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1. Immunosuppression and outcomes in adult patients with de novo acute myeloid leukemia with normal karyotypes

Author

Ferraro, Francesca, Miller, Christopher A., Christensen, Keegan A., Helton, Nichole M., O’Laughlin, Margaret, Fronick, Catrina C., Fulton, Robert S., Kohlschmidt, Jessica, Eisfeld, Ann-Kathrin, Bloomfield, Clara D., Ramakrishnan, Sai Mukund, Day, Ryan B., Wartman, Lukas D., Uy, Geoffrey L., Welch, John S., Christopher, Matthew J., Heath, Sharon E., Baty, Jack D., Schuelke, Matthew J., Payton, Jacqueline E., Spencer, David H., Rettig, Michael P., Link, Daniel C., Walter, Matthew J., Westervelt, Peter, DiPersio, John F., and Ley, Timothy J.

Published
2021

8. The Origin and Evolution of Mutations in Acute Myeloid Leukemia

Author

Welch, John S., Ley, Timothy J., Link, Daniel C., Miller, Christopher A., Larson, David E., Koboldt, Daniel C., Wartman, Lukas D., Lamprecht, Tamara L., Liu, Fulu, Xia, Jun, Kandoth, Cyriac, Fulton, Robert S., McLellan, Michael D., Dooling, David J., Wallis, John W., Chen, Ken, Harris, Christopher C., Schmidt, Heather K., Kalicki-Veizer, Joelle M., Lu, Charles, Zhang, Qunyuan, Lin, Ling, O’Laughlin, Michelle D., McMichael, Joshua F., Delehaunty, Kim D., Fulton, Lucinda A., Magrini, Vincent J., McGrath, Sean D., Demeter, Ryan T., Vickery, Tammi L., Hundal, Jasreet, Cook, Lisa L., Swift, Gary W., Reed, Jerry P., Alldredge, Patricia A., Wylie, Todd N., Walker, Jason R., Watson, Mark A., Heath, Sharon E., Shannon, William D., Varghese, Nobish, Nagarajan, Rakesh, Payton, Jacqueline E., Baty, Jack D., Kulkarni, Shashikant, Klco, Jeffery M., Tomasson, Michael H., Westervelt, Peter, Walter, Matthew J., Graubert, Timothy A., DiPersio, John F., Ding, Li, Mardis, Elaine R., and Wilson, Richard K.

Published
2012
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9. Role of TP53 mutations in the origin and evolution of therapy--related acute myeloid leukaemia

Author

Wong, Terrence N., Ramsingh, Giridharan, Young, Andrew L., Miller, Christopher A., Touma, Waseem, Welch, John S., Lamprecht, Tamara L., Shen, Dong, Hundal, Jasreet, Fulton, Robert S., Heath, Sharon, Baty, Jack D., Klco, Jeffery M., Ding, Li, Mardis, Elaine R., Westervelt, Peter, DiPersio, John F., Walter, Matthew J., Graubert, Timothy A., Ley, Timothy J., Druley, Todd E., Link, Daniel C., and Wilson, Richard K.

Subjects
Care and treatment, Genetic aspects, Research, Risk factors, Health aspects, Gene mutation -- Health aspects, Acute myelocytic leukemia -- Risk factors -- Genetic aspects -- Care and treatment -- Research, Gene mutations -- Health aspects
Abstract

