11 results
Relating Response Inhibition, Brain Connectivity, and Freezing of Gait in People with Parkinson’s Disease
- Daniel S. Peterson, Katrijn Smulders, Martina Mancini, John G. Nutt, Fay B. Horak, Brett W. Fling
-
- Journal:
- Journal of the International Neuropsychological Society / Volume 27 / Issue 7 / August 2021
- Published online by Cambridge University Press:
- 09 December 2020, pp. 733-743
-
- Article
- Export citation
-
Objective:
Freezing of gait (FoG) in Parkinson’s disease (PD) has been associated with response inhibition. However, the relationship between response inhibition, neural dysfunction, and PD remains unclear. We assessed response inhibition and microstructural integrity of brain regions involved in response inhibition [right hemisphere inferior frontal cortex (IFC), bilateral pre-supplementary motor areas (preSMA), and subthalamic nuclei (STN)] in PD subjects with and without FoG and elderly controls.
Method:Twenty-one people with PD and FoG (PD-FoG), 18 without FoG (PD-noFoG), and 19 age-matched controls (HC) completed a Stop-Signal Task (SST) and MRI scan. Probabilistic fiber tractography assessed structural integrity (fractional anisotropy, FA) among IFC, preSMA, and STN regions.
Results:Stop-signal performance did not differ between PD and HC, nor between PD-FoG and PD-noFoG. Differences in white matter integrity were observed across groups (.001 < p < .064), but were restricted to PD versus HC groups; no differences in FA were observed between PD-FoG and PD-noFoG (p > .096). Interestingly, worse FoG was associated with higher (better) mean FA in the r-preSMA, (β = .547, p = .015). Microstructural integrity of the r-IFC, r-preSMA, and r-STN tracts correlated with stop-signal performance in HC (p ≤ .019), but not people with PD.
Conclusion:These results do not support inefficient response inhibition in PD-FoG. Those with PD exhibited white matter loss in the response inhibition network, but this was not associated with FoG, nor with response inhibition deficits, suggesting FoG-specific neural changes may occur outside the response inhibition network. As shown previously, white matter loss was associated with response inhibition in elderly controls, suggesting PD may disturb this relationship.
Evaluation of optimal droplet size for control of Palmer amaranth (Amaranthus palmeri) with acifluorfen
- Lucas X. Franca, Darrin M. Dodds, Thomas R. Butts, Greg R. Kruger, Daniel B. Reynolds, J. Anthony Mills, Jason A. Bond, Angus L. Catchot, Daniel G. Peterson
-
- Journal:
- Weed Technology / Volume 34 / Issue 4 / August 2020
- Published online by Cambridge University Press:
- 20 January 2020, pp. 511-519
-
- Article
- Export citation
-
Acifluorfen is a nonsystemic PPO-inhibiting herbicide commonly used for POST Palmer amaranth control in soybean, peanut, and rice across the southern United States. Concerns have been raised regarding herbicide selection pressure and particle drift, increasing the need for application practices that optimize herbicide efficacy while mitigating spray drift. Field research was conducted in 2016, 2017, and 2018 in Mississippi and Nebraska to evaluate the influence of a range of spray droplet sizes [150 μm (Fine) to 900 μm (Ultra Coarse)], using acifluorfen to create a novel Palmer amaranth management recommendation using pulse width modulation (PWM) technology. A pooled site-year generalized additive model (GAM) analysis suggested that 150-μm (Fine) droplets should be used to obtain the greatest Palmer amaranth control and dry biomass reduction. Nevertheless, GAM models indicated that only 7.2% of the variability observed in Palmer amaranth control was due to differences in spray droplet size. Therefore, location-specific GAM analyses were performed to account for geographical differences to increase the accuracy of prediction models. GAM models suggested that 250-μm (Medium) droplets optimize acifluorfen efficacy on Palmer amaranth in Dundee, MS, and 310-μm (Medium) droplets could sustain 90% of maximum weed control. Specific models for Beaver City, NE, indicated that 150-μm (Fine) droplets provide maximum Palmer amaranth control, and 340-μm (Medium) droplets could maintain 90% of greatest weed control. For Robinsonville, MS, optimal Palmer amaranth control could be obtained with 370-μm (Coarse) droplets, and 90% maximum control could be sustained with 680 μm (Ultra Coarse) droplets. Differences in optimal droplet size across location could be a result of convoluted interactions between droplet size, weather conditions, population density, plant morphology, and soil fertility levels. Future research should adopt a holistic approach to identify and investigate the influence of environmental and application parameters to optimize droplet size recommendations.
