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Your search keyword '"Krolewski, A. S."' showing total 296 results
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296 results on '"Krolewski, A. S."'

2. Results of untargeted analysis using the SOMAscan proteomics platform indicates novel associations of circulating proteins with risk of progression to kidney failure in diabetes

Author

Kobayashi, Hiroki, Looker, Helen C., Satake, Eiichiro, Saulnier, Pierre Jean, Md Dom, Zaipul I., O’Neil, Kristina, Ihara, Katsuhito, Krolewski, Bozena, Galecki, Andrzej T., Niewczas, Monika A., Wilson, Jonathan M., Doria, Alessandro, Duffin, Kevin L., Nelson, Robert G., and Krolewski, Andrzej S.

Published
2022
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3. A dominant negative ADIPOQ mutation in a diabetic family with renal disease, hypoadiponectinemia, and hyperceramidemia

Author

Simeone, Christopher A., Wilkerson, Joseph L., Poss, Annelise M., Banks, James A., Varre, Joseph V., Guevara, Jose Lazaro, Hernandez, Edgar Javier, Gorsi, Bushra, Atkinson, Donald L., Turapov, Tursun, Frodsham, Scott G., Morales, Julio C. Fierro, O’Neil, Kristina, Moore, Barry, Yandell, Mark, Summers, Scott A., Krolewski, Andrzej S., Holland, William L., and Pezzolesi, Marcus G.

Published
2022
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6. Integrated analysis of blood DNA methylation, genetic variants, circulating proteins, microRNAs, and kidney failure in type 1 diabetes.

Author

Chen, Zhuo, Satake, Eiichiro, Pezzolesi, Marcus G., Md Dom, Zaipul I., Stucki, Devorah, Kobayashi, Hiroki, Syreeni, Anna, Johnson, Adam T., Wu, Xiwei, Dahlström, Emma H., King, Jaxon B., Groop, Per-Henrik, Rich, Stephen S., Sandholm, Niina, Krolewski, Andrzej S., and Natarajan, Rama

Subjects
TYPE 1 diabetes, KIDNEY failure, DNA methylation, GENETIC variation, DNA analysis, CIRCULATING tumor DNA
Abstract

Variation in DNA methylation (DNAmet) in white blood cells and other cells/tissues has been implicated in the etiology of progressive diabetic kidney disease (DKD). However, the specific mechanisms linking DNAmet variation in blood cells with risk of kidney failure (KF) and utility of measuring blood cell DNAmet in personalized medicine are not clear. We measured blood cell DNAmet in 277 individuals with type 1 diabetes and DKD using Illumina EPIC arrays; 51% of the cohort developed KF during 7 to 20 years of follow-up. Our epigenome-wide analysis identified DNAmet at 17 CpGs (5′-cytosine-phosphate-guanine-3′ loci) associated with risk of KF independent of major clinical risk factors. DNAmet at these KF-associated CpGs remained stable over a median period of 4.7 years. Furthermore, DNAmet variations at seven KF-associated CpGs were strongly associated with multiple genetic variants at seven genomic regions, suggesting a strong genetic influence on DNAmet. The effects of DNAmet variations at the KF-associated CpGs on risk of KF were partially mediated by multiple KF-associated circulating proteins and KF-associated circulating miRNAs. A prediction model for risk of KF was developed by adding blood cell DNAmet at eight selected KF-associated CpGs to the clinical model. This updated model significantly improved prediction performance (c-statistic = 0.93) versus the clinical model (c-statistic = 0.85) at P = 6.62 × 10−14. In conclusion, our multiomics study provides insights into mechanisms through which variation of DNAmet may affect KF development and shows that blood cell DNAmet at certain CpGs can improve risk prediction for KF in T1D. Editor's summary: Individuals with type 1 diabetes (T1D) are at increased risk of developing kidney disease, and a proportion of those who do then progress to kidney failure. Chen et al. examined the genomic DNA methylation of blood cells from patients with diabetic kidney disease and found methylation at specific CpGs that positively or negatively associated with subsequent kidney failure over the following years or decades. Some of these methylation sites were validated in a similar but independent patient cohort, suggesting that such sites may be useful for identifying individuals with T1D who are at risk of progressing to end-stage kidney disease. —Catherine Charneski [ABSTRACT FROM AUTHOR]

