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  1. Article ; Online: Jump-Starting Kidney Research: Fostering Disruptive Innovation to Advance Nephrology.

    Norton, Jenna M / Star, Robert A

    Clinical journal of the American Society of Nephrology : CJASN

    2020  Volume 16, Issue 2, Page(s) 313–315

    MeSH term(s) Acute Kidney Injury/therapy ; Biomedical Research/economics ; Disruptive Technology ; Financing, Government ; Humans ; Intersectoral Collaboration ; National Institute of Diabetes and Digestive and Kidney Diseases (U.S.)/economics ; Nephrology ; Renal Insufficiency, Chronic/therapy ; United States
    Language English
    Publishing date 2020-08-10
    Publishing country United States
    Document type Journal Article
    ZDB-ID 2226665-3
    ISSN 1555-905X ; 1555-9041
    ISSN (online) 1555-905X
    ISSN 1555-9041
    DOI 10.2215/CJN.06570520
    Database MEDical Literature Analysis and Retrieval System OnLINE

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  2. Article ; Online: Enlightening kidney pathophysiology.

    Hewitt, Stephen M / Star, Robert A

    Nature materials

    2019  Volume 18, Issue 10, Page(s) 1034–1035

    MeSH term(s) Acute Kidney Injury/diagnosis ; Biomarkers/metabolism ; Drug-Related Side Effects and Adverse Reactions ; Early Diagnosis ; Humans ; Kidney/drug effects ; Kidney/physiopathology
    Chemical Substances Biomarkers
    Language English
    Publishing date 2019-11-08
    Publishing country England
    Document type News
    ZDB-ID 2088679-2
    ISSN 1476-4660 ; 1476-1122
    ISSN (online) 1476-4660
    ISSN 1476-1122
    DOI 10.1038/s41563-019-0490-5
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  3. Article ; Online: Opportunities for Research for COVID-19 in the Mission of NIDDK.

    Cefalu, William T / James, Stephen P / Star, Robert A

    Diabetes care

    2020  Volume 43, Issue 7, Page(s) 1435–1437

    Keywords covid19
    Language English
    Publishing date 2020-05-14
    Publishing country United States
    Document type Journal Article
    ZDB-ID 441231-x
    ISSN 1935-5548 ; 0149-5992
    ISSN (online) 1935-5548
    ISSN 0149-5992
    DOI 10.2337/dci20-0025
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  4. Article ; Online: BAM15 treats mouse sepsis and kidney injury, linking mortality, mitochondrial DNA, tubule damage, and neutrophils.

    Tsuji, Naoko / Tsuji, Takayuki / Yamashita, Tetsushi / Hayase, Naoki / Hu, Xuzhen / Yuen, Peter St / Star, Robert A

    The Journal of clinical investigation

    2023  Volume 133, Issue 7

    Abstract: Sepsis pathogenesis is complex and heterogeneous; hence, a precision-medicine strategy is needed. Acute kidney injury (AKI) following sepsis portends higher mortality. Overproduction of mitochondrial ROS (mtROS) is a potential mediator of sepsis and ... ...

    Abstract Sepsis pathogenesis is complex and heterogeneous; hence, a precision-medicine strategy is needed. Acute kidney injury (AKI) following sepsis portends higher mortality. Overproduction of mitochondrial ROS (mtROS) is a potential mediator of sepsis and sepsis-induced AKI. BAM15, a chemical uncoupler, dissipates mitochondrial proton gradients without generating mtROS. We injected BAM15 into mice at 0, 6, or 12 hours after cecal ligation and puncture (CLP), and these mice were treated with fluids and antibiotics. BAM15 reduced mortality, even after 12 hours, when mice were ill, and BAM15 reduced kidney damage and splenic apoptosis. Serial plasma and urinary mitochondrial DNA (mtDNA) levels increased after CLP and decreased after BAM15 administration (at 0 or 6 hours). In vitro septic serum proportionately increased mtROS overproduction and mtDNA release from kidney tubule cells, which BAM15 prevented. BAM15 decreased neutrophil apoptosis and mtDNA release; neutrophil depletion counteracted BAM15 benefits. Further, mtDNA injection in vivo replicated inflammation and kidney injury, which was prevented by BAM15. A large dose of exogenous mtDNA reversed protection by BAM15. We conclude that BAM15 is an effective preventive and therapeutic candidate in experimental sepsis and that BAM15 and mtDNA, a potential drug-companion diagnostic/drug-efficacy pair for clinical sepsis, are mechanistically linked via mtROS.
    MeSH term(s) Mice ; Animals ; DNA, Mitochondrial/genetics ; Neutrophils/pathology ; Kidney/pathology ; Acute Kidney Injury/pathology ; Sepsis/genetics ; Mice, Inbred C57BL
    Chemical Substances DNA, Mitochondrial
    Language English
    Publishing date 2023-04-03
    Publishing country United States
    Document type Journal Article ; Research Support, N.I.H., Intramural ; Research Support, Non-U.S. Gov't
    ZDB-ID 3067-3
    ISSN 1558-8238 ; 0021-9738
    ISSN (online) 1558-8238
    ISSN 0021-9738
    DOI 10.1172/JCI152401
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  5. Article ; Online: The Application of Guanidinium to Improve Biomolecule Quality in Fixed, Paraffin-embedded Tissue.