t-AML and t-MDS are clonal haematopoietic disorders that typically develop 1-5 years after exposure to chemotherapy or radiotherapy (1). To understand better how prior cytotoxic therapy contributes to the high [...], Therapy-related acute myeloid leukaemia (t-AML) and therapy-related myelodysplastic syndrome (t-MDS) are well-recognized complications of cytotoxic chemotherapy and/or radiotherapy (1). There are several features that distinguish t-AML from denovo AML, including a higher incidence of TP53 mutations (2,3), abnormalities of chromosomes 5 or 7, complex cytogenetics and a reduced response to chemotherapy (4). However, it is not clear how prior exposure to cytotoxic therapy influences leukaemogenesis. In particular, the mechanism by which TP53 mutations are selectively enriched in t-AML/t-MDS is unknown. Here, by sequencing the genomes of 22 patients with t-AML, we show that the total number of somatic single-nucleotide variants and the percentage of chemotherapy-related transversions are similar in t-AML and denovo AML, indicating that previous chemotherapy does not induce genome-wide DNA damage. W e identified four cases of t-AML/ t-MDS in which the exact TP53 mutation found at diagnosis was also present at low frequencies (0.003-0.7%) in mobilized blood leukocytes or bone marrow 3-6 years before the development of t-AML/tMDS, including two cases in which the relevant TP53 mutation was detected before any chemotherapy. Moreover, functional TP53 mutations were identified in small populations of peripheral blood cells of healthy chemotherapy-naive elderly individuals. Finally, in mouse bone marrow chimaeras containing both wild-type and [Tp53.sup.+/-] haematopoietic stem/progenitor cells (HSPCs), the [Tp53.sup.+/-] HSPCs preferentially expanded after exposure to chemotherapy. These data suggest that cytotoxic therapy does not directly induce TP53 mutations. Rather, they support a model in which rare HSPCs carrying age-related TP53 mutations are resistant to chemotherapy and expand preferentially after treatment. The early acquisition of TP53 mutations in the founding HSPC clone probably contributes to the frequent cytogenetic abnormalities and poor responses to chemotherapy that are typical of patients with t-AML/t-MDS.

Published
2015

10. Adverse Outcomes in Acute Myeloid Leukemia Are Associated with Tumor Cell-Mediated Immunosuppression

Author

Ferraro, Francesca, primary, Miller, Christopher A, additional, Christensen, Keegan A, additional, Helton, Nichole M, additional, O'Laughlin, Michelle, additional, Fulton, Robert, additional, Kohlschmidt, Jessica, additional, Eisfeld, Ann-Kathrin, additional, Clara, Bloomfield, additional, Ramakrishnan, Sai Mukund, additional, Wartman, Lukas D, additional, Welch, John, additional, Christopher, Matthew, additional, Heath, Sharon E, additional, Westervelt, Peter, additional, Baty, Jack D, additional, Payton, Jacqueline E., additional, Retting, Michael, additional, Link, Daniel C., additional, Walter, Matthew J., additional, DiPersio, John F., additional, Day, Ryan, additional, Uy, Geoffrey L., additional, Schuelke, Matthew, additional, Spencer, David H, additional, and Ley, Timothy J, additional

Published
2021
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11. Air pollution and survival within the Washington University-EPRI Veterans Cohort: risks based on modeled estimates of ambient levels of hazardous and criteria air pollutants

Author

Lipfert, Frederick W., Wyzga, Ronald E., Baty, Jack D., and Miller, J.Philip

Subjects
Smog -- Social aspects -- Case studies -- Methods, Data entry -- Methods -- Case studies -- Social aspects, Environmental services industry, Environmental issues, Science and technology
Abstract

ABSTRACT For this paper, we considered relationships between mortality, vehicular traffic density, and ambient levels of 12 hazardous air pollutants, elemental carbon (EC), oxides of nitrogen ([NO.sub.x]), sulfur dioxide ([SO.sub.2]), [...]

Published
2009

12. Immunosuppression and Outcomes in Acute Myeloid Leukemia

Author

Ferraro, Francesca, primary, Miller, Christopher, additional, Christensen, Keegan, additional, Helton, Nichole M., additional, O'Laughlin, Margareth, additional, Fronick, Catrina C, additional, Fulton, Robert S, additional, Kohlschmidt, Jessica, additional, Eisfeld, Ann-Kathrin, additional, Bloomfield, Clara D, additional, Ramakrishnan, Sai M, additional, Day, Ryan B, additional, Wartman, Lukas D, additional, Uy, Geoffrey L, additional, Welch, John S, additional, Christopher, Matthew J, additional, Heath, Sharon E, additional, Baty, Jack D, additional, Schuelke, Matthew J, additional, Payton, Jacqueline E, additional, Spencer, David H, additional, Rettig, Michael P, additional, Link, Daniel C, additional, Walter, Matthew J, additional, Peter, Westervelt, additional, DiPersio, John F, additional, and Ley, Timothy J, additional

Published
2021
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13. Genome Sequencing as an Alternative to Cytogenetic Analysis in Myeloid Cancers

