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urine clu  (BioVendor Instruments)


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    Structured Review

    BioVendor Instruments urine clu
    Urine Clu, supplied by BioVendor Instruments, used in various techniques. Bioz Stars score: 92/100, based on 8 PubMed citations. ZERO BIAS - scores, article reviews, protocol conditions and more
    https://www.bioz.com/product/clusterin+rat+elisa/Clusterin+Rat+ELISA/pmc09140233-114-7-15
    Average 92 stars, based on 8 article reviews
    urine clu - by Bioz Stars, 2026-09
    92/100 stars

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    Article Title: Evaluation of Renal Biomarkers, Including Symmetric Dimethylarginine, following Gentamicin-Induced Proximal Tubular Injury in the Rat
    Article Snippet: n C, KIM-1, NGAL, and OPN was measured. Urine biomarker results were normalized to uCr concentration. Urine cystatin C, µ ALB, and NGAL were measured using the Luminex (Fl-labeled beads) platform. Urine CLU was performed on a Biovendor ELISA (RD391034200CS; Asheville, NC). Testing of serum cystatin C was conducted using a Biovendor ELISA (RD391009200R). Urine KIM-1 and urine OPN were performed using R&D Systems ELISAs (RKM100 for KIM1 and MOST00 f



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    Thermo Fisher rat clusterin elisa kit #erclu
    Temporo-spatial evolution of prolonged <t>clusterin</t> immunoreactivity in the cortex, dentate gyrus, and thalamus ipsilateral to the injury. (A) A brightfield photomicrograph of a Nissl-stained coronal section from a rat perfused for immunohistochemistry at 1 month after TBI. The lesion core is indicated by an arrow. Dashed boxes indicate the brain regions with prominent clusterin immunoreactivity (ir) in layer IV of the ipsilateral cortex (Cx; panels B,E,H,K), molecular layer of the dentate gyrus (DG; panels C,F,I,L), and dorsal aspect of the thalamus (Th; panels D,G,J,M). Higher-power darkfield photomicrographs show that at 7 d post-TBI, punctate clusterin immunoreactivity (arrowheads) was prominently present in (B) layer IV of the perilesional cortex, (C) in the molecular layer of ipsilateral dentate gyrus, and faintly in (D) the ipsilateral dorsal thalamus. At 14 d post-TBI, (G) the thalamic immunostaining increased. Cortical (E,H) and hippocampal (F,I) staining persisted prominently for up to 1 month post-TBI, becoming substantially weaker by ( cortex K , hippocampus L) 12 months post-TBI. In contrast, (J,M) thalamic staining remained prominent from 1 month until 12 months post-TBI. No immunostaining was observed in the corresponding contralateral brain areas. Abbreviations: CA3, cornu Ammonis 3; d, days; DLG, dorsal lateral geniculate nucleus; G, granule cell layer of the dentate gyrus; H, hilus; LDVL, laterodorsal thalamic nucleus, ventrolateral part; M, molecular layer of the dentate gyrus; mo, months; Rt, reticular thalamic nucleus; TBI, traumatic brain injury; VPL, ventral posterolateral thalamic nucleus; VPM, ventral posteromedial thalamic nucleus. Scale bar equals 100 µm for all panels.
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    Temporo-spatial evolution of prolonged <t>clusterin</t> immunoreactivity in the cortex, dentate gyrus, and thalamus ipsilateral to the injury. (A) A brightfield photomicrograph of a Nissl-stained coronal section from a rat perfused for immunohistochemistry at 1 month after TBI. The lesion core is indicated by an arrow. Dashed boxes indicate the brain regions with prominent clusterin immunoreactivity (ir) in layer IV of the ipsilateral cortex (Cx; panels B,E,H,K), molecular layer of the dentate gyrus (DG; panels C,F,I,L), and dorsal aspect of the thalamus (Th; panels D,G,J,M). Higher-power darkfield photomicrographs show that at 7 d post-TBI, punctate clusterin immunoreactivity (arrowheads) was prominently present in (B) layer IV of the perilesional cortex, (C) in the molecular layer of ipsilateral dentate gyrus, and faintly in (D) the ipsilateral dorsal thalamus. At 14 d post-TBI, (G) the thalamic immunostaining increased. Cortical (E,H) and hippocampal (F,I) staining persisted prominently for up to 1 month post-TBI, becoming substantially weaker by ( cortex K , hippocampus L) 12 months post-TBI. In contrast, (J,M) thalamic staining remained prominent from 1 month until 12 months post-TBI. No immunostaining was observed in the corresponding contralateral brain areas. Abbreviations: CA3, cornu Ammonis 3; d, days; DLG, dorsal lateral geniculate nucleus; G, granule cell layer of the dentate gyrus; H, hilus; LDVL, laterodorsal thalamic nucleus, ventrolateral part; M, molecular layer of the dentate gyrus; mo, months; Rt, reticular thalamic nucleus; TBI, traumatic brain injury; VPL, ventral posterolateral thalamic nucleus; VPM, ventral posteromedial thalamic nucleus. Scale bar equals 100 µm for all panels.
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    BioVendor Instruments clusterin
    Overview of the Accepted Biomarkers for the Detection of Nephrotoxicity Including their Physiological Function, the Area of Toxicity Prediction, as well as Preclinical and Clinical Data Available
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    Image Search Results


