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Your search keyword '"P.W. Conrad"' showing total 4 results
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4 results on '"P.W. Conrad"'

1. Oxidative Stress and Cardiovascular Risk in Type 1 Diabetes Mellitus: Insights From the DCCT/EDIC Study

Author

W.H. Wilson Tang, Paula McGee, John M. Lachin, Daniel Y. Li, Byron Hoogwerf, Stanley L. Hazen, D.M. Nathan, B. Zinman, O. Crofford, S. Genuth, J. Brown‐Friday, J. Crandall, H. Engel, S. Engel, H. Martinez, M. Phillips, M. Reid, H. Shamoon, J. Sheindlin, R. Gubitosi‐Klug, L. Mayer, S. Pendegast, H. Zegarra, D. Miller, L. Singerman, S. Smith‐Brewer, M. Novak, J. Quin, Saul Genuth, M. Palmert, E. Brown, J. McConnell, P. Pugsley, P. Crawford, W. Dahms, N.S. Gregory, M.E. Lackaye, S. Kiss, R. Chan, A. Orlin, M. Rubin, D. Brillon, V. Reppucci, T. Lee, M. Heinemann, S. Chang, B. Levy, L. Jovanovic, M. Richardson, B. Bosco, A. Dwoskin, R. Hanna, S. Barron, R. Campbell, A. Bhan, D. Kruger, J.K. Jones, P.A. Edwards, J.D. Carey, E. Angus, A. Thomas, A. Galprin, M. McLellan, F. Whitehouse, R. Bergenstal, M. Johnson, K. Gunyou, L. Thomas, J. Laechelt, P. Hollander, M. Spencer, D. Kendall, R. Cuddihy, P. Callahan, S. List, J. Gott, N. Rude, B. Olson, M. Franz, G. Castle, R. Birk, J. Nelson, D. Freking, L. Gill, W. Mestrezat, D. Etzwiler, K. Morgan, L.P. Aiello, E. Golden, P. Arrigg, V. Asuquo, R. Beaser, L. Bestourous, J. Cavallerano, R. Cavicchi, O. Ganda, O. Hamdy, R. Kirby, T. Murtha, D Schlossman, S. Shah, G. Sharuk, P. Silva, P. Silver, M. Stockman, J. Sun, E. Weimann, H. Wolpert, L.M. Aiello, A. Jacobson, L. Rand, J. Rosenzwieg, M.E. Larkin, M. Christofi, K. Folino, J. Godine, P. Lou, C. Stevens, E. Anderson, H. Bode, S. Brink, C. Cornish, D. Cros, L. Delahanty, eManbey, C. Haggan, J. Lynch, C. McKitrick, D. Norman, D. Moore, M. Ong, C. Taylor, D. Zimbler, S. Crowell, S. Fritz, K. Hansen, C. Gauthier‐Kelly, F.J. Service, G. Ziegler, A. Barkmeier, L. Schmidt, B. French, R. Woodwick, R. Rizza, W.F. Schwenk, M. Haymond, J. Pach, J. Mortenson, B. Zimmerman, A. Lucas, R. Colligan, L. Luttrell, M. Lopes‐Virella, S. Caulder, C. Pittman, N. Patel, K. Lee, M. Nutaitis, J. Fernandes, K. Hermayer, S. Kwon, A Blevins, J. Parker, J. Colwell, D. Lee, J. Soule, P. Lindsey, M. Bracey, A. Farr, S. Elsing, T. Thompson, J. Selby, T. Lyons, S. Yacoub‐Wasef, M. Szpiech, D. Wood, R. Mayfield, M. Molitch, D. Adelman, S. Colson, L. Jampol, A. Lyon, M. Gill, Z. Strugula, L. Kaminski, R. Mirza, E. Simjanoski, D. Ryan, C. Johnson, A. Wallia, S. Ajroud‐Driss, P. Astelford, N. Leloudes, A. Degillio, B. Schaefer, S. Mudaliar, G Lorenzi, M. Goldbaum, K. Jones, M. Prince, M. Swenson, I. Grant, R. Reed, R. Lyon, O. Kolterman, M. Giotta, T. Clark, G. Friedenberg, W.I. Sivitz, B. Vittetoe, J. Kramer, M. Bayless, R. Zeitler, H. Schrott, N. Olson, L. Snetselaar, R. Hoffman, J. MacIndoe, T. Weingeist, C. Fountain, R. Miller, S. Johnsonbaugh, M. Patronas, M. Carney, S. Mendley, P. Salemi, R. Liss, M. Hebdon, D. Counts, T. Donner, J. Gordon, R. Hemady, A. Kowarski, D. Ostrowski, S. Steidl, B. Jones, W.H. Herman, C.L. Martin, R. Pop‐Busui, D.A. Greene, M.J. Stevens, N. Burkhart, T. Sandford, J. Floyd, J. Bantle, N. Flaherty, J. Terry, D. Koozekanani, S. Montezuma, N. Wimmergren, B. Rogness, M. Mech, T. Strand, J. Olson, L. McKenzie, C. Kwong, F. Goetz, R. Warhol, D. Hainsworth, D. Goldstein, S. Hitt, J. Giangiacomo, D.S