Hydrogen Sulfide Exerted a Pro-Angiogenic Role by Promoting the Phosphorylation of VEGFR2 at Tyr797 and Ser799 Sites in Hypoxia-Reoxygenation Injury.

The protective effects of hydrogen sulfide (H2S) against ischemic brain injury and its role in promoting angiogenesis have been established. However, the specific mechanism underlying these effects remains unclear. This study is designed to investigate the regulatory impact and mechanism of H2S on VEGFR2 phosphorylation. Following expression and purification, the recombinant His-VEGFR2 protein was subjected to LC-PRM/MS analysis to identify the phosphorylation sites of VEGFR2 upon NaHS treatment. Adenovirus infection was used to transfect primary rat brain artery endothelial cells (BAECs) with the Ad-VEGFR2WT, Ad-VEGFR2Y797F, and Ad-VEGFR2S799A plasmids. The expression of VEGFR2 and recombinant Flag-VEGFR2, along with Akt phosphorylation, cell proliferation, and LDH levels, was assessed. The migratory capacity and tube-forming potential of BAECs were assessed using wound healing, transwell, and tube formation assays. NaHS notably enhanced the phosphorylation of VEGFR2 at Tyr797 and Ser799 sites. These phosphorylation sites were identified as crucial for mediating the protective effects of NaHS against hypoxia-reoxygenation (H/R) injury. NaHS significantly enhanced the Akt phosphorylation, migratory capacity, and tube formation of BAECs and upregulated the expression of VEGFR2 and recombinant proteins. These findings suggest that Tyr797 and Ser799 sites of VEGFR2 serve as crucial mediators of H2S-induced pro-angiogenic effects and protection against H/R injury.

Hydrogen Sulfide Protects against Rat Ischemic Brain Injury by Promoting RhoA Phosphorylation at Serine 188.

The protective role of hydrogen sulfide against cerebral ischemia-reperfusion injury involves the inhibition of the RhoA-/Rho-associated coiled-coil kinase (ROCK) pathway. However, the specific mechanism remains elusive. This study investigates the impact of hydrogen sulfide on RhoA phosphorylation at serine 188 (Ser188) in vivo, aiming to test the hypothesis that hydrogen sulfide exerts neuroprotection by enhancing RhoA phosphorylation at Ser188, subsequently inhibiting the RhoA/ROCK pathway. Recombinant RhoAwild-pEGFP-N1 and RhoAS188A-pEGFP-N1 plasmids were constructed and administered via stereotaxic injection into the rat hippocampus. A rat global cerebral ischemia-reperfusion model was induced by bilateral carotid artery ligation to elucidate the neuroprotective mechanisms of hydrogen sulfide. Both RhoAwild-pEGFP-N1 and RhoAS188A-pEGFP-N1 plasmids expressed RhoAwild and RhoAS188A proteins, respectively, in rat hippocampal tissues, alongside the intrinsic RhoA protein. Systemic administration of the exogenous hydrogen sulfide donor sodium hydrosulfide led to an increase in Ser188 phosphorylation of transfected RhoAwild and intrinsic RhoA protein within the hippocampus. However, this effect was not observed in tissues transfected with RhoAS188A. Sodium hydrosulfide-mediated RhoA phosphorylation correlated with decreased RhoA and ROCK2 activity in rat hippocampal tissues. Furthermore, sodium hydrosulfide administration reduced cerebral ischemia-reperfusion-induced neuronal damage and apoptosis in rat hippocampal tissues transfected with RhoAwild. However, this neuroprotective effect was attenuated in rats transfected with RhoAS188A. These findings suggest that the neuroprotective mechanism of hydrogen sulfide against cerebral ischemia/reperfusion injury involves increased RhoA phosphorylation at Ser188. Promoting this phosphorylation may represent a potential intrinsic therapeutic target for ischemic stroke.

RNA sequencing identifies key genes involved in intramuscular fat deposition in chickens at different developmental stages.

