Neuroimaging studies increasingly use naturalistic stimuli like video clips to trigger complex brain activations, but the complexity of such stimuli makes it difficult to assign specific functions to the resulting brain activations, particularly for higher-level content like social interactions. To address this challenge, researchers have turned to deep neural networks, e.g., convolutional neural networks (CNNs). CNNs have shown success in image recognition due to their different levels of features enabling high performance. In this study, we used pre-trained VGG-16, a popular CNN model, to analyze video data and extract hierarchical features from low-level shallow layers to high-level deeper layers, linking these activations to different levels of activation of the human brain. We hypothesized that activations in different layers of VGG-16 would be associated with different levels of brain activation and visual processing hierarchy in the brain. We were also curious about which brain regions would be associated with deeper convolutional layers in VGG-16. The study analyzed a functional MRI (fMRI) dataset where participants watched the cartoon movie Partly Cloudy. Frames of the videos were fed into VGG-16, and activation maps from different kernels and layers were extracted. Time series of the average activation patterns for each kernel were created and fed into a voxel-wise model to study brain activations. Results showed that lower convolutional layers (1 convolutional layer) were mostly associated with lower visual regions, but some kernels (6, 19, 24, 42, 55, and 58) surprisingly showed associations with activations in the posterior cingulate cortex, part of the default mode network. Deeper convolutional layers were associated with more anterior and lateral portions of the visual cortex (e.g., the lateral occipital complex) and the supramarginal gyrus. Analyzing activation features associated with different brain regions showed the promise and limitations of using CNNs to link video content to brain functions.
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http://dx.doi.org/10.1101/2024.01.20.576341 | DOI Listing |
It is known that inhibition of the endoplasmic reticulum transmembrane signaling protein (ERN1) suppresses the glioblastoma cells proliferation. The present study aims to investigate the impact of inhibition of ERN1 endoribonuclease and protein kinase activities on the , , and gene expression in U87MG glioblastoma cells with an intent to reveal the role of ERN1 signaling in the regulation of expression of these genes. The U87MG glioblastoma cells with inhibited ERN1 endoribonuclease (dnrERN1) or both enzymatic activities of ERN1 (endoribonuclease and protein kinase; dnERN1) were used.
View Article and Find Full Text PDFEndocr Regul
January 2025
1Department of Molecular Biology, Palladin Institute of Biochemistry, National Academy of Sciences of Ukraine, Kyiv, Ukraine.
For the effective growth of malignant tumors, including glioblastoma, the necessary factors involve endoplasmic reticulum (ER) stress, hypoxia, and the availability of nutrients, particularly glucose. The ER degradation enhancing alpha-mannosidase like protein 1 (EDEM1) is involved in ER-associated degradation (ERAD) targeting misfolded glycoproteins for degradation in an N-glycan-independent manner. EDEM1 was also identified as a new modulator of insulin synthesis and secretion.
View Article and Find Full Text PDFHepatology
March 2025
Department of Liver Surgery and Transplantation, Liver Cancer Institute and Zhongshan Hospital, Fudan University, Shanghai, China.
Background And Aims: Portal vein tumor thrombosis (PVTT), an indicator of clinical metastasis, significantly shortens hepatocellular carcinoma (HCC) patients' lifespan, and no effective treatment has been established. We aimed to illustrate mechanisms underlying PVTT formation and tumor metastasis, and identified potential targets for clinical intervention.
Approach And Results: Multi-omics data of 159 HCC patients (including 37 cases with PVTT) was analyzed to identify contributors to PVTT formation and tumor metastasis.
Sci Transl Med
March 2025
Clinical Neuroscience Research Center, Department of Neurosurgery and Neurology, Tulane University School of Medicine, New Orleans, LA 70112, USA.
Traumatic brain injury (TBI) rapidly triggers proinflammatory activation of microglia, contributing to secondary brain damage post-TBI. Although the governing role of energy metabolism in shaping the inflammatory phenotype and function of immune cells has been increasingly recognized, the specific alterations in microglial bioenergetics post-TBI remain poorly understood. Itaconate, a metabolite produced by the enzyme aconitate decarboxylase 1 [IRG1; encoded by immune responsive gene 1 ()], is a pivotal metabolic regulator in immune cells, particularly in macrophages.
View Article and Find Full Text PDFSci Robot
March 2025
NeuroX Institute and Brain Mind Institute, School of Life Sciences, Swiss Federal Institute of Technology (EPFL), Lausanne, Switzerland.
Rehabilitation robotics aims to promote activity-dependent reorganization of the nervous system. However, people with paralysis cannot generate sufficient activity during robot-assisted rehabilitation and, consequently, do not benefit from these therapies. Here, we developed an implantable spinal cord neuroprosthesis operating in a closed loop to promote robust activity during walking and cycling assisted by robotic devices.
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