human custom procartaplextm kit Search Results


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Thermo Fisher human custom procartaplextm kit
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Thermo Fisher human custom procartaplex assay kit
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Thermo Fisher ldh b human procartaplextm simplex kit
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BioPorto Inc ngal human elisa kit kit036ruo
Univariate association between biomarkers and UTI in urine by decreasing accuracy (AUC).
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Bio-Techne corporation sample activation kit 1
Univariate association between biomarkers and UTI in urine by decreasing accuracy (AUC).
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Bio-Techne corporation human luminex® discovery assay
Univariate association between biomarkers and UTI in urine by decreasing accuracy (AUC).
Human Luminex® Discovery Assay, supplied by Bio-Techne corporation, used in various techniques. Bioz Stars score: 97/100, based on 1 PubMed citations. ZERO BIAS - scores, article reviews, protocol conditions and more
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MBL Life science human il-18 elisa kit
A. HRV16 infection causes NLRP1 cleavage. HeLa-Ohio cells stably expressing NLRP1-HA and a vector control were infected with HRV16 at MOI=1 in duplicates. Rupintrivir (10 nM) was added at the time of infection and cell pellets were harvested 24 hours after inoculation. B. The effect of HRV16 infection on ASC-GFP speck formation in HeLa-Ohio-ASC-GFP cells expressing wild-type NLRP1 or NLRP1 Q130A . ***, p<0.0005 (Two-way ANOVA). n= 3, >100 cells per condition. C. Expression of NLR sensors, inflammasome effectors and RLR sensors in primary human airway epithelial cells. Expression values of Nasal #2 (GSE55458), Bronchial #2 (GSE107971) and Alveolar #2 (GSE83501) and were log-transformed prior to color mapping. D. Comparative analysis of cytokines/chemokines in HRV16-infected and Talabostat-treated NHBEs. Three different lots of NHBEs were used. E. Cytokines/chemokines induced by HRV16 infection and Talabostat in NHBEs. NHBEs were infected with HRV16 (MOI=5) or treated with Talabostat (2 µM). Conditioned media were harvested 48 hours post infection and subjected to multiplex cytokines/chemokine analysis. Cytokines/chemokines that were induced at least 5 fold in each condition (p<0.05, Student’s t test, lognormal values) are highlighted in red. F. HRV16 infection causes robust <t>IL-18</t> secretion, while IL-1B secretion is variable. Cytokine levels were measured by ELISA. *, p<0.05; **, p<0.005 (Two-way ANOVA). n= 4 biological replicates for IL-18 and 3 biological replicates for IL-1B. G. HRV16 infection causes IL-18 processing and endogenous ASC oligomerization in NHBEs. Cell lysates and conditioned media were harvested 48 hours post HRV16 inoculation. H. HRV16-induced inflammasome assembly requires NLRP1. Cas9-control, NLRP1 and ASC KO NHBEs were infected with HRV16 as in e-g. Cell pellets were harvested 48 hours post infection. I. HRV16-induced IL-18 secretion requires NLRP1 and ASC. Conditioned media were harvested from control and KO NHBEs. IL-18 levels were measured with ELISA. *, p<0.05; **, p<0.005 (Two-way ANOVA), n=3 biological replicates. J. Proposed mechanism of HRV-triggered NLRP1 inflammasome activation and IL-18 secretion in human airway epithelial cells.
Human Il 18 Elisa Kit, supplied by MBL Life science, 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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Luminex milliplex
A. HRV16 infection causes NLRP1 cleavage. HeLa-Ohio cells stably expressing NLRP1-HA and a vector control were infected with HRV16 at MOI=1 in duplicates. Rupintrivir (10 nM) was added at the time of infection and cell pellets were harvested 24 hours after inoculation. B. The effect of HRV16 infection on ASC-GFP speck formation in HeLa-Ohio-ASC-GFP cells expressing wild-type NLRP1 or NLRP1 Q130A . ***, p<0.0005 (Two-way ANOVA). n= 3, >100 cells per condition. C. Expression of NLR sensors, inflammasome effectors and RLR sensors in primary human airway epithelial cells. Expression values of Nasal #2 (GSE55458), Bronchial #2 (GSE107971) and Alveolar #2 (GSE83501) and were log-transformed prior to color mapping. D. Comparative analysis of cytokines/chemokines in HRV16-infected and Talabostat-treated NHBEs. Three different lots of NHBEs were used. E. Cytokines/chemokines induced by HRV16 infection and Talabostat in NHBEs. NHBEs were infected with HRV16 (MOI=5) or treated with Talabostat (2 µM). Conditioned media were harvested 48 hours post infection and subjected to multiplex cytokines/chemokine analysis. Cytokines/chemokines that were induced at least 5 fold in each condition (p<0.05, Student’s t test, lognormal values) are highlighted in red. F. HRV16 infection causes robust <t>IL-18</t> secretion, while IL-1B secretion is variable. Cytokine levels were measured by ELISA. *, p<0.05; **, p<0.005 (Two-way ANOVA). n= 4 biological replicates for IL-18 and 3 biological replicates for IL-1B. G. HRV16 infection causes IL-18 processing and endogenous ASC oligomerization in NHBEs. Cell lysates and conditioned media were harvested 48 hours post HRV16 inoculation. H. HRV16-induced inflammasome assembly requires NLRP1. Cas9-control, NLRP1 and ASC KO NHBEs were infected with HRV16 as in e-g. Cell pellets were harvested 48 hours post infection. I. HRV16-induced IL-18 secretion requires NLRP1 and ASC. Conditioned media were harvested from control and KO NHBEs. IL-18 levels were measured with ELISA. *, p<0.05; **, p<0.005 (Two-way ANOVA), n=3 biological replicates. J. Proposed mechanism of HRV-triggered NLRP1 inflammasome activation and IL-18 secretion in human airway epithelial cells.
