computerized adaptive tests (cat) in the domains of physical function (pf) and pain interference (pi) Search Results


90
ProMIS Neurosciences pi cat v2.0
Summary of baseline and follow-up score.
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Biotium cf 488a annexin v
Summary of baseline and follow-up score.
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98
Vector Laboratories vectashield
Summary of baseline and follow-up score.
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ProMIS Neurosciences promis-cat pain interference
Summary of baseline and follow-up score.
Promis Cat Pain Interference, supplied by ProMIS Neurosciences, used in various techniques. Bioz Stars score: 90/100, based on 1 PubMed citations. ZERO BIAS - scores, article reviews, protocol conditions and more
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Vector Laboratories pi 1000 rrid ab 2336198 horse anti mouse peroxidase
Summary of baseline and follow-up score.
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Beijing Solarbio Science annexin v fitc pi apoptosis detection kit
Figure 3. Nicotinamide treatment induced <t>apoptosis</t> of HL-60 cells. (A) Flow cytometry images for determined apoptosis of HL-60 cells.
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Echelon Biosciences p 3916 100ug

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Echelon Biosciences control polypiposomes

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Dojindo Labs cellstain pi solution

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Becton Dickinson propidium iodide (pi
A, Dose dependent inhibition of 5hmC by TETi76 in different leukemia cells. Cells were treated with increasing concentrations of TETi76 in the presence of 100 μM sodium ascorbate for 12 hours. Genomic content of 5hmC and 5mC were detected by dot blot analysis using specific antibodies and the ratio of 5hmC/5mC are plotted. B, Heatmap of significantly up and down regulated genes in K562 TET2+/+ (K01) or K562 TET2−/− (K18) cells treated with 25 μM TETi76 or 100 μM ascorbic acid (AA) for 24 hours followed by RNAseq analysis. C, Venn diagram of pathway analysis of K562 TET2−/− (K18, MU) vs K562 TET2+/+ (K01, WT), K562 TET2+/+ (K01) treated with 25 μM TETi76 for 24 hours vs vehicle (DMSO) control (CTRL) or BeatAML RNAseq data of TET2 mutant (MU) vs TET2 wild type (WT) (vizome.org/aml/) performed by hallmark gene set enrichment analysis. D, Correlation Analysis of LD50 of TETi76 against different leukemia cells with TET-activity. The TET activities in different cells were measured by relative ratio of 5hmC/5mC in 15 different leukemia cell lines including 8 isogenic TET1/2/3 knockout cell lines. Each cell lines were treated with increasing concentrations of TETi76 for 72 hours and the LD50 was calculated from viable cell monitored by methylene blue exclusion on vi-cell counter. Pearson correlation coefficient (r) and significance were calculated in GraphPad Prism. E, Effect of TETi76 on cells expressing neomorphic IDH1/2 mutants. Commercially available TF1-IDH2R140Q, house-made K562-IDH1R132C (Fig. 1J) and their parental cells (TF1 and K562) were treated with different concentrations of TETi76 for 3 days. Both K562 and K562-IDH1R132C cells were supplied with 1 μg/ml doxycycline during TETi76 treatment. Relative cell growth was measured by CellTiter-Glo assay. F, TETi76 induces programmed cell death in TET2 deficient cells. SIGM5 cells were treated with TETi76 and the apoptotic cell population was determined by annexin V and <t>propidium</t> iodide staining using flow cytometer. TETi76 treatment demonstrate a dose and time dependent increase in early and late apoptotic cells. G, Western blot analysis of PARP1, Caspase-3, NRF2 and NQO1 after TETi76 treatment in SIGM5 cells. H, Colony forming abilities of K562 TET2+/+ and TET2−/− cells in the presence and absence of TETi76. I, Bone marrow from Tet2+/+, Tet2+/− and Tet2−/− mice were harvested and cultured in MethoCult in the presence or absence of TETi76. Data is representative of 3 independent experiments performed separately. Data are shown as mean or mean±SEM; statistical significance (p values) from two tailed t-test are indicated; * p<0.05; *** p<0.001; ns: not significant.
Propidium Iodide (Pi, supplied by Becton Dickinson, used in various techniques. Bioz Stars score: 90/100, based on 1 PubMed citations. ZERO BIAS - scores, article reviews, protocol conditions and more
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Becton Dickinson propidium iodide
Analysis of <t>apoptosis,</t> ROS level and cell cycle in U87MG cells. *P<0.05 and ***P<0.001. n=3. Lnc-NLC1-C, long non-coding RNA narcolepsy candidate region 1 gene C; ov, overexpression; sh, short hairpin RNA; NC, negative control; ROS, reactive oxygen species.
Propidium Iodide, supplied by Becton Dickinson, used in various techniques. Bioz Stars score: 90/100, based on 1 PubMed citations. ZERO BIAS - scores, article reviews, protocol conditions and more
https://www.bioz.com/product/computerized+adaptive+tests+(cat)+in+the+domains+of+physical+function+(pf)+and+pain+interference+(pi)/propidium+iodide/pmc08299021-75-20-30
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Image Search Results


Summary of baseline and follow-up score.

