scholarly journals A Computational Perspective of the Role of the Thalamus in Cognition

2019 ◽  
Vol 31 (7) ◽  
pp. 1380-1418 ◽  
Author(s):  
Nima Dehghani ◽  
Ralf D. Wimmer
Keyword(s):  
Cognitive Capacity ◽  
Contextual Modulation ◽  
Dynamic Selection ◽  
Thalamic Relay ◽  
Health And Disease ◽  
Experimental Approaches ◽  
Cortical Inputs ◽  
Reasonable Description ◽  
Cortical Representations

The thalamus has traditionally been considered as only a relay source of cortical inputs, with hierarchically organized cortical circuits serially transforming thalamic signals to cognitively relevant representations. Given the absence of local excitatory connections within the thalamus, the notion of thalamic relay seemed like a reasonable description over the past several decades. Recent advances in experimental approaches and theory provide a broader perspective on the role of the thalamus in cognitively relevant cortical computations and suggest that only a subset of thalamic circuit motifs fits the relay description. Here, we discuss this perspective and highlight the potential role for the thalamus, and specifically the mediodorsal (MD) nucleus, in the dynamic selection of cortical representations through a combination of intrinsic thalamic computations and output signals that change cortical network functional parameters. We suggest that through the contextual modulation of cortical computation, the thalamus and cortex jointly optimize the information and cost trade-off in an emergent fashion. We emphasize that coordinated experimental and theoretical efforts will provide a path to understanding the role of the thalamus in cognition, along with an understanding to augment cognitive capacity in health and disease.

Role of nuclear factor κB in liver health and disease

2010 ◽  
Vol 118 (12) ◽  
pp. 691-705 ◽  
Author(s):  
Stuart M. Robinson ◽  
Derek A. Mann
Keyword(s):  
Hepatocellular Carcinoma ◽  
Current Knowledge ◽  
Transcriptional Regulator ◽  
Cell Types ◽  
Nuclear Factor Κb ◽  
Nuclear Factor ◽  
Liver Health ◽  
Health And Disease ◽  
Experimental Approaches

NF-κB (nuclear factor κB) is a heterodimeric transcription factor that is constitutively expressed in all cell types and has a central role as a transcriptional regulator in response to cellular stress. In the present review, we discuss the role of NF-κB signalling in the maintenance of liver homoeostasis as well as in the pathogenesis of a wide variety of conditions affecting the liver, including viral hepatitis, steatohepatitis, cirrhosis and hepatocellular carcinoma. Much of the current knowledge of NF-κB signalling in the liver relates to the canonical pathway, the IKK [IκB (inhibitor of κB) kinase] complex and the RelA subunit. We explore the weaknesses of the experimental approaches to date and suggest that further work is needed to investigate in detail the discreet functions of each of the Rel subunits in liver physiology and disease.

Concluding Summary

2018 ◽  
Author(s):  
Carrie Figdor
Keyword(s):  
Social Sciences ◽  
External Factors ◽  
Cognitive Capacity ◽  
Human Cognition ◽  
Conceptual Foundation ◽  
The Social ◽  
New Research ◽  
Internal And External Factors ◽  
Conceptual Confusion

Chapter 10 provides a summary of the argument of the book. It elaborates some of the benefits of Literalism, such as less conceptual confusion and an expanded range of entities for research that might illuminate human cognition. It motivates distinguishing the questions of whether something has a cognitive capacity from whether it is intuitively like us. It provides a conceptual foundation for the social sciences appropriate for the increasing role of modeling in these sciences. It also promotes convergence in terms of the roles of internal and external factors in explaining both human and nonhuman behavior. Finally, it sketches some of the areas of new research that it supports, including group cognition and artificial intelligence.

Categorization flexibility and unconventional choices: is life an adventure?

2020 ◽  
Vol 54 (8) ◽  
pp. 1963-1986
Author(s):  
Tilottama G. Chowdhury ◽  
Feisal Murshed
Keyword(s):  
Interactive Effect ◽  
Interactive Effects ◽  
Cognitive Capacity ◽  
Purchase Behavior ◽  
Consumer Decision Making ◽  
Cross Sectional ◽  
Content Type ◽  
Cross Domain ◽  
Multiple Domains