    Temporo-spatial evolution of prolonged clusterin immunoreactivity in the cortex, dentate gyrus, and thalamus ipsilateral to the injury. (A) A brightfield photomicrograph of a Nissl-stained coronal section from a rat perfused for immunohistochemistry at 1 month after TBI. The lesion core is indicated by an arrow. Dashed boxes indicate the brain regions with prominent clusterin immunoreactivity (ir) in layer IV of the ipsilateral cortex (Cx; panels B,E,H,K), molecular layer of the dentate gyrus (DG; panels C,F,I,L), and dorsal aspect of the thalamus (Th; panels D,G,J,M). Higher-power darkfield photomicrographs show that at 7 d post-TBI, punctate clusterin immunoreactivity (arrowheads) was prominently present in (B) layer IV of the perilesional cortex, (C) in the molecular layer of ipsilateral dentate gyrus, and faintly in (D) the ipsilateral dorsal thalamus. At 14 d post-TBI, (G) the thalamic immunostaining increased. Cortical (E,H) and hippocampal (F,I) staining persisted prominently for up to 1 month post-TBI, becoming substantially weaker by ( cortex K , hippocampus L) 12 months post-TBI. In contrast, (J,M) thalamic staining remained prominent from 1 month until 12 months post-TBI. No immunostaining was observed in the corresponding contralateral brain areas. Abbreviations: CA3, cornu Ammonis 3; d, days; DLG, dorsal lateral geniculate nucleus; G, granule cell layer of the dentate gyrus; H, hilus; LDVL, laterodorsal thalamic nucleus, ventrolateral part; M, molecular layer of the dentate gyrus; mo, months; Rt, reticular thalamic nucleus; TBI, traumatic brain injury; VPL, ventral posterolateral thalamic nucleus; VPM, ventral posteromedial thalamic nucleus. Scale bar equals 100 µm for all panels.

    Journal: Scientific Reports

    Article Title: Dynamics of clusterin protein expression in the brain and plasma following experimental traumatic brain injury

