phenylethyl alcohol pea  (Millipore)


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    Name:
    Phenylethyl Alcohol
    Description:
    Pharmaceutical secondary standards for application in quality control provide pharma laboratories and manufacturers with a convenient and cost effective alternative to the preparation of in house working standards
    Catalog Number:
    phr1122
    Price:
    None
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    Structured Review

    Millipore phenylethyl alcohol pea
    Phenylethyl Alcohol
    Pharmaceutical secondary standards for application in quality control provide pharma laboratories and manufacturers with a convenient and cost effective alternative to the preparation of in house working standards
    https://www.bioz.com/result/phenylethyl alcohol pea/product/Millipore
    Average 98 stars, based on 1 article reviews
    Price from $9.99 to $1999.99
    phenylethyl alcohol pea - by Bioz Stars, 2020-11
    98/100 stars

    Related Products / Commonly Used Together

    olfactory sensitivity
    odor detection thresholds

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    Related Articles

    Concentration Assay:

    Article Title: Chemosensory Loss: Functional Consequences of the World Trade Center Disaster
    Article Snippet: .. Odor detection thresholds To measure olfactory sensitivity, phenylethyl alcohol (PEA) (Sigma-Aldrich, St. Louis, MO) was diluted into an odorless diluent [polyethylene glycol 200 (PEG 200); Sigma-Aldrich] and placed into glass bottles in a 20-step semi-log dilution series, starting with a concentration of 100% vol/vol liquid. ..

    other:

    Article Title: Suppressive Interaction Approach for Masking Stale Note of Instant Ripened Pu-Erh Tea Products
    Article Snippet: Chemical Standards and Reagents The standards 2-hexanone, benzeneacetaldehyde, linalool, linalool oxides, phenylethyl alcohol, 4-oxoisophorone, menthol, α -terpineol, safranal, geraniol, indole, and 2-ethyl-3-methylpyrazine were purchased from Sigma-Aldrich Co., Ltd. (St. Louis, MO, USA).

    Article Title: Chemosensory communication of aggression: women's fine-tuned neural processing of male aggression signals
    Article Snippet: The test required the participants to detect phenylethyl alcohol (99%, 1 : 100 (v/v) diluted in 1,2-propanediol, 99%; both substances: Sigma-Aldrich, St Louis, Missouri, USA), being present in one of three bottles in two consecutive trials, with the remaining two bottles containing the same volume of solvent (phenylethyl alcohol smells rose-like, and is regularly used as a standard in olfactory sensitivity testing, [ ]).

    Article Title: Inhibitory effects of acetophenone or phenylethyl alcohol as fumigant to protect soybean seeds against two aflatoxin-producing fungi
    Article Snippet: Pure commercial compounds (technical grade) of acetophenone (Fluka, for GC, ≥ 99.5%) and phenylethyl alcohol (Sigma–Aldrich ≥ 99%, FCC, Kosher, FG) were used in this study.

    Article Title: Chemosensory and Behavioural Responses of Ixodes scapularis to Natural Products: Role of Chemosensory Organs in Volatile Detection
    Article Snippet: ChemicalsGeraniol ( > 98%), phenylethyl alcohol (≥99%, FCC, FG), citral ( > 95%), β-citronellol (≥95%), propionic acid (≥99.5%, FCC, FG), isovaleric acid (≥99%), hexanal (98%), octanal (≥99%), hexanoic acid (≥99%) were purchased from Sigma-Aldrich (Saint Louis, MO, USA).

    Plasmid Purification:

    Article Title: Structural basis for divergent and convergent evolution of catalytic machineries in plant aromatic amino acid decarboxylase proteins
    Article Snippet: .. Reagents L-tryptophan, tryptamine, L-tyrosine, tyramine, tyrosol, L-phenylalanine, phenylethylamine, phenylacetaldehyde, phenylethyl alcohol, tyrosol, L-3,4-dihydroxyphenylalanine, dopamine, (S)-norcoclaurine, PLP, and sodium borohydride were purchased from Sigma-Aldrich. .. 4-hydroxyphenylacetaldehyde was purchased from Santa Cruz Biotechnology.