Purpose This paper proposes that categorization flexibility, operationalized as the cognitive capacity that cross-categorizes products in multiple situational categories across multiple domains, might favorably influence a consumer’s evaluation of unconventional options. Design/methodology/approach Experimental research design is used to test the theory. An exploratory study first establishes the effect of categorization flexibility in a non-food domain. Study 1 documents the moderating role of decision domain, showing that the effect works only under low- (vs high-) consequence domain. Studies 2A and 2B further refine the notion by showing that individuals can be primed in a relatively higher categorization flexibility frame of mind. Study 3 demonstrates the interactive effect of categorization flexibility and adventure priming in a high-consequence domain. Study 4 integrates the interactive effects of decisions with low- vs high-consequence, adventure priming and categorization flexibility within a single decision domain of high consequence. Findings Consumers with higher- (vs lower-) categorization flexibility tend to opt for unconventional choices when the decision domain entails low consequences, whereas such a result does not hold under decision domain of high consequences. The categorization flexibility effects in case of low-consequence decision domain holds true even when consumers are primed to be categorization flexible. Furthermore, with additional adventure priming, consumers show an increased preference for unconventional options even under a decision domain with high consequence. Research limitations/implications This study could not examine real purchase behavior as results are based on cross-sectional, behavioral intention data. In addition, it did not examine the underlying reason for presence of cross-domain categorization flexibility index. Practical implications The results suggest that stimuli may be tailored to consumers in ways that increase the salience and the perceived attractiveness of unconventional choices. Further, data reinforce the notion of cross-categorical interrelations among different domains, which could be leveraged by marketers. Originality/value This study represents the first documentation of the potential ways by which unconventional product choice might be a function of individuals’ categorization flexibility level across different types of decision domains. The findings yield implications that are novel to both categorization and consumer decision-making literature.

scholarly journals Chromosome Instability, Aging and Brain Diseases

Cells ◽  
2021 ◽  
Vol 10 (5) ◽  
pp. 1256
Author(s):  
Ivan Y. Iourov ◽  
Yuri B. Yurov ◽  
Svetlana G. Vorsanova ◽  
Sergei I. Kutsev
Keyword(s):  
Brain Aging ◽  
Chromosome Instability ◽  
Neuronal Cell Death ◽  
Neuronal Cell ◽  
Accelerated Aging ◽  
Brain Diseases ◽  
Aging Brain ◽  
Ontogenetic Changes ◽  
Health And Disease

Chromosome instability (CIN) has been repeatedly associated with aging and progeroid phenotypes. Moreover, brain-specific CIN seems to be an important element of pathogenic cascades leading to neurodegeneration in late adulthood. Alternatively, CIN and aneuploidy (chromosomal loss/gain) syndromes exhibit accelerated aging phenotypes. Molecularly, cellular senescence, which seems to be mediated by CIN and aneuploidy, is likely to contribute to brain aging in health and disease. However, there is no consensus about the occurrence of CIN in the aging brain. As a result, the role of CIN/somatic aneuploidy in normal and pathological brain aging is a matter of debate. Still, taking into account the effects of CIN on cellular homeostasis, the possibility of involvement in brain aging is highly likely. More importantly, the CIN contribution to neuronal cell death may be responsible for neurodegeneration and the aging-related deterioration of the brain. The loss of CIN-affected neurons probably underlies the contradiction between reports addressing ontogenetic changes of karyotypes within the aged brain. In future studies, the combination of single-cell visualization and whole-genome techniques with systems biology methods would certainly define the intrinsic role of CIN in the aging of the normal and diseased brain.

scholarly journals The Role of Cell Metabolism in Innate Immune Memory

2020 ◽  
pp. 1-9
Author(s):  
Anaisa Valido Ferreira ◽  
Jorge Domiguéz-Andrés ◽  
Mihai Gheorghe Netea
Keyword(s):  
Metabolic Pathways ◽  
Tricarboxylic Acid Cycle ◽  
Cell Metabolism ◽  
Innate Immune ◽  
Immune Memory ◽  
Functional Changes ◽  
Trained Immunity ◽  
Health And Disease

Immunological memory is classically attributed to adaptive immune responses, but recent studies have shown that challenged innate immune cells can display long-term functional changes that increase nonspecific responsiveness to subsequent infections. This phenomenon, coined <i>trained immunity</i> or <i>innate immune memory</i>, is based on the epigenetic reprogramming and the rewiring of intracellular metabolic pathways. Here, we review the different metabolic pathways that are modulated in trained immunity. Glycolysis, oxidative phosphorylation, the tricarboxylic acid cycle, amino acid, and lipid metabolism are interplaying pathways that are crucial for the establishment of innate immune memory. Unraveling this metabolic wiring allows for a better understanding of innate immune contribution to health and disease. These insights may open avenues for the development of future therapies that aim to harness or dampen the power of the innate immune response.

