Quantitative volatile organic compound sensing with liquid crystal core fibers

Polymer fibers with liquid crystals (LCs) in the core have potential as autonomous sensors of airborne volatile organic compounds (VOCs), with a high surface-to-volume ratio enabling fast and sensi- tive response and an attractive non-woven textile form factor. We demonstrate their ability to continuously and quantitatively mea- sure the concentration of toluene, cyclohexane, and isopropanol as representative VOCs, via the impact of each VOC on the LC bire- fringence. The response is fully reversible and repeatable over several cycles, the response time can be as low as seconds, and high sensitivity is achieved when the operating temperature is near the LC-isotropic transition temperature. We propose that a broad operating temperature range can be realized by combining fi- bers with different LC mixtures, yielding autonomous VOC sensors suitable for integration in apparel or in furniture that can compete with existing consumer-grade electronic VOC sensors in terms of sensitivity and response speed

An active vesicle priming machinery suppresses axon regeneration upon adult CNS injury

Axons in the adult mammalian central nervous system fail to regenerate after spinal cord injury. Neurons lose their capacity to regenerate during development, but the intracellular processes underlying this loss are unclear. We found that critical components of the presynaptic active zone prevent axon regeneration in adult mice. Transcriptomic analysis combined with live-cell imaging revealed that adult primary sensory neurons downregulate molecular constituents of the synapse as they acquire the ability to rapidly grow their axons. Pharmacogenetic reduction of neuronal excitability stimulated axon regeneration after adult spinal cord injury. Genetic gain- and loss-of-function experiments uncovered that essential synaptic vesicle priming proteins of the presynaptic active zone, but not clostridial-toxin-sensitive VAMP-family SNARE proteins, inhibit axon regeneration. Systemic administration of Baclofen reduced voltage-dependent Ca2+ influx in primary sensory neurons and promoted their regeneration after spinal cord injury. These findings indicate that functional presynaptic active zones constitute a major barrier to axon regeneration

Role of Cytosolic Serine Hydroxymethyl Transferase 1 (SHMT1) in Phosphate-Induced Vascular Smooth Muscle Cell Calcification

Background/Aims: Hyperphosphatemia promotes medial vascular calcification, at least partly, by induction of osteo-/chondrogenic transdifferentiation of vascular smooth muscle cells (VSMCs). The complex signaling pathways regulating this process are still incompletely understood. The present study investigated the role of cytosolic serine hydroxymethyl transferase 1 (SHMT1) in phosphate-induced vascular calcification. Methods: Endogenous expression of SHMT1 was suppressed by silencing in primary human aortic smooth muscle cells (HAoSMCs) followed by treatment without and with phosphate or antioxidants. Results: In HAoSMCs, SHMT1 mRNA expression was up-regulated by phosphate. Silencing of SHMT1 alone was sufficient to induce osteo-/chondrogenic transdifferentiation of HAoSMCs, as shown by increased tissue-nonspecific alkaline phosphatase (ALPL) activity and osteogenic markers MSX2, CBFA1 and ALPL mRNA expression. Furthermore, phosphate-induced ALPL mRNA expression and activity as well as calcification were augmented in SHMT1 silenced HAoSMCs as compared to negative control siRNA transfected HAoSMCs. Silencing of SHMT1 decreased total antioxidant capacity and up-regulated NADH/NADPH oxidase system components NOX4 and CYBA mRNA expression in HAoSMCs, effects paralleled by increased mRNA expression of matrix metalloproteinase MMP2 as well as BAX/BCL2 ratio. More importantly, additional treatment with antioxidants TEMPOL or TIRON blunted the increased osteogenic markers mRNA expression in SHMT1 silenced HAoSMCs. Conclusion: Silencing of SHMT1 promotes osteo-/chondrogenic signaling in VSMCs, at least in part, by inducing cellular oxidative stress. It thus aggravates phosphate-induced calcification of VSMCs. The present findings support a regulatory role of SHMT1 in vascular calcification during conditions of hyperphosphatemia such as chronic kidney disease

Regulation of neuronal development and function by ROS.

Reactive oxygen species (ROS) have long been studied as destructive agents in the context of nervous system ageing, disease and degeneration. Their roles as signalling molecules under normal physiological conditions is less well understood. Recent studies have provided ample evidence of ROS-regulating neuronal development and function, from the establishment of neuronal polarity to growth cone pathfinding; from the regulation of connectivity and synaptic transmission to the tuning of neuronal networks. Appreciation of the varied processes that are subject to regulation by ROS might help us understand how changes in ROS metabolism and buffering could progressively impact on neuronal networks with age and disease

Quantitative volatile organic compound sensing with liquid crystal core fibers

Polymer fibers with liquid crystals (LCs) in the core have potential as autonomous sensors of airborne volatile organic compounds (VOCs), with a high surface-to-volume ratio enabling fast and sensitive response and an attractive non-woven textile form factor. We demonstrate their ability to continuously and quantitatively measure the concentration of toluene, cyclohexane, and isopropanol as representative VOCs, via the impact of each VOC on the LC birefringence. The response is fully reversible and repeatable over several cycles, the response time can be as low as seconds, and high sensitivity is achieved when the operating temperature is near the LC-isotropic transition temperature. We propose that a broad operating temperature range can be realized by combining fibers with different LC mixtures, yielding autonomous VOC sensors suitable for integration in apparel or in furniture that can compete with existing consumer-grade electronic VOC sensors in terms of sensitivity and response speed