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  • 94
    Millipore anti dcc
    Spine density and presynaptic release properties of axotomized neurons treated with exogenous netrin-1. a Representative dendrites before and 48 h post-axotomy treated with vehicle (HBS) or netrin-1 (Ntn1) beginning at 40 h post-axotomy (inverted fluorescence). Arrows : new spines; red asterisks : eliminated spines. Scale bars , 10 µm. b Quantification of spine density illustrated in a . Axotomy : n = 33 dendrites; 7 neurons; #spines/TDL: 392/3696 µm ( before ), 263/3447 µm ( after ). Axotomy + netrin-1 : n = 29 dendrites, 6 neurons; #spines/TDL: 293/3281 µm ( before ), 363/3417 µm ( after ). c Percent responsive FM puncta per neuron field at 48 h post-axotomy with HBS or netrin-1. n = 8–11 fields/chambers per condition over 5 experiments. d Number of responsive and unresponsive FM puncta from c . Significantly fewer unresponsive puncta followed axotomy compared to uninjured control (HBS). e , f Number of vGLUT1 and <t>vGAT</t> puncta per neuron area (uninjured control, axotomized + HBS, or axotomized + netrin-1) at 14 DIV. n = 8–9 neurons; 3 chambers per condition over 3 experiments. g Representative <t>DCC</t> immunostaining ( turquoise ) in uninjured control, post-axotomy, and post-axotomy + netrin-1 in cultures with similar spine densities. Neurons were retrogradely labeled with fluorescent protein (FP, magenta ) using an mCherry modified rabies virus. Scale bar , 10 µm. h Quantification of DCC immunofluorescence per spine region-of-interest (ROI). ROI: 2 µm diameter circular region surrounding each spine. Control, n = 295 ROIs; axotomy, n = 293 ROIs; axotomy + Ntn1, n = 210 ROIs. 8 neuron fields/3 chambers per condition; 3 experiments. i Quantification of spine density following 24 h of control antibody (IgG ab.) or DCC function blocking antibody (DCC ab.). IgG: n = 33 dendrites; 8 neurons; #spines/TDL: 464/4864 µm (before), 419/4712 µm (after). DCC ab: n = 34 dendrites; 7 neurons; #spines/TDL: 404/4433 µm (before), 222/3647 µm (after). j Representative FP-labeled dendritic segments immunostained for vGAT (inverted) and vGLUT1 (inverted) following 24 h application of IgG or DCC antibodies (outlined dendrites, solid magenta line ). Neurons were fixed at 15–16 DIV, older than the cultures in e , f . Scale bar , 10 µm. Quantification shown on the right. n = 23 neuron fields per condition; 3 chambers per condition over 3 experiments. b , i Repeated-measure two-way ANOVA, Bonferroni post hoc test; analyses included 1 chamber per condition for 3 experiments. c , j Unpaired two-tailed t -test. d – f , h One-way ANOVA, Bonferroni post hoc test. Error bars , s.e.m. * p
    Anti Dcc, supplied by Millipore, used in various techniques. Bioz Stars score: 94/100, based on 3 PubMed citations. ZERO BIAS - scores, article reviews, protocol conditions and more
    https://www.bioz.com/result/anti dcc/product/Millipore
    Average 94 stars, based on 3 article reviews
    Price from $9.99 to $1999.99
    anti dcc - by Bioz Stars, 2020-11
    94/100 stars
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    99
    Millipore calpeptin
    Maitotoxin treatment of SH-SY5Y cells leads to sequential cleavage of αII/βII spectrin and cell death (A) Cultured SH-SY5Y cell were treated with 0.04nM maitotoxin, and the time-course of spectrin breakdown monitored by Western blotting after SDS-PAGE analysis of cell lysates (20 μg/lane) with Pab-RAFA (anti-αII spectrin); α-bdp-1 antibody; and Pab-10D (anti-βII spectrin). Control cells were incubated for three hours without maitotoxin (ctrl). Duplicate experiments are shown for each time point. Note the rapid breakdown of αII spectrin vs. the delayed loss of βII spectrin. The positions of MW markers (÷1000) are depicted on the right; prominent bdp’s are marked on the left. ( B ) Densitometric