Published
2024
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7. A signature of circulating inflammatory proteins and development of end-stage renal disease in diabetes

Author

Niewczas, Monika A., Pavkov, Meda E., Skupien, Jan, Smiles, Adam, Md Dom, Zaipul I., Wilson, Jonathan M., Park, Jihwan, Nair, Viji, Schlafly, Andrew, Saulnier, Pierre-Jean, Satake, Eiichiro, Simeone, Christopher A., Shah, Hetal, Qiu, Chengxiang, Looker, Helen C., Fiorina, Paolo, Ware, Carl F., Sun, Jennifer K., Doria, Alessandro, Kretzler, Matthias, Susztak, Katalin, Duffin, Kevin L., Nelson, Robert G., and Krolewski, Andrzej S.

Published
2019
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15. The pseudokinase tribbles homolog 3 interacts with ATF4 to negatively regulate insulin exocytosis in human and mouse β cells

Author

Liew, Chong Wee, Bochenski, Jacek, Kawamori, Dan, Hu, Jiang, Leech, Colin A., Wanic, Krzysztof, Malecki, Maciej, Warram, James H., Qi, Ling, Krolewski, Andrzej S., and Kulkarni, Rohit N.

Subjects
Pancreatic beta cells -- Genetic aspects, Insulin -- Dosage and administration, Type 2 diabetes -- Development and progression -- Drug therapy -- Genetic aspects, Health care industry
Abstract

Insufficient insulin secretion and reduced pancreatic β cell mass are hallmarks of type 2 diabetes (T2DM). Here, we confirm that a previously identified polymorphism (rs2295490/Q84R) in exon 2 of the [...]

Published
2010
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18. Mutations at the BLK locus linked to maturity onset diabetes of the young and [beta]-cell dysfunction

Author

Borowiec, Maciej, Liew, Chong W., Thompson, Ryan, Boonyasrisawat, Watip, Hu, Jiang, Mlynarski, Wojciech M., Khattabi, Ilham El, Kim, Sung-Hoon, Marselli, Lorella, Rich, Stephen S., Krolewski, Andrzej S., Bonner-Weir, Susan, Sharma, Arun, Sale, Michele, Mychaleckyj, Josyf C., Kulkarni, Rohit N., and Doria, Alessandro

Subjects
Diabetes -- Development and progression, Diabetes -- Genetic aspects, Pancreatic beta cells -- Genetic aspects, Pancreatic beta cells -- Health aspects, Science and technology
Abstract

Maturity-onset diabetes of the young (MODY) is a subtype of diabetes defined by an autosomal pattern of inheritance and a young age at onset, often before age 25. MODY is genetically heterogeneous, with 8 distinct MODY genes identified to date and more believed to exist. We resequenced 732 kb of genomic sequence at 8p23 in 6 MODY families unlinked to known MODY genes that showed evidence of linkage at that location. Of the 410 sequence differences that we identified, 5 had a frequency < 1% in the general population and segregated with diabetes in 3 of the families, including the 2 showing the strongest support for linkage at this location. The 5 mutations were all placed within 100 kb corresponding to the BLK gene. One resulted in an Ala71Thr substitution; the other 4 were noncoding and determined decreased in vitro promoter activity in reporter gene experiments. We found that BLK--a nonreceptor tyrosine-kinase of the src family of proto-oncogenes--is expressed in [beta]-cells where it enhances insulin synthesis and secretion in response to glucose by up-regulating transcription factors Pdx1 and Nkx6.1. These actions are greatly attenuated by the Ala71Thr mutation. These findings point to BLK as a previously unrecognized modulator of [beta]-cell function, the deficit of which may lead to the development of diabetes. beta cells | genetics | MODY | tyrosine kinase