    Chung, Joon-Yong / Kim, Kyungeun / Ylaya, Kris / Walker-Bawa, Katharine E / Perry, Candice / Star, Robert A / Hewitt, Stephen M

    The journal of histochemistry and cytochemistry : official journal of the Histochemistry Society

    2023  Volume 71, Issue 2, Page(s) 87–101

    Abstract: Neutral buffered formalin (NBF) is the most common fixative in clinical applications. However, NBF damages proteins and nucleic acids, limiting the quality of proteomic and nucleic acid-based assays. Prior studies have demonstrated that BE70, a fixative ... ...

    Abstract Neutral buffered formalin (NBF) is the most common fixative in clinical applications. However, NBF damages proteins and nucleic acids, limiting the quality of proteomic and nucleic acid-based assays. Prior studies have demonstrated that BE70, a fixative of buffered 70% ethanol, has many benefits over NBF but the degradation of proteins and nucleic acids in archival paraffin blocks remain a challenge. Thus, we evaluated the addition of guanidinium salts to BE70 with the hypothesis that this may protect RNA and protein. Guanidinium salt supplemented BE70 (BE70G)-fixed tissue is comparable with that of BE70 via histology and immunohistochemistry. Western blot analysis also revealed that HSP70, AKT, and glyceraldehyde 3-phosphate dehydrogenase (GAPDH) expression signals in BE70G-fixed tissue were higher than those in BE70-fixed tissue. The quality of nucleic acids extracted from BE70G-fixed, paraffin-embedded tissue was also superior, and BE70G provides improved protein and RNA quality at shorter fixation times than its predecessors. The degradation of proteins, AKT and GAPDH, in archival tissue blocks is also decreased with the addition of guanidinium salt to BE70. In conclusion, BE70G fixative improves the quality of molecular analysis with more rapid fixation of tissue and enhanced long-term storage of paraffin blocks at room temperature for evaluation of protein epitopes.
    MeSH term(s) Fixatives ; Guanidine ; Proteomics ; Paraffin Embedding ; Paraffin ; Proto-Oncogene Proteins c-akt ; Formaldehyde ; RNA/analysis ; Nucleic Acids ; Tissue Fixation
    Chemical Substances Fixatives ; Guanidine (JU58VJ6Y3B) ; Paraffin (8002-74-2) ; Proto-Oncogene Proteins c-akt (EC 2.7.11.1) ; Formaldehyde (1HG84L3525) ; RNA (63231-63-0) ; Nucleic Acids
    Language English
    Publishing date 2023-03-04
    Publishing country United States
    Document type Journal Article ; Research Support, N.I.H., Intramural
    ZDB-ID 218208-7
    ISSN 1551-5044 ; 0022-1554
    ISSN (online) 1551-5044
    ISSN 0022-1554
    DOI 10.1369/00221554231159451
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  7. Article ; Online: Gut Leakage of Fungal-Derived Inflammatory Mediators: Part of a Gut-Liver-Kidney Axis in Bacterial Sepsis.

    Amornphimoltham, Panomwat / Yuen, Peter S T / Star, Robert A / Leelahavanichkul, Asada

    Digestive diseases and sciences

    2019  Volume 64, Issue 9, Page(s) 2416–2428

    Abstract: Sepsis is a life-threatening response to systemic infection. In addition to frank gastrointestinal (GI) rupture/puncture, sepsis can also be exacerbated by translocation of pathogen-associated molecular patterns (PAMPs) from the GI tract to the systemic ... ...