Droplet size impact on lactofen and acifluorfen efficacy for Palmer amaranth (Amaranthus palmeri) control
- Lucas X. Franca, Darrin M. Dodds, Thomas R. Butts, Greg R. Kruger, Daniel B. Reynolds, J. Anthony Mills, Jason A. Bond, Angus L. Catchot, Daniel G. Peterson
-
- Journal:
- Weed Technology / Volume 34 / Issue 3 / June 2020
- Published online by Cambridge University Press:
- 26 December 2019, pp. 416-423
-
- Article
- Export citation
-
Herbicide applications performed with pulse width modulation (PWM) sprayers to deliver specific spray droplet sizes could maintain product efficacy, minimize potential off-target movement, and increase flexibility in field operations. Given the continuous expansion of herbicide-resistant Palmer amaranth populations across the southern and midwestern United States, efficacious and cost-effective means of application are needed to maximize Palmer amaranth control. Experiments were conducted in two locations in Mississippi (2016, 2017, and 2018) and one location in Nebraska (2016 and 2017) for a total of 7 site-years. The objective of this study was to evaluate the influence of a range of spray droplet sizes [150 (Fine) to 900 μm (Ultra Coarse)] on lactofen and acifluorfen efficacy for Palmer amaranth control. The results of this research indicated that spray droplet size did not influence lactofen efficacy on Palmer amaranth. Palmer amaranth control and percent dry-biomass reduction remained consistent with lactofen applied within the aforementioned droplet size range. Therefore, larger spray droplets should be used as part of a drift mitigation approach. In contrast, acifluorfen application with 300-μm (Medium) spray droplets provided the greatest Palmer amaranth control. Although percent biomass reduction was numerically greater with 300-μm (Medium) droplets, results did not differ with respect to spray droplet size, possibly as a result of initial plant injury, causing weight loss, followed by regrowth. Overall, 900-μm (Ultra Coarse) droplets could be used effectively without compromising lactofen efficacy on Palmer amaranth, and 300-μm (Medium) droplets should be used to achieve maximum Palmer amaranth control with acifluorfen.
Molecular evolution in immune genes across the avian tree of life
- Diana C. Outlaw, V. Woody Walstrom, Haley N. Bodden, Chuan-yu Hsu, Mark Arick II, Daniel G. Peterson
-
- Journal:
- Parasitology Open / Volume 5 / 2019
- Published online by Cambridge University Press:
- 24 June 2019, e3
- Print publication:
- 2019
-
- Article
-
- You have access Access
- Open access
- HTML
- Export citation
-
All organisms encounter pathogens, and birds are especially susceptible to infection by malaria parasites and other haemosporidians. It is important to understand how immune genes, primarily innate immune genes which are the first line of host defense, have evolved across birds, a highly diverse group of tetrapods. Here, we find that innate immune genes are highly conserved across the avian tree of life and that although most show evidence of positive or diversifying selection within specific lineages or clades, the number of sites is often proportionally low in this broader context of putative constraint. Rather, evidence shows a much higher level of negative or purifying selection in these innate immune genes – rather than adaptive immune genes – which is consistent with birds' long coevolutionary history with pathogens and the need to maintain a rapid response to infection. We further explored avian responses to haemosporidians by comparing differential gene expression in wild birds (1) uninfected with haemosporidians, (2) infected with Plasmodium and (3) infected with Haemoproteus (Parahaemoproteus). We found patterns of significant differential expression with some genes unique to infection with each genus and a few shared between ‘treatment’ groups, but none that overlapped with the genes included in the phylogenetic study.