evaluation of the extent of spectrin breakdown of the gels shown in (A). The extent of maitotoxin-induced cell death was also evaluated in parallel experiments of maitotoxin treated cells, as measured by flow cytometry after Ethidium-1 staining. Data points are the mean ±SD of three determinations. Background cell death (non-viable cells at t=0) was subtracted from all points. (Inset) Western blot with Pab RAFA of SH-SY5Y cells after 0.03 nM maitotoxin treatment, ± inhibition of calpain or caspase. The maitotoxin induced cleavage of spectrin was entirely inhibited by the calpain inhibitor <t>calpeptin,</t> but not by the caspase inhibitor Z-D-DCB. Lane 1, control SH-SY5Y cells; lane 2, cells after 3 hrs of maitotoxin treatment; lane 3, 3 hrs. maitotoxin + calpeptin; lane 4, 3hrs. maitotoxin + caspase inhibitor.
    Calpeptin, supplied by Millipore, used in various techniques. Bioz Stars score: 99/100, based on 23 PubMed citations. ZERO BIAS - scores, article reviews, protocol conditions and more
    https://www.bioz.com/result/calpeptin/product/Millipore
    Average 99 stars, based on 23 article reviews
    Price from $9.99 to $1999.99
    calpeptin - by Bioz Stars, 2020-11
    99/100 stars
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    Spine density and presynaptic release properties of axotomized neurons treated with exogenous netrin-1. a Representative dendrites before and 48 h post-axotomy treated with vehicle (HBS) or netrin-1 (Ntn1) beginning at 40 h post-axotomy (inverted fluorescence). Arrows : new spines; red asterisks : eliminated spines. Scale bars , 10 µm. b Quantification of spine density illustrated in a . Axotomy : n = 33 dendrites; 7 neurons; #spines/TDL: 392/3696 µm ( before ), 263/3447 µm ( after ). Axotomy + netrin-1 : n = 29 dendrites, 6 neurons; #spines/TDL: 293/3281 µm ( before ), 363/3417 µm ( after ). c Percent responsive FM puncta per neuron field at 48 h post-axotomy with HBS or netrin-1. n = 8–11 fields/chambers per condition over 5 experiments. d Number of responsive and unresponsive FM puncta from c . Significantly fewer unresponsive puncta followed axotomy compared to uninjured control (HBS). e , f Number of vGLUT1 and vGAT puncta per neuron area (uninjured control, axotomized + HBS, or axotomized + netrin-1) at 14 DIV. n = 8–9 neurons; 3 chambers per condition over 3 experiments. g Representative DCC immunostaining ( turquoise ) in uninjured control, post-axotomy, and post-axotomy + netrin-1 in cultures with similar spine densities. Neurons were retrogradely labeled with fluorescent protein (FP, magenta ) using an mCherry modified rabies virus. Scale bar , 10 µm. h Quantification of DCC immunofluorescence per spine region-of-interest (ROI). ROI: 2 µm diameter circular region surrounding each spine. Control, n = 295 ROIs; axotomy, n = 293 ROIs; axotomy + Ntn1, n = 210 ROIs. 8 neuron fields/3 chambers per condition; 3 experiments. i Quantification of spine density following 24 h of control antibody (IgG ab.) or DCC function blocking antibody (DCC ab.). IgG: n = 33 dendrites; 8 neurons; #spines/TDL: 464/4864 µm (before), 419/4712 µm (after). DCC ab: n = 34 dendrites; 7 neurons; #spines/TDL: 404/4433 µm (before), 222/3647 µm (after). j Representative FP-labeled dendritic segments immunostained for vGAT (inverted) and vGLUT1 (inverted) following 24 h application of IgG or DCC antibodies (outlined dendrites, solid magenta line ). Neurons were fixed at 15–16 DIV, older than the cultures in e , f . Scale bar , 10 µm. Quantification shown on the right. n = 23 neuron fields per condition; 3 chambers per condition over 3 experiments. b , i Repeated-measure two-way ANOVA, Bonferroni post hoc test; analyses included 1 chamber per condition for 3 experiments. c , j Unpaired two-tailed t -test. d – f , h One-way ANOVA, Bonferroni post hoc test. Error bars , s.e.m. * p