Author

Duncavage, Eric J., primary, Schroeder, Molly C., additional, O’Laughlin, Michele, additional, Wilson, Roxanne, additional, MacMillan, Sandra, additional, Bohannon, Andrew, additional, Kruchowski, Scott, additional, Garza, John, additional, Du, Feiyu, additional, Hughes, Andrew E.O., additional, Robinson, Josh, additional, Hughes, Emma, additional, Heath, Sharon E., additional, Baty, Jack D., additional, Neidich, Julie, additional, Christopher, Matthew J., additional, Jacoby, Meagan A., additional, Uy, Geoffrey L., additional, Fulton, Robert S., additional, Miller, Christopher A., additional, Payton, Jacqueline E., additional, Link, Daniel C., additional, Walter, Matthew J., additional, Westervelt, Peter, additional, DiPersio, John F., additional, Ley, Timothy J., additional, and Spencer, David H., additional

Published
2021
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18. Chromosome 8 allelic loss and the outcome of patients with squamous cell carcinoma of the supraglottic larynx

Author

Scholnick, Steven B., Haughey, Bruce H., Sunwoo, John B., El-Mofty, Samir K., Baty, Jack D., Piccirillo, Jay F., and Zequeira, Maria R.

Subjects
Squamous cell carcinoma -- Prognosis, Disease susceptibility -- Genetic aspects, Laryngeal cancer -- Prognosis, Health
Abstract

Background: Loss of genetic heterogeneity (allelic loss or loss of heterozygosity) on chromosome arm 8p is frequent in squamous cell carcinomas of the head and neck and has been associated with poor prognosis. We have previously demonstrated that there are three minimal regions of allelic loss on this chromosome arm. The location of each region is marked by a microsatellite locus: D8S264 (8p23), D8S552 (8p23-p22), and D8S133 (8p21). These findings imply the existence of at least three putative tumor suppressor genes on this chromosome arm that may become inactivated during the progression of squamous cell carcinoma. Purpose: We used allelic loss data from these three loci to determine if inactivation of these putative suppressors is associated with poor prognosis for patients with squamous cell carcinoma of the supraglottic larynx. We also used multivariate statistics to compare the prognostic power of allelic loss at these genetic markers with that of demographic, clinical, and histopathologic parameters. Methods: We examined the D8S264, D8S552, and D8S133 microsatellites in tumors from a retrospective population of 59 patients. All patients had histologically confirmed squamous cell carcinoma of the supraglottic larynx and had been treated surgically. DNA was extracted from matched sets of normal and microdissected tumor tissue and used for polymerase chain reaction amplification of the microsatellite markers. Reaction products were separated by denaturing gel electrophoresis and visualized by autoradiography. Patient data were obtained from the original pathology report and from the tumor registry of the Department of Otolaryngology-Head and Neck Surgery, Washington University School of Medicine, St. Louis, MO. Histopathologic data were obtained by reviewing the portion of the resection specimen used for DNA extraction. Parameters whose association with reduced disease-free interval and reduced disease-specific survival was statistically significant were identified by use of the Kaplan-Meier method and the logrank statistic. Multivariate Cox proportional hazards models were used to identify independent predictors of poor prognosis. All statistical tests were two-sided. Results: In this patient population, allelic loss at the D8S264 locus was associated with both shorter disease-free interval (logrank P = .028) and reduced disease-specific survival (logrank P = .004). Allelic loss at the next most centromeric locus, D8S552, had a statistically significant association with only reduced disease-specific survival (logrank P = .034), whereas allelic loss at the most centromeric region, D8S133, showed no statistically significant association with reductions in either interval. Multivariate Cox models suggested that D8S264 was the only 8p marker of the three microsatellites with a statistically significant and independent association with shortened disease-free interval (relative risk [RR] = 3.38; P = .0107) and reduced disease-specific survival (RR = 3.41; P = .0105). Conclusions: Allelic loss in the p23 region of chromosome 8 appears to be a statistically significant, independent predictor of poor prognosis in patients with supraglottic squamous cell carcinoma.

