bar, 50 µm. G, Quantification of the ratio of MAP2‐positive area to DAPI‐positive area. n = 6 independent experiments. H, Quantification of MAP2 + fragmented branch density, calculated as the number of MAP2 + fragmented branches normalized to MAP2 + area. n = 6 independent experiments. I–M, Calcium imaging analysis of neuronal network activity in Day 80 organoids. I, Schematic of calcium imaging workflow and representative Fluo‐4 AM raw data. Scale bar, 50 µm. J, Representative heatmaps showing calcium transients (ΔF/F 0 ) in individual ROIs ( n = 40 cells per organoid) over a 5‐minute recording period. K–M, Quantitative analysis of (K) spontaneous calcium firing frequency (events/cell), (L) synchronization index quantified by the mean Pearson correlation coefficient of Δ F / F 0 traces across all cell pairs within each organoid, and (M) percentage of active versus inactive cells. n = 120 ROIs from n = 3 organoids across three independent differentiations. Statistical comparisons were performed based on the biological replicates ( n = 3) rather than technical ROIs. All data are presented as mean ± standard error of the mean. Statistical significance was determined using one‐way analysis of variance. ns, not significant. * P < 0.05, ** P < 0.01, *** P < 0.001, **** P < 0.0001. AD, Alzheimer's disease; APP, amyloid precursor protein; CHOL, cholesterol treatment; CHOL+SEMA, cholesterol + semaglutide treatment; CTR, control group; DAPI, 4′,6‐diamidino‐2‐phenylindole; MAP2, microtubule associated protein 2; p‐tau, phosphorylated tau; ROI, region of interest.

    Journal: Alzheimer's & Dementia

    Article Title: GLP‐1R agonist semaglutide protects human forebrain organoids from cholesterol‐induced neurotoxicity

    doi: 10.1002/alz.71888

    Figure Lengend Snippet: Semaglutide exerts limited neuroprotective effects in Day 80 forebrain organoids. A–B, Morphological evaluation of late‐stage forebrain organoids. Organoids were treated for 15 days (from Day 65 to Day 80) and analyzed on Day 80. A, Representative bright‐field images. Scale bar, 1 mm. B, Quantification of organoid area on Day 80. n = 11 organoids per group. C–E, Western blot analysis of AD‐associated pathological proteins. Representative bands show the expression of APP (≈ 110 kDa), p‐tau217 (≈ 55 kDa), and total tau (≈ 55 kDa), with β‐actin (42 kDa) as a loading control. D–E, Quantitative analysis of (D) relative APP levels and (E) p‐tau217/tau ratio. n = 4 independent experiments. F–H, Representative immunofluorescence images of MAP2 (green) and DAPI (blue) in Day 80 organoids. Middle panels show the MAP2 channel only, and lower panels show high‐magnification views of the boxed regions. Scale bar, 50 µm. G, Quantification of the ratio of MAP2‐positive area to DAPI‐positive area. n = 6 independent experiments. H, Quantification of MAP2 + fragmented branch density, calculated as the number of MAP2 + fragmented branches normalized to MAP2 + area. n = 6 independent experiments. I–M, Calcium imaging analysis of neuronal network activity in Day 80 organoids. I, Schematic of calcium imaging workflow and representative Fluo‐4 AM raw data. Scale bar, 50 µm. J, Representative heatmaps showing calcium transients (ΔF/F 0 ) in individual ROIs ( n = 40 cells per organoid) over a 5‐minute recording period. K–M, Quantitative analysis of (K) spontaneous calcium firing frequency (events/cell), (L) synchronization index quantified by the mean Pearson correlation coefficient of Δ F / F 0 traces across all cell pairs within each organoid, and (M) percentage of active versus inactive cells. n = 120 ROIs from n = 3 organoids across three independent differentiations. Statistical comparisons were performed based on the biological replicates ( n = 3) rather than technical ROIs. All data are presented as mean ± standard error of the mean. Statistical significance was determined using one‐way analysis of variance. ns, not significant. * P < 0.05, ** P < 0.01, *** P < 0.001, **** P < 0.0001. AD, Alzheimer's disease; APP, amyloid precursor protein; CHOL, cholesterol treatment; CHOL+SEMA, cholesterol + semaglutide treatment; CTR, control group; DAPI, 4′,6‐diamidino‐2‐phenylindole; MAP2, microtubule associated protein 2; p‐tau, phosphorylated tau; ROI, region of interest.

    Article Snippet: High‐throughput single‐cell encapsulation, library preparation, and paired‐end sequencing were performed on the MGI DNBelab C‐TaiM4 and DNBSEQ‐T7 platforms (BGI/Innomics).

    Techniques: Organoids, Western Blot, Analysis, Expressing, Control, Immunofluorescence, Imaging, Activity Assay