    Journal: Nature Communications

    Article Title: Distal axotomy enhances retrograde presynaptic excitability onto injured pyramidal neurons via trans-synaptic signaling

    doi: 10.1038/s41467-017-00652-y

    Figure Lengend Snippet: Spine density and presynaptic release properties of axotomized neurons treated with exogenous netrin-1. a Representative dendrites before and 48 h post-axotomy treated with vehicle (HBS) or netrin-1 (Ntn1) beginning at 40 h post-axotomy (inverted fluorescence). Arrows : new spines; red asterisks : eliminated spines. Scale bars , 10 µm. b Quantification of spine density illustrated in a . Axotomy : n = 33 dendrites; 7 neurons; #spines/TDL: 392/3696 µm ( before ), 263/3447 µm ( after ). Axotomy + netrin-1 : n = 29 dendrites, 6 neurons; #spines/TDL: 293/3281 µm ( before ), 363/3417 µm ( after ). c Percent responsive FM puncta per neuron field at 48 h post-axotomy with HBS or netrin-1. n = 8–11 fields/chambers per condition over 5 experiments. d Number of responsive and unresponsive FM puncta from c . Significantly fewer unresponsive puncta followed axotomy compared to uninjured control (HBS). e , f Number of vGLUT1 and vGAT puncta per neuron area (uninjured control, axotomized + HBS, or axotomized + netrin-1) at 14 DIV. n = 8–9 neurons; 3 chambers per condition over 3 experiments. g Representative DCC immunostaining ( turquoise ) in uninjured control, post-axotomy, and post-axotomy + netrin-1 in cultures with similar spine densities. Neurons were retrogradely labeled with fluorescent protein (FP, magenta ) using an mCherry modified rabies virus. Scale bar , 10 µm. h Quantification of DCC immunofluorescence per spine region-of-interest (ROI). ROI: 2 µm diameter circular region surrounding each spine. Control, n = 295 ROIs; axotomy, n = 293 ROIs; axotomy + Ntn1, n = 210 ROIs. 8 neuron fields/3 chambers per condition; 3 experiments. i Quantification of spine density following 24 h of control antibody (IgG ab.) or DCC function blocking antibody (DCC ab.). IgG: n = 33 dendrites; 8 neurons; #spines/TDL: 464/4864 µm (before), 419/4712 µm (after). DCC ab: n = 34 dendrites; 7 neurons; #spines/TDL: 404/4433 µm (before), 222/3647 µm (after). j Representative FP-labeled dendritic segments immunostained for vGAT (inverted) and vGLUT1 (inverted) following 24 h application of IgG or DCC antibodies (outlined dendrites, solid magenta line ). Neurons were fixed at 15–16 DIV, older than the cultures in e , f . Scale bar , 10 µm. Quantification shown on the right. n = 23 neuron fields per condition; 3 chambers per condition over 3 experiments. b , i Repeated-measure two-way ANOVA, Bonferroni post hoc test; analyses included 1 chamber per condition for 3 experiments. c , j Unpaired two-tailed t -test. d – f , h One-way ANOVA, Bonferroni post hoc test. Error bars , s.e.m. * p

    Article Snippet: Coverslips were incubated with anti-MAP2 (1:1000; Millipore # AB5622), anti-beta tubulin III (1:2000; Aves #TUJ), anti-GAD67 (1:2000; Aves labs # GAD), anti-vGLUT1 (1:100; NeuroMab, clone N28/9, cat. #75-066), anti-vGAT (1:1000; Synaptic Systems #131 003), anti-DCC (1:100; Calbiochem #OP45), or anti-synapsin1 (1:500; Calbiochem #574778) primary antibodies in 1% blocking solution for overnight at 4 °C.

