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Atypical Hemolytic Uremic Syndrome Recurrence after Renal Transplantation: C3-Glomerulonephritis as an Initial Presentation.

Transplantation direct

Bouatou Y, Bacchi VF, Villard J, Moll S, Martin PY, Hadaya K.
PMID: 27500215
Transplant Direct. 2015 Mar 26;1(2):e9. doi: 10.1097/TXD.0000000000000518. eCollection 2015 Mar.

Risk for atypical hemolytic uremic syndrome (aHUS) recurrence after renal transplantation is low with an isolated membrane cofactor protein mutation (MCP). We report the case of a 32-year-old woman with a MCP who underwent kidney transplantation with a good...

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Bouatou Y, Bacchi VF, Villard J, et al. Atypical Hemolytic Uremic Syndrome Recurrence after Renal Transplantation: C3-Glomerulonephritis as an Initial Presentation. Transplant Direct. 2015;1(2):e9doi: 10.1097/TXD.0000000000000518.
Bouatou, Y., Bacchi, V. F., Villard, J., Moll, S., Martin, P. Y., & Hadaya, K. (2015). Atypical Hemolytic Uremic Syndrome Recurrence after Renal Transplantation: C3-Glomerulonephritis as an Initial Presentation. Transplantation direct, 1(2), e9. https://doi.org/10.1097/TXD.0000000000000518
Bouatou, Yassine, et al. "Atypical Hemolytic Uremic Syndrome Recurrence after Renal Transplantation: C3-Glomerulonephritis as an Initial Presentation." Transplantation direct vol. 1,2 (2015): e9. doi: https://doi.org/10.1097/TXD.0000000000000518
Bouatou Y, Bacchi VF, Villard J, Moll S, Martin PY, Hadaya K. Atypical Hemolytic Uremic Syndrome Recurrence after Renal Transplantation: C3-Glomerulonephritis as an Initial Presentation. Transplant Direct. 2015 Mar 26;1(2):e9. doi: 10.1097/TXD.0000000000000518. eCollection 2015 Mar. PMID: 27500215; PMCID: PMC4946455.
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Factor H-Related (FHR)-1 and FHR-2 Form Homo- and Heterodimers, while FHR-5 Circulates Only As Homodimer in Human Plasma.

Frontiers in immunology

van Beek AE, Pouw RB, Brouwer MC, van Mierlo G, Geissler J, Ooijevaar-de Heer P, de Boer M, van Leeuwen K, Rispens T, Wouters D, Kuijpers TW.
PMID: 29093712
Front Immunol. 2017 Oct 18;8:1328. doi: 10.3389/fimmu.2017.01328. eCollection 2017.

The complement factor H-related (FHR) proteins are hypothesized to fine-tune the regulatory role of complement factor H (FH) in the alternative pathway of the complement system. Moreover, FHR-1, FHR-2, and FHR-5 have been proposed to be dimers, which further...

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van Beek AE, Pouw RB, Brouwer MC, et al. Factor H-Related (FHR)-1 and FHR-2 Form Homo- and Heterodimers, while FHR-5 Circulates Only As Homodimer in Human Plasma. Front Immunol. 2017;8:1328doi: 10.3389/fimmu.2017.01328.
van Beek, A. E., Pouw, R. B., Brouwer, M. C., van Mierlo, G., Geissler, J., Ooijevaar-de Heer, P., de Boer, M., van Leeuwen, K., Rispens, T., Wouters, D., & Kuijpers, T. W. (2017). Factor H-Related (FHR)-1 and FHR-2 Form Homo- and Heterodimers, while FHR-5 Circulates Only As Homodimer in Human Plasma. Frontiers in immunology, 81328. https://doi.org/10.3389/fimmu.2017.01328
van Beek, Anna E, et al. "Factor H-Related (FHR)-1 and FHR-2 Form Homo- and Heterodimers, while FHR-5 Circulates Only As Homodimer in Human Plasma." Frontiers in immunology vol. 8 (2017): 1328. doi: https://doi.org/10.3389/fimmu.2017.01328
van Beek AE, Pouw RB, Brouwer MC, van Mierlo G, Geissler J, Ooijevaar-de Heer P, de Boer M, van Leeuwen K, Rispens T, Wouters D, Kuijpers TW. Factor H-Related (FHR)-1 and FHR-2 Form Homo- and Heterodimers, while FHR-5 Circulates Only As Homodimer in Human Plasma. Front Immunol. 2017 Oct 18;8:1328. doi: 10.3389/fimmu.2017.01328. eCollection 2017. PMID: 29093712; PMCID: PMC5651247.
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A case of adult atypical haemolytic uraemic syndrome related to anti-factor H autoantibodies successfully treated by plasma exchange, corticosteroids and rituximab.