Milliplex, supplied by Luminex, 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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Luminex fluorokine
A. HRV16 infection causes NLRP1 cleavage. HeLa-Ohio cells stably expressing NLRP1-HA and a vector control were infected with HRV16 at MOI=1 in duplicates. Rupintrivir (10 nM) was added at the time of infection and cell pellets were harvested 24 hours after inoculation. B. The effect of HRV16 infection on ASC-GFP speck formation in HeLa-Ohio-ASC-GFP cells expressing wild-type NLRP1 or NLRP1 Q130A . ***, p<0.0005 (Two-way ANOVA). n= 3, >100 cells per condition. C. Expression of NLR sensors, inflammasome effectors and RLR sensors in primary human airway epithelial cells. Expression values of Nasal #2 (GSE55458), Bronchial #2 (GSE107971) and Alveolar #2 (GSE83501) and were log-transformed prior to color mapping. D. Comparative analysis of cytokines/chemokines in HRV16-infected and Talabostat-treated NHBEs. Three different lots of NHBEs were used. E. Cytokines/chemokines induced by HRV16 infection and Talabostat in NHBEs. NHBEs were infected with HRV16 (MOI=5) or treated with Talabostat (2 µM). Conditioned media were harvested 48 hours post infection and subjected to multiplex cytokines/chemokine analysis. Cytokines/chemokines that were induced at least 5 fold in each condition (p<0.05, Student’s t test, lognormal values) are highlighted in red. F. HRV16 infection causes robust <t>IL-18</t> secretion, while IL-1B secretion is variable. Cytokine levels were measured by ELISA. *, p<0.05; **, p<0.005 (Two-way ANOVA). n= 4 biological replicates for IL-18 and 3 biological replicates for IL-1B. G. HRV16 infection causes IL-18 processing and endogenous ASC oligomerization in NHBEs. Cell lysates and conditioned media were harvested 48 hours post HRV16 inoculation. H. HRV16-induced inflammasome assembly requires NLRP1. Cas9-control, NLRP1 and ASC KO NHBEs were infected with HRV16 as in e-g. Cell pellets were harvested 48 hours post infection. I. HRV16-induced IL-18 secretion requires NLRP1 and ASC. Conditioned media were harvested from control and KO NHBEs. IL-18 levels were measured with ELISA. *, p<0.05; **, p<0.005 (Two-way ANOVA), n=3 biological replicates. J. Proposed mechanism of HRV-triggered NLRP1 inflammasome activation and IL-18 secretion in human airway epithelial cells.
Fluorokine, supplied by Luminex, 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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Vector Laboratories immpact aec peroxidase (hrp) substrate
A. HRV16 infection causes NLRP1 cleavage. HeLa-Ohio cells stably expressing NLRP1-HA and a vector control were infected with HRV16 at MOI=1 in duplicates. Rupintrivir (10 nM) was added at the time of infection and cell pellets were harvested 24 hours after inoculation. B. The effect of HRV16 infection on ASC-GFP speck formation in HeLa-Ohio-ASC-GFP cells expressing wild-type NLRP1 or NLRP1 Q130A . ***, p<0.0005 (Two-way ANOVA). n= 3, >100 cells per condition. C. Expression of NLR sensors, inflammasome effectors and RLR sensors in primary human airway epithelial cells. Expression values of Nasal #2 (GSE55458), Bronchial #2 (GSE107971) and Alveolar #2 (GSE83501) and were log-transformed prior to color mapping. D. Comparative analysis of cytokines/chemokines in HRV16-infected and Talabostat-treated NHBEs. Three different lots of NHBEs were used. E. Cytokines/chemokines induced by HRV16 infection and Talabostat in NHBEs. NHBEs were infected with HRV16 (MOI=5) or treated with Talabostat (2 µM). Conditioned media were harvested 48 hours post infection and subjected to multiplex cytokines/chemokine analysis. Cytokines/chemokines that were induced at least 5 fold in each condition (p<0.05, Student’s t test, lognormal values) are highlighted in red. F. HRV16 infection causes robust <t>IL-18</t> secretion, while IL-1B secretion is variable. Cytokine levels were measured by ELISA. *, p<0.05; **, p<0.005 (Two-way ANOVA). n= 4 biological replicates for IL-18 and 3 biological replicates for IL-1B. G. HRV16 infection causes IL-18 processing and endogenous ASC oligomerization in NHBEs. Cell lysates and conditioned media were harvested 48 hours post HRV16 inoculation. H. HRV16-induced inflammasome assembly requires NLRP1. Cas9-control, NLRP1 and ASC KO NHBEs were infected with HRV16 as in e-g. Cell pellets were harvested 48 hours post infection. I. HRV16-induced IL-18 secretion requires NLRP1 and ASC. Conditioned media were harvested from control and KO NHBEs. IL-18 levels were measured with ELISA. *, p<0.05; **, p<0.005 (Two-way ANOVA), n=3 biological replicates. J. Proposed mechanism of HRV-triggered NLRP1 inflammasome activation and IL-18 secretion in human airway epithelial cells.
Immpact Aec Peroxidase (Hrp) Substrate, supplied by Vector Laboratories, used in various techniques. Bioz Stars score: 95/100, based on 1 PubMed citations. ZERO BIAS - scores, article reviews, protocol conditions and more
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Image Search Results