    Abstract Sepsis is a life-threatening response to systemic infection. In addition to frank gastrointestinal (GI) rupture/puncture, sepsis can also be exacerbated by translocation of pathogen-associated molecular patterns (PAMPs) from the GI tract to the systemic circulation (gut origin of sepsis). In the human gut, Gram-negative bacteria and Candida albicans are abundant, along with their major PAMP components, endotoxin (LPS) and (1 → 3)-β-D-glucan (BG). Whereas the influence of LPS in bacterial sepsis has been studied extensively, exploration of the role of BG in bacterial sepsis is limited. Post-translocation, PAMPs enter the circulation through lymphatics and the portal vein, and are detoxified and then excreted via the liver and the kidney. Sepsis-induced liver and kidney injury might therefore affect the kinetics and increase circulating PAMPs. In this article, we discuss the current knowledge of the impact of PAMPs from both gut mycobiota and microbiota, including epithelial barrier function and the "gut-liver-kidney axis," on bacterial sepsis severity.
    MeSH term(s) Animals ; Bacterial Infections/metabolism ; Candida/metabolism ; Gastrointestinal Tract/microbiology ; Humans ; Intestinal Mucosa/metabolism ; Intestinal Mucosa/microbiology ; Kidney/metabolism ; Lipopolysaccharides/blood ; Lipopolysaccharides/metabolism ; Liver/metabolism ; Pathogen-Associated Molecular Pattern Molecules/metabolism ; Sepsis/immunology ; Sepsis/metabolism ; Sepsis/microbiology ; beta-Glucans/blood ; beta-Glucans/metabolism
    Chemical Substances Lipopolysaccharides ; Pathogen-Associated Molecular Pattern Molecules ; beta-Glucans ; polysaccharide-K (3X48A86C8K)
    Language English
    Publishing date 2019-03-13
    Publishing country United States
    Document type Journal Article ; Research Support, Non-U.S. Gov't ; Review
    ZDB-ID 304250-9
    ISSN 1573-2568 ; 0163-2116
    ISSN (online) 1573-2568
    ISSN 0163-2116
    DOI 10.1007/s10620-019-05581-y
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  8. Article ; Online: How Community Engagement Is Enhancing NIDDK Research.

    Kimmel, Paul L / Jefferson, Nichole / Norton, Jenna M / Star, Robert A

    Clinical journal of the American Society of Nephrology : CJASN

    2019  Volume 14, Issue 5, Page(s) 768–770

    MeSH term(s) Apolipoprotein L1/genetics ; Biomedical Research ; Humans ; National Institute of Diabetes and Digestive and Kidney Diseases (U.S.) ; Nephrology ; Precision Medicine ; Residence Characteristics ; United States
    Chemical Substances Apolipoprotein L1
    Language English
    Publishing date 2019-03-27
    Publishing country United States
    Document type Journal Article
    ZDB-ID 2226665-3
    ISSN 1555-905X ; 1555-9041
    ISSN (online) 1555-905X
    ISSN 1555-9041
    DOI 10.2215/CJN.14591218
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  9. Article: Macrophage Depletion Protects Against Cisplatin-Induced Ototoxicity and Nephrotoxicity.

    Sung, Cathy Yea Won / Hayase, Naoki / Yuen, Peter S T / Lee, John / Fernandez, Katharine / Hu, Xuzhen / Cheng, Hui / Star, Robert A / Warchol, Mark E / Cunningham, Lisa L

    bioRxiv : the preprint server for biology

    2023  

    Abstract: Cisplatin is a widely used and highly effective anti-cancer drug with significant side effects including ototoxicity and nephrotoxicity. Macrophages, the major resident immune cells in the cochlea and kidney, are important drivers of both inflammatory ... ...

    Abstract Cisplatin is a widely used and highly effective anti-cancer drug with significant side effects including ototoxicity and nephrotoxicity. Macrophages, the major resident immune cells in the cochlea and kidney, are important drivers of both inflammatory and tissue repair responses. To investigate the roles of macrophages in cisplatin-induced ototoxicity and nephrotoxicity, we used PLX3397, an FDA-approved inhibitor of the colony-stimulating factor 1 receptor (CSF1R), to eliminate tissue-resident macrophages during the course of cisplatin administration. Mice treated with cisplatin alone (cisplatin/vehicle) had significant hearing loss (ototoxicity) as well as kidney injury (nephrotoxicity). Macrophage ablation using PLX3397 resulted in significantly reduced hearing loss measured by auditory brainstem responses (ABR) and distortion-product otoacoustic emissions (DPOAE). Sensory hair cells in the cochlea were protected against cisplatin-induced death in mice treated with PLX3397. Macrophage ablation also protected against cisplatin-induced nephrotoxicity, as evidenced by markedly reduced tubular injury and fibrosis as well as reduced plasma blood urea nitrogen (BUN) and neutrophil gelatinase-associated lipocalin (NGAL) levels. Mechanistically, our data suggest that the protective effect of macrophage ablation against cisplatin-induced ototoxicity and nephrotoxicity is mediated by reduced platinum accumulation in both the inner ear and the kidney. Together our data indicate that ablation of tissue-resident macrophages represents a novel strategy for mitigating cisplatin-induced ototoxicity and nephrotoxicity.
    Language English
    Publishing date 2023-11-17
    Publishing country United States
    Document type Preprint
    DOI 10.1101/2023.11.16.567274
    Database MEDical Literature Analysis and Retrieval System OnLINE

