How are visuomotor mismatch responses in primary visual cortex embedded into cortical processing? We here show that mismatch responses can be understood as the result of a cooperation of motor and visual areas to jointly explain optic flow. This cooperation requires that optic flow is not explained redundantly by both areas, meaning that optic flow inputs to V1 that are predictable from motor neurons should be canceled (i.e., explained away). As a result, neurons in V1 represent only external causes of optic flow, which could allow the animal to easily detect movements that are independent of its own locomotion. We implement the proposed model in a spiking neural network, where coding errors are computed in dendrites and synaptic weights are learned with voltage-dependent plasticity rules. We find that both positive and negative mismatch responses arise, providing an alternative to the prevailing idea that visuomotor mismatch responses are linked to dedicated neurons for error computation. These results also provide a new perspective on several other recent observations of cross-modal neural interactions in cortex.
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Sci Adv
January 2025
Istituto per l'Endocrinologia e l'Oncologia Sperimentale "G. Salvatore", IEOS-CNR, Napoli, Italy.
CD4FOXP3 regulatory T cells (T) suppress immune responses to tumors, and their accumulation in the tumor microenvironment (TME) correlates with poor clinical outcome in several cancers, including breast cancer (BC). However, the properties of intratumoral T remain largely unknown. Here, we found that a functionally distinct subpopulation of T, expressing the FOXP3 Exon2 splicing variants, is prominent in patients with hormone receptor-positive BC with poor prognosis.
View Article and Find Full Text PDFJ Immunother Precis Oncol
February 2025
Department of Investigational Therapeutics, Division of Cancer Medicine, The University of Texas MD Anderson Cancer Center, Houston, TX, USA.
BRAF mutation leads to constitutive activation of the MAPK pathway and is associated with the immune-activating molecular subtype of colorectal cancer. Targeted therapy for mutant metastatic colorectal cancer (CRC) has significantly improved outcomes for these patients when combined with anti-epithelial growth factor receptor (EGFR) therapy. However, most patients ultimately develop disease progression.
View Article and Find Full Text PDFNPJ Precis Oncol
January 2025
College of Medicine, Chang Gung University, Taoyuan, Taiwan, ROC.
Anaplastic thyroid carcinoma (ATC) is an aggressive cancer that requirements rapid diagnosis and multimodal treatment. Next-generation sequencing (NGS) aids in personalized therapies and improved trial enrollment. The role of liquid-based NGS in ATC remains unclear.
View Article and Find Full Text PDFAJNR Am J Neuroradiol
January 2025
From the Department of Radiology, Medical Physics (MML, TJC), Department of Interventional Radiology (NS, GAC), Department of Surgery and Large Animal Studies (MAN), and the Department of Statistics (MG), University of Chicago, Chicago, IL, USA; Department of Anesthesiology (SPR), University of Illinois, Chicago, IL, USA; Department of Radiology (MSS), University of Massachusetts Chan Medical School, Worcester, MA, USA; Department of Radiology, Biomedical Engineering and Imaging Institute (Current affiliation MML), Icahn School of Medicine at Mount Sinai, New York, NY, USA; Mount Carmel Health Systems (Current affiliation GAC), Columbus, OH, USA.
Background And Purpose: In acute ischemic stroke, the amount of "local" CBF distal to the occlusion, i.e. all blood flow within a region whether supplied antegrade or delayed and dispersed through the collateral network, may contain valuable information regarding infarct growth rate and treatment response.
View Article and Find Full Text PDFJ Pain
January 2025
Innovative Clinical Training, Trials & Healthcare Initiative, Zermatt CH-3920, Switzerland.
In order to disentangle the effects of drugs from placebo responses, several approaches have been used, such as a placebo run-in phase in which only placebo nonresponders, or poor responders, are considered for further randomization to either placebo or active treatment. This study is aimed at investigating the variability of placebo nonresponders obtained through the classical placebo run-in paradigm (group RUN) and through mismatch conditioning (group MIS), as done in our previous study. To do this, we simulated a real clinical trial in the laboratory, in which the placebo responders of both groups were discarded and the remaining nonresponders of both groups RUN and MIS were randomized to either continuing on placebo (groups RUN-P and MIS-P, respectively) or receiving topical 0.
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