Published
1996

21. Immune Escape of Relapsed AML Cells after Allogeneic Transplantation

Author

Christopher, Matthew J., primary, Petti, Allegra A., additional, Rettig, Michael P., additional, Miller, Christopher A., additional, Chendamarai, Ezhilarasi, additional, Duncavage, Eric J., additional, Klco, Jeffery M., additional, Helton, Nicole M., additional, O’Laughlin, Michelle, additional, Fronick, Catrina C., additional, Fulton, Robert S., additional, Wilson, Richard K., additional, Wartman, Lukas D., additional, Welch, John S., additional, Heath, Sharon E., additional, Baty, Jack D., additional, Payton, Jacqueline E., additional, Graubert, Timothy A., additional, Link, Daniel C., additional, Walter, Matthew J., additional, Westervelt, Peter, additional, Ley, Timothy J., additional, and DiPersio, John F., additional

Published
2018
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22. Improving Risk Assessment of AML with a Precision Genomic Strategy to Assess Mutation Clearance

Author

Jacoby, Meagan, primary, Spencer, David H, additional, Hughes, Emma, additional, Fulton, Robert S, additional, O'Laughlin, Michelle, additional, Fronick, Catrina, additional, Loken, Michael R., additional, Baty, Jack D, additional, Schroeder, Mark A., additional, Ghobadi, Armin, additional, Uy, Geoffrey L., additional, Vij, Ravi, additional, Kahl, Brad S, additional, Cashen, Amanda F, additional, Walter, Matthew J., additional, Wartman, Lukas D, additional, Welch, John S., additional, DiPersio, John F., additional, Westervelt, Peter, additional, and Ley, Timothy J, additional

Published
2018
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23. Cellular stressors contribute to the expansion of hematopoietic clones of varying leukemic potential

Author

Wong, Terrence N., primary, Miller, Christopher A., additional, Jotte, Matthew R. M., additional, Bagegni, Nusayba, additional, Baty, Jack D., additional, Schmidt, Amy P., additional, Cashen, Amanda F., additional, Duncavage, Eric J., additional, Helton, Nichole M., additional, Fiala, Mark, additional, Fulton, Robert S., additional, Heath, Sharon E., additional, Janke, Megan, additional, Luber, Kierstin, additional, Westervelt, Peter, additional, Vij, Ravi, additional, DiPersio, John F., additional, Welch, John S., additional, Graubert, Timothy A., additional, Walter, Matthew J., additional, Ley, Timothy J., additional, and Link, Daniel C., additional

Published
2018
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24. TP53 and Decitabine in Acute Myeloid Leukemia and Myelodysplastic Syndromes

Author

Welch, John S., primary, Petti, Allegra A., additional, Miller, Christopher A., additional, Fronick, Catrina C., additional, O’Laughlin, Michelle, additional, Fulton, Robert S., additional, Wilson, Richard K., additional, Baty, Jack D., additional, Duncavage, Eric J., additional, Tandon, Bevan, additional, Lee, Yi-Shan, additional, Wartman, Lukas D., additional, Uy, Geoffrey L., additional, Ghobadi, Armin, additional, Tomasson, Michael H., additional, Pusic, Iskra, additional, Romee, Rizwan, additional, Fehniger, Todd A., additional, Stockerl-Goldstein, Keith E., additional, Vij, Ravi, additional, Oh, Stephen T., additional, Abboud, Camille N., additional, Cashen, Amanda F., additional, Schroeder, Mark A., additional, Jacoby, Meagan A., additional, Heath, Sharon E., additional, Luber, Kierstin, additional, Janke, Megan R., additional, Hantel, Andrew, additional, Khan, Niloufer, additional, Sukhanova, Madina J., additional, Knoebel, Randall W., additional, Stock, Wendy, additional, Graubert, Timothy A., additional, Walter, Matthew J., additional, Westervelt, Peter, additional, Link, Daniel C., additional, DiPersio, John F., additional, and Ley, Timothy J., additional

Published
2016
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25. Genomic and epigenomic landscapes of adult de novo acute myeloid leukemia

