Bibliografías temáticas / Whole-brain map

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Literatura académica sobre el tema "Whole-brain map"

Autor: Grafiati

Publicado: 10 de marzo de 2023

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Artículos de revistas sobre el tema "Whole-brain map"

Brittin, Christopher A., Steven J. Cook, David H. Hall, Scott W. Emmons, and Netta Cohen. "A multi-scale brain map derived from whole-brain volumetric reconstructions." Nature 591, no. 7848 (2021): 105–10. http://dx.doi.org/10.1038/s41586-021-03284-x.

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Lee, Dongha, and Hae-Jeong Park. "A populational connection map for the whole brain white matter." IBRO Reports 6 (September 2019): S153. http://dx.doi.org/10.1016/j.ibror.2019.07.486.

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Bernat, James L. "THE BIOPHILOSOPHICAL BASIS OF WHOLE-BRAIN DEATH." Social Philosophy and Policy 19, no. 2 (2002): 324–42. http://dx.doi.org/10.1017/s0265052502192132.

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Notwithstanding these wise pronouncements, my project here is to characterize the biological phenomenon of death of the higher animal species, such as vertebrates. My claim is that the formulation of “whole-brain death” provides the most congruent map for our correct understanding of the concept of death. This essay builds upon the foundation my colleagues and I have laid since 1981 to characterize the concept of death and refine when this event occurs. Although our society's well-accepted program of multiple organ procurement for transplantation requires the organ donor first to be dead, the concept of brain death is not merely a social contrivance to permit us to obtain the benefits of organ procurement. Rather, the concept of whole-brain death stands independently as the most accurate biological representation of the demise of the human organism.

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Shi, Yuhang, S. Johanna Vannesjo, Karla L. Miller, and Stuart Clare. "Template-based field map prediction for rapid whole brain B0 shimming." Magnetic Resonance in Medicine 80, no. 1 (2017): 171–80. http://dx.doi.org/10.1002/mrm.27020.

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Jung, Youjin, Raymond P. Viviano, Sanneke van Rooden, Jeroen van der Grond, Serge A. R. B. Rombouts, and Jessica S. Damoiseaux. "White Matter Hyperintensities and Apolipoprotein E Affect the Association Between Mean Arterial Pressure and Objective and Subjective Cognitive Functioning in Older Adults." Journal of Alzheimer's Disease 84, no. 3 (2021): 1337–50. http://dx.doi.org/10.3233/jad-210695.

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Background: White matter hyperintensities (WMH) show a robust relationship with arterial pressure as well as objective and subjective cognitive functioning. In addition, APOE ɛ4 carriership may influence how arterial pressure affects cognitive functioning. Objective: To determine the role of region-specific WMH burden and APOE ɛ4 carriership on the relationship between mean arterial pressure (MAP) and cognitive function as well as subjective cognitive decline (SCD). Methods: The sample consisted of 87 cognitively unimpaired middle-aged to older adults aged 50–85. We measured WMH volume for the whole brain, anterior thalamic radiation (ATR), forceps minor, and superior longitudinal fasciculus (SLF). We examined whether WMH burden mediated the relationship between MAP and cognition (i.e., TMT-A score for processing speed; Stroop performance for executive function) as well as SCD (i.e., Frequency of Forgetting (FoF)), and whether APOE ɛ4 carriership moderated that mediation. Results: WMH burden within SLF mediated the effect of MAP on Stroop performance. Both whole brain and ATR WMH burden mediated the effect of MAP on FoF score. In the MAP–WMH–Stroop relationship, the mediation effect of SLF WMH and the effect of MAP on SLF WMH were significant only in APOE ɛ4 carriers. In the MAP–WMH–FoF relationship, the effect of MAP on whole brain WMH burden was significant only in ɛ4 carriers. Conclusion: WMH burden and APOE genotype explain the link between blood pressure and cognitive function and may enable a more accurate assessment of the effect of high blood pressure on cognitive decline and risk for dementia.