Published
2009

21. Association Between a Genetic Variant Related to Glutamic Acid Metabolism and Coronary Heart Disease in Individuals With Type 2 Diabetes

Author

Qi, Lu, Qi, Qibin, Prudente, Sabrina, Mendonca, Christine, Andreozzi, Francesco, di Pietro, Natalia, Sturma, Mariella, Novelli, Valeria, Mannino, Gaia Chiara, Formoso, Gloria, Gervino, Ernest V., Hauser, Thomas H., Muehlschlegel, Jochen D., Niewczas, Monika A., Krolewski, Andrzej S., Biolo, Gianni, Pandolfi, Assunta, Rimm, Eric, Sesti, Giorgio, Trischitta, Vincenzo, Hu, Frank, and Doria, Alessandro

Published
2013
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23. Regression of microalbuminuria in type 1 diabetes

Author

Perkins, Bruce A., Ficociello, Linda H., Silva, Kristen H., Finkelstein, Dianne M., Warram, James H., and Krolewski, Andrzej S.

Subjects
Diabetic nephropathies -- Development and progression, Albuminuria -- Development and progression
Abstract

Many diabetics who have a protein called albumin in their urine?will not necessarily develop diabetic kidney disease, according to a study of 386 patients. In fact, they may even stop excreting albumin in their urine. Diabetics with low blood pressure, low cholesterol levels, and low glycosylated hemoglobin levels were three times more likely to stop excreting albumin in their urine than other diabetics. Albumin in the urine is a sign that a person may be developing kidney disease.

Published
2003

29. Genome-Wide Association Scan for Diabetic Nephropathy Susceptibility Genes in Type 1 Diabetes

Author

Pezzolesi, Marcus G., Poznik, G. David, Mychaleckyj, Josyf C., Paterson, Andrew D., Barati, Michelle T., Klein, Jon B., Ng, Daniel P.K., Placha, Grzegorz, Canani, Luis H., Bochenski, Jacek, Waggott, Daryl, Merchant, Michael L., Krolewski, Bozena, Mirea, Lucia, Wanic, Krzysztof, Katavetin, Pisut, Kure, Masahiko, Wolkow, Pawel, Dunn, Jonathon S., Smiles, Adam, Walker, William H., Boright, Andrew P., Bull, Shelley B., Doria, Alessandro, Rogus, John J., Rich, Stephen S., Warram, James H., and Krolewski, Andrzej S.

Published
2009

47. Glycosylated hemoglobin and the risk of microalbuminuria in patients with insulin-dependent diabetes mellitus

Author

Krolewski, Andrzej S., Laffel, Lori M.B., Krolewski, Martin, Quinn, Maryanne, and Warram, James H.

Subjects
Blood sugar -- Measurement, Glycosylated hemoglobin -- Measurement, Albuminuria -- Risk factors, Type 1 diabetes -- Physiological aspects
Abstract

Maintaining glycosylated hemoglobin levels in diabetic patients at approximately 10% may reduce their risk of end-stage kidney disease. Measuring glycosylated hemoglobin is another way of measuring blood sugar. A 10% level is approximately equivalent to a blood sugar of 200 milligrams per deciliter. Researchers measured a glycosylated hemoglobin called hemoglobin A1 in 1,613 diabetic patients who had been diagnosed with microalbuminuria. Microalbuminuria is an increase in albumin excretion in the urine, which can be a sign of early kidney disease. The risk of microalbuminuria increased as the level of hemoglobin A1 increased. Twelve percent of those with the lowest hemoglobin A1 levels had microalbuminuria, compared to 36% of those with the highest levels. A 10% hemoglobin A1 level appeared to be the cut-off point below which diabetic patients had little risk of microalbuminuria and above which they had a greatly increased risk of microalbuminuria.

Published
1995

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