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urine albumin concentration  (Assaypro)


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    Assaypro urine albumin concentration
    Urine Albumin Concentration, supplied by Assaypro, used in various techniques. Bioz Stars score: 94/100, based on 55 PubMed citations. ZERO BIAS - scores, article reviews, protocol conditions and more
    https://www.bioz.com/result/urine albumin concentration/product/Assaypro
    Average 94 stars, based on 55 article reviews
    urine albumin concentration - by Bioz Stars, 2026-03
    94/100 stars

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    Fig. 5 In vivo therapeutic effects of Dex@NBs-TRPC6. (A) Schematic diagram of in vivo treatment and therapy protocol. Normal <t>mouse</t> without any treat ment was dedicated as control group. (B) Albuminuria <t>(urine</t> <t>albumin-to-creatinine</t> ratio) was determined in control group, ADR + NS group and three Dex-treated ADR groups. n = 9–10 mice per group. (C) Representative kidney images of PAS staining. Upper: glomerular morphology, scale bar = 20 μm; Lower: tubule-interstitial morphology, scale bar = 50 μm. (D) Quantitative analysis of glomerulosclerosis severity. (E) Quantitative analysis of tubular injury. (F) RT-PCR analysis of mRNA expression of Kim-1. (G) RT-PCR analysis of mRNA expression of NGAL. n = 9. (H) Representative images of TEM of glomerular basement membrane. Top: scale bar = 2 μm, Bottom: scale bar = 500 nm. (I) Quantitative analysis of foot process width. n = 6 mice per group in all histo logical analysis. (J) Upper: immunofluorescence staining of WT1 expressed in nuclei of mouse podocytes, scale bar = 20 μm. Lower: immunofluorescence staining of podocin expressed along the glomerular basement membrane, scale bar = 20 μm. (K) Quantitative analysis of WT1 positive cell numbers per glomerulus, n = 6. (L) Quantitative analysis of fluorescence intensity of podocin, n = 6. Data are presented as mean ± SEM, one-way ANOVA. *p < 0.05, **p < 0.01, vs. Control group, #p < 0.05, ##p < 0.01, vs. ADR + NS group, $p < 0.05, $$p < 0.01 as indicated
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    Fig. 5 In vivo therapeutic effects of Dex@NBs-TRPC6. (A) Schematic diagram of in vivo treatment and therapy protocol. Normal <t>mouse</t> without any treat ment was dedicated as control group. (B) Albuminuria <t>(urine</t> <t>albumin-to-creatinine</t> ratio) was determined in control group, ADR + NS group and three Dex-treated ADR groups. n = 9–10 mice per group. (C) Representative kidney images of PAS staining. Upper: glomerular morphology, scale bar = 20 μm; Lower: tubule-interstitial morphology, scale bar = 50 μm. (D) Quantitative analysis of glomerulosclerosis severity. (E) Quantitative analysis of tubular injury. (F) RT-PCR analysis of mRNA expression of Kim-1. (G) RT-PCR analysis of mRNA expression of NGAL. n = 9. (H) Representative images of TEM of glomerular basement membrane. Top: scale bar = 2 μm, Bottom: scale bar = 500 nm. (I) Quantitative analysis of foot process width. n = 6 mice per group in all histo logical analysis. (J) Upper: immunofluorescence staining of WT1 expressed in nuclei of mouse podocytes, scale bar = 20 μm. Lower: immunofluorescence staining of podocin expressed along the glomerular basement membrane, scale bar = 20 μm. (K) Quantitative analysis of WT1 positive cell numbers per glomerulus, n = 6. (L) Quantitative analysis of fluorescence intensity of podocin, n = 6. Data are presented as mean ± SEM, one-way ANOVA. *p < 0.05, **p < 0.01, vs. Control group, #p < 0.05, ##p < 0.01, vs. ADR + NS group, $p < 0.05, $$p < 0.01 as indicated
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    Fig. 5 In vivo therapeutic effects of Dex@NBs-TRPC6. (A) Schematic diagram of in vivo treatment and therapy protocol. Normal <t>mouse</t> without any treat ment was dedicated as control group. (B) Albuminuria <t>(urine</t> <t>albumin-to-creatinine</t> ratio) was determined in control group, ADR + NS group and three Dex-treated ADR groups. n = 9–10 mice per group. (C) Representative kidney images of PAS staining. Upper: glomerular morphology, scale bar = 20 μm; Lower: tubule-interstitial morphology, scale bar = 50 μm. (D) Quantitative analysis of glomerulosclerosis severity. (E) Quantitative analysis of tubular injury. (F) RT-PCR analysis of mRNA expression of Kim-1. (G) RT-PCR analysis of mRNA expression of NGAL. n = 9. (H) Representative images of TEM of glomerular basement membrane. Top: scale bar = 2 μm, Bottom: scale bar = 500 nm. (I) Quantitative analysis of foot process width. n = 6 mice per group in all histo logical analysis. (J) Upper: immunofluorescence staining of WT1 expressed in nuclei of mouse podocytes, scale bar = 20 μm. Lower: immunofluorescence staining of podocin expressed along the glomerular basement membrane, scale bar = 20 μm. (K) Quantitative analysis of WT1 positive cell numbers per glomerulus, n = 6. (L) Quantitative analysis of fluorescence intensity of podocin, n = 6. Data are presented as mean ± SEM, one-way ANOVA. *p < 0.05, **p < 0.01, vs. Control group, #p < 0.05, ##p < 0.01, vs. ADR + NS group, $p < 0.05, $$p < 0.01 as indicated
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    Fig. 5 In vivo therapeutic effects of Dex@NBs-TRPC6. (A) Schematic diagram of in vivo treatment and therapy protocol. Normal <t>mouse</t> without any treat ment was dedicated as control group. (B) Albuminuria <t>(urine</t> <t>albumin-to-creatinine</t> ratio) was determined in control group, ADR + NS group and three Dex-treated ADR groups. n = 9–10 mice per group. (C) Representative kidney images of PAS staining. Upper: glomerular morphology, scale bar = 20 μm; Lower: tubule-interstitial morphology, scale bar = 50 μm. (D) Quantitative analysis of glomerulosclerosis severity. (E) Quantitative analysis of tubular injury. (F) RT-PCR analysis of mRNA expression of Kim-1. (G) RT-PCR analysis of mRNA expression of NGAL. n = 9. (H) Representative images of TEM of glomerular basement membrane. Top: scale bar = 2 μm, Bottom: scale bar = 500 nm. (I) Quantitative analysis of foot process width. n = 6 mice per group in all histo logical analysis. (J) Upper: immunofluorescence staining of WT1 expressed in nuclei of mouse podocytes, scale bar = 20 μm. Lower: immunofluorescence staining of podocin expressed along the glomerular basement membrane, scale bar = 20 μm. (K) Quantitative analysis of WT1 positive cell numbers per glomerulus, n = 6. (L) Quantitative analysis of fluorescence intensity of podocin, n = 6. Data are presented as mean ± SEM, one-way ANOVA. *p < 0.05, **p < 0.01, vs. Control group, #p < 0.05, ##p < 0.01, vs. ADR + NS group, $p < 0.05, $$p < 0.01 as indicated
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    Fig. 5 In vivo therapeutic effects of Dex@NBs-TRPC6. (A) Schematic diagram of in vivo treatment and therapy protocol. Normal mouse without any treat ment was dedicated as control group. (B) Albuminuria (urine albumin-to-creatinine ratio) was determined in control group, ADR + NS group and three Dex-treated ADR groups. n = 9–10 mice per group. (C) Representative kidney images of PAS staining. Upper: glomerular morphology, scale bar = 20 μm; Lower: tubule-interstitial morphology, scale bar = 50 μm. (D) Quantitative analysis of glomerulosclerosis severity. (E) Quantitative analysis of tubular injury. (F) RT-PCR analysis of mRNA expression of Kim-1. (G) RT-PCR analysis of mRNA expression of NGAL. n = 9. (H) Representative images of TEM of glomerular basement membrane. Top: scale bar = 2 μm, Bottom: scale bar = 500 nm. (I) Quantitative analysis of foot process width. n = 6 mice per group in all histo logical analysis. (J) Upper: immunofluorescence staining of WT1 expressed in nuclei of mouse podocytes, scale bar = 20 μm. Lower: immunofluorescence staining of podocin expressed along the glomerular basement membrane, scale bar = 20 μm. (K) Quantitative analysis of WT1 positive cell numbers per glomerulus, n = 6. (L) Quantitative analysis of fluorescence intensity of podocin, n = 6. Data are presented as mean ± SEM, one-way ANOVA. *p < 0.05, **p < 0.01, vs. Control group, #p < 0.05, ##p < 0.01, vs. ADR + NS group, $p < 0.05, $$p < 0.01 as indicated

