Search

Your search keyword '"Phillips, Carrie L"' showing total 216 results
Start Over Author "Phillips, Carrie L"
216 results on '"Phillips, Carrie L"'

1. The chromatin landscape of healthy and injured cell types in the human kidney

Author

Gisch, Debora L., Brennan, Michelle, Lake, Blue B., Basta, Jeannine, Keller, Mark S., Melo Ferreira, Ricardo, Akilesh, Shreeram, Ghag, Reetika, Lu, Charles, Cheng, Ying-Hua, Collins, Kimberly S., Parikh, Samir V., Rovin, Brad H., Robbins, Lynn, Stout, Lisa, Conklin, Kimberly Y., Diep, Dinh, Zhang, Bo, Knoten, Amanda, Barwinska, Daria, Asghari, Mahla, Sabo, Angela R., Ferkowicz, Michael J., Sutton, Timothy A., Kelly, Katherine J., De Boer, Ian H., Rosas, Sylvia E., Kiryluk, Krzysztof, Hodgin, Jeffrey B., Alakwaa, Fadhl, Winfree, Seth, Jefferson, Nichole, Türkmen, Aydın, Gaut, Joseph P., Gehlenborg, Nils, Phillips, Carrie L., El-Achkar, Tarek M., Dagher, Pierre C., Hato, Takashi, Zhang, Kun, Himmelfarb, Jonathan, Kretzler, Matthias, Mollah, Shamim, Jain, Sanjay, Rauchman, Michael, and Eadon, Michael T.