Author

Ley, Timothy, Miller, Christopher, Ding, Li, Raphael, Benjamin J., Mungall, Andrew J., Robertson, A. Gordon, Hoadley, Katherine, Triche, Timothy J., Laird, Peter W., Baty, Jack D., Fulton, Lucinda L., Fulton, Robert, Heath, Sharon E., Kalicki Veizer, Joelle, Kandoth, Cyriac, Klco, Jeffery M., Koboldt, Daniel C., Kanchi, Krishna Latha, Shashikant, Kulkarni, M. S., P. h. D., F. A. C. M. G., Lamprecht, Tamara L., B. S., Washington, University, Louis, S. t., Larson, David E., P. h. D., Ling, Lin, M. S., Charles, Lu, Mclellan, Michael D., Mcmichael, Joshua F., the Genome Institute at Washington University, Jacqueline, Payton, M. D., P. h. D., Heather, Schmidt, Spencer, David H., Tomasson, Michael H., M. D., Siteman Cancer Center, S. t. Louis, Wallis, John W., Wartman, Lukas D., Watson, Mark A., John, Welch, Wendl, Michael C., Adrian, Ally, B. S. c., Miruna, Balasundaram, B. A. S. c., Inanc, Birol, Yaron, Butterfield, Readman, Chiu, M. S. c., Andy, Chu, Eric, Chuah, Hye Jung Chun, Richard, Corbett, Noreen, Dhalla, Ranabir, Guin, An, He, Carrie, Hirst, Martin, Hirst, Holt, Robert A., Steven, Jones, Aly, Karsan, Darlene, Lee, Haiyan I., Li, Marra, Marco A., Michael, Mayo, Moore, Richard A., Karen, Mungall, Jeremy, Parker, Erin, Pleasance, Patrick, Plettner, Jacquie, Schein, Dominik, Stoll, Lucas, Swanson, Angela, Tam, Nina, Thiessen, Richard, Varhol, Natasja, Wye, Yongjun, Zhao, M. S. c., D. V. M., British Columbia Cancer Agency's Genome Sciences Centre, Vancouver, Canada, Stacey, Gabriel, Gad, Getz, Carrie, Sougnez, Lihua, Zou, Broad Institute of Harvard, Massachusetts Institute of Technology, Cambridge, Ma, Mark D. M. Leiserson, B. A., Vandin, Fabio, Hsin Ta Wu, Brown, University, Center for Computational Molecular Biology, Providence, Ri, Frederick, Applebaum, Fred Hutchinson Cancer Research Center, Division of Medical Oncology, Seattle Cancer Care Alliance, Seattle, Baylin, Stephen B., Johns Hopkins University, Baltimore, Rehan, Akbani, Broom, Bradley M., Ken, Chen, Motter, Thomas C., B. A., Khanh, Nguyen, Weinstein, John N., Nianziang, Zhang, Anderson Cancer Center, University of Texas M. D., Houston, Ferguson, Martin L., Mlf, Consulting, Biotechnology Consultant, Boston, Christopher, Adams, Aaron, Black, Jay, Bowen, Julie Gastier Foster, Thomas, Grossman, Tara, Lichtenberg, Lisa, Wise, the Research Institute at Nationwide Children's Hospital, Columbus, Oh, Tanja, Davidsen, Demchok, John A., Mills Shaw, Kenna R., Margi, Sheth, National Cancer Institute, Bethesda, Md, Sofia, Heidi J., P. h. D., M. P. H., National Human Genome Research Institute, Liming, Yang, Downing, James R., Jude Children's Research Hospital, S. t., Memphis, Greg, Eley, Sciementis, Llc, Statham, Ga, Shelley, Alonso, Brenda, Ayala, Julien, Baboud, Mark, Backus, Barletta, Sean P., Berton, Dominique L., M. S. C. S., Chu, Anna L., Stanley, Girshik, Jensen, Mark A., Ari, Kahn, Prachi, Kothiyal, Nicholls, Matthew C., Pihl, Todd D., Pot, David A., Rohini, Raman, B. E., Sanbhadti, Rashmi N., Snyder, Eric E., Deepak, Srinivasan, Jessica, Walton, Yunhu, Wan, Zhining, Wang, Sra, International, Fairfax, Va, Issa, Jean Pierre J., Temple, University, Philadelphia, Michelle Le Beau, University of Chicago, Chicago, Martin, Carroll, University of Pennsylvania, Hagop Kantarjian, M. D., Steven, Kornblau, Bootwalla, Moiz S., B. S. c., M. S., Lai, Phillip H., Hui, Shen, Van Den Berg, David J., Weisenberger, Daniel J., University of Southern California, Epigenome, Center, Los, Angeles, Daniel C. Link, M. D., Walter, Matthew J., Ozenberger, Bradley A., Mardis, Elaine R., Peter, Westervelt, Graubert, Timothy A., Dipersio, John F., and Wilson, Richard K.

