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  1. Article ; Online: Successful treatment of disseminated coccidioidomycosis with direct kidney allograft infection.

    Rosenstiel, Paul / Kapturczak, Matthias

    Nephrology (Carlton, Vic.)

    2023  Volume 28, Issue 3, Page(s) 208–209

    MeSH term(s) Humans ; Coccidioidomycosis/therapy ; Transplantation, Homologous ; Nephritis, Interstitial ; Pyelonephritis ; Allografts ; Kidney
    Language English
    Publishing date 2023-01-17
    Publishing country Australia
    Document type Letter
    ZDB-ID 1303661-0
    ISSN 1440-1797 ; 1320-5358
    ISSN (online) 1440-1797
    ISSN 1320-5358
    DOI 10.1111/nep.14141
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    Zs.A 4822: Show issues Location:
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  2. Article ; Online: Diagnosis of AApoAIV medullary amyloidosis at radical nephrectomy.

    Rosenstiel, Paul E / Alves, Tahira

    Kidney international

    2022  Volume 101, Issue 2, Page(s) 423

    MeSH term(s) Amyloidosis/diagnosis ; Humans ; Kidney Neoplasms/surgery ; Nephrectomy
    Language English
    Publishing date 2022-01-20
    Publishing country United States
    Document type Case Reports
    ZDB-ID 120573-0
    ISSN 1523-1755 ; 0085-2538
    ISSN (online) 1523-1755
    ISSN 0085-2538
    DOI 10.1016/j.kint.2021.06.016
    Database MEDical Literature Analysis and Retrieval System OnLINE

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  3. Article ; Online: A Patient Presenting with AKI, Proteinuria, and Anasarca.

    Rosenstiel, Paul / Luitel, Deepa / Luna, Maria

    Kidney360

    2023  Volume 4, Issue 2, Page(s) 287–288

    MeSH term(s) Humans ; Proteinuria ; Edema ; Acute Kidney Injury
    Language English
    Publishing date 2023-02-23
    Publishing country United States
    Document type Case Reports ; Journal Article
    ISSN 2641-7650
    ISSN (online) 2641-7650
    DOI 10.34067/KID.0000000000000034
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  4. Article ; Online: An Unusual Cause of Kidney Allograft Dysfunction.

    Rosenstiel, Paul E / Markowitz, Glen S / Amante, Brigani

    Kidney360

    2021  Volume 2, Issue 7, Page(s) 1207–1208

    MeSH term(s) Allografts ; Foscarnet ; Kidney/diagnostic imaging ; Transplantation, Homologous/adverse effects
    Chemical Substances Foscarnet (364P9RVW4X)
    Language English
    Publishing date 2021-07-29
    Publishing country United States
    Document type Journal Article
    ISSN 2641-7650
    ISSN (online) 2641-7650
    DOI 10.34067/KID.0001062021
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  5. Article: Development of antibiotic resistance in clinically relevant microorganisms in central Europe. Results of a longitudinal study of the Study Group "Bacterial Resistance" of the Paul-Ehrlich Society for Chemotherapy from the period of 1975-1995

    Kresken, M. / Hafner, D. / Rosenstiel, N. von

    Bundesgesundheitsblatt

    1999  

    Keywords Bacteria ; Pathogen ; Krankheitsbekaempfung ; Untersuchung ; Infektion ; Identifizierung ; Chemikalienresistenz ; Antibiotikum ; Risiko
    Language German
    Edition v. 42(1) p. 17-25
    Document type Article
    ISSN 0007-5914
    Database ELFIS - Nutrition, agriculture and forestry information system

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  6. Article ; Online: Loss of NOD2 in macrophages improves colitis and tumorigenesis in a lysozyme-dependent manner.

    Chauvin, Camille / Radulovic, Katarina / Boulard, Olivier / Delacre, Myriam / Waldschmitt, Nadine / Régnier, Paul / Legris, Gauthier / Bouchez, Clément / Sleimi, Mohamed-Yassine / Rosenstiel, Philip / Darrasse-Jèze, Guillaume / Chamaillard, Mathias / Poulin, Lionel F

    Frontiers in immunology

    2023  Volume 14, Page(s) 1252979

    Abstract: Background: Crohn's disease (CD) is a complex and poorly understood myeloid-mediated disorder. Genetic variants with loss of function in the : Methods: To ablate Nod2 specifically within the myeloid compartment, we generated : Results: Upon DSS ... ...

