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644 citation(s) found for "Hugo".

Adrenoleukodystrophy
Moser, Hugo W., Moser, Ann B. , Frayer, Karen K., Chen, Winston, Kishimoto, Yasuo, Schulman, Joseph D. , O’Neill, Brian Patrick

Neurology | May 13, 2012 | Volume: 51 | Issue: 2 | Pages: 334

10.1212/wnl.51.2.334-a | PMID 9709997 Get It

Familial spastic paraparesis
Swanson, Jerry W., Brown, Frank R., Griffin, John W., Moser, Hugo W., O’Neill, Brian Patrick

Neurology | May 13, 2012 | Volume: 35 | Issue: 8 | Pages: 1233-1233

10.1212/wnl.35.8.1233 | PMID 4022363 Get It

Adrenoleukodystrophy
Moser, Hugo W., Saxena, Krishna M., Marmion, Lee C., O’Neill, Brian Patrick

Neurology | May 13, 2012 | Volume: 34 | Issue: 6 | Pages: 798-798

10.1212/wnl.34.6.798 | PMID 6539445 Get It

Adrenoleuko‐dystrophy (ALD)
Marler, John R., Forbes, Glenn S. , Moser, Hugo W., O’Neill, Brian Patrick

Neurology | May 13, 2012 | Volume: 33 | Issue: 9 | Pages: 1203-1203

10.1212/wnl.33.9.1203 | PMID 6684256 Get It

Familial X‐linked Addison disease as an expression of adrenoleukodystrophy (ALD)
Moser, Hugo W., Saxena, Krishna M., O’Neill, Brian Patrick

Neurology | May 13, 2012 | Volume: 32 | Issue: 5 | Pages: 543-543

10.1212/wnl.32.5.543 | PMID 6280107 Get It

Adrenoleukodystrophy
Moser, Hugo W., Marmion, Lee C., O’Neill, Brian Patrick

Neurology | May 13, 2012 | Volume: 32 | Issue: 5 | Pages: 540-540

10.1212/wnl.32.5.540 | PMID 6280106 Get It

Pretransplant Fasting Glucose Predicts New-Onset Diabetes after Liver Transplantation
Carey, Elizabeth J. , Aqel, Bashar , Byrne, Thomas , Douglas, David D., Rakela, Jorge , Vargas, Hugo E. , Moss, Adyr A. , Reddy, Kunam S. , Chakkera, Harini A. , Aqel, Bashar A. , Mulligan, David C. , Vargas, Hugo E , Chakkera, Harini A

Journal of Transplantation | January 29, 2012 | Volume: 2012 | Issue: No issue available | Pages: 1-6

10.1155/2012/614781 | PMID 22461975 Get It

New-onset diabetes after transplantation (NODAT) is common after liver transplant and associated with poorer outcomes. The aim of this study was to identify risk factors for NODAT in liver transplant recipients off corticosteroids. In 225 adult nondiabetic liver transplant recipients, the mean age was 51.7 years, the majority were men (71%), and half had HCV (49%). The mean calculated MELD score at transplantation was 18.7, and 19% underwent living-donor transplant (LDLT). One year after transplantation, 17% developed NODAT, and an additional 16% had impaired fasting glucose. The incidence of NODAT in patients with HCV was 26%. In multivariate analysis, HCV, pretransplant FPG, and LDLT were significant. Each 10 mg/dL increase in pretransplant FPG was associated with a twofold increase in future development of NODAT. The incidence of NODAT after liver transplant in patients off corticosteroids is 17%. Risk factors for developing NODAT include HCV and pretransplant FPG; LDLT is protective.
Interpreting Changes in Troponin—Clinical Judgment Is Essential
Katus, Hugo A. , Jaffe, Allan S. , Giannitsis, Evangelos , Jaffe, Allan S.