Subjects
Myeloid, Adult, Epigenomics, Male, NPM1, Gene Expression, CpG Islands, DNA Methylation, Female, Gene Fusion, Genome, Human, Humans, Leukemia, Myeloid, Acute, MicroRNAs, Middle Aged, Sequence Analysis, DNA, Mutation, Acute, Enasidenib, Biology, CEBPA, Genetics, Genome, Leukemia, Massive parallel sequencing, MicroRNA sequencing, Myeloid leukemia, DNA, General Medicine, KMT2A, biology.protein, Sequence Analysis, Nucleophosmin, Human, Comparative genomic hybridization
Abstract

BACKGROUND—Many mutations that contribute to the pathogenesis of acute myeloid leukemia (AML) are undefined. The relationships between patterns of mutations and epigenetic phenotypes are not yet clear. METHODS—We analyzed the genomes of 200 clinically annotated adult cases of de novo AML, using either whole-genome sequencing (50 cases) or whole-exome sequencing (150 cases), along with RNA and microRNA sequencing and DNA-methylation analysis. RESULTS—AML genomes have fewer mutations than most other adult cancers, with an average of only 13 mutations found in genes. Of these, an average of 5 are in genes that are recurrently mutated in AML. A total of 23 genes were significantly mutated, and another 237 were mutated in two or more samples. Nearly all samples had at least 1 nonsynonymous mutation in one of nine categories of genes that are almost certainly relevant for pathogenesis, including transcriptionfactor fusions (18% of cases), the gene encoding nucleophosmin (NPM1) (27%), tumorsuppressor genes (16%), DNA-methylation–related genes (44%), signaling genes (59%), chromatin-modifying genes (30%), myeloid transcription-factor genes (22%), cohesin-complex genes (13%), and spliceosome-complex genes (14%). Patterns of cooperation and mutual exclusivity suggested strong biologic relationships among several of the genes and categories. CONCLUSIONS—We identified at least one potential driver mutation in nearly all AML samples and found that a complex interplay of genetic events contributes to AML pathogenesis in individual patients. The databases from this study are widely available to serve as a foundation for further investigations of AML pathogenesis, classification, and risk stratification. (Funded by the National Institutes of Health.) The molecular pathogenesis of acute myeloid leukemia (AML) has been studied with the use of cytogenetic analysis for more than three decades. Recurrent chromosomal structural variations are well established as diagnostic and prognostic markers, suggesting that acquired genetic abnormalities (i.e., somatic mutations) have an essential role in pathogenesis. 1,2 However, nearly 50% of AML samples have a normal karyotype, and many of these genomes lack structural abnormalities, even when assessed with high-density comparative genomic hybridization or single-nucleotide polymorphism (SNP) arrays 3-5 (see Glossary). Targeted sequencing has identified recurrent mutations in FLT3, NPM1, KIT, CEBPA, and TET2. 6-8 Massively parallel sequencing enabled the discovery of recurrent mutations in DNMT3A 9,10 and IDH1. 11 Recent studies have shown that many patients with

Published
2013

27. Cellular Stressors Contribute to the Expansion of Multiple Hematopoietic Clones of Varying Leukemic Potential

Author

Wong, Terrence N, Miller, Christopher A, Jotte, Matthew RM, Bagegni, Nusayba, Baty, Jack D, Schmidt, Amy E, Cashen, Amanda F, Duncavage, Eric J., Helton, Nichole M, Fiala, Mark A., Fulton, Robert S, Heath, Sharon E, Janke, Megan, Luber, Kierstin, Westervelt, Peter, Vij, Ravi, DiPersio, John F, Welch, John S., Graubert, Timothy A., Walter, Matthew J., Ley, Timothy James J, and Link, Daniel C.

Published
2017
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28. Role of TP53 mutations in the origin and evolution of therapy-related acute myeloid leukaemia

Author

Wong, Terrence N., primary, Ramsingh, Giridharan, additional, Young, Andrew L., additional, Miller, Christopher A., additional, Touma, Waseem, additional, Welch, John S., additional, Lamprecht, Tamara L., additional, Shen, Dong, additional, Hundal, Jasreet, additional, Fulton, Robert S., additional, Heath, Sharon, additional, Baty, Jack D., additional, Klco, Jeffery M., additional, Ding, Li, additional, Mardis, Elaine R., additional, Westervelt, Peter, additional, DiPersio, John F., additional, Walter, Matthew J., additional, Graubert, Timothy A., additional, Ley, Timothy J., additional, Druley, Todd E., additional, Link, Daniel C., additional, and Wilson, Richard K., additional

Published
2014
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41. Cognitive speed in nondemented Parkinson's disease

Author

*, MARCIA C. SMITH, **, GOLDMAN, WILLIAM P., JANER, KEVIN W., and BATY, JACK D.