    Abstract Background: Crohn's disease (CD) is a complex and poorly understood myeloid-mediated disorder. Genetic variants with loss of function in the
    Methods: To ablate Nod2 specifically within the myeloid compartment, we generated
    Results: Upon DSS colitis model,
    Conclusion: Our results indicate that loss of Nod2 signaling in myeloid cells aids in the tissue repair of the inflamed large intestine through lysozyme secretion by myeloid cells. These results may pave the way to design new therapeutics to limit the inflammatory and tumorigenic functions of NOD2.
    MeSH term(s) Animals ; Mice ; Azoxymethane ; Colitis/chemically induced ; Colitis/genetics ; Colitis/metabolism ; Crohn Disease ; Macrophages/metabolism ; Muramidase/genetics ; Nod2 Signaling Adaptor Protein/genetics
    Chemical Substances Azoxymethane (MO0N1J0SEN) ; Muramidase (EC 3.2.1.17) ; Nod2 protein, mouse ; Nod2 Signaling Adaptor Protein
    Language English
    Publishing date 2023-10-09
    Publishing country Switzerland
    Document type Journal Article ; Research Support, Non-U.S. Gov't
    ZDB-ID 2606827-8
    ISSN 1664-3224 ; 1664-3224
    ISSN (online) 1664-3224
    ISSN 1664-3224
    DOI 10.3389/fimmu.2023.1252979
    Database MEDical Literature Analysis and Retrieval System OnLINE

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  7. Article ; Online: Adrenergic Signaling in Muscularis Macrophages Limits Infection-Induced Neuronal Loss.

    Matheis, Fanny / Muller, Paul A / Graves, Christina L / Gabanyi, Ilana / Kerner, Zachary J / Costa-Borges, Diego / Ahrends, Tomasz / Rosenstiel, Philip / Mucida, Daniel

    Cell

    2020  Volume 180, Issue 1, Page(s) 64–78.e16

    Abstract: Enteric-associated neurons (EANs) are closely associated with immune cells and continuously monitor and modulate homeostatic intestinal functions, including motility and nutrient sensing. Bidirectional interactions between neuronal and immune cells are ... ...

    Abstract Enteric-associated neurons (EANs) are closely associated with immune cells and continuously monitor and modulate homeostatic intestinal functions, including motility and nutrient sensing. Bidirectional interactions between neuronal and immune cells are altered during disease processes such as neurodegeneration or irritable bowel syndrome. We investigated the effects of infection-induced inflammation on intrinsic EANs (iEANs) and the role of intestinal muscularis macrophages (MMs) in this context. Using murine models of enteric infections, we observed long-term gastrointestinal symptoms, including reduced motility and loss of excitatory iEANs, which was mediated by a Nlrp6- and Casp11-dependent mechanism, depended on infection history, and could be reversed by manipulation of the microbiota. MMs responded to luminal infection by upregulating a neuroprotective program via β
    MeSH term(s) Adrenergic Agents ; Animals ; Arginase/metabolism ; Caspases, Initiator/immunology ; Caspases, Initiator/metabolism ; Enteric Nervous System/immunology ; Enteric Nervous System/metabolism ; Female ; Gastrointestinal Diseases ; Gastrointestinal Microbiome ; Infections ; Inflammation/immunology ; Intestinal Mucosa/immunology ; Intestinal Mucosa/metabolism ; Intestine, Small/immunology ; Intestines/immunology ; Macrophages/immunology ; Macrophages/metabolism ; Male ; Mice ; Mice, Inbred C57BL ; Microbiota ; Neurons/physiology ; Receptors, Adrenergic, beta-2/immunology ; Receptors, Adrenergic, beta-2/metabolism ; Receptors, Cell Surface/immunology ; Receptors, Cell Surface/metabolism ; Signal Transduction
    Chemical Substances Adrenergic Agents ; Nod-like receptor pyrin domain-containing protein 6, mouse ; Receptors, Adrenergic, beta-2 ; Receptors, Cell Surface ; Casp4 protein, mouse (EC 3.4.22.-) ; Caspases, Initiator (EC 3.4.22.-) ; Arg1 protein, mouse (EC 3.5.3.1) ; Arginase (EC 3.5.3.1)
    Language English
    Publishing date 2020-01-13
    Publishing country United States
    Document type Journal Article ; Research Support, N.I.H., Extramural ; Research Support, Non-U.S. Gov't
    ZDB-ID 187009-9
    ISSN 1097-4172 ; 0092-8674
    ISSN (online) 1097-4172
    ISSN 0092-8674
    DOI 10.1016/j.cell.2019.12.002
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    Zs.A 1167: Show issues Location:
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    Zs.MG 58: Show issues

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  8. Article ; Online: Endoplasmic reticulum stress in the intestinal epithelium initiates purine metabolite synthesis and promotes Th17 cell differentiation in the gut.

