3 results
Evaluation of chemical control and seasonal application options for smutgrass (Sporobolus indicus)
- Zachary S. Howard, Scott A. Nolte, Mark Hussey, Morgan L. Treadwell, Brent Sellers
-
- Journal:
- Weed Technology / Volume 37 / Issue 5 / October 2023
- Published online by Cambridge University Press:
- 29 September 2023, pp. 530-536
-
- Article
-
- You have access Access
- Open access
- HTML
- Export citation
-
Smutgrass is a non-native perennial weed that is problematic because of its poor palatability to cattle and its difficulty to control once established. Limited literature exists to explain the effectiveness of herbicides other than hexazinone for smutgrass control and forage injury. This study aimed to evaluate seasonal applications of labeled herbicides used on forage for maximum smutgrass control. The second objective was to evaluate preemergent herbicides and hexazinone for their ability to control smutgrass germinating from seed. Hexazinone, nicosulfuron + metsulfuron-methyl, and glyphosate + imazapic were the most effective postemergence treatments, while quinclorac exhibited little activity on smutgrass. Common bermudagrass forage fully recovered from all treatments by 3 mo after treatment. Hexazinone, nicosulfuron + metsulfuron methyl, glyphosate, and imazapic were applied postemergence to smutgrass in spring, summer, and fall. Summer applications of hexazinone resulted in the greatest level of control, while spring treatments provided the least control. Applications of hexazinone or glyphosate resulted in the most effective smutgrass control. However, fall applications resulted in the least forage injury. Results of the study of preemergence herbicides indicate that treatments with indaziflam and hexazinone provide adequate control of germinating smutgrass seedlings in the greenhouse at 0.25×, 0.5×, and 0.75× of the lowest recommended labeled rate for seedling grass control. Indaziflam treatments prevented the emergence of any visible smutgrass seedling tissue, compared to hexazinone, which fully controlled the germinating seedlings by 21 d after treatment, whereas pendimethalin significantly reduced seedling numbers at the 0.5× and 0.75× rates.
Evidence of causal effect of major depression on alcohol dependence: findings from the psychiatric genomics consortium
- Renato Polimanti, Roseann E. Peterson, Jue-Sheng Ong, Stuart MacGregor, Alexis C. Edwards, Toni-Kim Clarke, Josef Frank, Zachary Gerring, Nathan A. Gillespie, Penelope A. Lind, Hermine H. Maes, Nicholas G. Martin, Hamdi Mbarek, Sarah E. Medland, Fabian Streit, Major Depressive Disorder Working Group of the Psychiatric Genomics Consortium, Substance Use Disorder Working Group of the Psychiatric Genomics Consortium, 23andMe Research Team, Arpana Agrawal, Howard J. Edenberg, Kenneth S. Kendler, Cathryn M. Lewis, Patrick F. Sullivan, Naomi R. Wray, Joel Gelernter, Eske M. Derks
-
- Journal:
- Psychological Medicine / Volume 49 / Issue 7 / May 2019
- Published online by Cambridge University Press:
- 01 April 2019, pp. 1218-1226
-
- Article
- Export citation
-
Background
Despite established clinical associations among major depression (MD), alcohol dependence (AD), and alcohol consumption (AC), the nature of the causal relationship between them is not completely understood. We leveraged genome-wide data from the Psychiatric Genomics Consortium (PGC) and UK Biobank to test for the presence of shared genetic mechanisms and causal relationships among MD, AD, and AC.
MethodsLinkage disequilibrium score regression and Mendelian randomization (MR) were performed using genome-wide data from the PGC (MD: 135 458 cases and 344 901 controls; AD: 10 206 cases and 28 480 controls) and UK Biobank (AC-frequency: 438 308 individuals; AC-quantity: 307 098 individuals).
ResultsPositive genetic correlation was observed between MD and AD (rgMD−AD = + 0.47, P = 6.6 × 10−10). AC-quantity showed positive genetic correlation with both AD (rgAD−AC quantity = + 0.75, P = 1.8 × 10−14) and MD (rgMD−AC quantity = + 0.14, P = 2.9 × 10−7), while there was negative correlation of AC-frequency with MD (rgMD−AC frequency = −0.17, P = 1.5 × 10−10) and a non-significant result with AD. MR analyses confirmed the presence of pleiotropy among these four traits. However, the MD-AD results reflect a mediated-pleiotropy mechanism (i.e. causal relationship) with an effect of MD on AD (beta = 0.28, P = 1.29 × 10−6). There was no evidence for reverse causation.
ConclusionThis study supports a causal role for genetic liability of MD on AD based on genetic datasets including thousands of individuals. Understanding mechanisms underlying MD-AD comorbidity addresses important public health concerns and has the potential to facilitate prevention and intervention efforts.
Contributors
-
- By Agoston T. Agoston, Syed Z. Ali, Mahul B. Amin, Daniel A. Arber, Pedram Argani, Sylvia L. Asa, Rebecca N. Baergen, Zubair W. Baloch, Andrew M. Bellizzi, Kurt Benirschke, Allen Burke, Kenneth B. Calder, Karen L. Chang, Rebecca D. Chernock, Wang Cheung, Thomas V. Colby, Byron P. Croker, Ronald A. DeLellis, Edward F. DiCarlo, Ralph C. Eagle, Hormoz Ehya, Brett M. Elicker, Tarik M. Elsheikh, Robert E. Fechner, Linda D. Ferrell, Melina B. Flanagan, Douglas B. Flieder, Christopher S. Foster, Lillian Gaber, Karuna Garg, Kim R. Geisinger, Ryan M. Gill, Eric F. Glassy, David J. Glembocki, Zachary D. Goodman, Robert O. Greer, David J. Grignon, Gerardo E. Guiter, Kymberly A. Gyure, Ian S. Hagemann, Michael R. Henry, Jason L. Hornick, Ralph H. Hruban, Phyllis C. Huettner, Peter A. Humphrey, Olga B. Ioffe, Edward C. Klatt, Michael J. Klein, Ernest E. Lack, James N. Lampros, Lester J. Layfield, Robin D. LeGallo, Kevin O. Leslie, James S. Lewis, Virginia A. LiVolsi, Alberto M. Marchevsky, Anne Marie McNicol, Mitra Mehrad, Elizabeth Montgomery, Cesar A. Moran, Christopher A. Moskaluk, George J. Netto, G. Petur Nielsen, Robert D. Odze, Arthur S. Patchefsky, James W. Patterson, Elizabeth N. Pavlisko, John D. Pfeifer, Celeste N. Powers, Richard A. Prayson, Anja C. Roden, Victor L. Roggli, Andrew E. Rosenberg, Sherif Said, Margie A. Scott, Raja R. Seethala, Carlie S. Sigel, Jan F. Silverman, Bruce R. Smoller, Edward B. Stelow, Nora C. J. Sun, Mark W. Teague, Satish K. Tickoo, Thomas M. Ulbright, Paul E. Wakely, Jun Wang, Lawrence M. Weiss, Mark R. Wick, Howard H. Wu, Rhonda K. Yantiss, Charles Zaloudek, Yaxia Zhang, Xiaohui Sheila Zhao
- Edited by Mark R. Wick, University of Virginia, Virginia A. LiVolsi, University of Pennsylvania School of Medicine, John D. Pfeifer, Washington University School of Medicine, St Louis, Edward B. Stelow, University of Virginia, Paul E. Wakely, Jr
-
- Book:
- Silverberg's Principles and Practice of Surgical Pathology and Cytopathology
- Published online:
- 13 March 2015
- Print publication:
- 26 March 2015, pp vii-x
-
- Chapter
- Export citation