Univariate association between biomarkers and UTI in urine by decreasing accuracy (AUC).

Journal: Frontiers in Pediatrics

Article Title: Biomarkers for febrile urinary tract infection in children

doi: 10.3389/fped.2023.1163546

Figure Lengend Snippet: Univariate association between biomarkers and UTI in urine by decreasing accuracy (AUC).

Article Snippet: These markers were measured in urine using a commercially available 34-plex plate (ProcartaPlex, EPX340-12167-901, Thermo Fisher Scientific; see for a listing of these markers) and Bioporto NGAL Human ELISA kit (KIT036RUO; Bioporto).

Techniques: Biomarker Discovery

Box and whisker plot of urinary NGAL level in children with and without UTI. Dots represent outliers. Diamonds represent group means. NGAL, neutrophil gelatinase–associated lipocalin; UTI, urinary tract infection.

Journal: Frontiers in Pediatrics

Article Title: Biomarkers for febrile urinary tract infection in children

doi: 10.3389/fped.2023.1163546

Figure Lengend Snippet: Box and whisker plot of urinary NGAL level in children with and without UTI. Dots represent outliers. Diamonds represent group means. NGAL, neutrophil gelatinase–associated lipocalin; UTI, urinary tract infection.

Article Snippet: These markers were measured in urine using a commercially available 34-plex plate (ProcartaPlex, EPX340-12167-901, Thermo Fisher Scientific; see for a listing of these markers) and Bioporto NGAL Human ELISA kit (KIT036RUO; Bioporto).