BACKGROUND: Intramuscular fat (IMF) is an important factor in meat quality, and triglyceride (TG) and Phospholipids (PLIP), as the main components of IMF, are of great significance to the improvement of meat quality. RESULTS: In this study, we used 30 RNA sequences generated from the transcriptome of chicken breast muscle tissues at different developmental stages to construct a gene expression matrix to map RNA sequence reads to the chicken genome and identify the transcript of origin. We used weighted gene co-expression network analysis (WGCNA) and identified 27 co-expression modules, 10 of which were related to TG and PLIP. We identified 150 highly-connected hub genes related to TG and PLIP, respectively, which were found to be mainly enriched in the adipocytokine signaling pathway, MAPK signaling pathway, mTOR signaling pathway, FoxO signaling pathway, and TGF-beta signaling pathway. Additionally, using the BioMart database, we identified 134 and 145 candidate genes related to fat development in the TG-related module and PLIP-related module, respectively. Among them, RPS6KB1, BRCA1, CDK1, RPS3, PPARGC1A, ACSL1, NDUFAB1, NDUFA9, ATP5B and PRKAG2 were identified as candidate genes related to fat development and highly-connected hub genes in the module, suggesting that these ten genes may be important candidate genes affecting IMF deposition. CONCLUSIONS: RPS6KB1, BRCA1, CDK1, RPS3, PPARGC1A, ACSL1, NDUFAB1, NDUFA9, ATP5B and PRKAG2 may be important candidate genes affecting IMF deposition. The purpose of this study was to identify the co-expressed gene modules related to chicken IMF deposition using WGCNA and determine key genes related to IMF deposition, so as to lay a foundation for further research on the molecular regulation mechanism underlying chicken fat deposition.

Stretchable, Programmable and Magnet-Insensitive Protonic Display Based on Integrated Ionic Circuit.

As a new approach to "More than Moore", integrated ionic circuits serve as a possible alternative to traditional electronic circuits, yet the integrated ionic circuit composed of functional ionic elements and ionic connections is still challenging. Herein, a stretchable and transparent ionic display module of the integrated ionic circuit has been successfully prepared and demonstrated by pixelating a proton-responsive hydrogel. It is programmed to excite the hydrogel color change by a Faraday process occurring at the electrode at the specific pixel points, which enables the display of digital information and even color information. Importantly, the display module exhibits stable performance under strong magnetic field conditions (1.7 T). The transparent and stretchable nature of such ionic modules also allows them to be utilized in a broad range of scenarios, which paves the way for integrated ionic circuits.

Flavonoids and ischemic stroke-induced neuroinflammation: Focus on the glial cells.

Ischemic stroke is one of the most cases worldwide, with high rate of morbidity and mortality. In the pathological process of ischemic stroke, neuroinflammation is an essential process that defines the functional prognosis. After stroke onset, microglia, astrocytes and the infiltrating immune cells contribute to a complicated neuroinflammation cascade and play the complicated roles in the pathophysiological variations of ischemic stroke. Both microglia and astrocytes undergo both morphological and functional changes, thereby deeply participate in the neuronal inflammation via releasing pro-inflammatory or anti-inflammatory factors. Flavonoids are plant-specific secondary metabolites and can protect against cerebral ischemia injury via modulating the inflammatory responses. For instances, quercetin can inhibit the expression and release of pro-inflammatory cytokines, such as tumor necrosis factor (TNF)-α, IL-6 and IL-1ß, in the cerebral nervous system (CNS). Apigenin and rutin can promote the polarization of microglia to anti-inflammatory genotype and then inhibit neuroinflammation. In this review, we focused on the dual roles of activated microglia and reactive astrocyte in the neuroinflammation following ischemic stroke and discussed the anti-neuroinflammation of some flavonoids. Importantly, we aimed to reveal the new strategies for alleviating the cerebral ischemic stroke.

Biomimetic Ion Channel Regulation for Temperature-Pressure Decoupled Tactile Perception.

