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yeast c utilis atcc 9950  (ATCC)


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    ATCC yeast c utilis atcc 9950
    Yeast C Utilis Atcc 9950, supplied by ATCC, used in various techniques. Bioz Stars score: 95/100, based on 53 PubMed citations. ZERO BIAS - scores, article reviews, protocol conditions and more
    https://www.bioz.com/product/c-900/Candida+utilis%3B+NRRL+Y-900/pm41666662-350-25-28
    Average 95 stars, based on 53 article reviews
    yeast c utilis atcc 9950 - by Bioz Stars, 2026-10
    95/100 stars

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    Activity Assay:

    Article Title: Essential oil profile and biological activity of the paleoendemic species Salvia dorystaechas B.T. Drew
    Article Snippet: S. dorystaechas extracts were evaluated for their antibacterial activity against Escherichia coli NRRL B-3008, Staphylococcus aureus ATCC 6538, Pseudomonas aeruginosa ATCC 27853, Salmonella typhimurium ATCC 13311, Serratia marcescens NRRL B-2544, Klebsiella pneumoniae NCTC 9633. .. Anticandidal activity was also screened by using Candida albicans ATCC 10231 and ATCC 90028, C. utilis NRRL Y- 900, C. tropicalis ATCC 750, and C. parapsilosis ATCC 22019. ..

    Article Title: Effect of selenium on the cellular structure and oxidative response of the yeasts Saccharomyces cerevisiae and Rhodotorula glutinis.
    Article Snippet: Background: Selenium is an element with diverse biological effects that, at higher concentrations, can cause oxidative stress and cell damage.. Therefore, it is essential to understand its impact on yeast cells, which can serve as a model for studying selenium toxicity.. Objective: This study aimed to evaluate the effect of selenium on the physiology, cellular structure, and oxidative response of the yeasts Saccharomyces cerevisiae ATCC 7090 and Rhodotorula glutinis CCY 20–2–26.

    Article Title: Probiotics and Postbiotics Derived from Saline/Marine Plant-Based Feedstocks.
    Article Snippet: .. E. cava C. utilis ATCC 9950 Phlorotannin (anti-inflamma- tory) Fermentation in liquid phase at 30 °C, 120 RPM for 24 h [128] E. cava C. utilis Phenolics/antioxidants (postbiotics) Fermentation in liquid phase at 30 °C, 120 RPM for 24 h [129] E. cava S. cerevisiae Bioactive polysaccharides Fermentation in liquid phase at 30 °C, 1200 RPM for 24 h [114] C. utilis Eisenia bicyclis C. utilis YM-1 Antimicrobial activity (postbiotics) Fermentation in liquid phase at 30 °C, 120 RPM for 24 h [130] S. japonica Red yeast rice (Monascus purpureus) Phenolics, flavonoids, and antioxidants (postbiotic) Solid stare fermentation [131] S. japonica Monascus purpureus KCCM 60168 Phenolics, flavonoids, and antioxidants (postbiotic) Wet fermentation with 50% moisture content at 30 °C, 20 days [132] Monascus kaoliang KCCM 60154 Undaria pinnatifida Monascus purpureus KCCM 60168 Phenolics, flavonoids, and antioxidants (postbiotic) Wet fermentation with 50% moisture content at 30 °C, 20 days [132] Monascus kaoliang KCCM 60154 Durvillaea spp. .. Co-culture of Pleurotus, Lentinula, Hericium, and Ganoderma Mycoprotein, amino acids, antioxidants (postbiotics) Fermentation in liquid phase [133] K. alvarezii A. oryzae Phenolics, flavonoids, and antioxidants (postbiotic) Solid-state fermentation with 70% moisture content at 30 °C for 2 to 6 days [134] K. alvarezii S. cerevisiae Probiotic feed additive Fermentation in liquid phase at 28 °C, 125 RPM for 48 h [135] Macrocystis pyrifera Paradendryphiella salina 100654 Mycoprotein, phenolics, antioxidants (postbiotics) Fermentation in liquid phase at 25 °C, 200 RPM for 8 days [85] Ulva spp.

    Purification:

    Article Title: Production of yeast cell wall polysaccharides‐β‐glucan and chitin by using food waste substrates: Biosynthesis, production, extraction, and purification methods
    Article Snippet: .. Bzducha‐Wróbel et al. ( ) extracted water‐insoluble yeast cell wall and purified yeast β‐glucan from C. utilis ATCC 9950 following biomass cultivation using waste potato juice water and glycerol. ..



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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.
    Dnbelab C Series Highthroughput Single Cell Rna Library Preparation Set, 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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    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.
    Rlp, supplied by Mini-Circuits, used in various techniques. Bioz Stars score: 94/100, based on 1 PubMed citations. ZERO BIAS - scores, article reviews, protocol conditions and more
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    genome survey genome assembly hi c 1d library bgi dnbseq t7 clean  (Complete Genomics Inc)
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    Complete Genomics Inc genome survey genome assembly hi c 1d library bgi dnbseq t7 clean
    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.
    Hi C, 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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    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