Multiple Herbicide–Resistant Junglerice (Echinochloa colona): Identification of Genes Potentially Involved in Resistance through Differential Gene Expression Analysis
- Alice A. Wright, Marianela Rodriguez-Carres, Rajkumar Sasidharan, Liisa Koski, Daniel G. Peterson, Vijay K. Nandula, Jeffery D. Ray, Jason A. Bond, David R. Shaw
-
- Journal:
- Weed Science / Volume 66 / Issue 3 / May 2018
- Published online by Cambridge University Press:
- 16 March 2018, pp. 347-354
-
- Article
-
- You have access Access
- HTML
- Export citation
-
Herbicide resistance, and in particular multiple-herbicide resistance, poses an ever-increasing threat to food security. A biotype of junglerice [Echinochloa colona (L.) Link] with resistance to four herbicides, imazamox, fenoxaprop-P-ethyl, quinclorac, and propanil, each representing a different mechanism of action, was identified in Sunflower County, MS. Dose responses were performed on the resistant biotype and a biotype sensitive to all four herbicides to determine the level of resistance. Application of a cytochrome P450 inhibitor, malathion, with the herbicides imazamox and quinclorac resulted in increased susceptibility in the resistant biotype. Differential gene expression analysis of resistant and sensitive plants revealed that 170 transcripts were upregulated in resistant plants relative to sensitive plants and 160 transcripts were upregulated in sensitive plants. In addition, 507 transcripts were only expressed in resistant plants and 562 only in sensitive plants. A subset of these transcripts were investigated further using quantitative PCR (qPCR) to compare gene expression in resistant plants with expression in additional sensitive biotypes. The qPCR analysis identified two transcripts, a kinase and a glutathione S-transferase that were significantly upregulated in resistant plants compared with the sensitive plants. A third transcript, encoding an F-box protein, was downregulated in the resistant plants relative to the sensitive plants. As no cytochrome P450s were differentially expressed between the resistant and sensitive plants, a single-nucleotide polymorphism analysis was performed, revealing several nonsynonymous point mutations of interest. These candidate genes will require further study to elucidate the resistance mechanisms present in the resistant biotype.
Characterization of Fenoxaprop-P-Ethyl–Resistant Junglerice (Echinochloa colona) from Mississippi
- Alice A. Wright, Vijay K. Nandula, Logan Grier, Kurt C. Showmaker, Jason A. Bond, Daniel G. Peterson, Jeffery D. Ray, David R. Shaw
-
- Journal:
- Weed Science / Volume 64 / Issue 4 / December 2016
- Published online by Cambridge University Press:
- 20 January 2017, pp. 588-595
-
- Article
- Export citation
-
A population of junglerice from Sunflower County, MS, exhibited resistance to fenoxaprop-P-ethyl. An 11-fold difference in ED50 (the effective dose needed to reduce growth by 50%) values was observed when comparing the resistant population (249 g ae ha–1) with susceptible plants (20 g ae ha–1) collected from a different field. The resistant population was controlled by clethodim and sethoxydim at the field rate. Sequencing of the acetyl coenzyme A carboxylase, which encodes the enzyme targeted by fenoxaprop-P-ethyl, did not reveal the presence of any known resistance-conferring point mutations. An enzyme assay confirmed that the acetyl coenzyme A carboxylase in the resistant population is herbicide sensitive. Further investigations with two cytochrome P450 inhibitors, malathion and piperonyl butoxide, and a glutathione-S-transferase inhibitor, 4-chloro-7-nitrobenzofurazan, did not indicate involvement of any metabolic enzymes inhibited by these compounds. The absence of a known target-site point mutation and the sensitivity of the ACCase enzyme to herbicide show that fenoxaprop-P-ethyl resistance in this population is due to a non–target-site mechanism or mechanisms.
