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software nis-elementary ts br 3.2  (Nikon)

 
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    Nikon software nis-elementary ts br 3.2
    Biopsy findings of three cases
    Software Nis Elementary Ts Br 3.2, supplied by Nikon, 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/result/software nis-elementary ts br 3.2/product/Nikon
    Average 90 stars, based on 1 article reviews
    software nis-elementary ts br 3.2 - by Bioz Stars, 2026-04
    90/100 stars

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    1) Product Images from "Early graft loss due to acute thrombotic microangiopathy accompanied by complement gene variants in living-related kidney transplantation: case series report"

    Article Title: Early graft loss due to acute thrombotic microangiopathy accompanied by complement gene variants in living-related kidney transplantation: case series report

    Journal: BMC Nephrology

    doi: 10.1186/s12882-022-02868-7

    Biopsy findings of three cases
    Figure Legend Snippet: Biopsy findings of three cases

    Techniques Used: Biomarker Discovery

    Hypothesis based on our case series: both recipients and donors carried the complement genetic abnormality, contributing to the continuous injury of endothelial cells and leading to early graft loss after activation of TMA by triggers in our case series. Advice for these patients: (1) before transplantation, recipients with kidney disease of unknown etiology may consider complement genetic testing. A deceased donor kidney transplant should be recommended if testing reveals complement genetic variant in both donor and recipient; (2) after transplantation, intensive monitoring and timely treatment of triggers are critical. Besides, surveillance allograft biopsy, more testing, and exome sequence may help to diagnosis; (3) since diagnosis of post-transplant TMA, early anti-complement treatment is necessary. LKT, living-relative kidney disease; DD, deceased donor; ABMR, antibody-mediated rejection; CNIs, calcineurin inhibitors; TMA, thrombotic microangiopathy; LDH, lactic dehydrogenase; PE, plasma exchange
    Figure Legend Snippet: Hypothesis based on our case series: both recipients and donors carried the complement genetic abnormality, contributing to the continuous injury of endothelial cells and leading to early graft loss after activation of TMA by triggers in our case series. Advice for these patients: (1) before transplantation, recipients with kidney disease of unknown etiology may consider complement genetic testing. A deceased donor kidney transplant should be recommended if testing reveals complement genetic variant in both donor and recipient; (2) after transplantation, intensive monitoring and timely treatment of triggers are critical. Besides, surveillance allograft biopsy, more testing, and exome sequence may help to diagnosis; (3) since diagnosis of post-transplant TMA, early anti-complement treatment is necessary. LKT, living-relative kidney disease; DD, deceased donor; ABMR, antibody-mediated rejection; CNIs, calcineurin inhibitors; TMA, thrombotic microangiopathy; LDH, lactic dehydrogenase; PE, plasma exchange

    Techniques Used: Activation Assay, Transplantation Assay, Variant Assay, Sequencing, Biomarker Discovery, Clinical Proteomics



    Similar Products

    software nis-elementary ts br 3.2  (Nikon)
    90
    Nikon software nis-elementary ts br 3.2
    Biopsy findings of three cases
    Software Nis Elementary Ts Br 3.2, supplied by Nikon, 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/result/software nis-elementary ts br 3.2/product/Nikon
    Average 90 stars, based on 1 article reviews
    software nis-elementary ts br 3.2 - by Bioz Stars, 2026-04
    90/100 stars
    		  Buy from Supplier

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    Biopsy findings of three cases

    Journal: BMC Nephrology

    Article Title: Early graft loss due to acute thrombotic microangiopathy accompanied by complement gene variants in living-related kidney transplantation: case series report

    doi: 10.1186/s12882-022-02868-7

    Figure Lengend Snippet: Biopsy findings of three cases

    Article Snippet: Light microscopy (equipment, Nikon ECLIPSE 80i; software, NIS-Elementary TS BR 3.2) on transplant biopsy revealed glomerulitis, acute tubulointerstitial nephritis (ATIN), and typical TMA.

    Techniques: Biomarker Discovery

    Hypothesis based on our case series: both recipients and donors carried the complement genetic abnormality, contributing to the continuous injury of endothelial cells and leading to early graft loss after activation of TMA by triggers in our case series. Advice for these patients: (1) before transplantation, recipients with kidney disease of unknown etiology may consider complement genetic testing. A deceased donor kidney transplant should be recommended if testing reveals complement genetic variant in both donor and recipient; (2) after transplantation, intensive monitoring and timely treatment of triggers are critical. Besides, surveillance allograft biopsy, more testing, and exome sequence may help to diagnosis; (3) since diagnosis of post-transplant TMA, early anti-complement treatment is necessary. LKT, living-relative kidney disease; DD, deceased donor; ABMR, antibody-mediated rejection; CNIs, calcineurin inhibitors; TMA, thrombotic microangiopathy; LDH, lactic dehydrogenase; PE, plasma exchange

    Journal: BMC Nephrology

    Article Title: Early graft loss due to acute thrombotic microangiopathy accompanied by complement gene variants in living-related kidney transplantation: case series report

    doi: 10.1186/s12882-022-02868-7

    Figure Lengend Snippet: Hypothesis based on our case series: both recipients and donors carried the complement genetic abnormality, contributing to the continuous injury of endothelial cells and leading to early graft loss after activation of TMA by triggers in our case series. Advice for these patients: (1) before transplantation, recipients with kidney disease of unknown etiology may consider complement genetic testing. A deceased donor kidney transplant should be recommended if testing reveals complement genetic variant in both donor and recipient; (2) after transplantation, intensive monitoring and timely treatment of triggers are critical. Besides, surveillance allograft biopsy, more testing, and exome sequence may help to diagnosis; (3) since diagnosis of post-transplant TMA, early anti-complement treatment is necessary. LKT, living-relative kidney disease; DD, deceased donor; ABMR, antibody-mediated rejection; CNIs, calcineurin inhibitors; TMA, thrombotic microangiopathy; LDH, lactic dehydrogenase; PE, plasma exchange

    Article Snippet: Light microscopy (equipment, Nikon ECLIPSE 80i; software, NIS-Elementary TS BR 3.2) on transplant biopsy revealed glomerulitis, acute tubulointerstitial nephritis (ATIN), and typical TMA.

    Techniques: Activation Assay, Transplantation Assay, Variant Assay, Sequencing, Biomarker Discovery, Clinical Proteomics