Published
2024
Full Text
View/download PDF

5. Molecular Signatures of Glomerular Neovascularization in a Patient with Diabetic Kidney Disease

Author

Ferkowicz, Michael J., Verma, Ashish, Barwinska, Daria, Melo Ferreira, Ricardo, Henderson, Joel M., Kirkpatrick, Mary, Silva, Paolo S., Steenkamp, Devin W., Phillips, Carrie L., Waikar, Sushrut S., Sutton, Timothy A., Lake, Blue, Zhang, Kun, Lecker, Stewart, Morales, Alexander, Stillman, Isaac, Bogen, Steve, Amodu, Afolarin A., Beck, Laurence, Henderson, Joel, Ilori, Titlayo, Maikhor, Shana, Onul, Ingrid, Schmidt, Insa, Verma, Ashish, Waikar, Sushrut, Yadati, Pranav, Yu, Guanghao, Colona, Mia R., McMahon, Gearoid, Weins, Astrid, Hacohen, Nir, Greka, Anna, Hoover, Paul J., Marshall, Jamie L., Aulisio, Mark, Bush, William, Chen, Yijiang, Crawford, Dana, Madabhushi, Anant, Viswanathan, Vidya S., Bush, Lakeshia, Cooperman, Leslie, Gadegbeku, Crystal, Herlitz, Leal, Jolly, Stacey, Nguyen, Jane, O’Malley, Charles, O’Toole, John, Palmer, Ellen, Poggio, Emilio, Spates-Harden, Kassandra, Sedor, John, Sendrey, Dianna, Taliercio, Jonathan, Appelbaum, Paul, Balderes, Olivia, Barasch, Jonathan, Berroue, Cecilia, Bomback, Andrew, Canetta, Pietro A., D’Agati, Vivette, Kiryluk, Krzysztof, Kudose, Satoru, Mehl, Karla, Sabatello, Maya, Shang, Ning, Varela, German, de Pinho Gonçalves, Joana, Lardenoije, Roy, Migas, Lukasz, Van de Plas, Raf, Barisoni, Laura, Rennke, Helmut, Azeloglu, Evren, Campbell, Kirk, Coca, Steven, He, Cijang, He, John, Iyengar, Srinivas Ravi, Lefferts, Seanee, Nadkarni, Girish, Patel, Marissa, Tokita, Joji, Ward, Stephen, Xiong, Yuguang, Verdoes, Abraham, Sabo, Angela, Barwinska, Daria, Gisch, Debora Lidia, Williams, James, Kelly, Katherine, Dunn, Kenneth, Asghari, Mahla, Eadon, Michael, Ferkowicz, Michael, Dagher, Pierre, Ferreira, Ricardo Melo, Winfree, Seth, Bledsoe, Sharon, Wofford, Stephanie, El-Achkar, Tarek, Sutton, Timothy, Bowen, William, Cheng, Ying-Hua, Slade, Austen, Record, Elizabeth, Cheng, Yinghua, Borner, Katy, Herr, Bruce, Jain, Yashvardhan, Quardokus, Ellen, Atta, Mohamed, Bernard, Lauren, Menez, Steven, Parikh, Chirag, Corona Villalobos, Celia Pamela, Wang, Ashley, Wen, Yumeng, Xu, Alan, Chen, Sarah, Donohoe, Isabel, Johansen, Camille, Rosas, Sylvia, Sun, Jennifer, Ardayfio, Joseph, Bebiak, Jack, Brown, Keith, Campbell, Taneisha, Fox, Monica, Hayashi, Lynda, Jefferson, Nichole, Richard Knight, Jennifer Jones, Koewler, Robert, Pinkeney, Roy, Saul, John, Shpigel, Anna, Stutzke, Christy, Prasad, Pottumarthi, Madhavan, Sethu M., Parikh, Samir, Rovin, Brad, Shapiro, John P., Anderton, Christopher, Lukowski, Jessica, Pasa-Tolic, Ljiljana, Velickovic, Dusan, Oliver, George, Mao, Weiguang, Sealfon, Rachel, Troyanskaya, Olga, Wong, Aaron, Pollack, Ari, Goltsev, Yury, Ginley, Brandon, Lutnick, Brendon, Anjani, Kavya, Laszik, Zoltan G., Mukatash, Tariq, Nolan, Garry, Beyda, David, Bracamonte, Erika, Brosius, Frank, Campos, Baltazar, Marquez, Nicole, Mendoza, Katherine, Scott, Raymond, Thajudeen, Bijin, Tsosie, Rebecca, Woodhead, Gregory, Saunders, Milda, Alloway, Rita R., Lee, Paul J., Rike, Adele, Shi, Tiffany, Woodle, E. Steve, Bjornstad, Petter, Hsieh, Elena, Kendrick, Jessica, Pyle, Laura, Thurman, Joshua, Vinovskis, Carissa, Wrobel, Julia, Lucarelli, Nicholas, Sarder, Pinaki, Bui, James, Carmona-Powell, Eunice, Gaba, Ron, Kelly, Tanika, Lash, James, Meza, Natalie, Redmond, Devona, Renteria, Amada, Ricardo, Ana, Setty, Suman, Srivastava, Anand, Alakwaa, Fadhl, Ascani, Heather, Balis, Ul, Bitzer, Markus, Blanc, Victoria, Bonevich, Nikki, Conser, Ninive, Demeke, Dawit, Dull, Rachel, Eddy, Sean, Frey, Renee, Hartman, John, He, Yongqun Oliver, Hodgin, Jeffrey, Kretzler, Matthias, Lienczewski, Chrysta, Luo, Jinghui, Mariani, Laura, McCown, Phillip, Menon, Rajasree, Nair, Viji, Otto, Edgar, Reamy, Rebecca, Rose, Michael, Schaub, Jennifer, Steck, Becky, Wright, Zachary, Coleman, Alyson, Henderson-Brown, Dorisann, Berge, Jerica, Caramori, Maria Luiza, Adeyi, Oyedele, Nachman, Patrick, Safadi, Sami, Flanagan, Siobhan, Ma, Sisi, Klett, Susan, Wolf, Susan, Harindhanavudhi, Tasma, Rao, Via, Bream, Peter, Froment, Anne, Kelley, Sara, Mottl, Amy, Roy-Chaudhury, Prabir, Zeitler, Evan, Bender, Filitsa, Elder, Michele, Gilliam, Matthew, Hall, Daniel E., Kellum, John A., Murugan, Raghavan, Palevsky, Paul, Rosengart, Matthew, Tan, Roderick, Tublin, Mitchell, Winters, James, Bansal, Shweta, Montellano, Richard, Pamreddy, Annapurna, Sharma, Kumar, Venkatachalam, Manjeri, Ye, Hongping, Zhang, Guanshi, Basit, Mujeeb, Cai, Qi, Hendricks, Allen, Hedayati, Susan, and Asra