    Journal: Journal of nanobiotechnology

    Article Title: TRPC6-targeted dexamethasone nanobubbles with ultrasound-guided theranostics for adriamycin-induced nephropathy.

    doi: 10.1186/s12951-025-03487-8

    Figure Lengend Snippet: Fig. 5 In vivo therapeutic effects of Dex@NBs-TRPC6. (A) Schematic diagram of in vivo treatment and therapy protocol. Normal mouse without any treat ment was dedicated as control group. (B) Albuminuria (urine albumin-to-creatinine ratio) was determined in control group, ADR + NS group and three Dex-treated ADR groups. n = 9–10 mice per group. (C) Representative kidney images of PAS staining. Upper: glomerular morphology, scale bar = 20 μm; Lower: tubule-interstitial morphology, scale bar = 50 μm. (D) Quantitative analysis of glomerulosclerosis severity. (E) Quantitative analysis of tubular injury. (F) RT-PCR analysis of mRNA expression of Kim-1. (G) RT-PCR analysis of mRNA expression of NGAL. n = 9. (H) Representative images of TEM of glomerular basement membrane. Top: scale bar = 2 μm, Bottom: scale bar = 500 nm. (I) Quantitative analysis of foot process width. n = 6 mice per group in all histo logical analysis. (J) Upper: immunofluorescence staining of WT1 expressed in nuclei of mouse podocytes, scale bar = 20 μm. Lower: immunofluorescence staining of podocin expressed along the glomerular basement membrane, scale bar = 20 μm. (K) Quantitative analysis of WT1 positive cell numbers per glomerulus, n = 6. (L) Quantitative analysis of fluorescence intensity of podocin, n = 6. Data are presented as mean ± SEM, one-way ANOVA. *p < 0.05, **p < 0.01, vs. Control group, #p < 0.05, ##p < 0.01, vs. ADR + NS group, $p < 0.05, $$p < 0.01 as indicated

    Article Snippet: Mouse urine albumin concentration was measured using an ELISA kit (Bethyl Laboratories.

    Techniques: In Vivo, Control, Staining, Reverse Transcription Polymerase Chain Reaction, Expressing, Membrane, Immunofluorescence, Fluorescence