    doi: 10.1038/s41598-019-56683-6

    Figure Lengend Snippet: Temporo-spatial evolution of prolonged clusterin immunoreactivity in the cortex, dentate gyrus, and thalamus ipsilateral to the injury. (A) A brightfield photomicrograph of a Nissl-stained coronal section from a rat perfused for immunohistochemistry at 1 month after TBI. The lesion core is indicated by an arrow. Dashed boxes indicate the brain regions with prominent clusterin immunoreactivity (ir) in layer IV of the ipsilateral cortex (Cx; panels B,E,H,K), molecular layer of the dentate gyrus (DG; panels C,F,I,L), and dorsal aspect of the thalamus (Th; panels D,G,J,M). Higher-power darkfield photomicrographs show that at 7 d post-TBI, punctate clusterin immunoreactivity (arrowheads) was prominently present in (B) layer IV of the perilesional cortex, (C) in the molecular layer of ipsilateral dentate gyrus, and faintly in (D) the ipsilateral dorsal thalamus. At 14 d post-TBI, (G) the thalamic immunostaining increased. Cortical (E,H) and hippocampal (F,I) staining persisted prominently for up to 1 month post-TBI, becoming substantially weaker by ( cortex K , hippocampus L) 12 months post-TBI. In contrast, (J,M) thalamic staining remained prominent from 1 month until 12 months post-TBI. No immunostaining was observed in the corresponding contralateral brain areas. Abbreviations: CA3, cornu Ammonis 3; d, days; DLG, dorsal lateral geniculate nucleus; G, granule cell layer of the dentate gyrus; H, hilus; LDVL, laterodorsal thalamic nucleus, ventrolateral part; M, molecular layer of the dentate gyrus; mo, months; Rt, reticular thalamic nucleus; TBI, traumatic brain injury; VPL, ventral posterolateral thalamic nucleus; VPM, ventral posteromedial thalamic nucleus. Scale bar equals 100 µm for all panels.

    Article Snippet: Duplicate samples from each rat and standards were analysed with the rat clusterin ELISA kit (#ERCLU, ThermoFisher Scientific), according to manufacturer’s instructions.

    Techniques: Staining, Immunohistochemistry, Immunostaining

    Post-TBI expression of clusterin is prominent in the extracellular space. Double-immunofluorescence revealed that in the perilesional cortex, ipsilateral dentate gyrus, and ipsilateral thalamus, clusterin-immunoreactivity did not colocalise with the (A–C) neuronal marker NeuN, (D–F) astrocyte marker GFAP, microglial markers (G–I) CD68 or (J–L) OX42, or (M–O) the mitochondrial marker MT-CO1. In the ipsilateral dorsal thalamus, robust clusterin immunoreactivity surrounded the cells labelled with microglial markers (I) CD68 and (L) OX42, and (O) mitochondria labelled with MT-CO1. All images were taken from rats perfused at 1 month post-TBI. Abbreviations: CD68, cluster of differentiation 68; Clu, clusterin; GFAP, glial fibrillary acidic protein; MT-CO1, mitochondrially encoded cytochrome c oxidase 1; NeuN, neuronal nuclei; OX42, antibody against CD11b/c; Scale bar = 50 µm for all panels.

    Journal: Scientific Reports

    Article Title: Dynamics of clusterin protein expression in the brain and plasma following experimental traumatic brain injury

    doi: 10.1038/s41598-019-56683-6

    Figure Lengend Snippet: Post-TBI expression of clusterin is prominent in the extracellular space. Double-immunofluorescence revealed that in the perilesional cortex, ipsilateral dentate gyrus, and ipsilateral thalamus, clusterin-immunoreactivity did not colocalise with the (A–C) neuronal marker NeuN, (D–F) astrocyte marker GFAP, microglial markers (G–I) CD68 or (J–L) OX42, or (M–O) the mitochondrial marker MT-CO1. In the ipsilateral dorsal thalamus, robust clusterin immunoreactivity surrounded the cells labelled with microglial markers (I) CD68 and (L) OX42, and (O) mitochondria labelled with MT-CO1. All images were taken from rats perfused at 1 month post-TBI. Abbreviations: CD68, cluster of differentiation 68; Clu, clusterin; GFAP, glial fibrillary acidic protein; MT-CO1, mitochondrially encoded cytochrome c oxidase 1; NeuN, neuronal nuclei; OX42, antibody against CD11b/c; Scale bar = 50 µm for all panels.