    Duan, Jinzhi / Matute, Juan D / Unger, Lukas W / Hanley, Thomas / Schnell, Alexandra / Lin, Xi / Krupka, Niklas / Griebel, Paul / Lambden, Conner / Sit, Brandon / Grootjans, Joep / Pyzik, Michal / Sommer, Felix / Kaiser, Sina / Falk-Paulsen, Maren / Grasberger, Helmut / Kao, John Y / Fuhrer, Tobias / Li, Hai /
    Paik, Donggi / Lee, Yunjin / Refetoff, Samuel / Glickman, Jonathan N / Paton, Adrienne W / Bry, Lynn / Paton, James C / Sauer, Uwe / Macpherson, Andrew J / Rosenstiel, Philip / Kuchroo, Vijay K / Waldor, Matthew K / Huh, Jun R / Kaser, Arthur / Blumberg, Richard S

    Immunity

    2023  Volume 56, Issue 5, Page(s) 1115–1131.e9

    Abstract: Intestinal IL-17-producing T helper (Th17) cells are dependent on adherent microbes in the gut for their development. However, how microbial adherence to intestinal epithelial cells (IECs) promotes Th17 cell differentiation remains enigmatic. Here, we ... ...

    Abstract Intestinal IL-17-producing T helper (Th17) cells are dependent on adherent microbes in the gut for their development. However, how microbial adherence to intestinal epithelial cells (IECs) promotes Th17 cell differentiation remains enigmatic. Here, we found that Th17 cell-inducing gut bacteria generated an unfolded protein response (UPR) in IECs. Furthermore, subtilase cytotoxin expression or genetic removal of X-box binding protein 1 (Xbp1) in IECs caused a UPR and increased Th17 cells, even in antibiotic-treated or germ-free conditions. Mechanistically, UPR activation in IECs enhanced their production of both reactive oxygen species (ROS) and purine metabolites. Treating mice with N-acetyl-cysteine or allopurinol to reduce ROS production and xanthine, respectively, decreased Th17 cells that were associated with an elevated UPR. Th17-related genes also correlated with ER stress and the UPR in humans with inflammatory bowel disease. Overall, we identify a mechanism of intestinal Th17 cell differentiation that emerges from an IEC-associated UPR.
    MeSH term(s) Endoplasmic Reticulum Stress/drug effects ; Intestinal Mucosa/drug effects ; Intestinal Mucosa/metabolism ; Th17 Cells/cytology ; Th17 Cells/metabolism ; Cell Differentiation ; Humans ; Animals ; Mice ; Mice, Transgenic ; Anti-Bacterial Agents/pharmacology
    Chemical Substances purine (W60KTZ3IZY) ; Anti-Bacterial Agents
    Language English
    Publishing date 2023-03-13
    Publishing country United States
    Document type Journal Article ; Research Support, N.I.H., Extramural ; Research Support, Non-U.S. Gov't
    ZDB-ID 1217235-2
    ISSN 1097-4180 ; 1074-7613
    ISSN (online) 1097-4180
    ISSN 1074-7613
    DOI 10.1016/j.immuni.2023.02.018
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    Zs.A 4227: Show issues Location:
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  9. Article ; Online: Longitudinal multi-omics analysis identifies early blood-based predictors of anti-TNF therapy response in inflammatory bowel disease.

    Mishra, Neha / Aden, Konrad / Blase, Johanna I / Baran, Nathan / Bordoni, Dora / Tran, Florian / Conrad, Claudio / Avalos, Diana / Jaeckel, Charlot / Scherer, Michael / Sørensen, Signe B / Overgaard, Silja H / Schulte, Berenice / Nikolaus, Susanna / Rey, Guillaume / Gasparoni, Gilles / Lyons, Paul A / Schultze, Joachim L / Walter, Jörn /
    Andersen, Vibeke / Dermitzakis, Emmanouil T / Schreiber, Stefan / Rosenstiel, Philip

    Genome medicine

    2022  Volume 14, Issue 1, Page(s) 110

    Abstract: Background and aims: Treatment with tumor necrosis factor α (TNFα) antagonists in IBD patients suffers from primary non-response rates of up to 40%. Biomarkers for early prediction of therapy success are missing. We investigated the dynamics of gene ... ...