    Techniques: Fluorescence, Droplet Countercurrent Chromatography, Immunostaining, Labeling, Modification, Immunofluorescence, Blocking Assay, Two Tailed Test

    Netrin-1 triggers the dissociation of a DSCAM/DCC complex. (A) DSCAM (red) and DCC (green) proteins co-localize in precrossing commissural axons in transverse section of the E12 rat spinal cord. Lower panels are close ups (20x) of the ventral spinal cord

    Journal:

    Article Title: DSCAM is a netrin receptor that collaborates with DCC in mediating turning responses to netrin-1

    doi: 10.1016/j.cell.2008.05.030

    Figure Lengend Snippet: Netrin-1 triggers the dissociation of a DSCAM/DCC complex. (A) DSCAM (red) and DCC (green) proteins co-localize in precrossing commissural axons in transverse section of the E12 rat spinal cord. Lower panels are close ups (20x) of the ventral spinal cord

    Article Snippet: Anti-DCC (AF5, Calbiochem; 2 μg/ml), DSCAM-Fc or Fc was added to the medium 30 min before initiating the gradient.

    Techniques: Droplet Countercurrent Chromatography

    DSCAM binds netrin-1. (A) COS cells expressing DSCAM or DCC, but not Robo1 bind netrin-1 (top). Receptor expression was verified by immunocytochemistry (bottom). (B–D) Netrin-1 specifically binds to DSCAM. (B) DSCAMecto-Fc or control [(BSA)] protein

    Journal:

    Article Title: DSCAM is a netrin receptor that collaborates with DCC in mediating turning responses to netrin-1

    doi: 10.1016/j.cell.2008.05.030

    Figure Lengend Snippet: DSCAM binds netrin-1. (A) COS cells expressing DSCAM or DCC, but not Robo1 bind netrin-1 (top). Receptor expression was verified by immunocytochemistry (bottom). (B–D) Netrin-1 specifically binds to DSCAM. (B) DSCAMecto-Fc or control [(BSA)] protein

    Article Snippet: Anti-DCC (AF5, Calbiochem; 2 μg/ml), DSCAM-Fc or Fc was added to the medium 30 min before initiating the gradient.

    Techniques: Expressing, Droplet Countercurrent Chromatography, Immunocytochemistry

    DSCAM guides growth cones independent of DCC

    Journal:

    Article Title: DSCAM is a netrin receptor that collaborates with DCC in mediating turning responses to netrin-1

    doi: 10.1016/j.cell.2008.05.030

    Figure Lengend Snippet: DSCAM guides growth cones independent of DCC

    Article Snippet: Anti-DCC (AF5, Calbiochem; 2 μg/ml), DSCAM-Fc or Fc was added to the medium 30 min before initiating the gradient.

    Techniques: Droplet Countercurrent Chromatography

    Maitotoxin treatment of SH-SY5Y cells leads to sequential cleavage of αII/βII spectrin and cell death (A) Cultured SH-SY5Y cell were treated with 0.04nM maitotoxin, and the time-course of spectrin breakdown monitored by Western blotting after SDS-PAGE analysis of cell lysates (20 μg/lane) with Pab-RAFA (anti-αII spectrin); α-bdp-1 antibody; and Pab-10D (anti-βII spectrin). Control cells were incubated for three hours without maitotoxin (ctrl). Duplicate experiments are shown for each time point. Note the rapid breakdown of αII spectrin vs. the delayed loss of βII spectrin. The positions of MW markers (÷1000) are depicted on the right; prominent bdp’s are marked on the left. ( B ) Densitometric evaluation of the extent of spectrin breakdown of the gels shown in (A). The extent of maitotoxin-induced cell death was also evaluated in parallel experiments of maitotoxin treated cells, as measured by flow cytometry after Ethidium-1 staining. Data points are the mean ±SD of three determinations. Background cell death (non-viable cells at t=0) was subtracted from all points. (Inset) Western blot with Pab RAFA of SH-SY5Y cells after 0.03 nM maitotoxin treatment, ± inhibition of calpain or caspase. The maitotoxin induced cleavage of spectrin was entirely inhibited by the calpain inhibitor calpeptin, but not by the caspase inhibitor Z-D-DCB. Lane 1, control SH-SY5Y cells; lane 2, cells after 3 hrs of maitotoxin treatment; lane 3, 3 hrs. maitotoxin + calpeptin; lane 4, 3hrs. maitotoxin + caspase inhibitor.