Schade, J.L. Canady, M.R. Burge, A. Das, R.B. Avery, L.H. Ketai, J.E. Chapin, M.L. Schluter, J. Rich, C. Johannes, D. Hornbeck, M. Schutta, P.A. Bourne, A. Brucker, S. Braunstein, S. Schwartz, B.J. Maschak‐Carey, L. Baker, T. Orchard, L. Cimino, T. Songer, B. Doft, S. Olson, D. Becker, D. Rubinstein, R.L. Bergren, J. Fruit, R. Hyre, C. Palmer, N. Silvers, L. Lobes, P. Paczan Rath, P.W. Conrad, S. Yalamanchi, J. Wesche, M. Bratkowksi, S. Arslanian, J. Rinkoff, J. Warnicki, D. Curtin, D. Steinberg, G. Vagstad, R. Harris, L. Steranchak, J. Arch, K. Kelly, P. Ostrosaka, M. Guiliani, M. Good, T. Williams, K. Olsen, A. Campbell, C. Shipe, R. Conwit, D. Finegold, M. Zaucha, A. Drash, A. Morrison, J.I. Malone, M.L. Bernal, P.R. Pavan, N. Grove, E.A. Tanaka, D. McMillan, J. Vaccaro‐Kish, L. Babbione, H. Solc, T.J. DeClue, S. Dagogo‐Jack, C. Wigley, H. Ricks, A. Kitabchi, E. Chaum, M.B. Murphy, S. Moser, D. Meyer, A. Iannacone, S. Yoser, M. Bryer‐Ash, S. Schussler, H. Lambeth, P. Raskin, S. Strowig, M. Basco, S. Cercone, A. Barnie, R. Devenyi, M. Mandelcorn, M. Brent, S. Rogers, A. Gordon, N. Bakshi, B. Perkins, L. Tuason, F. Perdikaris, R. Ehrlich, D. Daneman, K. Perlman, S Ferguson, J. Palmer, R. Fahlstrom, I.H. de Boer, J. Kinyoun, L. Van Ottingham, S. Catton, J. Ginsberg, C. McDonald, J. Harth, M. Driscoll, T. Sheidow, J. Mahon, C. Canny, D. Nicolle, P. Colby, J. Dupre, I. Hramiak, N.W. Rodger, M. Jenner, T. Smith, W. Brown, M. May, J. Lipps Hagan, A. Agarwal, T. Adkins, R. Lorenz, S. Feman, L. Survant, N.H. White, L. Levandoski, G. Grand, M. Thomas, D. Joseph, K. Blinder, G. Shah, D. Burgess, I. Boniuk, J. Santiago, W. Tamborlane, P. Gatcomb, K. Stoessel, P. Ramos, K. Fong, P. Ossorio, J. Ahern, L. Meadema‐Mayer, C. Beck, K. Farrell, J Quin, P. Gaston, R. Trail, J. Lachin, J. Backlund, I. Bebu, B. Braffett, L. Diminick, X. Gao, W. Hsu, K. Klumpp, H. Pan, V. Trapani, P. Cleary, P. McGee, W. Sun, S. Villavicencio, K. Anderson, L. Dews, Naji Younes, B. Rutledge, K. Chan, D. Rosenberg, B. Petty, A. Determan, D. Kenny, C. Williams, C. Cowie, C. Siebert, M. Steffes, V. Arends, J. Bucksa, M. Nowicki, B. Chavers, D. O'Leary, J. Polak, A. Harrington, L. Funk, R Crow, B. Gloeb, S. Thomas, C. O'Donnell, E.Z. Soliman, Z.M. Zhang, Y. Li, C. Campbell, L. Keasler, S. Hensley, J. Hu, M. Barr, T. Taylor, R. Prineas, E.L. Feldman, J.W. Albers, P. Low, C. Sommer, K. Nickander, T. Speigelberg, M. Pfiefer, M. Schumer, M. Moran, J. Farquhar, C. Ryan, D. Sandstrom, M. Geckle, E. Cupelli, F. Thoma, B. Burzuk, T. Woodfill, R. Danis, B. Blodi, D. Lawrence, H. Wabers, S. Gangaputra, S. Neill, M. Burger, J. Dingledine, V. Gama, R. Sussman, M. Davis, L. Hubbard, M. Budoff, S. Darabian, P. Rezaeian, N. Wong, M. Fox, R. Oudiz, L Kim, R. Detrano, K. Cruickshanks, D. Dalton, K. Bainbridge, J. Lima, D. Bluemke, E. Turkbey, der Geest, C. Liu, A. Malayeri, A. Jain, C. Miao, H. Chahal, R. Jarboe, V. Monnier, D. Sell, C. Strauch, S. Hazen, A. Pratt, W. Tang, J. Brunzell, J. Purnell, R. Natarajan, F. Miao, L. Zhang, Z. Chen, A. Paterson, A. Boright, S. Bull, L. Sun, S. Scherer, T.J. Lyons, A. Jenkins, R. Klein, G. Virella, A. Jaffa, R. Carter, J. Stoner, W.T. Garvey, D. Lackland, M. Brabham, D. McGee, D. Zheng, R.K. Mayfield, J. Maynard, H. Wessells, A Sarma, R. Dunn, S. Holt, J. Hotaling, C. Kim, Q. Clemens, J. Brown, and K. McVary