    Abstract Background and aims: Treatment with tumor necrosis factor α (TNFα) antagonists in IBD patients suffers from primary non-response rates of up to 40%. Biomarkers for early prediction of therapy success are missing. We investigated the dynamics of gene expression and DNA methylation in blood samples of IBD patients treated with the TNF antagonist infliximab and analyzed the predictive potential regarding therapy outcome.
    Methods: We performed a longitudinal, blood-based multi-omics study in two prospective IBD patient cohorts receiving first-time infliximab therapy (discovery: 14 patients, replication: 23 patients). Samples were collected at up to 7 time points (from baseline to 14 weeks after therapy induction). RNA-sequencing and genome-wide DNA methylation data were analyzed and correlated with clinical remission at week 14 as a primary endpoint.
    Results: We found no consistent ex ante predictive signature across the two cohorts. Longitudinally upregulated transcripts in the non-remitter group comprised TH2- and eosinophil-related genes including ALOX15, FCER1A, and OLIG2. Network construction identified transcript modules that were coherently expressed at baseline and in non-remitting patients but were disrupted at early time points in remitting patients. These modules reflected processes such as interferon signaling, erythropoiesis, and platelet aggregation. DNA methylation analysis identified remission-specific temporal changes, which partially overlapped with transcriptomic signals. Machine learning approaches identified features from differentially expressed genes cis-linked to DNA methylation changes at week 2 as a robust predictor of therapy outcome at week 14, which was validated in a publicly available dataset of 20 infliximab-treated CD patients.
    Conclusions: Integrative multi-omics analysis reveals early shifts of gene expression and DNA methylation as predictors for efficient response to anti-TNF treatment. Lack of such signatures might be used to identify patients with IBD unlikely to benefit from TNF antagonists at an early time point.
    MeSH term(s) Biomarkers ; Humans ; Inflammatory Bowel Diseases/drug therapy ; Inflammatory Bowel Diseases/genetics ; Infliximab/therapeutic use ; Interferons/therapeutic use ; Prospective Studies ; RNA ; Tumor Necrosis Factor Inhibitors ; Tumor Necrosis Factor-alpha
    Chemical Substances Biomarkers ; Tumor Necrosis Factor Inhibitors ; Tumor Necrosis Factor-alpha ; RNA (63231-63-0) ; Interferons (9008-11-1) ; Infliximab (B72HH48FLU)
    Language English
    Publishing date 2022-09-24
    Publishing country England
    Document type Journal Article ; Research Support, Non-U.S. Gov't
    ZDB-ID 2484394-5
    ISSN 1756-994X ; 1756-994X
    ISSN (online) 1756-994X
    ISSN 1756-994X
    DOI 10.1186/s13073-022-01112-z
    Database MEDical Literature Analysis and Retrieval System OnLINE

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  10. Article ; Online: Predicting Post-Transplant Recurrence of IgA Nephropathy: The Importance of Crescents.

    Avasare, Rupali S / Rosenstiel, Paul E / Zaky, Ziad S / Tsapepas, Demetra S / Appel, Gerald B / Markowitz, Glen S / Bomback, Andrew S / Canetta, Pietro A

    American journal of nephrology

    2017  Volume 45, Issue 2, Page(s) 99–106

    Abstract: Background: Most studies that have assessed the predictors of recurrent IgA nephropathy (IgAN) in the renal allograft have focused on post-transplant features. Identifying high-risk pre-transplant features of IgAN is useful for counseling patients and ... ...

    Abstract Background: Most studies that have assessed the predictors of recurrent IgA nephropathy (IgAN) in the renal allograft have focused on post-transplant features. Identifying high-risk pre-transplant features of IgAN is useful for counseling patients and may help in tailoring post-transplant immunosuppression.
    Methods: We investigated the pre-transplant clinical and biopsy features of 62 patients with IgAN who received transplants at Columbia University Medical Center from 2001 to 2012 and compared the characteristics and outcomes of patients with IgAN recurrence to those without recurrence. The primary outcome was time to recurrent IgAN. Secondary outcomes were a composite of doubling of creatinine or allograft failure, and recurrent IgAN as a cause of allograft dysfunction.
    Results: Of the 62 patients, 14 had recurrent IgAN in the allograft. Mean time to recurrence was 2.75 years. Those with recurrent disease were younger at the time of native kidney biopsy (29 vs. 41 years, p < 0.0009). Black race and Hispanic ethnicity composed a higher proportion of the recurrent disease group. On multivariable analysis, significant predictors of recurrent IgAN included age at diagnosis (hazards ratio (HR) 0.911, 95% CI 0.85-0.98), burden of crescents on native biopsy (HR 1.21 per 10% increase in crescents, 95% CI 1.00-1.47) and allograft rejection (HR 3.59, 95% CI 1.10-11.7).
    Conclusions: Features of native IgAN can help predict the risk of recurrent disease in the renal allograft. In particular, immunologically active disease represented by earlier age of onset and greater burden of crescents on native biopsy is more likely to recur after transplant.
    Language English
    Publishing date 2017
    Publishing country Switzerland
    Document type Journal Article
    ZDB-ID 604540-6
    ISSN 1421-9670 ; 0250-8095
    ISSN (online) 1421-9670
    ISSN 0250-8095
    DOI 10.1159/000453081
    Database MEDical Literature Analysis and Retrieval System OnLINE

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