Abstract

Studies of speed of cognitive processing in Parkinson's disease (PD) have yielded mixed results. This may relate in part to a differential effect on cognitive speed by the type of information to be processed. In the present study, we compared medication fasted, nondemented individuals with mild idiopathic PD (N = 26) with age-matched controls (N = 12) on a test requiring easy and hard same–different discriminations for verbal, quantitative, and spatial information, as well as on a traditional memory scanning paradigm. A voice-activated relay rather than a key press was used to eliminate the need for limb and finger movements. Simple reaction time and movement time were also measured in a task requiring subjects to move a hand held stylus to a designated target. The PD group performed as fast as the control group across all tasks except movement time. Thus, in our paradigm, the presence of PD alone does not predict cognitive slowing in the presence of motor slowing. (JINS, 1998, 4, 584–592.)

Published
1998

42. Oxytocin and Oxytocinase in the Obese and Nonobese Parturients during Induction and Augmentation of Labor.

Author

De Tina A, Juang J, McElrath TF, Baty JD, and Palanisamy A

Abstract

Objective  To investigate differences in oxytocin (OXT) biodistribution between nonobese and obese parturients during labor. Study Design  Patients with body mass index (BMI) of either ≥ 18 ≤ 24.9 kg/m 2 ("nonobese") or ≥ 30 kg/m 2 ("obese") undergoing elective induction of labor were included ( N  = 25 each). Blood samples were collected at baseline (T 0 ), and 20 minutes after maximal OXT augmentation or adequate uterine contractions (T 1 ) for OXT and oxytocinase assays. A mixed-model repeated-measures analysis of variance was used to test for group versus time interaction and analysis of covariance to detect a difference in OXT level at T 1 . Data presented as mean ± standard deviation or median (interquartile range), with p  < 0.05 considered significant. Results  The mean BMIs (kg/m 2 ) were 22.1 ± 1.6 and 35.9 ± 5.1 in the nonobese and obese groups, respectively. No differences were observed in either the duration of OXT infusion, total dose of OXT, or plasma OXT (pg/mL) either at T 0 or T 1 . However, plasma oxytocinase (ng/mL) was significantly lower at T 0 (1.41 [0.67, 3.51] vs. 0.40 [0.29, 1.12]; p  = 0.03) in the obese group. Conclusion  We provide preliminary evidence that the disposition of OXT may not be different between obese and nonobese women during labor.

Published
2019
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43. Long-term motor outcome analysis using a motor score composite following surgical brachial plexus repair.

Author

Ashley WW Jr, Baty JD, Hollander T, Noetzel MJ, and Park TS

Subjects
Brachial Plexus surgery, Female, Humans, Infant, Male, Models, Neurological, Predictive Value of Tests, Recovery of Function physiology, Retrospective Studies, Time Factors, Birth Injuries physiopathology, Birth Injuries surgery, Brachial Plexus injuries, Brachial Plexus physiopathology, Motor Activity physiology, Outcome Assessment, Health Care methods
Abstract

Object: Due to the complex and variable nature of brachial plexus injury, outcome analysis can be cumbersome and imprecise. Many scales have been devised, but no single scale is used uniformly. Moreover, despite several studies in which the authors have reported brachial plexus surgical data, no highly predictive clinical model has been defined., Methods: In this study the authors performed a retrospective analysis of 114 consecutive brachial plexus surgeries performed by the senior author during the past 14 years at St. Louis Children's Hospital. Of these, 63 are included in this study. The authors defined the motor score composite (MSC) and used this novel metric to perform a detailed analysis of their surgical outcomes. The mean MSC was 0.50 preoperatively, 0.71 at 1 year postoperatively, and 0.80 at 2 years postoperatively. By 2 years postoperatively, 89% of the patients attained a good or excellent recovery. Age at surgery, time to visit, location, and severity were predictive of outcome. Using MSC data, the authors developed a prognostic model that enabled the prediction (with 88% accuracy) of surgical outcomes using preoperative variables., Conclusions: The MSC is an efficient metric for the reporting of data regarding outcomes of brachial plexus injury. It provides information about extent and severity of injury in a single proportion and facilitates complex data analysis. The authors used the MSC model to accurately predict surgical outcome. This metric could have wide applicability for the prediction of postoperative recovery to improve both surgical decision making and family counseling.

Published
2007
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