NDT plus

Lionet A, Provôt F, Glowacki F, Frémeaux-Bacchi V, Hazzan M.
PMID: 25984036
NDT Plus. 2009 Dec;2(6):458-60. doi: 10.1093/ndtplus/sfp109. Epub 2009 Aug 18.

Complement factor H auto-antibodies (CFH-ab) are a rare cause (6-10%) of atypical haemolytic uraemic syndrome (aHUS). All observations previously described were retrospective and occurred in children or teenagers. We report the first case of aHUS associated with anti-CFH antibodies...

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Lionet A, Provôt F, Glowacki F, et al. A case of adult atypical haemolytic uraemic syndrome related to anti-factor H autoantibodies successfully treated by plasma exchange, corticosteroids and rituximab. NDT Plus. 2009;2(6):458-60doi: 10.1093/ndtplus/sfp109.
Lionet, A., Provôt, F., Glowacki, F., Frémeaux-Bacchi, V., & Hazzan, M. (2009). A case of adult atypical haemolytic uraemic syndrome related to anti-factor H autoantibodies successfully treated by plasma exchange, corticosteroids and rituximab. NDT plus, 2(6), 458-60. https://doi.org/10.1093/ndtplus/sfp109
Lionet, Arnaud, et al. "A case of adult atypical haemolytic uraemic syndrome related to anti-factor H autoantibodies successfully treated by plasma exchange, corticosteroids and rituximab." NDT plus vol. 2,6 (2009): 458-60. doi: https://doi.org/10.1093/ndtplus/sfp109
Lionet A, Provôt F, Glowacki F, Frémeaux-Bacchi V, Hazzan M. A case of adult atypical haemolytic uraemic syndrome related to anti-factor H autoantibodies successfully treated by plasma exchange, corticosteroids and rituximab. NDT Plus. 2009 Dec;2(6):458-60. doi: 10.1093/ndtplus/sfp109. Epub 2009 Aug 18. PMID: 25984036; PMCID: PMC4421306.
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HTRA1 in Age-Related Macular Degeneration.

Asia-Pacific journal of ophthalmology (Philadelphia, Pa.)

Ng TK, Liang XY, Pang CP.
PMID: 26107018
Asia Pac J Ophthalmol (Phila). 2012 Jan-Feb;1(1):51-63. doi: 10.1097/APO.0b013e31823e57fe.

Age-related macular degeneration (AMD) is a leading cause of severe visual impairment and irreversible blindness in most developed countries, affecting more than 50 million of elderly people worldwide. Current treatments, such as intravitreal injection of antiangiogenic agents, mitigate the...

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Ng TK, Liang XY, Pang CP. HTRA1 in Age-Related Macular Degeneration. Asia Pac J Ophthalmol (Phila). 2012;1(1):51-63doi: 10.1097/APO.0b013e31823e57fe.
Ng, T. K., Liang, X. Y., & Pang, C. P. (2012). HTRA1 in Age-Related Macular Degeneration. Asia-Pacific journal of ophthalmology (Philadelphia, Pa.), 1(1), 51-63. https://doi.org/10.1097/APO.0b013e31823e57fe
Ng, Tsz Kin, et al. "HTRA1 in Age-Related Macular Degeneration." Asia-Pacific journal of ophthalmology (Philadelphia, Pa.) vol. 1,1 (2012): 51-63. doi: https://doi.org/10.1097/APO.0b013e31823e57fe
Ng TK, Liang XY, Pang CP. HTRA1 in Age-Related Macular Degeneration. Asia Pac J Ophthalmol (Phila). 2012 Jan-Feb;1(1):51-63. doi: 10.1097/APO.0b013e31823e57fe. PMID: 26107018.
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Correction: Bacillus anthracis Spore Surface Protein BclA Mediates Complement Factor H Binding to Spores and Promotes Spore Persistence.