scholarly journals Role of Insulin in Health and Disease: An Update

2021 ◽  
Vol 22 (12) ◽  
pp. 6403
Author(s):  
Md Saidur Rahman ◽  
Khandkar Shaharina Hossain ◽  
Sharnali Das ◽  
Sushmita Kundu ◽  
Elikanah Olusayo Adegoke ◽  
...  
Keyword(s):  
Insulin Signaling ◽  
Basic Research ◽  
Future Research ◽  
Protective Effects ◽  
Glucose Levels ◽  
Physiological Processes ◽  
Blood Glucose Levels ◽  
Wide Range ◽  
Health And Disease

Insulin is a polypeptide hormone mainly secreted by β cells in the islets of Langerhans of the pancreas. The hormone potentially coordinates with glucagon to modulate blood glucose levels; insulin acts via an anabolic pathway, while glucagon performs catabolic functions. Insulin regulates glucose levels in the bloodstream and induces glucose storage in the liver, muscles, and adipose tissue, resulting in overall weight gain. The modulation of a wide range of physiological processes by insulin makes its synthesis and levels critical in the onset and progression of several chronic diseases. Although clinical and basic research has made significant progress in understanding the role of insulin in several pathophysiological processes, many aspects of these functions have yet to be elucidated. This review provides an update on insulin secretion and regulation, and its physiological roles and functions in different organs and cells, and implications to overall health. We cast light on recent advances in insulin-signaling targeted therapies, the protective effects of insulin signaling activators against disease, and recommendations and directions for future research.

scholarly journals A modular tool to query and inducibly disrupt biomolecular condensates

2021 ◽  
Vol 12 (1) ◽  
Author(s):  
Carmen N. Hernández-Candia ◽  
Sarah Pearce ◽  
Chandra L. Tucker
Keyword(s):  
Amyotrophic Lateral Sclerosis ◽  
Huntington's Disease ◽  
Huntington’S Disease ◽  
Cellular Function ◽  
Biological Role ◽  
Cellular Biology ◽  
Condensate Formation ◽  
Health And Disease ◽  
Lateral Sclerosis

AbstractDynamic membraneless compartments formed by protein condensates have multifunctional roles in cellular biology. Tools that inducibly trigger condensate formation have been useful for exploring their cellular function, however, there are few tools that provide inducible control over condensate disruption. To address this need we developed DisCo (Disassembly of Condensates), which relies on the use of chemical dimerizers to inducibly recruit a ligand to the condensate-forming protein, triggering condensate dissociation. We demonstrate use of DisCo to disrupt condensates of FUS, associated with amyotrophic lateral sclerosis, and to prevent formation of polyglutamine-containing huntingtin condensates, associated with Huntington’s disease. In addition, we combined DisCo with a tool to induce condensates with light, CRY2olig, achieving bidirectional control of condensate formation and disassembly using orthogonal inputs of light and rapamycin. Our results demonstrate a method to manipulate condensate states that will have broad utility, enabling better understanding of the biological role of condensates in health and disease.

Role of PRAS40 in Akt and mTOR signaling in health and disease

2012 ◽  
Vol 302 (12) ◽  
pp. E1453-E1460 ◽  
Author(s):  
Claudia Wiza ◽  
Emmani B. M. Nascimento ◽  
D. Margriet Ouwens
Keyword(s):  
Mammalian Target Of Rapamycin ◽  
Mtor Signaling ◽  
Cellular Growth ◽  
S6 Kinase ◽  
Binding Partners ◽  
Health And Disease ◽  
Mtor Complex 1 ◽  
Mtor Activity

The proline-rich Akt substrate of 40 kDa (PRAS40) acts at the intersection of the Akt- and mammalian target of rapamycin (mTOR)-mediated signaling pathways. The protein kinase mTOR is the catalytic subunit of two distinct signaling complexes, mTOR complex 1 (mTORC1) and mTORC2, that link energy and nutrients to the regulation of cellular growth and energy metabolism. Activation of mTOR in response to nutrients and growth factors results in the phosphorylation of numerous substrates, including the phosphorylations of S6 kinase by mTORC1 and Akt by mTORC2. Alterations in Akt and mTOR activity have been linked to the progression of multiple diseases such as cancer and type 2 diabetes. Although PRAS40 was first reported as substrate for Akt, investigations toward mTOR-binding partners subsequently identified PRAS40 as both component and substrate of mTORC1. Phosphorylation of PRAS40 by Akt and by mTORC1 itself results in dissociation of PRAS40 from mTORC1 and may relieve an inhibitory constraint on mTORC1 activity. Adding to the complexity is that gene silencing studies indicate that PRAS40 is also necessary for the activity of the mTORC1 complex. This review summarizes the regulation and potential function(s) of PRAS40 in the complex Akt- and mTOR-signaling network in health and disease.

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