The ability to inhibit inappropriate responses is central to cognitive control, but whether the same brain mechanisms mediate inhibition across different tasks is not known. We present evidence for a common set of frontal and parietal regions engaged in response inhibition across three tasks: a go/no-go task, a flanker task, and a stimulus-response compatibility task. Regions included bilateral anterior insula/frontal operculum and anterior prefrontal, right dorsolateral and premotor, and parietal cortices. Insula activity was positively correlated with interference costs in behavioral performance in each task. Principal components analysis showed a coherent pattern of individual differences in these regions that was also positively correlated with performance in all three tasks. However, correlations among tasks were low, for both brain activity and performance. We suggest that common interference detection and/or resolution mechanisms are engaged across tasks, and that inter-task correlations in behavioral performance are low because they conflate measurements of common mechanisms with measurements of individual biases unique to each task.
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http://dx.doi.org/10.1016/j.neuroimage.2005.01.054 | DOI Listing |
Plant Physiol
January 2025
School of Life Science, Ningxia University, Yinchuan 750021, Ningxia, China.
Cold stress severely impacts the quality and yield of grapevine (Vitis L.). In this study, we extend our previous work to elucidate the role and regulatory mechanisms of Vitis amurensis MYB transcription factor 4a (VaMYB4a) in grapevine's response to cold stress.
View Article and Find Full Text PDFACS Appl Mater Interfaces
January 2025
Department of Gerontology, The Second Affiliated Hospital of Chongqing Medical University, Chongqing 400010, People's Republic of China.
20% acute pancreatitis (AP) develops into severe AP (SAP), a global health crisis, with an increased mortality rate to 30%-50%. Mitochondrial damage and immune disorders are direct factors, which exacerbate the occurrence and progression of AP. So far, mitochondrial and immunity injury in SAP remains largely elusive, with no established treatment options available.
View Article and Find Full Text PDFPLoS One
January 2025
Department of Clinical Science, SUS, Division of Islet Cell Physiology, University of Lund, Malmö, Sweden.
The impact of islet neuronal nitric oxide synthase (nNOS) on glucose-stimulated insulin secretion (GSIS) is less understood. We investigated this issue by performing simultaneous measurements of the activity of nNOS versus inducible NOS (iNOS) in GSIS using isolated murine islets. Additionally, the significance of extracellular NO on GSIS was studied.
View Article and Find Full Text PDFJ Med Chem
January 2025
State Key Laboratory for Chemo/Bio-Sensing and Chemometrics, College of Chemistry and Chemical Engineering, Hunan University, Changsha 410082, China.
Blocking mitosis is a promising strategy to induce tumor cell death. However, AMPK- and PFKFB3-mediated glycolysis can maintain ATP supply and help tumor cells overcome antimitotic drugs. Inhibiting glycolysis provides an opportunity to decrease the resistance of tumor cells to antimitotic drugs.
View Article and Find Full Text PDFCell Rep
January 2025
MOE Key Laboratory of Biosystems Homeostasis & Protection, and Zhejiang Provincial Key Laboratory of Cancer Molecular Cell Biology, Life Sciences Institute, Zhejiang University, Hangzhou, Zhejiang 310058, China; Center for Life Sciences, Shaoxing Institute, Zhejiang University, Shaoxing, Zhejiang 321000, China; Cancer Center, Zhejiang University, Hangzhou, Zhejiang 310058, China; The Second Affiliated Hospital, Zhejiang University, Hangzhou, Zhejiang 310009, China. Electronic address:
Transforming growth factor β (TGF-β) is well known to play paradoxical roles in tumorigenesis as it has both growth-inhibitory and pro-metastatic effects. However, the underlying mechanisms of how TGF-β drives the opposing responses remain largely unknown. Here, we report that ERBB4, a member of the ERBB receptor tyrosine kinase family, specifically promotes TGF-β's metastatic response but not its anti-growth response.
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