Clinical Chemistry | December 28, 2011 | Volume: 58 | Issue: 1 | Pages: 39-43

10.1373/clinchem.2011.173138 | PMID 22205772 Get It

The Alzheimer's Association external quality control program for cerebrospinal fluid biomarkers
Mattsson, Niklas , Andréasson, Ulf , Batish, Sat Dev, Bernardini, Sergio , Bocchio‐Chiavetto, Luisella , Blankenstein, Marinus A. , Carrillo, María C. , Chalbot, Sonia, Coart, Els, Chiasserini, Davide , Cutler, Neal E., Dahlfors, Gunilla, Duller, Stefan, Fagan, Anne M. , Frisoni, Giovanni B. , Galimberti, Daniela , Hampel, Harald , Handberg, Aase , Heneka, Michael T. , Herskovits, A. Zara , Herukka, Sanna‐Kaisa , Humpel, Christian , Iqbal, Khalid , Kaeser, Stephan A. , Kaiser, Elmar, Kapaki, Elisabeth, Kidd, Daniel, Klivènyi, Péter , Knudsen, Cindy Soendersoe, Kummer, Markus P. , Lui, James, Lladó, Albert , Li, Qiao‐Xin , Martins, Ralph N. , Masters, Colin L. , McAuliffe, John C., Mercken, Marc, Moghekar, Abhay , Molinuevo, José Luís , Montine, Thomas J. , Nowatzke, William, O’Brien, Richard , Otto, Markus , Parnetti, Lucilla , Petersen, Ronald C. , Prvulovic, David, Reus, Herman P.M. de, Scarpini, Elio , Stefani, Alessandro , Schröder, Johannes , Shaw, Leslie M. , Skinningsrud, Anders, Skrogstad, Brith, Spreer, Annette, Trojanowski, John Q. , Tumani, Hayrettin , Umek, Robert M., Broeck, Bianca Van, Vanderstichele, Hugo, Vécsei, László , Blennow, Kaj , Frisoni, Giovanni B. , Persson, Staffan , Arai, Hiroyuki N. , Forlenza, Orestes Vicente , Galasko, Douglas , Holtzman, David M. , Hyman, Bradley T. , Jucker, Mathias , Lewczuk, Piotr , Paraskevas, George P. , Rissman, Robert A. , Soininen, Hilkka S. , Talib, Leda Leme , Teunissen, Charlotte E. , Verbeek, Marcel M. , Windisch, Manfred , Zhang, Jing , Zetterberg, Henrik , Parnetti, Lucilla , Molinuevo, José Luis , Masters, Colin L , Otto, Markus , Galimberti, Daniela

Alzheimer's & Dementia | July 25, 2011 | Volume: 7 | Issue: 4 | Pages: 386

10.1016/j.jalz.2011.05.2243 | PMID 21784349 Get It

BackgroundThe cerebrospinal fluid (CSF) biomarkers amyloid β (Aβ)‐42, total‐tau (T‐tau), and phosphorylated‐tau (P‐tau) demonstrate good diagnostic accuracy for Alzheimer's disease (AD). However, there are large variations in biomarker measurements between studies, and between and within laboratories. The Alzheimer's Association has initiated a global quality control program to estimate and monitor variability of measurements, quantify batch‐to‐batch assay variations, and identify sources of variability. In this article, we present the results from the first two rounds of the program.MethodsThe program is open for laboratories using commercially available kits for Aβ, T‐tau, or P‐tau. CSF samples (aliquots of pooled CSF) are sent for analysis several times a year from the Clinical Neurochemistry Laboratory at the Mölndal campus of the University of Gothenburg, Sweden. Each round consists of three quality control samples.ResultsForty laboratories participated. Twenty‐six used INNOTEST enzyme‐linked immunosorbent assay kits, 14 used Luminex xMAP with the INNO‐BIA AlzBio3 kit (both measure Aβ‐(1‐42), P‐tau(181P), and T‐tau), and 5 used Meso Scale Discovery with the Aβ triplex (AβN‐42, AβN‐40, and AβN‐38) or T‐tau kits. The total coefficients of variation between the laboratories were 13% to 36%. Five laboratories analyzed the samples six times on different occasions. Within‐laboratory precisions differed considerably between biomarkers within individual laboratories.ConclusionsMeasurements of CSF AD biomarkers show large between‐laboratory variability, likely caused by factors related to analytical procedures and the analytical kits. Standardization of laboratory procedures and efforts by kit vendors to increase kit performance might lower variability, and will likely increase the usefulness of CSF AD biomarkers.
Autologous transplantation gives encouraging results for young adults with favorable-risk acute myeloid leukemia, but is not improved with gemtuzumab ozogamicin
Fernández, Hugo F. , Sun, Zhuoxin , Litzow, Mark R. , Luger, Selina M. , Paietta, Elisabeth , Racevskis, Janis, Dewald, Gordon W., Ketterling, Rhett P. , Rowe, Jacob M. , Tallman, Martin S. , Lazarus, Hillard M. , Ketterling, Rhett P

Blood | March 18, 2011 | Volume: 117 | Issue: 20 | Pages: 5306-5313

10.1182/blood-2010-09-309229 | PMID 21415269 Get It

AbstractWe report the results of a prospective, randomized phase 3 trial evaluating the use of gemtuzumab ozogamicin (GO) in an intensive consolidation approach in 657 patients 17-60 years of age. Patients in first complete remission (CR1) after cytarabine and standard- or high-dose daunorubicin induction received 2 cycles of consolidation with high-dose cytarabine followed by peripheral blood progenitor cell collection. The 352 patients who entered consolidation were randomized to receive GO (n = 132) or not (n = 138) and then proceeded to autologous hematopoietic cell transplantation (HCT). GO was given to 67 patients. Median follow-up was 50.9 months. Results of the intention-to-treat analysis demonstrated a 4-year disease-free survival (DFS) of 33.6% versus 35.9% (P = .54) and an overall survival (OS) of 41.3% versus 41.9% (P = .52) for those randomized to receive GO versus no GO, respectively. Patients with favorable- and intermediate-risk acute myeloid leukemia (AML) treated with high-dose daunorubicin and autologous HCT had 4-year DFS rates of 60% and 40% and OS rates of 80% and 49.3%, respectively. For younger AML patients in CR1, autologous HCT should be considered in favorable- and intermediate-cytogenetic risk patients who do not have an allogeneic donor. The addition of a single dose of GO in this setting did not improve outcomes. This trial is registered at http://www.clinicaltrials.gov as NCT00049517.