Published
2024
Full Text
View/download PDF

6. Circulating uromodulin inhibits systemic oxidative stress by inactivating the TRPM2 channel

Author

LaFavers, Kaice A, Macedo, Etienne, Garimella, Pranav S, Lima, Camila, Khan, Shehnaz, Myslinski, Jered, McClintick, Jeanette, Witzmann, Frank A, Winfree, Seth, Phillips, Carrie L, Hato, Takashi, Dagher, Pierre C, Wu, Xue-Ru, El-Achkar, Tarek M, and Micanovic, Radmila

Subjects
Prevention, Aging, Kidney Disease, Renal and urogenital, Adult, Animals, Doxycycline, Female, HEK293 Cells, Humans, Male, Mice, Middle Aged, Oxidative Stress, Reactive Oxygen Species, Signal Transduction, TRPM Cation Channels, Uromodulin, Biological Sciences, Medical and Health Sciences
Abstract

High serum concentrations of kidney-derived protein uromodulin [Tamm-Horsfall protein (THP)] have recently been shown to be independently associated with low mortality in both older adults and cardiac patients, but the underlying mechanism remains unclear. Here, we show that THP inhibits the generation of reactive oxygen species (ROS) both in the kidney and systemically. Consistent with this experimental data, the concentration of circulating THP in patients with surgery-induced acute kidney injury (AKI) correlated with systemic oxidative damage. THP in the serum dropped after AKI and was associated with an increase in systemic ROS. The increase in oxidant injury correlated with postsurgical mortality and need for dialysis. Mechanistically, THP inhibited the activation of the transient receptor potential cation channel, subfamily M, member 2 (TRPM2) channel. Furthermore, inhibition of TRPM2 in vivo in a mouse model mitigated the systemic increase in ROS during AKI and THP deficiency. Our results suggest that THP is a key regulator of systemic oxidative stress by suppressing TRPM2 activity, and our findings might help explain how circulating THP deficiency is linked with poor outcomes and increased mortality.

Published
2019

15. Alterations in Protein Translation and Carboxylic Acid Catabolic Processes in Diabetic Kidney Disease

Author

Collins, Kimberly S., primary, Eadon, Michael T., additional, Cheng, Ying-Hua, additional, Barwinska, Daria, additional, Melo Ferreira, Ricardo, additional, McCarthy, Thomas W., additional, Janosevic, Danielle, additional, Syed, Farooq, additional, Maier, Bernhard, additional, El-Achkar, Tarek M., additional, Kelly, Katherine J., additional, Phillips, Carrie L., additional, Hato, Takashi, additional, Sutton, Timothy A., additional, and Dagher, Pierre C., additional

Published
2022
Full Text
View/download PDF

21. Early monitoring of acute tubular necrosis in the rat kidney by [sup.23]Na-MRI

Author

Atthe, Bharath K., Babsky, Andriy M., Hopewell, Paige N., Phillips, Carrie L., Molitoris, Bruce A., and Bansal, Navin

Subjects
Acute renal failure -- Risk factors, Acute renal failure -- Diagnosis, Acute renal failure -- Care and treatment, Magnetic resonance imaging -- Usage, Sodium in the body -- Physiological aspects, Sodium in the body -- Measurement, Biological sciences
Abstract

