Dynamics of aesthetic experience are reflected in the default-mode network

Publication date: Available online 10 December 2018

Source: NeuroImage

Author(s): Amy M. Belfi, Edward A. Vessel, Aenne Brielmann, Ayse Ilkay Isik, Anjan Chatterjee, Helmut Leder, Denis G. Pelli, G. Gabrielle Starr

Abstract

Neuroaesthetics is a rapidly developing interdisciplinary field of research that aims to understand the neural substrates of aesthetic experience: While understanding aesthetic experience has been an objective of philosophers for centuries, it has only more recently been embraced by neuroscientists. Recent work in neuroaesthetics has revealed that aesthetic experience with static visual art engages visual, reward and default-mode networks. Very little is known about the temporal dynamics of these networks during aesthetic appreciation. Previous behavioral and brain imaging research suggests that critical aspects of aesthetic experience have slow dynamics, taking more than a few seconds, making them amenable to study with fMRI. Here, we identified key aspects of the dynamics of aesthetic experience while viewing art for various durations. In the first few seconds following image onset, activity in the DMN (and high-level visual and reward regions) was greater for very pleasing images; in the DMN this activity counteracted a suppressive effect that grew longer and deeper with increasing image duration. In addition, for very pleasing art, the DMN response returned to baseline in a manner time-locked to image offset. Conversely, for non-pleasing art, the timing of this return to baseline was inconsistent. This differential response in the DMN may therefore reflect the internal dynamics of the participant's state: The participant disengages from art-related processing and returns to stimulus-independent thought. These dynamics suggest that the DMN tracks the internal state of a participant during aesthetic experience.

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Metabolism Plays a Key Role during Macrophage Activation

Monocyte and macrophage diversity is evidenced by the modulation of cell surface markers and differential production of soluble mediators. These immune cells play key roles in controlling tissue homeostasis, infections, and excessive inflammation. Macrophages remove dead cells in a process named efferocytosis, contributing to the healthy tissue maintenance. Recently, it became clear that the main macrophage functions are under metabolic control. Modulation of glucose, fatty acid, and amino acid metabolism is associated with various macrophage activations in response to external stimuli. Deciphering these metabolic pathways provided critical information about macrophage functions.

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Activation of GABAB Receptor Suppresses Diabetic Neuropathic Pain through Toll-Like Receptor 4 Signaling Pathway in the Spinal Dorsal Horn

Diabetic neuropathic pain (DNP) is a prevalent complication in diabetes patients. Neuronal inflammation and activation of Toll-like receptor 4 (TLR4) are involved in the occurrence of DNP. However, the underlying mechanisms remain unclear. Downregulation of gamma-aminobutyric acid B (GABAB) receptor contributes to the DNP. GABAB receptor interacts with NF-κB, a downstream signaling factor of TLR4, in a neuropathic pain induced by chemotherapy. In this study, we determined the role of TLR4/Myd88/NF-κB signaling pathways coupled to GABAB receptors in the generation of DNP. Intrathecal injection of baclofen (GABAB receptor agonist), LPS-RS ultrapure (TLR4 antagonist), MIP (MyD88 antagonist), or SN50 (NF-κB inhibitor) significantly increased paw withdrawal threshold (PWT) and paw withdrawal thermal latency (PWTL) in DNP rats, while intrathecal injection of saclofen (GABAB receptor blocker) decreased PWT and PWTL in DNP rats. The expression of TLR4, Myd88, NF-κBp65, and their downstream components IL-1 and TNF-α was significantly higher in the spinal cord tissue in DNP rats compared to control rats. Following inhibition of TLR4, Myd88, and NF-κB, the expression of IL-1 and TNF-α decreased. Activation of GABAB receptors downregulated the expression of TLR4, Myd88, NF-κBp65, IL-1, and TNF-α. Blockade of GABAB receptors significantly upregulated expression of TLR4, Myd88, NF-κBp65, IL-1, and TNF-α. These data suggest that activation of the TLR4/Myd88/NF-κB signaling pathway is involved in the occurrence of DNP in rats. Activation of GABAB receptor in the spinal cord may suppress the TLR4/Myd88/NF-κB signaling pathway and alleviate the DNP.

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Improved resin‐to‐dentin bond strength and durability via non‐thermal atmospheric pressure plasma drying of etched dentin

This study aimed to evaluate the improvement in strength and durability of the bond between dentin and composite resins following plasma drying of the etched dentin surface using non‐thermal atmospheric pressure plasma. Plasma drying was applied to the etched dentin before applying adhesive. Conventional wet‐bonding and helium (He) gas‐dried bonding schemes were used as control groups. The bond strength of the composite resin to dentin was measured as the microtensile bond strength at 24 h after bonding and after 10,000 cycles of thermocycling. Hybrid layer formation was observed using micro‐Raman spectroscopy and scanning electron microscopy. Although the bond‐strength values were not statistically different either at 24 h after bonding or after thermocycling, the bond strength of the plasma‐dried bonding group was significantly higher than the conventional wet‐bonding group and He gas‐dried bonding group. Micro‐Raman spectral analysis revealed effective penetration of the adhesive and an improved polymerization rate of the adhesive after plasma drying. Plasma drying increased the penetration of hydrophobic resin into the collagen mesh structure, which improved mechanical bonding and long‐term durability between dentin and composite resin.