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Morone, Flaviano, Kevin Roth, Byungjoon Min, H. Eugene Stanley, and Hernán A. Makse. "Model of brain activation predicts the neural collective influence map of the brain." Proceedings of the National Academy of Sciences 114, no. 15 (2017): 3849–54. http://dx.doi.org/10.1073/pnas.1620808114.

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Efficient complex systems have a modular structure, but modularity does not guarantee robustness, because efficiency also requires an ingenious interplay of the interacting modular components. The human brain is the elemental paradigm of an efficient robust modular system interconnected as a network of networks (NoN). Understanding the emergence of robustness in such modular architectures from the interconnections of its parts is a longstanding challenge that has concerned many scientists. Current models of dependencies in NoN inspired by the power grid express interactions among modules with fragile couplings that amplify even small shocks, thus preventing functionality. Therefore, we introduce a model of NoN to shape the pattern of brain activations to form a modular environment that is robust. The model predicts the map of neural collective influencers (NCIs) in the brain, through the optimization of the influence of the minimal set of essential nodes responsible for broadcasting information to the whole-brain NoN. Our results suggest intervention protocols to control brain activity by targeting influential neural nodes predicted by network theory.

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Deleo, Francesco, Seok-Jun Hong, Fatemeh Fadaie, et al. "Whole-brain multimodal MRI phenotyping of periventricular nodular heterotopia." Neurology 95, no. 17 (2020): e2418-e2426. http://dx.doi.org/10.1212/wnl.0000000000010648.

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ObjectiveTo test the hypothesis that in periventricular nodular heterotopia (PVNH) structure and function of cortical areas overlying the heterotopic gray matter are preferentially affected.MethodsWe studied a group of 40 patients with PVNH and normal-appearing cortex and compared their quantitative MRI markers of brain development, structure, and function to those of 43 age- and sex-matched healthy controls. Inspired by models of neocortical development suggesting that neuronal migration follows a curvilinear path to preserve topologic correspondence between the outer ventricular zone and the cortical surface, we computationally defined the overlying cortex using the Laplace equation and generated synthetic streamlines that link the ventricles, where nodules are located, and the neocortex.ResultsWe found multilobar cortical thickening encompassing prefrontal, latero-basal temporal, and temporoparietal cortices largely corresponding with the PVNH group-averaged map of the overlying cortex, the latter colocalized with areas of abnormal function, as defined by resting-state fMRI. Patients also presented hippocampal functional hyperconnectivity and malrotation, the latter positively correlating with neocortical maldevelopment indexed by increased folding complexity of the parahippocampus. In clusters of thickness and curvature findings, there were no significant differences between unilateral and bilateral PVNH; contrasting brain-wide metrics between cohorts was also unrevealing. There was no relationship between imaging markers and disease duration except for positive correlation with functional anomalies.ConclusionOur quantitative image analysis demonstrates widespread structural and functional alterations in PVNH with differential interaction with the overlying cortex and the hippocampus. Right hemispheric predominance may be explained by an early insult, likely genetically determined, on brain morphogenesis.

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Tao, Jingshan, Yong Cai, Yisheng Dai, Yingdi Xie, Hailing Liu, and Xiaojin Zang. "Value of 4D CT Angiography Combined with Whole Brain CT Perfusion Imaging Feature Analysis under Deep Learning in Imaging Examination of Acute Ischemic Stroke." Computational Intelligence and Neuroscience 2022 (June 13, 2022): 1–9. http://dx.doi.org/10.1155/2022/2286413.

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This study was aimed at investigating the application of deep learning 4D computed tomography angiography (CTA) combined with whole brain CT perfusion (CTP) imaging in acute ischemic stroke (AIS). A total of 46 patients with ischemic stroke were selected from the hospital as the research objects. Image quality was analyzed after the 4D CTA images were obtained by perfusion imaging. The results showed that whole brain perfusion imaging based on FCN can achieve automatic segmentation. FCN segmentation results took a short time, an average of 2-3 seconds, and the Dice similarity coefficient (DSC) and mean absolute distance (MAD) were lower than those of other algorithms. FCN segmentation distance was 17.87. The parameters of the central area, the peripheral area, and the mirror area of the perfusion map were compared, and the mean transit time (MTT) and time to peak (TTP) of the lesion were prolonged compared with the mirror area. Moreover, the peripheral CBV was increased, and the differences between the parameters were significant ( P < 0.05 ). In conclusion, using the deep learning FCN network, 4D CTA combined with whole brain CTP imaging technology can effectively analyze the perfusion state and achieve clinically personalized treatment.

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Jehl, Markus, Ekaterina Mikhaylova, Valerie Treyer, et al. "Attenuation Correction Using Template PET Registration for Brain PET: A Proof-of-Concept Study." Journal of Imaging 9, no. 1 (2022): 2. http://dx.doi.org/10.3390/jimaging9010002.

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NeuroLF is a dedicated brain PET system with an octagonal prism shape housed in a scanner head that can be positioned around a patient’s head. Because it does not have MR or CT capabilities, attenuation correction based on an estimation of the attenuation map is a crucial feature. In this article, we demonstrate this method on [18F]FDG PET brain scans performed with a low-resolution proof of concept prototype of NeuroLF called BPET. We perform an affine registration of a template PET scan to the uncorrected emission image, and then apply the resulting transform to the corresponding template attenuation map. Using a whole-body PET/CT system as reference, we quantitively show that this method yields comparable image quality (0.893 average correlation to reference scan) to using the reference µ-map as obtained from the CT scan of the imaged patient (0.908 average correlation). We conclude from this initial study that attenuation correction using template registration instead of a patient CT delivers similar results and is an option for patients undergoing brain PET.

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Yang, Hsiao T., and Kevin J. Cummings. "Brain stem serotonin protects blood pressure in neonatal rats exposed to episodic anoxia." Journal of Applied Physiology 115, no. 12 (2013): 1733–41. http://dx.doi.org/10.1152/japplphysiol.00970.2013.

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In neonatal rodents, a loss of brain stem serotonin [5-hydroxytryptamine (5-HT)] in utero or at birth compromises anoxia-induced gasping and the recovery of heart rate (HR) and breathing with reoxygenation (i.e., autoresuscitation). How mean arterial pressure (MAP) is influenced after an acute loss of brain stem 5-HT content is unknown. We hypothesized that a loss of 5-HT for ∼1 day would compromise MAP during episodic anoxia. We injected 6-fluorotryptophan (20 mg/kg ip) into rat pups (postnatal days 9–10 or 11–13, n = 22 treated, 24 control), causing a ∼70% loss of brain stem 5-HT. Pups were exposed to a maximum of 15 anoxic episodes, separated by 5 min of room air to allow autoresuscitation. In younger pups, we measured breathing frequency and tidal volume using “head-out” plethysmography and HR from the electrocardiogram. In older pups, we used whole body plethysmography to detect gasping, while monitoring MAP. Gasp latency and the time required for respiratory, HR, and MAP recovery following each episode were determined. Despite normal gasp latency, breathing frequency and a larger tidal volume ( P < 0.001), 5-HT-deficient pups survived one-half the number of episodes as controls ( P < 0.001). The anoxia-induced decrease in MAP experienced by 5-HT-deficient pups was double that of controls ( P = 0.017), despite the same drop in HR ( P = 0.48). MAP recovery was delayed ∼10 s by 5-HT deficiency ( P = 0.001). Our data suggest a loss of brain stem 5-HT leads to a pronounced, premature loss of MAP in response to episodic anoxia. These data may help explain why some sudden infant death syndrome cases die from what appears to be cardiovascular collapse during apparent severe hypoxia.

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