Journal: JSES International

Article Title: Many patients fail to achieve MCID for PROMIS upper extremity and pain interference following nonoperative management of rotator cuff tears

doi: 10.1016/j.jseint.2023.06.014

Figure Lengend Snippet: Summary of baseline and follow-up score.

Article Snippet: PROMIS PI CAT v2.0 (n = 107) , , , .

Techniques:

Figure 3. Nicotinamide treatment induced apoptosis of HL-60 cells. (A) Flow cytometry images for determined apoptosis of HL-60 cells.

Journal: Medical Science Monitor

Article Title: Nicotinamide Inhibits Glycolysis of HL-60 Cells by Modulating Sirtuin 1 (SIRT1)/Peroxisome Proliferator-Activated Receptor γ Coactivator 1α (PGC-1α)/Hypoxia-Inducible Factor-2α (HIF2α) Signaling Pathway

doi: 10.12659/msm.920810

Figure Lengend Snippet: Figure 3. Nicotinamide treatment induced apoptosis of HL-60 cells. (A) Flow cytometry images for determined apoptosis of HL-60 cells.

Article Snippet: The apoptosis was detected using the Annexin V-FITC/PI Apoptosis Detection Kit (Cat. No. CA1020, SolarBio.

Techniques: Flow Cytometry

Journal: Cell

Article Title: Friction Mediates Scission of Tubular Membranes Scaffolded by BAR Proteins

doi: 10.1016/j.cell.2017.05.047

Figure Lengend Snippet:

Article Snippet: L-α-phosphatidylinositol-4,5-bisphosphate (PI(4,5)P 2 ,) , Avanti Polar Lipids , cat# 840046P.

Techniques: Recombinant, Modification, Electron Microscopy, Software

A, Dose dependent inhibition of 5hmC by TETi76 in different leukemia cells. Cells were treated with increasing concentrations of TETi76 in the presence of 100 μM sodium ascorbate for 12 hours. Genomic content of 5hmC and 5mC were detected by dot blot analysis using specific antibodies and the ratio of 5hmC/5mC are plotted. B, Heatmap of significantly up and down regulated genes in K562 TET2+/+ (K01) or K562 TET2−/− (K18) cells treated with 25 μM TETi76 or 100 μM ascorbic acid (AA) for 24 hours followed by RNAseq analysis. C, Venn diagram of pathway analysis of K562 TET2−/− (K18, MU) vs K562 TET2+/+ (K01, WT), K562 TET2+/+ (K01) treated with 25 μM TETi76 for 24 hours vs vehicle (DMSO) control (CTRL) or BeatAML RNAseq data of TET2 mutant (MU) vs TET2 wild type (WT) (vizome.org/aml/) performed by hallmark gene set enrichment analysis. D, Correlation Analysis of LD50 of TETi76 against different leukemia cells with TET-activity. The TET activities in different cells were measured by relative ratio of 5hmC/5mC in 15 different leukemia cell lines including 8 isogenic TET1/2/3 knockout cell lines. Each cell lines were treated with increasing concentrations of TETi76 for 72 hours and the LD50 was calculated from viable cell monitored by methylene blue exclusion on vi-cell counter. Pearson correlation coefficient (r) and significance were calculated in GraphPad Prism. E, Effect of TETi76 on cells expressing neomorphic IDH1/2 mutants. Commercially available TF1-IDH2R140Q, house-made K562-IDH1R132C (Fig. 1J) and their parental cells (TF1 and K562) were treated with different concentrations of TETi76 for 3 days. Both K562 and K562-IDH1R132C cells were supplied with 1 μg/ml doxycycline during TETi76 treatment. Relative cell growth was measured by CellTiter-Glo assay. F, TETi76 induces programmed cell death in TET2 deficient cells. SIGM5 cells were treated with TETi76 and the apoptotic cell population was determined by annexin V and propidium iodide staining using flow cytometer. TETi76 treatment demonstrate a dose and time dependent increase in early and late apoptotic cells. G, Western blot analysis of PARP1, Caspase-3, NRF2 and NQO1 after TETi76 treatment in SIGM5 cells. H, Colony forming abilities of K562 TET2+/+ and TET2−/− cells in the presence and absence of TETi76. I, Bone marrow from Tet2+/+, Tet2+/− and Tet2−/− mice were harvested and cultured in MethoCult in the presence or absence of TETi76. Data is representative of 3 independent experiments performed separately. Data are shown as mean or mean±SEM; statistical significance (p values) from two tailed t-test are indicated; * p<0.05; *** p<0.001; ns: not significant.