Subjects
medicine.medical_specialty, endocrine system diseases, 030209 endocrinology & metabolism, Disease, 030204 cardiovascular system & hematology, Lower risk, medicine.disease_cause, 03 medical and health sciences, 0302 clinical medicine, Internal medicine, Diabetes mellitus, medicine, Diseases of the circulatory (Cardiovascular) system, Coronary Heart Disease, Glycemic, Original Research, free radical, Inflammation, Type 1 diabetes, biology, business.industry, Paraoxonase, medicine.disease, paraoxonase, 3. Good health, RC666-701, Cohort, diabetes mellitus, biology.protein, Cardiology and Cardiovascular Medicine, business, Oxidant Stress, Oxidative stress, F2Isoprostane, Biomarkers
Abstract

Background Hyperglycemia leading to increased oxidative stress is implicated in the increased risk for the development of macrovascular and microvascular complications in patients with type 1 diabetes mellitus. Methods and Results A random subcohort of 349 participants was selected from the DCCT / EDIC (Diabetes Control and Complications Trial/Epidemiology of Diabetes Interventions and Complications) cohort. This included 320 controls and 29 cardiovascular disease cases that were augmented with 98 additional known cases to yield a case cohort of 447 participants (320 controls, 127 cases). Biosamples from DCCT baseline, year 1, and closeout of DCCT , and 1 to 2 years post‐ DCCT ( EDIC years 1 and 2) were measured for markers of oxidative stress, including plasma myeloperoxidase, paraoxonase activity, urinary F 2α isoprostanes, and its metabolite, 2,3 dinor‐8 iso prostaglandin F 2α . Following adjustment for glycated hemoblobin and weighting the observations inversely proportional to the sampling selection probabilities, higher paraoxonase activity, reflective of antioxidant activity, and 2,3 dinor‐8 iso prostaglandin F 2α , an oxidative marker, were significantly associated with lower risk of cardiovascular disease (−4.5% risk for 10% higher paraoxonase, P iso prostaglandin F 2α , P =0.0092). In contrast, the oxidative markers myeloperoxidase and F 2α isoprostanes were not significantly associated with cardiovascular disease after adjustment for glycated hemoblobin. There were no significant differences between DCCT intensive and conventional treatment groups in the change in all biomarkers across time segments. Conclusions Heightened antioxidant activity (rather than diminished oxidative stress markers) is associated with lower cardiovascular disease risk in type 1 diabetes mellitus, but these biomarkers did not change over time with intensification of glycemic control. Clinical Trial Registration URL : https://www.clinicaltrials.gov . Unique identifiers: NCT 00360815 and NCT 00360893.