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High-pitch CT, decreasing need for sedation and its potential side effects: some practical considerations and future directions

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Gut Microbiome Dysbiosis and Immunometabolism: New Frontiers for Treatment of Metabolic Diseases

Maintenance of healthy human metabolism depends on a symbiotic consortium among bacteria, archaea, viruses, fungi, and host eukaryotic cells throughout the human gastrointestinal tract. Microbial communities provide the enzymatic machinery and the metabolic pathways that contribute to food digestion, xenobiotic metabolism, and production of a variety of bioactive molecules. These include vitamins, amino acids, short-chain fatty acids (SCFAs), and metabolites, which are essential for the interconnected pathways of glycolysis, the tricarboxylic acid/Krebs cycle, oxidative phosphorylation (OXPHOS), and amino acid and fatty acid metabolism. Recent studies have been elucidating how nutrients that fuel the metabolic processes impact on the ways immune cells, in particular, macrophages, respond to different stimuli under physiological and pathological conditions and become activated and acquire a specialized function. The two major inflammatory phenotypes of macrophages are controlled through differential consumption of glucose, glutamine, and oxygen. M1 phenotype is triggered by polarization signal from bacterial lipopolysaccharide (LPS) and Th1 proinflammatory cytokines such as interferon-γ, TNF-α, and IL-1β, or both, whereas M2 phenotype is triggered by Th2 cytokines such as interleukin-4 and interleukin-13 as well as anti-inflammatory cytokines, IL-10 and TGFβ, or glucocorticoids. Glucose utilization and production of chemical mediators including ATP, reactive oxygen species (ROS), nitric oxide (NO), and NADPH support effector activities of M1 macrophages. Dysbiosis is an imbalance of commensal and pathogenic bacteria and the production of microbial antigens and metabolites. It is now known that the gut microbiota-derived products induce low-grade inflammatory activation of tissue-resident macrophages and contribute to metabolic and degenerative diseases, including diabetes, obesity, metabolic syndrome, and cancer. Here, we update the potential interplay of host gut microbiome dysbiosis and metabolic diseases. We also summarize on advances on fecal therapy, probiotics, prebiotics, symbiotics, and nutrients and small molecule inhibitors of metabolic pathway enzymes as prophylactic and therapeutic agents for metabolic diseases.

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The Process of Acclimation to Chronic Hypoxia Leads to Submandibular Gland and Periodontal Alterations: An Insight on the Role of Inflammatory Mediators

The exposition to hypoxia is a stressful stimulus, and the organism develops acclimation mechanisms to ensure homeostasis, but if this fails, it leads to the development of pathological processes. Considering the large number of people under hypoxic conditions, it is of utmost importance to study the mechanisms implicated in hypoxic acclimation in oral tissues and the possible alteration of some important inflammatory markers that regulate salivary and periodontal function. It is the aim of the present study to analyze submandibular (SMG) and periodontal status of animals chronically exposed to continuous (CCH) or intermittent (CIH) hypoxia in order to elucidate the underlying molecular mechanisms that may lead to hypoxic acclimation. Adult Wistar rats were exposed to CCH or CIH simulating 4200 meters of altitude during 90 days. Salivary secretion was decreased in animals exposed to hypoxia, being lower in CIH, together with increased prostaglandin E2 (PGE2) content, TBARS concentration, and the presence of apoptotic nuclei and irregular secretion granules in SMG. AQP-5 mRNA levels decreased in both hypoxic groups. Only the CCH group showed higher HIF-1α staining, while CIH alone exhibited interradicular bone loss and increased concentration of the bone resorption marker CTX-I. In summary, animals exposed to CIH show a worse salivary secretion rate, which related with higher levels of PGE2, suggesting a negative role of this inflammatory mediator during hypoxia acclimation. We link the weak immunorreactivity of HIF-1α in CIH with improper hypoxia acclimation, which is necessary to sustaining SMG physiology under this environmental condition. The alveolar bone loss observed in CIH rats could be due mainly to a direct effect of PGE2, as suggested by its higher content in gingival tissue, but also to the indirect effect of hyposalivation. This study may eventually contribute to finding therapeutics to treat the decreased salivary flow, improving in that way oral health.

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