PLoS pathogens

Wang Y, Jenkins SA, Gu C, Shree A, Martinez-Moczygemba M, Herold J, Botto M, Wetsel RA, Xu Y.
PMID: 30735542
PLoS Pathog. 2019 Feb 08;15(2):e1007579. doi: 10.1371/journal.ppat.1007579. eCollection 2019 Feb.

[This corrects the article DOI: 10.1371/journal.ppat.1005678.].

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Wang Y, Jenkins SA, Gu C, et al. Correction: Bacillus anthracis Spore Surface Protein BclA Mediates Complement Factor H Binding to Spores and Promotes Spore Persistence. PLoS Pathog. 2019;15(2):e1007579doi: 10.1371/journal.ppat.1007579.
Wang, Y., Jenkins, S. A., Gu, C., Shree, A., Martinez-Moczygemba, M., Herold, J., Botto, M., Wetsel, R. A., & Xu, Y. (2019). Correction: Bacillus anthracis Spore Surface Protein BclA Mediates Complement Factor H Binding to Spores and Promotes Spore Persistence. PLoS pathogens, 15(2), e1007579. https://doi.org/10.1371/journal.ppat.1007579
Wang, Yanyu, et al. "Correction: Bacillus anthracis Spore Surface Protein BclA Mediates Complement Factor H Binding to Spores and Promotes Spore Persistence." PLoS pathogens vol. 15,2 (2019): e1007579. doi: https://doi.org/10.1371/journal.ppat.1007579
Wang Y, Jenkins SA, Gu C, Shree A, Martinez-Moczygemba M, Herold J, Botto M, Wetsel RA, Xu Y. Correction: Bacillus anthracis Spore Surface Protein BclA Mediates Complement Factor H Binding to Spores and Promotes Spore Persistence. PLoS Pathog. 2019 Feb 08;15(2):e1007579. doi: 10.1371/journal.ppat.1007579. eCollection 2019 Feb. PMID: 30735542; PMCID: PMC6368309.
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Serum complement factor I is associated with disease activity of systemic lupus erythematosus.

Oncotarget

Tseng MH, Lin SH, Wu CY, Chien HP, Yang HY, Chen YC, Chou YC, Huang JL.
PMID: 29492211
Oncotarget. 2018 Jan 03;9(9):8502-8511. doi: 10.18632/oncotarget.23907. eCollection 2018 Feb 02.

Although aberrant complement activation is involved in the pathogenesis of systemic lupus erythematosus (SLE), the role of complement regulatory proteins in disease activity of SLE remains limited. We enrolled the pediatric-onset SLE patients from our cohort study over 10...

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Tseng MH, Lin SH, Wu CY, et al. Serum complement factor I is associated with disease activity of systemic lupus erythematosus. Oncotarget. 2018;9(9):8502-8511doi: 10.18632/oncotarget.23907.
Tseng, M. H., Lin, S. H., Wu, C. Y., Chien, H. P., Yang, H. Y., Chen, Y. C., Chou, Y. C., & Huang, J. L. (2018). Serum complement factor I is associated with disease activity of systemic lupus erythematosus. Oncotarget, 9(9), 8502-8511. https://doi.org/10.18632/oncotarget.23907
Tseng, Min-Hua, et al. "Serum complement factor I is associated with disease activity of systemic lupus erythematosus." Oncotarget vol. 9,9 (2018): 8502-8511. doi: https://doi.org/10.18632/oncotarget.23907
Tseng MH, Lin SH, Wu CY, Chien HP, Yang HY, Chen YC, Chou YC, Huang JL. Serum complement factor I is associated with disease activity of systemic lupus erythematosus. Oncotarget. 2018 Jan 03;9(9):8502-8511. doi: 10.18632/oncotarget.23907. eCollection 2018 Feb 02. PMID: 29492211; PMCID: PMC5823600.
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Comparative proteomic analysis in serum of former uranium miners with and without radon induced squamous lung cancer.