Techniques: Whisker Assay, Infection

A. HRV16 infection causes NLRP1 cleavage. HeLa-Ohio cells stably expressing NLRP1-HA and a vector control were infected with HRV16 at MOI=1 in duplicates. Rupintrivir (10 nM) was added at the time of infection and cell pellets were harvested 24 hours after inoculation. B. The effect of HRV16 infection on ASC-GFP speck formation in HeLa-Ohio-ASC-GFP cells expressing wild-type NLRP1 or NLRP1 Q130A . ***, p<0.0005 (Two-way ANOVA). n= 3, >100 cells per condition. C. Expression of NLR sensors, inflammasome effectors and RLR sensors in primary human airway epithelial cells. Expression values of Nasal #2 (GSE55458), Bronchial #2 (GSE107971) and Alveolar #2 (GSE83501) and were log-transformed prior to color mapping. D. Comparative analysis of cytokines/chemokines in HRV16-infected and Talabostat-treated NHBEs. Three different lots of NHBEs were used. E. Cytokines/chemokines induced by HRV16 infection and Talabostat in NHBEs. NHBEs were infected with HRV16 (MOI=5) or treated with Talabostat (2 µM). Conditioned media were harvested 48 hours post infection and subjected to multiplex cytokines/chemokine analysis. Cytokines/chemokines that were induced at least 5 fold in each condition (p<0.05, Student’s t test, lognormal values) are highlighted in red. F. HRV16 infection causes robust IL-18 secretion, while IL-1B secretion is variable. Cytokine levels were measured by ELISA. *, p<0.05; **, p<0.005 (Two-way ANOVA). n= 4 biological replicates for IL-18 and 3 biological replicates for IL-1B. G. HRV16 infection causes IL-18 processing and endogenous ASC oligomerization in NHBEs. Cell lysates and conditioned media were harvested 48 hours post HRV16 inoculation. H. HRV16-induced inflammasome assembly requires NLRP1. Cas9-control, NLRP1 and ASC KO NHBEs were infected with HRV16 as in e-g. Cell pellets were harvested 48 hours post infection. I. HRV16-induced IL-18 secretion requires NLRP1 and ASC. Conditioned media were harvested from control and KO NHBEs. IL-18 levels were measured with ELISA. *, p<0.05; **, p<0.005 (Two-way ANOVA), n=3 biological replicates. J. Proposed mechanism of HRV-triggered NLRP1 inflammasome activation and IL-18 secretion in human airway epithelial cells.

Journal: bioRxiv

Article Title: Direct cleavage of human NLRP1 by enteroviral 3C protease triggers inflammasome activation in airway epithelium

doi: 10.1101/2020.10.14.325076

Figure Lengend Snippet: A. HRV16 infection causes NLRP1 cleavage. HeLa-Ohio cells stably expressing NLRP1-HA and a vector control were infected with HRV16 at MOI=1 in duplicates. Rupintrivir (10 nM) was added at the time of infection and cell pellets were harvested 24 hours after inoculation. B. The effect of HRV16 infection on ASC-GFP speck formation in HeLa-Ohio-ASC-GFP cells expressing wild-type NLRP1 or NLRP1 Q130A . ***, p<0.0005 (Two-way ANOVA). n= 3, >100 cells per condition. C. Expression of NLR sensors, inflammasome effectors and RLR sensors in primary human airway epithelial cells. Expression values of Nasal #2 (GSE55458), Bronchial #2 (GSE107971) and Alveolar #2 (GSE83501) and were log-transformed prior to color mapping. D. Comparative analysis of cytokines/chemokines in HRV16-infected and Talabostat-treated NHBEs. Three different lots of NHBEs were used. E. Cytokines/chemokines induced by HRV16 infection and Talabostat in NHBEs. NHBEs were infected with HRV16 (MOI=5) or treated with Talabostat (2 µM). Conditioned media were harvested 48 hours post infection and subjected to multiplex cytokines/chemokine analysis. Cytokines/chemokines that were induced at least 5 fold in each condition (p<0.05, Student’s t test, lognormal values) are highlighted in red. F. HRV16 infection causes robust IL-18 secretion, while IL-1B secretion is variable. Cytokine levels were measured by ELISA. *, p<0.05; **, p<0.005 (Two-way ANOVA). n= 4 biological replicates for IL-18 and 3 biological replicates for IL-1B. G. HRV16 infection causes IL-18 processing and endogenous ASC oligomerization in NHBEs. Cell lysates and conditioned media were harvested 48 hours post HRV16 inoculation. H. HRV16-induced inflammasome assembly requires NLRP1. Cas9-control, NLRP1 and ASC KO NHBEs were infected with HRV16 as in e-g. Cell pellets were harvested 48 hours post infection. I. HRV16-induced IL-18 secretion requires NLRP1 and ASC. Conditioned media were harvested from control and KO NHBEs. IL-18 levels were measured with ELISA. *, p<0.05; **, p<0.005 (Two-way ANOVA), n=3 biological replicates. J. Proposed mechanism of HRV-triggered NLRP1 inflammasome activation and IL-18 secretion in human airway epithelial cells.

Article Snippet: Cytokine and chemokine measurements were carried out with human IL-1B ELISA kit (BD, #557953), human IL-18 ELISA kit (MBL Bioscience, #7620) and Immune Monitoring 65-Plex Human ProcartaPlex™ Panel (ThermoFisher EPX650-10065-901).

Techniques: Infection, Stable Transfection, Expressing, Plasmid Preparation, Transformation Assay, Multiplex Assay, Enzyme-linked Immunosorbent Assay, Activation Assay