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pass filter  (Mini-Circuits)


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    Mini-Circuits pass filter
    Pass Filter, supplied by Mini-Circuits, used in various techniques. Bioz Stars score: 94/100, based on 8 PubMed citations. ZERO BIAS - scores, article reviews, protocol conditions and more
    https://www.bioz.com/product/c-900/RLP-Series+SMT+Lumped+L-C+Low+Pass+Filters/10__3390_slash_sym18010179-53-39-43
    Average 94 stars, based on 8 article reviews
    pass filter - by Bioz Stars, 2026-10
    94/100 stars

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    Article Title: Development of a Micro-Radian Phasemeter and Verification Based on Single Pilot Tone for Space Gravitational Wave Detection
    Article Snippet: For this purpose, the Mini-Circuits RLP-30+ low-pass filter chip is selected, offering a cutoff frequency of −3 dB of 37 MHz, which fully encompasses the phasemeter measurement band while maintaining low insertion loss characteristics.

    Article Title: Simulation of Heterodyne Signal for Science Interferometers of Space-Borne Gravitational Wave Detector and Evaluation of Phase Measurement Noise
    Article Snippet: This design uses the RLP-83+ low-pass filter from Mini-Circuits, featuring a −3 dB cutoff frequency of 93 MHz.

    Article Title: Single electrons on solid neon as a solid-state qubit platform.
    Article Snippet: At the MXC plate, behind each thermocoax there is a two-stage RC low-pass filter with a cutoff frequency of around 400 Hz cascaded with a LC low-pass filter (Mini-Circuits RLP-30+) with a cutoff frequency of around 30 MHz.

    Article Title: A Noise Signal Simulator for Testing Broadband Systems
    Article Snippet: A two-channel broadband noise signal simulator of a radioastronomic receiving device designed to test signal conversion systems is described.. Both channels of the broadband signal simulator contain five switchable filters with 512and 1024-MHz bandwidths and a special unfiltered channel, which allows testing devices that have different input intermediate-frequency bands.. The simulator allows determination of parameters and tuning broadband systems of radio telescopes.

    Article Title: Sine wave gating silicon single-photon detectors for multiphoton entanglement experiments.
    Article Snippet: Further, this mixed signal passes through two band-stop filters (BSFs, BSF-C160+, Mini-Circuits) with a stop band frequency from 150 MHz to 170 MHz and a rejection of 48 dB and one low-pass filter (LPF, RLP-105+, Mini-Circuits) with a cutoff frequency of 116 MHz to eliminate the capacitive response signal and to extract the avalanche signal.

    Extraction:

    Article Title: Validation of Phase Extraction Precision Based on Ultra-Stable Hexagonal Optical Bench for Space-Borne Gravitational Wave Detection
    Article Snippet: .. The overall workflow of phase extraction [17] is as follows: the beat-note and the pilot tone are combined by a coupler (ZFSC-2-6+ from Mini-Circuits) and then fed into the analog board, where the signal sequentially passes through a low pass filter (RLP-83+ from Mini-Circuits), a differential operational amplifier (AD8138), and an Analog to Digital Converter (AD9253). ..



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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.
    Genome Survey Genome Assembly Hi C 1d Library Bgi Dnbseq T7 Clean, supplied by Complete Genomics Inc, used in various techniques. Bioz Stars score: 99/100, based on 1 PubMed citations. ZERO BIAS - scores, article reviews, protocol conditions and more
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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