How we decide what to eat: Toward an interdisciplinary model of gut–brain interactions

International audienceEveryday dietary decisions have important short-term and long-term consequences for health and well-being. How do we decide what to eat, and what physiological and neurobiological systems are involved in those decisions? Here, we integrate findings from thus-far separate literatures: (a) the cognitive neuroscience of dietary decision-making, and (b) growing evidence of gut-brain interactions and especially influences of the gut microbiome on diet and health outcomes. We review findings that suggest that dietary decisions and food consumption influence nutrient sensing, homeostatic signaling in the gut, and the composition of the gut microbiome. In turn, the microbiome can influence host health and behavior. Through reward signaling pathways, the microbiome could potentially affect food and drink decisions. Such bidirectional links between gut microbiome and the brain systems underlying dietary decision-making may lead to self-reinforcing feedback loops that determine long-term dietary patterns, body mass, and health outcomes. This article is categorized under: Economics > Individual Decision-Making Psychology > Brain Function and Dysfunction Psychology > Reasoning and Decision Making

The Role of Oxytocin for Marketing Placebo Effects

Our study explores the influence of the hypothalamic neuropeptide oxytocin on marketing placebo effects for experienced taste pleasantness and objective outcome measures like cognitive performance. We hypothesize that oxytocin increases placebo responses of marketing actions and that this effect is mediated by an increased trust in the marketer

SGK1-dependent stimulation of vascular smooth muscle cell osteo-/chondrogenic transdifferentiation by interleukin-18

The serum- and glucocorticoid-inducible kinase 1 (SGK1) is a key regulator of osteo-/chondrogenic transdifferentiation and subsequent calcification of vascular smooth muscle cells (VSMCs). The phenotypical transdifferentiation of VSMCs is associated with increased interleukin-18 (IL-18) levels and generalized inflammation. Therefore, the present study investigated the possible involvement of SGK1 in IL-18-induced vascular calcification. Experiments were performed in primary human aortic smooth muscle cells (HAoSMCs) treated with recombinant human IL-18 protein in control or high phosphate conditions and following SGK1 knockdown by siRNA or pharmacological inhibition of SGK1, PI3K, and PDK1. As a result, IL-18 treatment increased SGK1 mRNA and protein expression in HAoSMCs. IL-18 upregulated SGK1 mRNA expression in a dose-dependent manner. This effect was paralleled by upregulation of the mRNA expression of MSX2 and CBFA1, osteogenic transcription factors, and of tissue-nonspecific alkaline phosphatase (ALPL), an osteogenic enzyme, as markers of increased osteo-/chondrogenic transdifferentiation. Phosphate treatment increased SGK1 and osteogenic markers mRNA expression as well as ALPL activity and induced calcification of HAoSMCs, all effects significantly augmented by additional treatment with IL-18. Conversely, silencing of SGK1 or cotreatment with the SGK1 inhibitor EMD638683 blunted the effects of IL-18 on osteo-/chondrogenic transdifferentiation and calcification of HAoSMCs. The procalcific effects of IL-18 were similarly suppressed in the presence of PI3K or PDK1 inhibitors. In conclusion, SGK1 expression is upregulated by IL-18 in VSMCs and SGK1 participates in the intracellular signaling of IL-18-induced osteo-/chondrogenic transdifferentiation of VSMCs. Thus, SGK1 may serve as therapeutic target to limit the progression of medial vascular calcification during vascular inflammation.(VLID)4848456Version of recor

An fMRI-based brain marker of individual differences in delay discounting

International audienceIndividual differences in delay discounting-how much we discount future compared to immediate rewards-are associated with general life outcomes, psychopathology, and obesity. Here, we use machine learning on fMRI activity during an intertemporal choice task to develop a functional brain marker of these individual differences in human adults. Training and cross-validating the marker in one dataset (Study 1, N = 110 male adults) resulted in a significant prediction-outcome correlation (r = 0.49), generalized to predict individual differences in a completely independent dataset (Study 2: N = 145 male and female adults, r = 0.45), and predicted discounting several weeks later. Out-of-sample responses of the functional brain marker, but not discounting behavior itself, differed significantly between overweight and lean individuals in both studies, and predicted fasting-state blood levels of insulin, c-peptide, and leptin in Study 1. Significant predictive weights of the marker were found in cingulate, insula, and frontoparietal areas, among others, suggesting an interplay among regions associated with valuation, conflict processing, and cognitive control. This new functional brain marker is a step toward a generalizable brain model of individual differences in delay discounting. Future studies can evaluate it as a potential transdiagnostic marker of altered decision-making in different clinical and developmental populations.SIGNIFICANCE STATEMENT People differ substantially in how much they prefer smaller sooner rewards or larger later rewards such as spending money now versus saving it for retirement. These individual differences are generally stable over time and have been related to differences in mental and bodily health. What is their neurobiological basis? We applied machine learning to brain-imaging data to identify a novel brain activity pattern that accurately predicts how much people prefer sooner versus later rewards, and which can be used as a new brain-based measure of intertemporal decision-making in future studies. The resulting functional brain marker also predicts overweight and metabolism-related blood markers, providing new insight into the possible links between metabolism and the cognitive and brain processes involved in intertemporal decision-making