Reabsorption of water and other molecules is dependent on the corticomedullary sodium concentration gradient in the kidney. During the early course of acute tubular necrosis (ATN), this gradient is altered. Therefore, [sup.23]Na magnetic resonance imaging (MRI) was used to study the alterations in renal sodium distribution in the rat kidney during ischemia and reperfusion (IR) injury, which induces ATN. In-magnet ischemia was induced for 0 (control), 10, 20, 30 or 50 min in Wistar rats. [sup.23]Na images were collected every 10 min during baseline, ischemia, and 60-min reperfusion periods. [T.sub.1] and [T.sub.2] relaxation times were measured by both [sup.23]Na-MRI and -MRS on a separate cohort of animals during ischemia and reperfusion for correction of relaxation-related tissue sodium concentration (TSC). A marked decrease was observed in the medulla and cortex [sup.23]Na-MRI signal intensity (SI) during the early evolution of ATN caused by IR injury, with the sodium reabsorption function of the kidney being irreversibly damaged after 50 min of ischemia. Sodium relaxation time characteristics were similar in the medulla and cortex of normal kidney, but significantly decreased with IR. The changes in relaxation times in both compartments were identical; thus the medulla-to-cortex sodium SI ratio represents the TSC ratio of both compartments. The extent of IR damage observed with histological examination correlated with the [sup.23]Na-MRI data. [sup.23]Na-MRI has great potential for noninvasive, clinical diagnosis of evolving ATN in the setup of acute renal failure and in differentiating ATN from other causes of renal failure where tubular function is maintained. ischemia-reperfusion injury; relaxation times; tissue; sodium concentration doi: 10.1152/ajprenal.00388.2009.

Published
2009

23. Alterations in protein translation and carboxylic acid catabolic processes in diabetic kidney disease

Author

Collins, Kimberly S., primary, Eadon, Michael T., additional, Cheng, Ying-Hua, additional, Barwinska, Daria, additional, Ferreira, Ricardo Melo, additional, McCarthy, Thomas W., additional, Janosevic, Danielle, additional, Syed, Farooq, additional, Maier, Bernhard, additional, El-Achkar, Tarek M., additional, Kelly, Katherine J., additional, Phillips, Carrie L., additional, Hato, Takashi, additional, Sutton, Timothy A., additional, and Dagher, Pierre C., additional

Published
2021
Full Text
View/download PDF

24. Ischemia induces alterations in actin filaments in renal vascular smooth muscle cells

Author

Kwon, Osun, Phillips, Carrie L., and Molitoris, Bruce A.

Subjects
Acute renal failure -- Physiological aspects, Cytoskeleton -- Physiological aspects, Ischemia -- Physiological aspects, Actin -- Physiological aspects, Vascular smooth muscle -- Physiological aspects, Biological sciences
Abstract

Although altered renal vascular reactivity is known to occur after ischemia, the structural basis explaining the phenomenon has not been clarified. To evaluate for structural damage to the renal vasculature in ischemic acute renal failure (ARF), F-actin in the renal vasculature of rat kidneys and cultured vascular smooth muscle cells was examined using confocal fluorescence microscopy. The left renal artery was clamped for 15 or 45 min in Sprague-Dawley rats. In other experimental groups, 45 min of renal arterial clamping was followed by 1 or 3 h of reperfusion. Control kidneys were procured without any preceding interventional procedure. F-actin was labeled with either fluorescein or Texas red-conjugated phalloidin. Serial optical sections were collected by confocal microscopy, and image volumes were rendered three dimensionally. The degree of cytoskeletal damage in the vasculature was assessed by semiquantitative scoring of the staining for F-actin. Disorganization/disarray of F-actin, reflected by disruption and clumping of the actin filaments, was observed in arteries, arterioles, and the vasa rectae of the kidney after ischemia or ischemia-reperfusion. Smooth muscle cells from arteries and arterioles showed significant damage to F-actin after either 15 or 45 min of ischemia in a duration-dependent manner. The actin cytoskeleton tended to recover from damage from 45 min of ischemia 1 and 3 h after reperfusion. The vasa rectae did not demonstrate significant damage to F-actin after 15- or 45-min ischemia. However, significant damage to the vasa rectae was manifest 3 h after the reperfusion following 45 min of ischemia. In summary, disorganization/disarray of F-actin in vascular smooth muscle cells of the kidney was observed after ischemia or ischemia-reperfusion. A similar finding was observed in cultured vascular smooth muscle cells. We suggest that this disorganization of the actin cytoskeleton may play a contributory role in the loss of autoregulation of renal blood flow and the aberrant vascular reactivity in postischemic ARF. acute renal failure; vasculature; actin cytoskeleton; fluorescence microscopy; confocal microscopy