    Article Snippet: Duplicate samples from each rat and standards were analysed with the rat clusterin ELISA kit (#ERCLU, ThermoFisher Scientific), according to manufacturer’s instructions.

    Techniques: Expressing, Immunofluorescence, Marker

    Elevated Clu mRNA expression was observed in the brain at 3 months post-TBI. TaqMan RT-qPCR analysis revealed increased Clu mRNA expression in the (A) perilesional cortex (FC 3.3, p < 0.01) and (B) ipsilateral thalamus (FC 2.4, p < 0.05) of the rats at 3 months post-TBI as compared to sham-operated controls (n = 9 TBI, 6 sham; each dot in panels A-B refers to one animal). Clusterin Ct values were normalised to the housekeeping gene GAPDH. Statistical significances: *p < 0.05; **p < 0.01 (Mann-Whitney U test). Abbreviations: Clu, clusterin; Ct, cycle threshold; RT-qPCR, reverse transcription-quantitative polymerase chain reaction; sham, sham-operated controls.

    Journal: Scientific Reports

    Article Title: Dynamics of clusterin protein expression in the brain and plasma following experimental traumatic brain injury

    doi: 10.1038/s41598-019-56683-6

    Figure Lengend Snippet: Elevated Clu mRNA expression was observed in the brain at 3 months post-TBI. TaqMan RT-qPCR analysis revealed increased Clu mRNA expression in the (A) perilesional cortex (FC 3.3, p < 0.01) and (B) ipsilateral thalamus (FC 2.4, p < 0.05) of the rats at 3 months post-TBI as compared to sham-operated controls (n = 9 TBI, 6 sham; each dot in panels A-B refers to one animal). Clusterin Ct values were normalised to the housekeeping gene GAPDH. Statistical significances: *p < 0.05; **p < 0.01 (Mann-Whitney U test). Abbreviations: Clu, clusterin; Ct, cycle threshold; RT-qPCR, reverse transcription-quantitative polymerase chain reaction; sham, sham-operated controls.

    Article Snippet: Duplicate samples from each rat and standards were analysed with the rat clusterin ELISA kit (#ERCLU, ThermoFisher Scientific), according to manufacturer’s instructions.

    Techniques: Expressing, Quantitative RT-PCR, MANN-WHITNEY, Reverse Transcription, Real-time Polymerase Chain Reaction

    Acute reduction in plasma clusterin levels after TBI. ( A ) The dilution curve demonstrated linearity, indicating no significant matrix interference effect in the ELISA assay. (B) Clusterin levels in plasma derived from the cardiac puncture at very acute post-TBI time-points (<6 h, i.e ., 2 h-6 h post-TBI) were lower than that in controls (15%, p < 0.01) or that at 6 months post-TBI (21%, p < 0.01). At the other time-points, there was no difference between the TBI and control animals, or within the TBI groups. Moreover, at 6 months post-TBI, the plasma clusterin levels did not distinguish the rats with (open circles) or without (filled circles) spontaneous seizures (p > 0.05). (C) ROC analysis indicated that plasma clusterin levels sampled <6 h from TBI distinguished the animals with TBI from controls with an AUC of 0.851 (p < 0.05) and (D) from the 6 months post-TBI group with an AUC of 0.917 (p < 0.01). Statistical significances: **p < 0.01 compared with the control group; ##p < 0.01 compared to 6 months post-TBI (Mann-Whitney U test). Abbreviations: AUC, area under curve; C, controls; d, days; h, hours; mo, months; R 2 , coefficient of determination; wk, weeks.