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  10. Article ; Online: Readmission and Mortality After Hospitalization With Acute Kidney Injury.

    Schulman, Ivonne H / Chan, Kevin / Der, Jane S / Wilkins, Kenneth J / Corns, Helen L / Sayer, Bryan / Ngo, Duc Anh / Eggers, Paul / Norton, Jenna / Shah, Neha / Mendley, Susan / Parsa, Afshin / Star, Robert A / Kimmel, Paul L

    American journal of kidney diseases : the official journal of the National Kidney Foundation

    2023  Volume 82, Issue 1, Page(s) 63–74.e1

    Abstract: Rationale & objective: Acute kidney injury (AKI) carries high rates of morbidity and mortality. This study quantified various short- and long-term outcomes after hospitalization with AKI.: Study design: Retrospective propensity score (PS)-matched ... ...

    Abstract Rationale & objective: Acute kidney injury (AKI) carries high rates of morbidity and mortality. This study quantified various short- and long-term outcomes after hospitalization with AKI.
    Study design: Retrospective propensity score (PS)-matched cohort study.
    Setting & participants: Optum Clinformatics, a national claims database, was used to identify patients hospitalized with and without an AKI discharge diagnosis between January 2007 and September 2020.
    Exposure: Among patients with prior continuous enrollment for at least 2years without AKI hospitalization, 471,176 patients hospitalized with AKI were identified and PS-matched to 471,176 patients hospitalized without AKI.
    Outcome(s): All-cause and selected-cause rehospitalizations and mortality 90 and 365 days after index hospitalization.
    Analytical approach: After PS matching, rehospitalization and death incidences were estimated using the cumulative incidence function method and compared using Gray's test. The association of AKI hospitalization with each outcome was tested using Cox models for all-cause mortality and, with mortality as competing risk, cause-specific hazard modeling for all-cause and selected-cause rehospitalization. Overall and stratified analyses were performed to evaluate for interaction between an AKI hospitalization and preexisting chronic kidney disease (CKD).
    Results: After PS matching, AKI was associated with higher rates of rehospitalization for any cause (hazard ratio [HR], 1.62; 95% CI, 1.60-1.65), end-stage renal disease (HR, 6.21; 95% CI, 1.04-36.92), heart failure (HR, 2.81; 95% CI, 2.66, 2.97), sepsis (HR, 2.62; 95% CI, 2.49-2.75), pneumonia (HR, 1.47; 95% CI, 1.37-1.57), myocardial infarction (HR, 1.48; 95% CI, 1.33-1.65), and volume depletion (HR, 1.64; 95% CI, 1.37-1.96) at 90 days after discharge compared with the group without AKI, with similar findings at 365 days. Mortality rate was higher in the group with AKI than in the group without AKI at 90 (HR, 2.66; 95% CI, 2.61-2.72) and 365 days (HR, 2.11; 95% CI, 2.08-2.14). The higher risk of outcomes persisted when participants were stratified by CKD status (P<0.01).
    Limitations: Causal associations between AKI and the reported outcomes cannot be inferred.
    Conclusions: AKI during hospitalization in patients with and without CKD is associated with increased risk of 90- and 365-day all-cause/selected-cause rehospitalization and death.
    MeSH term(s) Humans ; Patient Readmission ; Cohort Studies ; Retrospective Studies ; Hospitalization ; Renal Insufficiency, Chronic/epidemiology ; Acute Kidney Injury/diagnosis ; Risk Factors
    Language English
    Publishing date 2023-04-27
    Publishing country United States
    Document type Journal Article ; Research Support, N.I.H., Intramural
    ZDB-ID 604539-x
    ISSN 1523-6838 ; 0272-6386
    ISSN (online) 1523-6838
    ISSN 0272-6386
    DOI 10.1053/j.ajkd.2022.12.008
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