Published
2018

2. Hypoxia Differentially Regulates the Mitogen- and Stress-Activated Protein Kinases

Author

David E. Millhorn, Dana Beitner-Johnson, and P.W Conrad

Subjects
MAPK/ERK pathway, biology, Kinase, p38 mitogen-activated protein kinases, Mitogen-activated protein kinase, biology.protein, medicine, Phosphorylation, Hypoxia (medical), medicine.symptom, Signal transduction, Protein kinase A, Cell biology
Abstract

Hypoxic/ischemic trauma is a primary factor in the pathology of various vascular, pulmonary, and cerebral disease states. Yet, the signaling mechanisms by which cells respond and adapt to changes in oxygen levels are not clearly established. The effects of hypoxia on the stress-and mitogen-activated protein kinase (SAPK and MAPK) signaling pathways were studied in PC12 cells. Exposure to moderate hypoxia (5%O2) was found to progressively stimulate phosphorylation and activation of p38γ in particular, and also p38α. two isoforms of the p38 family of stress-activated protein kinases. In contrast, hypoxia had no effect on enzyme activity of p38β, p38β2, p38δ or on JNK, another stress-activated protein kinase. Prolonged hypoxia also induced phosphorylation and activation of p42/p44 MAPK, although this activation was modest when compared to NGF and UV-induced activation. We further showed that activation of p38γ and MAPK during hypoxia requires calcium, as treatment with Ca2+-free media or the calmodulin antagonist, W13, blocked the activation of p38γ and MAPK, respectively. These studies demonstrate that an extremely typical physiological stress (hypoxia) causes selective activation of specific elements of the SAPKs and MAPKs, and identifies Ca+2/CaM as a critical upstream activator.

Published
2002
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3. Identification of hypoxia-responsive genes in a dopaminergic cell line by subtractive cDNA libraries and microarray analysis

Author

P.W Conrad, Yong Yuan, Dana Beitner-Johnson, David E. Millhorn, H.-W Kim, K Seta, Shuichi Kobayashi, and Randy T. Rust

Subjects
Programmed cell death, Microarray analysis techniques, cDNA library, Hypoxia (medical), Biology, Bioinformatics, Cell biology, Transplantation, Neurology, Dopaminergic Cell, Parenchyma, Gene expression, medicine, Neurology (clinical), Geriatrics and Gerontology, medicine.symptom
Abstract

Transplantation of dopamine-secreting cells harvested from fetal mesencephalon directly into the striatum has had limited success as a therapy for Parkinson's disease. A major problem is that the majority of the cells die during the first 3 weeks following transplantation. Hypoxia in the tissue surrounding the graft is a potential cause of the cell death. We have used subtractive cDNA libraries and microarray analysis to identify the gene expression profile that regulates tolerance to hypoxia. An improved understanding of the molecular basis of hypoxia-tolerance may allow investigators to engineer cells that can survive in the hypoxic environment of the brain parenchyma following transplantation.

Published
2001

4. Regulation of gene expression and secretory functions in oxygen-sensing pheochromocytoma cells

Author

Dana Beitner-Johnson, Shuichi Kobayashi, David E. Millhorn, P.W Conrad, Thomas L. Freeman, and Laura Conforti

Subjects
Pulmonary and Respiratory Medicine, Adenosine, Potassium Channels, Tyrosine 3-Monooxygenase, Physiology, Dopamine, Pheochromocytoma, Biology, PC12 Cells, Feedback, Membrane Potentials, Receptors, Dopamine, Neurotransmitter secretion, Gene expression, medicine, Animals, Homeostasis, Receptor, Regulation of gene expression, Tyrosine hydroxylase, Receptors, Purinergic P1, Depolarization, Cell Hypoxia, Cell biology, Rats, Gene Expression Regulation, Neoplastic, Oxygen, Biochemistry, Calcium, Intracellular, medicine.drug
Abstract

The cellular response to hypoxia is complex. Specialized oxygen chemosensitive cells that are excitable respond to reduced O2 by membrane depolarization, altered gene expression, and neurotransmitter secretion. We have used the O2-sensitive pheochromocytoma (PC12) cell line to investigate the cellular response to hypoxia. Here, we present evidence that membrane depolarization and increased intracellular free Ca2+ are major regulatory events in these cells. Membrane depolarization is mediated by the inhibition of a slow-inactivating voltage-dependent potassium (K) channel. Evidence from molecular biology and patch-clamp studies indicate that the O2-sensitive K channel is a member of the Kv1 family. We also reviewed findings on the regulation of gene expression in PC12 cells during hypoxia. An increase in intracellular free Ca2+ is required for hypoxia-induced transcription of a number of genes including tyrosine hydroxylase (TH), the rate-limiting enzyme in the synthesis of catecholamine neurotransmitters, and several of the immediate early genes. We also reviewed the role of dopamine (DA) and adenosine (ADO) receptors in regulation of membrane depolarization and gene expression.

Published
1999

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