Published
2002

25. Voxx: a PC-based, near real-time volume rendering system for biological microscopy

Author

Clendenon, Jeffrey L., Phillips, Carrie L., Sandoval, Ruben M., Fang, Shiaofen, and Dunn, Kenneth W.

Subjects
Physiology -- Research, Microscope and microscopy -- Equipment and supplies, Three-dimensional graphics -- Physiological aspects, Biological sciences
Abstract

Voxx: a PC-based, near real-time volume rendering system for biological microscopy. Am J Physiol Cell Physiol 282: C213-C218, 2002.--Confocal and two-photon fluorescence microscopy have advanced the exploration of complex, three-dimensional biological structures at submicron resolution. We have developed a voxel-based three-dimensional (3-D) imaging program (Voxx) capable of near real-time rendering that runs on inexpensive personal computers. This low-cost interactive 3-D imaging system provides a powerful tool for analyzing complex structures in cells and tissues and encourages a more thorough exploration of complex biological image data. confocal; three-dimensional; two-photon; voxels

Published
2002

28. Distal Tubular Hyperplasia

Author

Williamson, Sean R., primary, Al-Obaidy, Khaleel I., additional, Cheng, Liang, additional, Smith, Steven C., additional, Cox, Roni Michelle, additional, McKenney, Jesse K., additional, Gokden, Neriman, additional, Phillips, Carrie L., additional, Giannico, Giovanna A., additional, Gallan, Alexander J., additional, Przybycin, Christopher G., additional, and Grignon, David J., additional

Published
2021
Full Text
View/download PDF

29. Conditional Myh9 and Myh10 inactivation in adult mouse renal epithelium results in progressive kidney disease

Author

Otterpohl, Karla L., primary, Busselman, Brook W., additional, Ratnayake, Ishara, additional, Hart, Ryan G., additional, Hart, Kimberly R., additional, Evans, Claire M., additional, Phillips, Carrie L., additional, Beach, Jordan R., additional, Ahrenkiel, Phil, additional, Molitoris, Bruce A., additional, Surendran, Kameswaran, additional, and Chandrasekar, Indra, additional

Published
2020
Full Text
View/download PDF

32. Clinical, histopathologic and molecular features of idiopathic and diabetic nodular mesangial sclerosis in humans.

Author

Eadon, Michael T, Lampe, Sam, Baig, Mirza M, Collins, Kimberly S, Ferreira, Ricardo Melo, Mang, Henry, Cheng, Ying-Hua, Barwinska, Daria, El-Achkar, Tarek M, Schwantes-An, Tae-Hwi, Winfree, Seth, Temm, Constance J, Ferkowicz, Michael J, Dunn, Kenneth W, Kelly, Katherine J, Sutton, Timothy A, Moe, Sharon M, Moorthi, Ranjani N, Phillips, Carrie L, and Dagher, Pierre C