Journal of occupational medicine and toxicology (London, England)

Helmig S, Lochnit G, Schneider J.
PMID: 30923558
J Occup Med Toxicol. 2019 Mar 15;14:9. doi: 10.1186/s12995-019-0228-y. eCollection 2019.

SUMMARY: Former uranium miners of the Wismut Company, East Germany, have been exposed to ionizing radiation from radon decay products and therefore were at high risk for lung cancer. Since histological types of cancer in the so called Wismut...

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Helmig S, Lochnit G, Schneider J. Comparative proteomic analysis in serum of former uranium miners with and without radon induced squamous lung cancer. J Occup Med Toxicol. 2019;14:9doi: 10.1186/s12995-019-0228-y.
Helmig, S., Lochnit, G., & Schneider, J. (2019). Comparative proteomic analysis in serum of former uranium miners with and without radon induced squamous lung cancer. Journal of occupational medicine and toxicology (London, England), 149. https://doi.org/10.1186/s12995-019-0228-y
Helmig, Simone, et al. "Comparative proteomic analysis in serum of former uranium miners with and without radon induced squamous lung cancer." Journal of occupational medicine and toxicology (London, England) vol. 14 (2019): 9. doi: https://doi.org/10.1186/s12995-019-0228-y
Helmig S, Lochnit G, Schneider J. Comparative proteomic analysis in serum of former uranium miners with and without radon induced squamous lung cancer. J Occup Med Toxicol. 2019 Mar 15;14:9. doi: 10.1186/s12995-019-0228-y. eCollection 2019. PMID: 30923558; PMCID: PMC6419832.
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Impact of a Complement Factor H Gene Variant on Renal Dysfunction, Cardiovascular Events, and Response to ACE Inhibitor Therapy in Type 2 Diabetes.

Frontiers in genetics

Valoti E, Noris M, Perna A, Rurali E, Gherardi G, Breno M, Parvanova Ilieva A, Petrov Iliev I, Bossi A, Trevisan R, Dodesini AR, Ferrari S, Stucchi N, Benigni A, Remuzzi G, Ruggenenti P.
PMID: 31428128
Front Genet. 2019 Jul 26;10:681. doi: 10.3389/fgene.2019.00681. eCollection 2019.

Complement activation has been increasingly implicated in the pathogenesis of type 2 diabetes and its chronic complications. It is unknown whether complement factor H (CFH) genetic variants, which have been previously associated with complement-mediated organ damage likely due to...

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Valoti E, Noris M, Perna A, et al. Impact of a Complement Factor H Gene Variant on Renal Dysfunction, Cardiovascular Events, and Response to ACE Inhibitor Therapy in Type 2 Diabetes. Front Genet. 2019;10:681doi: 10.3389/fgene.2019.00681.
Valoti, E., Noris, M., Perna, A., Rurali, E., Gherardi, G., Breno, M., Parvanova Ilieva, A., Petrov Iliev, I., Bossi, A., Trevisan, R., Dodesini, A. R., Ferrari, S., Stucchi, N., Benigni, A., Remuzzi, G., & Ruggenenti, P. (2019). Impact of a Complement Factor H Gene Variant on Renal Dysfunction, Cardiovascular Events, and Response to ACE Inhibitor Therapy in Type 2 Diabetes. Frontiers in genetics, 10681. https://doi.org/10.3389/fgene.2019.00681
Valoti, Elisabetta, et al. "Impact of a Complement Factor H Gene Variant on Renal Dysfunction, Cardiovascular Events, and Response to ACE Inhibitor Therapy in Type 2 Diabetes." Frontiers in genetics vol. 10 (2019): 681. doi: https://doi.org/10.3389/fgene.2019.00681
Valoti E, Noris M, Perna A, Rurali E, Gherardi G, Breno M, Parvanova Ilieva A, Petrov Iliev I, Bossi A, Trevisan R, Dodesini AR, Ferrari S, Stucchi N, Benigni A, Remuzzi G, Ruggenenti P. Impact of a Complement Factor H Gene Variant on Renal Dysfunction, Cardiovascular Events, and Response to ACE Inhibitor Therapy in Type 2 Diabetes. Front Genet. 2019 Jul 26;10:681. doi: 10.3389/fgene.2019.00681. eCollection 2019. PMID: 31428128; PMCID: PMC6689971.
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Identification of potential therapeutic target genes in mouse mesangial cells associated with diabetic nephropathy using bioinformatics analysis.