Contributors
-
- By Tod C. Aeby, Melanie D. Altizer, Ronan A. Bakker, Meghann E. Batten, Anita K. Blanchard, Brian Bond, Megan A. Brady, Saweda A. Bright, Ellen L. Brock, Amy Brown, Ashley Carroll, Jori S. Carter, Frances Casey, Weldon Chafe, David Chelmow, Jessica M. Ciaburri, Stephen A. Cohen, Adrianne M. Colton, PonJola Coney, Jennifer A. Cross, Julie Zemaitis DeCesare, Layson L. Denney, Megan L. Evans, Nicole S. Fanning, Tanaz R. Ferzandi, Katie P. Friday, Nancy D. Gaba, Rajiv B. Gala, Andrew Galffy, Adrienne L. Gentry, Edward J. Gill, Philippe Girerd, Meredith Gray, Amy Hempel, Audra Jolyn Hill, Chris J. Hong, Kathryn A. Houston, Patricia S. Huguelet, Warner K. Huh, Jordan Hylton, Christine R. Isaacs, Alison F. Jacoby, Isaiah M. Johnson, Nicole W. Karjane, Emily E. Landers, Susan M. Lanni, Eduardo Lara-Torre, Lee A. Learman, Nikola Alexander Letham, Rachel K. Love, Richard Scott Lucidi, Elisabeth McGaw, Kimberly Woods McMorrow, Christopher A. Manipula, Kirk J. Matthews, Michelle Meglin, Megan Metcalf, Sarah H. Milton, Gaby Moawad, Christopher Morosky, Lindsay H. Morrell, Elizabeth L. Munter, Erin L. Murata, Amanda B. Murchison, Nguyet A. Nguyen, Nan G. O’Connell, Tony Ogburn, K. Nathan Parthasarathy, Thomas C. Peng, Ashley Peterson, Sarah Peterson, John G. Pierce, Amber Price, Heidi J. Purcell, Ronald M. Ramus, Nicole Calloway Rankins, Fidelma B. Rigby, Amanda H. Ritter, Barbara L. Robinson, Danielle Roncari, Lisa Rubinsak, Jennifer Salcedo, Mary T. Sale, Peter F. Schnatz, John W. Seeds, Kathryn Shaia, Karen Shelton, Megan M. Shine, Haller J. Smith, Roger P. Smith, Nancy A. Sokkary, Reni A. Soon, Aparna Sridhar, Lilja Stefansson, Laurie S. Swaim, Chemen M. Tate, Hong-Thao Thieu, Meredith S. Thomas, L. Chesney Thompson, Tiffany Tonismae, Angela M. Tran, Breanna Walker, Alan G. Waxman, C. Nathan Webb, Valerie L. Williams, Sarah B. Wilson, Elizabeth M. Yoselevsky, Amy E. Young
- Edited by David Chelmow, Virginia Commonwealth University, Christine R. Isaacs, Virginia Commonwealth University, Ashley Carroll, Virginia Commonwealth University
-
- Book:
- Acute Care and Emergency Gynecology
- Published online:
- 05 November 2014
- Print publication:
- 30 October 2014, pp ix-xiv
-
- Chapter
- Export citation
Contributors
-
- By Lenard A. Adler, Pinky Agarwal, Rehan Ahmed, Jagga Rao Alluri, Fawaz Al-Mufti, Samuel Alperin, Michael Amoashiy, Michael Andary, David J. Anschel, Padmaja Aradhya, Vandana Aspen, Esther Baldinger, Jee Bang, George D. Baquis, John J. Barry, Jason J. S. Barton, Julius Bazan, Amanda R. Bedford, Marlene Behrmann, Lourdes Bello-Espinosa, Ajay Berdia, Alan R. Berger, Mark Beyer, Don C. Bienfang, Kevin M. Biglan, Thomas M. Boes, Paul W. Brazis, Jonathan L. Brisman, Jeffrey A. Brown, Scott E. Brown, Ryan R. Byrne, Rina Caprarella, Casey A. Chamberlain, Wan-Tsu W. Chang, Grace M. Charles, Jasvinder Chawla, David Clark, Todd J. Cohen, Joe Colombo, Howard Crystal, Vladimir Dadashev, Sarita B. Dave, Jean Robert Desrouleaux, Richard L. Doty, Robert Duarte, Jeffrey S. Durmer, Christyn M. Edmundson, Eric R. Eggenberger, Steven Ender, Noam Epstein, Alberto J. Espay, Alan B. Ettinger, Niloofar (Nelly) Faghani, Amtul Farheen, Edward Firouztale, Rod Foroozan, Anne L. Foundas, David Elliot Friedman, Deborah I. Friedman, Steven J. Frucht, Oded Gerber, Tal Gilboa, Martin Gizzi, Teneille G. Gofton, Louis J. Goodrich, Malcolm H. Gottesman, Varda Gross-Tsur, Deepak Grover, David A. Gudis, John J. Halperin, Maxim D. Hammer, Andrew R. Harrison, L. Anne Hayman, Galen V. Henderson, Steven Herskovitz, Caitlin Hoffman, Laryssa A. Huryn, Andres M. Kanner, Gary P. Kaplan, Bashar Katirji, Kenneth R. Kaufman, Annie Killoran, Nina Kirz, Gad E. Klein, Danielle G. Koby, Christopher P. Kogut, W. Curt