Subjects
FALSE discovery rate, RENAL biopsy, DIABETES, TRANSCRIPTOMES
Abstract

Background Idiopathic nodular mesangial sclerosis, also called idiopathic nodular glomerulosclerosis (ING), is a rare clinical entity with an unclear pathogenesis. The hallmark of this disease is the presence of nodular mesangial sclerosis on histology without clinical evidence of diabetes mellitus or other predisposing diagnoses. To achieve insights into its pathogenesis, we queried the clinical, histopathologic and transcriptomic features of ING and nodular diabetic nephropathy (DN). Methods All renal biopsy reports accessioned at Indiana University Health from 2001 to 2016 were reviewed to identify 48 ING cases. Clinical and histopathologic features were compared between individuals with ING and DN (n  = 751). Glomeruli of ING (n  = 5), DN (n  = 18) and reference (REF) nephrectomy (n  = 9) samples were isolated by laser microdissection and RNA was sequenced. Immunohistochemistry of proline-rich 36 (PRR36) protein was performed. Results ING subjects were frequently hypertensive (95.8%) with a smoking history (66.7%). ING subjects were older, had lower proteinuria and had less hyaline arteriolosclerosis than DN subjects. Butanoate metabolism was an enriched pathway in ING samples compared with either REF or DN samples. The top differentially expressed gene, PRR36 , had increased expression in glomeruli 248-fold [false discovery rate (FDR) P = 5.93 × 10−6] compared with the REF and increased 109-fold (FDR P = 1.85 × 10−6) compared with DN samples. Immunohistochemistry revealed a reduced proportion of cells with perinuclear reaction in ING samples as compared to DN. Conclusions Despite similar clinical and histopathologic characteristics in ING and DN, the uncovered transcriptomic signature suggests that ING has distinct molecular features from nodular DN. Further study is warranted to understand these relationships. [ABSTRACT FROM AUTHOR]

Published
2022
Full Text
View/download PDF

46. AA cardiomyopathy

Author

Dasgupta, Noel R., primary, Cummings, Oscar W., additional, Phillips, Carrie L., additional, and Benson, Merrill D., additional

Published
2017
Full Text
View/download PDF

48. CONTRASTING HISTOPATHOLOGY AND CRYSTAL DEPOSITS IN KIDNEYS OF IDIOPATHIC STONE FORMERS WHO PRODUCE HYDROXY APATITE, BRUSHITE, OR CALCIUM OXALATE STONES

Author

Evan, Andrew P, Lingeman, James E, Worcester, Elaine M, Sommer, Andre J, Phillips, Carrie L, Williams, James C, and Coe, Fredric L

Subjects
Adult, Calcium Phosphates, Male, Adolescent, Calcium Oxalate, X-Ray Microtomography, Middle Aged, Article, Kidney Calculi, Young Adult, Durapatite, Microscopy, Electron, Transmission, Humans, Female, Aged
Abstract

Our previous work has shown that stone formers who form calcium phosphate (CaP) stones that contain any brushite (BRSF) have a distinctive renal histopathology and surgical anatomy when compared with idiopathic calcium oxalate stone formers (ICSF). Here we report on another group of idiopathic CaP stone formers, those forming stone containing primarily hydroxyapatite, in order to clarify in what ways their pathology differs from BRSF and ICSF. Eleven hydroxyapatite stone formers (HASF) (2 males, 9 females) were studied using intra-operative digital photography and biopsy of papillary and cortical regions to measure tissue changes associated with stone formation. Our main finding is that HASF and BRSF differ significantly from each other and that both differ greatly from ICSF. Both BRSF and ICSF patients have significant levels of Randall's plaque compared with HASF. Intra-tubular deposit number is greater in HASF than BRSF and nonexistent in ICSF while deposit size is smaller in HASF than BRSF. Cortical pathology is distinctly greater in BRSF than HASF. Four attached stones were observed in HASF, three in 25 BRSF and 5-10 per ICSF patient. HASF and BRSF differ clinically in that both have higher average urine pH, supersaturation of CaP, and calcium excretion than ICSF. Our work suggests that HASF and BRSF are two distinct and separate diseases and both differ greatly from ICSF.

Published
2014

Catalog

Books, media, physical & digital resources
See catalog results