Experimental and therapeutic medicine

Mou X, Zhou DY, Liu YH, Liu K, Zhou D.
PMID: 31105790
Exp Ther Med. 2019 Jun;17(6):4617-4627. doi: 10.3892/etm.2019.7524. Epub 2019 Apr 23.

The aim of the present study was to identify genes under the effect of transforming growth factor-β (TGF-β1), high glucose (HG) and glucosamine (GlcN) in MES-13 mesangial cells and elucidate the molecular mechanisms of diabetic nephropathy (DN). The gene...

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Mou X, Zhou DY, Liu YH, et al. Identification of potential therapeutic target genes in mouse mesangial cells associated with diabetic nephropathy using bioinformatics analysis. Exp Ther Med. 2019;17(6):4617-4627doi: 10.3892/etm.2019.7524.
Mou, X., Zhou, D. Y., Liu, Y. H., Liu, K., & Zhou, D. (2019). Identification of potential therapeutic target genes in mouse mesangial cells associated with diabetic nephropathy using bioinformatics analysis. Experimental and therapeutic medicine, 17(6), 4617-4627. https://doi.org/10.3892/etm.2019.7524
Mou, Xin, et al. "Identification of potential therapeutic target genes in mouse mesangial cells associated with diabetic nephropathy using bioinformatics analysis." Experimental and therapeutic medicine vol. 17,6 (2019): 4617-4627. doi: https://doi.org/10.3892/etm.2019.7524
Mou X, Zhou DY, Liu YH, Liu K, Zhou D. Identification of potential therapeutic target genes in mouse mesangial cells associated with diabetic nephropathy using bioinformatics analysis. Exp Ther Med. 2019 Jun;17(6):4617-4627. doi: 10.3892/etm.2019.7524. Epub 2019 Apr 23. PMID: 31105790; PMCID: PMC6507521.
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Case Report: A Rare Truncating Variant of the .

Frontiers in genetics

Guzzo G, Sadallah S, Fodstad H, Venetz JP, Rotman S, Teta D, Gauthier T, Pantaleo G, Superti-Furga A, Pascual M.
PMID: 34220921
Front Genet. 2021 May 20;12:529236. doi: 10.3389/fgene.2021.529236. eCollection 2021.

IgA nephropathy (IgAN) is the most common primary glomerulonephritis worldwide. Despite appropriate therapy, 20-40% of affected-patients evolve toward end-stage kidney disease (ESKD). Mesangial IgA deposits are the hallmark of IgAN, and complement deposition (C3) seems to differentiate latent IgA...

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Guzzo G, Sadallah S, Fodstad H, et al. Case Report: A Rare Truncating Variant of the . Front Genet. 2021;12:529236doi: 10.3389/fgene.2021.529236.
Guzzo, G., Sadallah, S., Fodstad, H., Venetz, J. P., Rotman, S., Teta, D., Gauthier, T., Pantaleo, G., Superti-Furga, A., & Pascual, M. (2021). Case Report: A Rare Truncating Variant of the . Frontiers in genetics, 12529236. https://doi.org/10.3389/fgene.2021.529236
Guzzo, Gabriella, et al. "Case Report: A Rare Truncating Variant of the ." Frontiers in genetics vol. 12 (2021): 529236. doi: https://doi.org/10.3389/fgene.2021.529236
Guzzo G, Sadallah S, Fodstad H, Venetz JP, Rotman S, Teta D, Gauthier T, Pantaleo G, Superti-Furga A, Pascual M. Case Report: A Rare Truncating Variant of the . Front Genet. 2021 May 20;12:529236. doi: 10.3389/fgene.2021.529236. eCollection 2021. PMID: 34220921; PMCID: PMC8244589.
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Pediatric atypical hemolytic-uremic syndrome due to auto-antibodies against factor H: is there an interest to combine eculizumab and mycophenolate mofetil?.