Journal: Blood cancer discovery

Article Title: A Therapeutic Strategy for Preferential Targeting of TET2 Mutant and TET-dioxygenase Deficient Cells in Myeloid Neoplasms

doi: 10.1158/2643-3230.BCD-20-0173

Figure Lengend Snippet: A, Dose dependent inhibition of 5hmC by TETi76 in different leukemia cells. Cells were treated with increasing concentrations of TETi76 in the presence of 100 μM sodium ascorbate for 12 hours. Genomic content of 5hmC and 5mC were detected by dot blot analysis using specific antibodies and the ratio of 5hmC/5mC are plotted. B, Heatmap of significantly up and down regulated genes in K562 TET2+/+ (K01) or K562 TET2−/− (K18) cells treated with 25 μM TETi76 or 100 μM ascorbic acid (AA) for 24 hours followed by RNAseq analysis. C, Venn diagram of pathway analysis of K562 TET2−/− (K18, MU) vs K562 TET2+/+ (K01, WT), K562 TET2+/+ (K01) treated with 25 μM TETi76 for 24 hours vs vehicle (DMSO) control (CTRL) or BeatAML RNAseq data of TET2 mutant (MU) vs TET2 wild type (WT) (vizome.org/aml/) performed by hallmark gene set enrichment analysis. D, Correlation Analysis of LD50 of TETi76 against different leukemia cells with TET-activity. The TET activities in different cells were measured by relative ratio of 5hmC/5mC in 15 different leukemia cell lines including 8 isogenic TET1/2/3 knockout cell lines. Each cell lines were treated with increasing concentrations of TETi76 for 72 hours and the LD50 was calculated from viable cell monitored by methylene blue exclusion on vi-cell counter. Pearson correlation coefficient (r) and significance were calculated in GraphPad Prism. E, Effect of TETi76 on cells expressing neomorphic IDH1/2 mutants. Commercially available TF1-IDH2R140Q, house-made K562-IDH1R132C (Fig. 1J) and their parental cells (TF1 and K562) were treated with different concentrations of TETi76 for 3 days. Both K562 and K562-IDH1R132C cells were supplied with 1 μg/ml doxycycline during TETi76 treatment. Relative cell growth was measured by CellTiter-Glo assay. F, TETi76 induces programmed cell death in TET2 deficient cells. SIGM5 cells were treated with TETi76 and the apoptotic cell population was determined by annexin V and propidium iodide staining using flow cytometer. TETi76 treatment demonstrate a dose and time dependent increase in early and late apoptotic cells. G, Western blot analysis of PARP1, Caspase-3, NRF2 and NQO1 after TETi76 treatment in SIGM5 cells. H, Colony forming abilities of K562 TET2+/+ and TET2−/− cells in the presence and absence of TETi76. I, Bone marrow from Tet2+/+, Tet2+/− and Tet2−/− mice were harvested and cultured in MethoCult in the presence or absence of TETi76. Data is representative of 3 independent experiments performed separately. Data are shown as mean or mean±SEM; statistical significance (p values) from two tailed t-test are indicated; * p<0.05; *** p<0.001; ns: not significant.

Article Snippet: Cells were incubated with FITC-Annexin V (BD Pharmingen Catalog No.556420) in a binding buffer (BD Pharmingen catalog number 556454) containing propidium iodide (PI, BD Pharmingen catalog number 556463) and analyzed by flow cytometry (BD FACSVerse).

Techniques: Inhibition, Dot Blot, Mutagenesis, Activity Assay, Knock-Out, Expressing, Glo Assay, Staining, Flow Cytometry, Western Blot, Cell Culture, Two Tailed Test

Analysis of apoptosis, ROS level and cell cycle in U87MG cells. *P<0.05 and ***P<0.001. n=3. Lnc-NLC1-C, long non-coding RNA narcolepsy candidate region 1 gene C; ov, overexpression; sh, short hairpin RNA; NC, negative control; ROS, reactive oxygen species.

Journal: Oncology Letters

Article Title: lnc-NLC1-C inhibits migration, invasion and autophagy of glioma cells by targeting miR-383 and regulating PRDX-3 expression

doi: 10.3892/ol.2021.12901

Figure Lengend Snippet: Analysis of apoptosis, ROS level and cell cycle in U87MG cells. *P<0.05 and ***P<0.001. n=3. Lnc-NLC1-C, long non-coding RNA narcolepsy candidate region 1 gene C; ov, overexpression; sh, short hairpin RNA; NC, negative control; ROS, reactive oxygen species.

Article Snippet: After 200 µl binding buffer was added to the cells, 10 µl Annexin V-fluorescein isothiocyanate and 10 µl propidium iodide (part of the AnnexinV-FITC/PI Apoptosis Detection kit; cat. no. 556547; BD Biosciences) were added, and the cells were incubated at 4°C in the dark for 30 min and subjected to flow cytometry (FC500 MCL; Beckman Coulter, Inc.).

Techniques: Over Expression, shRNA, Negative Control