LaFrance, Patrick J.M. Lavin, Susan W. Law, James L. Levenson, Richard B. Lipton, Glenn Lopate, Daniel J. Luciano, Reema Maindiratta, Robert M. Mallery, Georgios Manousakis, Alan Mazurek, Luis J. Mejico, Dragana Micic, Ali Mokhtarzadeh, Walter J. Molofsky, Heather E. Moss, Mark L. Moster, Manpreet Multani, Siddhartha Nadkarni, George C. Newman, Rolla Nuoman, Paul A. Nyquist, Gaia Donata Oggioni, Odi Oguh, Denis Ostrovskiy, Kristina Y. Pao, Juwen Park, Anastas F. Pass, Victoria S. Pelak, Jeffrey Peterson, John Pile-Spellman, Misha L. Pless, Gregory M. Pontone, Aparna M. Prabhu, Michael T. Pulley, Philip Ragone, Prajwal Rajappa, Venkat Ramani, Sindhu Ramchandren, Ritesh A. Ramdhani, Ramses Ribot, Heidi D. Riney, Diana Rojas-Soto, Michael Ronthal, Daniel M. Rosenbaum, David B. Rosenfield, Durga Roy, Michael J. Ruckenstein, Max C. Rudansky, Eva Sahay, Friedhelm Sandbrink, Jade S. Schiffman, Angela Scicutella, Maroun T. Semaan, Robert C. Sergott, Aashit K. Shah, David M. Shaw, Amit M. Shelat, Claire A. Sheldon, Anant M. Shenoy, Yelizaveta Sher, Jessica A. Shields, Tanya Simuni, Rajpaul Singh, Eric E. Smouha, David Solomon, Mehri Songhorian, Steven A. Sparr, Egilius L. H. Spierings, Eve G. Spratt, Beth Stein, S.H. Subramony, Rosa Ana Tang, Cara Tannenbaum, Hakan Tekeli, Amanda J. Thompson, Michael J. Thorpy, Matthew J. Thurtell, Pedro J. Torrico, Ira M. Turner, Scott Uretsky, Ruth H. Walker, Deborah M. Weisbrot, Michael A. Williams, Jacques Winter, Randall J. Wright, Jay Elliot Yasen, Shicong Ye, G. Bryan Young, Huiying Yu, Ryan J. Zehnder
- Edited by Alan B. Ettinger, Albert Einstein College of Medicine, New York, Deborah M. Weisbrot, State University of New York, Stony Brook
-
- Book:
- Neurologic Differential Diagnosis
- Published online:
- 05 June 2014
- Print publication:
- 17 April 2014, pp xi-xx
-
- Chapter
- Export citation
Growth hormone alters lipid composition and increases the abundance of casein and lactalbumin mRNA in the MAC-T cell line
- Tasha L Johnson, Brent AS Fujimoto, Rafaél Jiménez-Flores, Daniel G Peterson
-
- Journal:
- Journal of Dairy Research / Volume 77 / Issue 2 / May 2010
- Published online by Cambridge University Press:
- 12 April 2010, pp. 199-204
- Print publication:
- May 2010
-
- Article
- Export citation
-
The MAC-T cell line has been used extensively to investigate bovine mammary epithelial cell function. A lactogenic phenotype is generally induced in this cell line by a combination of dexamethasone, insulin and prolactin and has typically been assessed by milk protein production. Few studies have focused on identifying other factors that may affect milk protein synthesis in the MAC-T cell line, and none have considered the lipid class distribution of MAC-T cells as a component of the lactogenic phenotype. Growth hormone (GH) has been shown to increase milk protein synthesis both in vivo and in mammary cell models, and has been shown to alter the lipogenic profile of mammary explant models. We tested the hypothesis that MAC-T cells would respond directly to GH and that the response would include alterations to the lipid class distribution as well as to milk protein gene expression, leading to a more appropriate model for mammary cell function than treatment with dexamethasone, insulin and prolactin alone. Differentiated cells expressed GH receptor mRNA, and addition of GH to the differentiation medium significantly induced production of α-s1 casein and α-lactalbumin mRNA. GH also significantly affected the proportion of triacylglycerol and sphingomyelin. These results indicate that GH is an important factor in inducing a lactogenic phenotype in the MAC-T cell line, and support the possibility of a direct effect of GH on milk synthesis in vivo.