Pediatric nephrology (Berlin, Germany)

Matrat L, Bacchetta J, Ranchin B, Tanné C, Sellier-Leclerc AL.
PMID: 33774745
Pediatr Nephrol. 2021 Jun;36(6):1647-1650. doi: 10.1007/s00467-021-05025-8. Epub 2021 Mar 28.

BACKGROUND: Atypical hemolytic and uremic syndrome (aHUS), a thrombotic micro-angiopathy (TMA) caused by deregulation in the complement pathway, is sometimes due to the presence of anti-complement factor H (CFH) auto-antibodies. The "standard" treatment for such aHUS combines plasma exchange...

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Matrat L, Bacchetta J, Ranchin B, et al. Pediatric atypical hemolytic-uremic syndrome due to auto-antibodies against factor H: is there an interest to combine eculizumab and mycophenolate mofetil?. Pediatr Nephrol. 2021;36(6):1647-1650doi: 10.1007/s00467-021-05025-8.
Matrat, L., Bacchetta, J., Ranchin, B., Tanné, C., & Sellier-Leclerc, A. L. (2021). Pediatric atypical hemolytic-uremic syndrome due to auto-antibodies against factor H: is there an interest to combine eculizumab and mycophenolate mofetil?. Pediatric nephrology (Berlin, Germany), 36(6), 1647-1650. https://doi.org/10.1007/s00467-021-05025-8
Matrat, Lucie, et al. "Pediatric atypical hemolytic-uremic syndrome due to auto-antibodies against factor H: is there an interest to combine eculizumab and mycophenolate mofetil?." Pediatric nephrology (Berlin, Germany) vol. 36,6 (2021): 1647-1650. doi: https://doi.org/10.1007/s00467-021-05025-8
Matrat L, Bacchetta J, Ranchin B, Tanné C, Sellier-Leclerc AL. Pediatric atypical hemolytic-uremic syndrome due to auto-antibodies against factor H: is there an interest to combine eculizumab and mycophenolate mofetil?. Pediatr Nephrol. 2021 Jun;36(6):1647-1650. doi: 10.1007/s00467-021-05025-8. Epub 2021 Mar 28. PMID: 33774745.
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Interaction of human complement factor H variants Tyr⁴⁰² and His⁴⁰² with Leptospira spp.

Frontiers in immunology

Silva AS, Valencia MM, Cianciarullo AM, Vasconcellos SA, Barbosa AS, Isaac L.
PMID: 22566834
Front Immunol. 2011 Oct 05;2:44. doi: 10.3389/fimmu.2011.00044. eCollection 2011.

Leptospirosis is a zoonosis caused by pathogenic bacteria from the genus Leptospira. The disease represents a serious public health problem in underdeveloped tropical countries. Leptospires infect hosts through small abrasions in the skin or mucous membranes and they rapidly...

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Silva AS, Valencia MM, Cianciarullo AM, et al. Interaction of human complement factor H variants Tyr⁴⁰² and His⁴⁰² with Leptospira spp. Front Immunol. 2011;2:44doi: 10.3389/fimmu.2011.00044.
Silva, A. S., Valencia, M. M., Cianciarullo, A. M., Vasconcellos, S. A., Barbosa, A. S., & Isaac, L. (2011). Interaction of human complement factor H variants Tyr⁴⁰² and His⁴⁰² with Leptospira spp. Frontiers in immunology, 244. https://doi.org/10.3389/fimmu.2011.00044
Silva, Aldacilene Souza, et al. "Interaction of human complement factor H variants Tyr⁴⁰² and His⁴⁰² with Leptospira spp." Frontiers in immunology vol. 2 (2011): 44. doi: https://doi.org/10.3389/fimmu.2011.00044
Silva AS, Valencia MM, Cianciarullo AM, Vasconcellos SA, Barbosa AS, Isaac L. Interaction of human complement factor H variants Tyr⁴⁰² and His⁴⁰² with Leptospira spp. Front Immunol. 2011 Oct 05;2:44. doi: 10.3389/fimmu.2011.00044. eCollection 2011. PMID: 22566834; PMCID: PMC3342064.
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