    Journal: Scientific Reports

    Article Title: Dynamics of clusterin protein expression in the brain and plasma following experimental traumatic brain injury

    doi: 10.1038/s41598-019-56683-6

    Figure Lengend Snippet: Acute reduction in plasma clusterin levels after TBI. ( A ) The dilution curve demonstrated linearity, indicating no significant matrix interference effect in the ELISA assay. (B) Clusterin levels in plasma derived from the cardiac puncture at very acute post-TBI time-points (<6 h, i.e ., 2 h-6 h post-TBI) were lower than that in controls (15%, p < 0.01) or that at 6 months post-TBI (21%, p < 0.01). At the other time-points, there was no difference between the TBI and control animals, or within the TBI groups. Moreover, at 6 months post-TBI, the plasma clusterin levels did not distinguish the rats with (open circles) or without (filled circles) spontaneous seizures (p > 0.05). (C) ROC analysis indicated that plasma clusterin levels sampled <6 h from TBI distinguished the animals with TBI from controls with an AUC of 0.851 (p < 0.05) and (D) from the 6 months post-TBI group with an AUC of 0.917 (p < 0.01). Statistical significances: **p < 0.01 compared with the control group; ##p < 0.01 compared to 6 months post-TBI (Mann-Whitney U test). Abbreviations: AUC, area under curve; C, controls; d, days; h, hours; mo, months; R 2 , coefficient of determination; wk, weeks.

    Article Snippet: Duplicate samples from each rat and standards were analysed with the rat clusterin ELISA kit (#ERCLU, ThermoFisher Scientific), according to manufacturer’s instructions.

    Techniques: Clinical Proteomics, Enzyme-linked Immunosorbent Assay, Derivative Assay, Control, MANN-WHITNEY

    Study design for clusterin analysis in brain tissue, plasma, and CSF. Spatiotemporal expression of clusterin protein in the brain after TBI was investigated in cohorts 1–2. Chronic expression of clusterin mRNA in the brain was assessed using RT-qPCR in cohort 3. Post-TBI plasma clusterin levels were assessed using ELISA in cohorts 4–5. In cohort 5, 5 of the 16 TBI rats had epilepsy. Consequently, the study was powered to diagnose post-traumatic epilepsy in the TBI group if the AUC was ≥0.900. Finally, clusterin levels in CSF was analysed using iTRAQ proteomics in the chronic cohort 2. Abbreviations: CSF, cerebrospinal fluid; d, days; ELISA, enzyme-linked immunosorbent assay; h, hours; IHC, immunohistochemistry; iTRAQ, isobaric tag for relative and absolute quantification; RNA-Seq, RNA sequencing; RT-qPCR, reverse transcription-quantitative polymerase chain reaction; sham, sham-operated controls; TBI, traumatic brain injury.

    Journal: Scientific Reports

    Article Title: Dynamics of clusterin protein expression in the brain and plasma following experimental traumatic brain injury

    doi: 10.1038/s41598-019-56683-6

    Figure Lengend Snippet: Study design for clusterin analysis in brain tissue, plasma, and CSF. Spatiotemporal expression of clusterin protein in the brain after TBI was investigated in cohorts 1–2. Chronic expression of clusterin mRNA in the brain was assessed using RT-qPCR in cohort 3. Post-TBI plasma clusterin levels were assessed using ELISA in cohorts 4–5. In cohort 5, 5 of the 16 TBI rats had epilepsy. Consequently, the study was powered to diagnose post-traumatic epilepsy in the TBI group if the AUC was ≥0.900. Finally, clusterin levels in CSF was analysed using iTRAQ proteomics in the chronic cohort 2. Abbreviations: CSF, cerebrospinal fluid; d, days; ELISA, enzyme-linked immunosorbent assay; h, hours; IHC, immunohistochemistry; iTRAQ, isobaric tag for relative and absolute quantification; RNA-Seq, RNA sequencing; RT-qPCR, reverse transcription-quantitative polymerase chain reaction; sham, sham-operated controls; TBI, traumatic brain injury.

    Article Snippet: Duplicate samples from each rat and standards were analysed with the rat clusterin ELISA kit (#ERCLU, ThermoFisher Scientific), according to manufacturer’s instructions.