    Journal: Biochemistry

    Article Title: Sequential Degradation of αII and βII Spectrin by Calpain in Glutamate or Maitotoxin-Stimulated Cells

    doi: 10.1021/bi061504y

    Figure Lengend Snippet: Maitotoxin treatment of SH-SY5Y cells leads to sequential cleavage of αII/βII spectrin and cell death (A) Cultured SH-SY5Y cell were treated with 0.04nM maitotoxin, and the time-course of spectrin breakdown monitored by Western blotting after SDS-PAGE analysis of cell lysates (20 μg/lane) with Pab-RAFA (anti-αII spectrin); α-bdp-1 antibody; and Pab-10D (anti-βII spectrin). Control cells were incubated for three hours without maitotoxin (ctrl). Duplicate experiments are shown for each time point. Note the rapid breakdown of αII spectrin vs. the delayed loss of βII spectrin. The positions of MW markers (÷1000) are depicted on the right; prominent bdp’s are marked on the left. ( B ) Densitometric evaluation of the extent of spectrin breakdown of the gels shown in (A). The extent of maitotoxin-induced cell death was also evaluated in parallel experiments of maitotoxin treated cells, as measured by flow cytometry after Ethidium-1 staining. Data points are the mean ±SD of three determinations. Background cell death (non-viable cells at t=0) was subtracted from all points. (Inset) Western blot with Pab RAFA of SH-SY5Y cells after 0.03 nM maitotoxin treatment, ± inhibition of calpain or caspase. The maitotoxin induced cleavage of spectrin was entirely inhibited by the calpain inhibitor calpeptin, but not by the caspase inhibitor Z-D-DCB. Lane 1, control SH-SY5Y cells; lane 2, cells after 3 hrs of maitotoxin treatment; lane 3, 3 hrs. maitotoxin + calpeptin; lane 4, 3hrs. maitotoxin + caspase inhibitor.

    Article Snippet: Calmodulin (bovine brain) and maitotoxin were from Sigma, calpeptin from Calbiochem, and Ethidium-1 from Molecular Probes.

    Techniques: Cell Culture, Western Blot, SDS Page, Incubation, Flow Cytometry, Cytometry, Staining, Inhibition

    QVD, Calpeptin and rapamycin treatments inhibit the FTS-induced p62 cleavage. (A) CTRL HCT-116 cells were treated with 75 μM FTS for 48 h, in the presence or in the absence of 25 μM QVD-OPH or 10 μM calpeptin (Calp) and then subjected to immunoblot analysis using anti-p62 antibodies. Left panel , representative blot is shown. Right panel , densitometric analysis of the results is presented as fold induction over the untreated cells (mean ± SE; *, p

    Journal: PLoS ONE

    Article Title: Continuous treatment with FTS confers resistance to apoptosis and affects autophagy

    doi: 10.1371/journal.pone.0171351

    Figure Lengend Snippet: QVD, Calpeptin and rapamycin treatments inhibit the FTS-induced p62 cleavage. (A) CTRL HCT-116 cells were treated with 75 μM FTS for 48 h, in the presence or in the absence of 25 μM QVD-OPH or 10 μM calpeptin (Calp) and then subjected to immunoblot analysis using anti-p62 antibodies. Left panel , representative blot is shown. Right panel , densitometric analysis of the results is presented as fold induction over the untreated cells (mean ± SE; *, p

    Article Snippet: FTS (SaliRasib, S-trans, trans-farnesylthiosalicylic acid) was provided by Concordia Pharmaceuticals (Fort Lauderdale, FL); chloroquine (CQ; C6628) and 5-fluorouracil (5-FU; F6627) were from Sigma-Aldrich; QVD-OPH was from R & D systems (Minneapolis, MN; OPH-001); calpeptin was from EMD Millipore (Darmstadt, Germany; 03-34-0051); and rapamycin was from Cayman Chemical (Ann Arbor, MI; 13346).

    Techniques: