scholarly journals Embodied higher cognition: insights from Merleau-Ponty’s interpretation of motor intentionality

2021 ◽  
Author(s):  
Jan Halák
Keyword(s):  
Conceptual Knowledge ◽  
Higher Order ◽  
The Body ◽  
Strong Continuity ◽  
Abstract Thought ◽  
Brain Injured ◽  
Motor Intentionality ◽  
The Brain ◽  
Gerstmann’S Syndrome

AbstractThis paper clarifies Merleau-Ponty’s original account of “higher-order” cognition as fundamentally embodied and enacted. Merleau-Ponty’s philosophy inspired theories that deemphasize overlaps between conceptual knowledge and motor intentionality or, on the contrary, focus exclusively on abstract thought. In contrast, this paper explores the link between Merleau-Ponty’s account of motor intentionality and his interpretations of our capacity to understand and interact productively with cultural symbolic systems. I develop my interpretation based on Merleau-Ponty’s analysis of two neuropathological modifications of motor intentionality, the case of the brain-injured war veteran Schneider, and a neurological disorder known as Gerstmann’s syndrome. Building on my analysis of Schneider’s sensorimotor compensatory performances in relation to his limitations in the domains of algebra, geometry, and language usage, I demonstrate a strong continuity between the sense of embodiment and enaction at all these levels. Based on Merleau-Ponty’s interpretations, I argue that “higher-order” cognition is impaired in Schneider insofar as his injury limits his sensorimotor capacity to dynamically produce comparatively more complex differentiations of any given phenomenal structure. I then show how Merleau-Ponty develops and specifies his interpretation of Schneider’s intellectual difficulties in relation to the ambiguous role of the body, and in particular the hand, in Gerstmann’s syndrome. I explain how Merleau-Ponty defends the idea that sensorimotor and quasi-representational cognition are mutually irreducible, while maintaining that symbol-based cognition is a fundamentally enactive and embodied process.

scholarly journals Millimeter (MM) wave and microwave frequency radiation produce deeply penetrating effects: the biology and the physics

2021 ◽  
Vol 0 (0) ◽  
Author(s):  
Martin L. Pall
Keyword(s):  
Magnetic Fields ◽  
Electric Fields ◽  
Cardiac Activity ◽  
Maximum Level ◽  
Voltage Sensor ◽  
The Body ◽  
Time Varying ◽  
The Brain ◽  
Mm Waves

Abstract Millimeter wave (MM-wave) electromagnetic fields (EMFs) are predicted to not produce penetrating effects in the body. The electric but not magnetic part of MM-EMFs are almost completely absorbed within the outer 1 mm of the body. Rodents are reported to have penetrating MM-wave impacts on the brain, the myocardium, liver, kidney and bone marrow. MM-waves produce electromagnetic sensitivity-like changes in rodent, frog and skate tissues. In humans, MM-waves have penetrating effects including impacts on the brain, producing EEG changes and other neurological/neuropsychiatric changes, increases in apparent electromagnetic hypersensitivity and produce changes on ulcers and cardiac activity. This review focuses on several issues required to understand penetrating effects of MM-waves and microwaves: 1. Electronically generated EMFs are coherent, producing much higher electrical and magnetic forces then do natural incoherent EMFs. 2. The fixed relationship between electrical and magnetic fields found in EMFs in a vacuum or highly permeable medium such as air, predicted by Maxwell’s equations, breaks down in other materials. Specifically, MM-wave electrical fields are almost completely absorbed in the outer 1 mm of the body due to the high dielectric constant of biological aqueous phases. However, the magnetic fields are very highly penetrating. 3. Time-varying magnetic fields have central roles in producing highly penetrating effects. The primary mechanism of EMF action is voltage-gated calcium channel (VGCC) activation with the EMFs acting via their forces on the voltage sensor, rather than by depolarization of the plasma membrane. Two distinct mechanisms, an indirect and a direct mechanism, are consistent with and predicted by the physics, to explain penetrating MM-wave VGCC activation via the voltage sensor. Time-varying coherent magnetic fields, as predicted by the Maxwell–Faraday version of Faraday’s law of induction, can put forces on ions dissolved in aqueous phases deep within the body, regenerating coherent electric fields which activate the VGCC voltage sensor. In addition, time-varying magnetic fields can directly put forces on the 20 charges in the VGCC voltage sensor. There are three very important findings here which are rarely recognized in the EMF scientific literature: coherence of electronically generated EMFs; the key role of time-varying magnetic fields in generating highly penetrating effects; the key role of both modulating and pure EMF pulses in greatly increasing very short term high level time-variation of magnetic and electric fields. It is probable that genuine safety guidelines must keep nanosecond timescale-variation of coherent electric and magnetic fields below some maximum level in order to produce genuine safety. These findings have important implications with regard to 5G radiation.

CCM3 Loss-Induced Lymphatic Defect Is Mediated by the Augmented VEGFR3-ERK1/2 Signaling

2021 ◽  
Author(s):  
Lingfeng Qin ◽  
Haifeng Zhang ◽  
Busu Li ◽  
Quan Jiang ◽  
Francesc Lopez ◽  
...  
Keyword(s):  
Nuclear Translocation ◽  
Fluorescein Isothiocyanate ◽  
The Body ◽  
Blue Dye ◽  
Transcriptional Level ◽  
Dependent Manner ◽  
Cavernous Malformations ◽  
Morphological Alterations ◽  
The Brain

Objective: Cerebral cavernous malformations (CCMs) can happen anywhere in the body, although they most commonly produce symptoms in the brain. The role of CCM genes in other vascular beds outside the brain and retina is not well-examined, although the 3 CCM-associated genes ( CCM1 , CCM2 , and CCM3 ) are ubiquitously expressed in all tissues. We aimed to determine the role of CCM gene in lymphatics. Approach and Results: Mice with an inducible pan–endothelial cell (EC) or lymphatic EC deletion of Ccm3 ( Pdcd10 ECKO or Pdcd10 LECKO ) exhibit dilated lymphatic capillaries and collecting vessels with abnormal valve structure. Morphological alterations were correlated with lymphatic dysfunction in Pdcd10 LECKO mice as determined by Evans blue dye and fluorescein isothiocyanate(FITC)-dextran transport assays. Pdcd10 LECKO lymphatics had increased VEGFR3 (vascular endothelial growth factor receptor-3)-ERK1/2 signaling with lymphatic hyperplasia. Mechanistic studies suggested that VEGFR3 is primarily regulated at a transcriptional level in Ccm3-deficient lymphatic ECs, in an NF-κB (nuclear factor κB)–dependent manner. CCM3 binds to importin alpha 2/KPNA2 (karyopherin subunit alpha 2), and a CCM3 deletion releases KPNA2 to activate NF-κB P65 by facilitating its nuclear translocation and P65-dependent VEGFR3 transcription. Moreover, increased VEGFR3 in lymphatic EC preferentially activates ERK1/2 signaling, which is critical for lymphatic EC proliferation. Importantly, inhibition of VEGFR3 or ERK1/2 rescued the lymphatic defects in structure and function. Conclusions: Our data demonstrate that CCM3 deletion augments the VEGFR3-ERK1/2 signaling in lymphatic EC that drives lymphatic hyperplasia and malformation and warrant further investigation on the potential clinical relevance of lymphatic dysfunction in patients with CCM.

scholarly journals The role of thickness inhomogeneities in hierarchical cortical folding

2020 ◽  
Author(s):  
Lucas da Costa Campos ◽  
Raphael Hornung ◽  
Gerhard Gompper ◽  
Jens Elgeti ◽  
Svenja Caspers
Keyword(s):  
Fetal Brain ◽  
Epileptic Seizures ◽  
Quantitative Model ◽  
Higher Order ◽  
Mammalian Brain ◽  
Cortical Folding ◽  
Differential Growth ◽  
The Brain ◽  
Short Life Expectancy

AbstractThe morphology of the mammalian brain cortex is highly folded. For long it has been known that specific patterns of folding are necessary for an optimally functioning brain. On the extremes, lissencephaly, a lack of folds in humans, and polymicrogyria, an overly folded brain, can lead to severe mental retardation, short life expectancy, epileptic seizures, and tetraplegia. The construction of a quantitative model on how and why these folds appear during the development of the brain is the first step in understanding the cause of these conditions. In recent years, there have been various attempts to understand and model the mechanisms of brain folding. Previous works have shown that mechanical instabilities play a crucial role in the formation of brain folds, and that the geometry of the fetal brain is one of the main factors in dictating the folding characteristics. However, modeling higher-order folding, one of the main characteristics of the highly gyrencephalic brain, has not been fully tackled. The effects of thickness inhomogeneity in the gyrogenesis of the mammalian brain are studied in silico. Finite-element simulations of rectangular slabs are performed. The slabs are divided into two distinct regions, where the outer layer mimics the gray matter, and the inner layer the underlying white matter. Differential growth is introduced by growing the top layer tangentially, while keeping the underlying layer untouched. The brain tissue is modeled as a neo-Hookean hyperelastic material. Simulations are performed with both, homogeneous and inhomogeneous cortical thickness. The homogeneous cortex is shown to fold into a single wavelength, as is common for bilayered materials, while the inhomogeneous cortex folds into more complex conformations. In the early stages of development of the inhomogeneous cortex, structures reminiscent of the deep sulci in the brain are obtained. As the cortex continues to develop, secondary undulations, which are shallower and more variable than the structures obtained in earlier gyrification stage emerge, reproducing well-known characteristics of higher-order folding in the mammalian, and particularly the human, brain.

3. Beyond amyloid

2020 ◽  
pp. 51-73
Author(s):  
Kathleen Taylor
Keyword(s):  
Alzheimer’S Disease ◽  
Immune Response ◽  
Lifestyle Factors ◽  
The Body ◽  
Amyloid Cascade Hypothesis ◽  
Brain Injured ◽  
Injured Patients ◽  
Amyloid P ◽  
Amyloid Cascade ◽  
The Brain

‘Beyond amyloid’ outlines recent challenges to the amyloid cascade hypothesis of Alzheimer’s disease. This theory’s enduring popularity has not been matched by success in the clinic. Some people without dementia appear to have high amyloid levels and some brain-injured patients with more amyloid have better outcomes than those with less. One possible explanation is that neurodegeneration begins long before symptoms appear. Other theories include amyloid as the defence rather than cause, and the idea of an immune response to infection causing inflammation in the brain. All this points towards the importance of method and the acknowledgement of the roles played by other parts of the body and lifestyle factors.

scholarly journals Concentrations of the Selected Biomarkers of Endothelial Dysfunction in Response to Antiepileptic Drugs: A Literature Review

2019 ◽  
Vol 25 ◽  
pp. 107602961985942 ◽  
Author(s):  
Beata Sarecka-Hujar ◽  
Izabela Szołtysek-Bołdys ◽  
Ilona Kopyta ◽  
Barbara Dolińska ◽  
Andrzej Sobczak
Keyword(s):  
Risk Factors ◽  
Cardiovascular Diseases ◽  
Endothelial Dysfunction ◽  
Literature Review ◽  
Antiepileptic Drug ◽  
Asymmetric Dimethylarginine ◽  
The Body ◽  
Biochemical Processes ◽  
The Brain

Epilepsy is a disease arising from morphological and metabolic changes in the brain. Approximately 60% of patients with seizures can be controlled with 1 antiepileptic drug (AED), while in others, polytherapy is required. The AED treatment affects a number of biochemical processes in the body, including increasing the risk of cardiovascular diseases (CVDs). It is indicated that the duration of AED therapy with some AEDs significantly accelerates the process of atherosclerosis. Most of AEDs increase levels of homocysteine (HCys) as well as may affect concentrations of new, nonclassical risk factors for atherosclerosis, that is, asymmetric dimethylarginine (ADMA) and homoarginine (hArg). Because of the role of these parameters in the pathogenesis of CVD, knowledge of HCys, ADMA, and hArg concentrations in patients with epilepsia treated with AED, both pediatric and adult, appears to be of significant importance.

scholarly journals Molecular Regulation of Striatal Development: A Review

2012 ◽  
Vol 2012 ◽  
pp. 1-14 ◽  
Author(s):  
A. E. Evans ◽  
C. M. Kelly ◽  
S. V. Precious ◽  
A. E. Rosser
Keyword(s):  
Complex Function ◽  
Dorsal Striatum ◽  
Higher Order ◽  
The Body ◽  
Specific Reference ◽  
Signalling Molecules ◽  
New Information ◽  
Brain Malformations ◽  
The Central Nervous System ◽  
The Brain

The central nervous system is composed of the brain and the spinal cord. The brain is a complex organ that processes and coordinates activities of the body in bilaterian, higher-order animals. The development of the brain mirrors its complex function as it requires intricate genetic signalling at specific times, and deviations from this can lead to brain malformations such as anencephaly. Research into how the CNS is specified and patterned has been studied extensively in chick, fish, frog, and mice, but findings from the latter will be emphasised here as higher-order mammals show most similarity to the human brain. Specifically, we will focus on the embryonic development of an important forebrain structure, the striatum (also known as the dorsal striatum or neostriatum). Over the past decade, research on striatal development in mice has led to an influx of new information about the genes involved, but the precise orchestration between the genes, signalling molecules, and transcription factors remains unanswered. We aim to summarise what is known to date about the tightly controlled network of interacting genes that control striatal development. This paper will discuss early telencephalon patterning and dorsal ventral patterning with specific reference to the genes involved in striatal development.

scholarly journals Co-occuring Toxoplasma Infection and Psychotic Symptoms : Case Report

2020 ◽  
Vol 1 (1) ◽  
Author(s):  
Carla R Marchira ◽  
Andrian F Kusumadewi ◽  
Patricia Wulandari
Keyword(s):  
Life Support ◽  
The United States ◽  
The Body ◽  
Psychotic Symptoms ◽  
Toxoplasma Infection ◽  
Case Presentation ◽  
The Family ◽  
Brain Neurotransmitter ◽  
The Brain

Abstract   Introduction Schizophrenia is a neuropsychiatric disease that is global and is experienced by 1% of the population in the United States and Europe. This study raises awareness of the role of infectious agents in the initiation of psychotic symptoms in schizophrenia. Case Presentation A 20-year-old man is taken by the family to the emergency department because he has decreased consciousness, and the body suddenly stiffens. Patients begin to experience changes in behavior in the form of difficulty sleeping, when invited to talk quietly, laughing alone and whispering without the other person. TORCH examination found an increase in anti-toxoplasma IgM and IgG. This patient is then given basic life support in the form of ABC (airway, breathing, circulation support) and seizure management. Also given risperidone 2 mg / 12 hours, pyrimethamine 1-II (1x200 mg), pyrimethamine day III-XXI (1x 25 mg), intravenous Cefotaxim 2g / 8 hours, Clindamycin 500 mg / 8 hours. The patient experienced improvement after the second week of treatment. Conclusion Toxoplasmosis causes lesions in the brain that cause changes in brain neurotransmitter pathways, which lead to changes in patient behavior.

scholarly journals Hyperammonemia in clinical practice: analysis of own clinical observations

2020 ◽  
Vol 4 (38) ◽  
pp. 23-26
Author(s):  
Z. M. Galeeva ◽  
O. F. Galiullin ◽  
E. G. Yeziukova ◽  
R. G. Tukhbatullina
Keyword(s):  
Clinical Practice ◽  
Drug Therapy ◽  
Human Body ◽  
Scientific Data ◽  
The Body ◽  
Mechanism Of Formation ◽  
Practice Analysis ◽  
Clinical Observations ◽  
The Brain

The article presents scientific data on the role of ammonia in the human body, examines in detail the mechanism of formation and utilization of ammonia in the body. The questions of etiology and separate forms of pathogenesis of hyperammonemia, and its influence on the processes of fibrosis in the liver and the role of stellate liver cells in it are highlighted separately. The data on the influence of hyperammonemia on cognitive functions of the brain with the development of encephalopathy are presented, which is of great importance in clinical practice, during medical examination. The data of own observations are given, the questions of drug therapy are highlighted.

scholarly journals Intersection of Brain Development and Paediatric Diffuse Midline Gliomas: Potential Role of Microenvironment in Tumour Growth

2018 ◽  
Vol 8 (11) ◽  
pp. 200 ◽  
Author(s):  
Katie Loveson ◽  
Helen Fillmore
Keyword(s):  
Tumour Growth ◽  
Median Overall Survival ◽  
Tumour Microenvironment ◽  
Diffuse Intrinsic Pontine Glioma ◽  
The Body ◽  
Paediatric Brain Tumour ◽  
Molecular Aberrations ◽  
The Brain ◽  
Complex Organ

Diffuse intrinsic pontine glioma (DIPG) is a devastating and incurable paediatric brain tumour with a median overall survival of 9 months. Until recently, DIPGs were treated similarly to adult gliomas, but due to the advancement in molecular and imaging technologies, our understanding of these tumours has increased dramatically. While extensive research is being undertaken to determine the function of the molecular aberrations in DIPG, there are significant gaps in understanding the biology and the influence of the tumour microenvironment on DIPG growth, specifically in regards to the developing pons. The precise orchestration and co-ordination of the development of the brain, the most complex organ in the body, is still not fully understood. Herein, we present a brief overview of brainstem development, discuss the developing microenvironment in terms of DIPG growth, and provide a basis for the need for studies focused on bridging pontine development and DIPG microenvironment. Conducting investigations in the context of a developing brain will lead to a better understanding of the role of the tumour microenvironment and will help lead to identification of drivers of tumour growth and therapeutic resistance.

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