    Techniques: Clinical Proteomics, Expressing, Quantitative RT-PCR, Enzyme-linked Immunosorbent Assay, Multiplex sample analysis, Immunohistochemistry, Quantitative Proteomics, RNA Sequencing, Reverse Transcription, Real-time Polymerase Chain Reaction

    Overview of the Accepted Biomarkers for the Detection of Nephrotoxicity Including their Physiological Function, the Area of Toxicity Prediction, as well as Preclinical and Clinical Data Available

    Journal: The AAPS Journal

    Article Title: Biomarkers for Drug-Induced Renal Damage and Nephrotoxicity--An Overview for Applied Toxicology

    doi: 10.1208/s12248-011-9301-x

    Figure Lengend Snippet: Overview of the Accepted Biomarkers for the Detection of Nephrotoxicity Including their Physiological Function, the Area of Toxicity Prediction, as well as Preclinical and Clinical Data Available

    Article Snippet: For example, ELISAs for the most promising markers such as Kim-1 (e.g., Argutus Medical Ltd.) or Clusterin (BioVendor R&D) are available.

    Techniques: Marker, Filtration, Expressing

    The Current Status of the Originally Qualified Seven Urinary Protein Biomarkers and There Voluntary Usability in Clinical Trials Recommended by the ICH-Regulated Agencies

    Journal: The AAPS Journal

    Article Title: Biomarkers for Drug-Induced Renal Damage and Nephrotoxicity--An Overview for Applied Toxicology

    doi: 10.1208/s12248-011-9301-x

    Figure Lengend Snippet: The Current Status of the Originally Qualified Seven Urinary Protein Biomarkers and There Voluntary Usability in Clinical Trials Recommended by the ICH-Regulated Agencies

    Article Snippet: For example, ELISAs for the most promising markers such as Kim-1 (e.g., Argutus Medical Ltd.) or Clusterin (BioVendor R&D) are available.

    Techniques: Biomarker Assay

    Summary of Commercial Available Multiplex Assays Based on the Luminex® xMAP® Technology and the MULTI-Array® Technology from MesoScale Discovery®

    Journal: The AAPS Journal

    Article Title: Biomarkers for Drug-Induced Renal Damage and Nephrotoxicity--An Overview for Applied Toxicology

    doi: 10.1208/s12248-011-9301-x

    Figure Lengend Snippet: Summary of Commercial Available Multiplex Assays Based on the Luminex® xMAP® Technology and the MULTI-Array® Technology from MesoScale Discovery®

    Article Snippet: For example, ELISAs for the most promising markers such as Kim-1 (e.g., Argutus Medical Ltd.) or Clusterin (BioVendor R&D) are available.

    Techniques: Multiplex Assay, Luminex

    33 Genes Provided by Althea DX4 for the qPCR-Based Detection of Renal Insult in Rat

    Journal: The AAPS Journal

    Article Title: Biomarkers for Drug-Induced Renal Damage and Nephrotoxicity--An Overview for Applied Toxicology

    doi: 10.1208/s12248-011-9301-x

    Figure Lengend Snippet: 33 Genes Provided by Althea DX4 for the qPCR-Based Detection of Renal Insult in Rat

    Article Snippet: For example, ELISAs for the most promising markers such as Kim-1 (e.g., Argutus Medical Ltd.) or Clusterin (BioVendor R&D) are available.

    Techniques: Binding Assay

    84 Genes Specific for Rat, Provided by SABiosciences Corp. Provided qPCR Arrays Specific for Mouse or Human Can Include Different Genes (Not Shown)

    Journal: The AAPS Journal

    Article Title: Biomarkers for Drug-Induced Renal Damage and Nephrotoxicity--An Overview for Applied Toxicology

    doi: 10.1208/s12248-011-9301-x

    Figure Lengend Snippet: 84 Genes Specific for Rat, Provided by SABiosciences Corp. Provided qPCR Arrays Specific for Mouse or Human Can Include Different Genes (Not Shown)

    Article Snippet: For example, ELISAs for the most promising markers such as Kim-1 (e.g., Argutus Medical Ltd.) or Clusterin (BioVendor R&D) are available.

    Techniques: Activity Assay, Binding Assay, Marker