Contributors
-
- By Kateri Berasi, Carol A. Boyer, Diane R. Brown, Robyn Lewis Brown, Tony N. Brown, Padraic J. Burns, Cleopatra Howard Caldwell, Daniel L. Carlson, Cheryl Corcoran, Manuela Costa, Stephen Crystal, Gary S. Cuddeback, William W. Eaton, Adrianne Frech, Virginia Aldigé Hiday, Stevan E. Hobfoll, Allan V. Horwitz, Robert J. Johnson, Verna M. Keith, Ronald C. Kessler, Corey L. M. Keyes, Jacinta P. Leavell, Harriet P. Lefley, Mary Clare Lennon, Laura Limonic, Bruce G. Link, Athena McLean, David Mechanic, Elizabeth G. Menaghan, Barret Michalec, John Mirowsky, Shirin Montazer, Joseph P. Morrissey, Carles Muntaner, Bernice A. Pescosolido, Christopher Peterson, Jo C. Phelan, Michael Polgar, Sarah Rosenfield, Catherine E. Ross, Ebony Sandusky, Jaime C. Sapag, Teresa L. Scheid, Mark F. Schmitz, Sharon Schwartz, Dena Smith, David T. Takeuchi, Peggy A. Thoits, R. Jay Turner, Edwina S. Uehara, Jerome C. Wakefield, James Walkup, Emily Walton, Blair Wheaton, David R. Williams, Kristi Williams
- Edited by Teresa L. Scheid, University of North Carolina, Charlotte, Tony N. Brown, Vanderbilt University, Tennessee
-
- Book:
- A Handbook for the Study of Mental Health
- Published online:
- 05 June 2012
- Print publication:
- 16 November 2009, pp xi-xiv
-
- Chapter
- Export citation
Contributors
-
- By James M. Bjork, Hilary P. Blumberg, Nathalie Boddaert, Susan Bookheimer, Silvia A. Bunge, Beata Buzas, B. J. Casey, Nadia Chabane, Eveline A. Crone, Mirella Dapretto, John A. Detre, Vaibhav A. Diwadkar, Jeffery N. Epstein, Monique Ernst, Guido K. W. Frank, David C. Glahn, David Goldman, Daniel A. Gorman, Ian H. Gotlib, Michael G. Hardin, Clinton D. Hermes, Rebecca M. Jones, Jutta Joormann, Jessica H. Kalmar, Walter H. Kaye, Matcheri S. Keshavan, Dae-Shik Kim, Liat Levita, Lisa H. Lu, Rachel Marsh, Kristin McNealy, Kevin A. Pelphrey, Susan B. Perlman, Bradley S. Peterson, Daniel S. Pine, Steven R. Pliszka, Konasale Prasad, Hengyi Rao, Allan L. Reiss, Perry Renshaw, Susan M. Rivera, Jason Royal, Judith M. Rumsey, Maulik P. Shah, Marisa M. Silveri, Elizabeth R. Sowell, Jeffrey A. Stanley, Henning U. Voss, Jiong-Jiong Wang, Ke Xu, Deborah Yurgelun-Todd, Monica Zilbovicius
- Edited by Judith M. Rumsey, National Institute of Mental Health, Bethesda, Maryland, Monique Ernst, National Institute of Mental Health, Bethesda, Maryland
-
- Book:
- Neuroimaging in Developmental Clinical Neuroscience
- Published online:
- 04 August 2010
- Print publication:
- 19 February 2009, pp vii-xii
-
- Chapter
- Export citation