The perception of temperature and pressure of skin plays a vital role in joint movement, hand grasp, emotional expression, and self-protection of human. Among many biomimetic materials, ionic gels are uniquely suited to simulate the function of skin due to its ionic transport mechanism. However, both the temperature and pressure sensing are heavily dependent on the changes in ionic conductivity, making it impossible to decouple the temperature and pressure signals. Here, a pressure-insensitive and temperature-modulated ion channel is designed by synergistic strategies for gel skeleton's compact packing and ultra-thin structure, mimicking the function of the temperature ion channel in human skin. This ion-confined gel can completely suppress the pressure response of the temperature sensing layer. Furthermore, a temperature-pressure decoupled ionic sensor is fabricated and it is demonstrated that the ionic sensor can sense complex signals of temperature and pressure. This novel and effective approach has great potential to overcome one of the current barriers in developing ionic skin and extending its applications.

H2S Regulates the Phenotypic Transformation of Astrocytes Following Cerebral Ischemia/Reperfusion via Inhibiting the RhoA/ROCK Pathway.

The role of hydrogen sulfide (H2S) on the phenotypic change of astrocytes following cerebral ischemia/reperfusion (I/R) in mice was investigated in present study. We tested the expression of glial fibrillary acidic protein (GFAP), A2 phenotype marker S100a10, and A1 phenotype marker C3 protein and assessed the change of BrdU/GFAP-positive cells, GFAP/C3-positive cells, and GFAP/S100a10-positive cells in mice hippocampal tissues to evaluate the change of astrocyte phenotypes following cerebral I/R. The role of H2S on the phenotypic change of astrocytes following cerebral I/R in mice was investigated by using H2S synthase cystathionine-γ-lyase (CSE) knockout mice (KO). The results revealed that cerebral I/R injury promoted the astrocytes proliferation of both A1 and A2 phenotypes, which were more significant in mice of H2S synthase CSE KO than in mice of wild type (WT). Interestingly, supplement with H2S could inhibit the A1 phenotype proliferation but promote the proliferation of A2 phenotype, suggesting that H2S could regulate the transformation of astrocytes to A2 phenotype following cerebral I/R, which is beneficial for neuronal recovery. Besides, we found that H2S-mediated change of astrocyte phenotype is related to inhibiting the RhoA/ROCK pathway. Furthermore, both H2S and ROCK inhibitor could ameliorate the brain injury of mice at 9 days after cerebral I/R. In conclusion, H2S regulates the phenotypic transformation of astrocytes to A2 phenotype following the cerebral I/R via inhibiting RhoA/ROCK pathway and then exerts the neuroprotective effect against the subacute brain injury.

Uniformly Hybrid Surface Containing Adjustable Hydrophobic/Hydrophilic Components Obtained by Programmed Strain for Synergistic Anti-Icing.

Sufficient efforts have been put into the design of anti-icing materials to eliminate the icing hazard. Among the currently approved anti-icing concepts, hydrophilic/hydrophobic hybrid anti-icing materials inspired by antifreeze proteins show excellent properties in inhibiting ice nucleation, inhibiting ice crystal growth, and reducing ice adhesion. However, it is still a great challenge to accurately regulate the hydrophilic and hydrophobic hybrid components of the coating surface to clarify the synergistic mechanism. This work proposes a strain-manipulated surface modification strategy, and an anti-icing coating with adjustable hydrophilic/hydrophobic hybrid components prepared by combining chemical vapor deposition and siloxane chemistry is obtained. According to the ice resistance experiment at -15 °C, the performance of anti-icing is closely related to the proportion of hydrophilic and hydrophobic hybrids. The icing delay time and ice adhesion strength of the material with the optimal hydrophilic/hydrophobic components are 280 s and 18.6 kPa, respectively. These unique properties can be attributed to the synergistic effect of hydrophilic and hydrophobic structures on the regulation of interfacial water.

Enhancing impacts of mesoscale eddies on Southern Ocean temperature variability and extremes.

As a major sink of anthropogenic heat and carbon, the Southern Ocean experienced pronounced warming with increasing extreme temperature events over the past decades. Mesoscale eddies that strongly influence the uptake, redistribution, and storage of heat in the ocean are expected to play important roles in these changes, yet observational evidence remains limited. Here, we employ a comprehensive analysis of over 500,000 historical hydrographic profile measurements combined with satellite-based eddy observations to show enhanced thermal eddy imprints in the Southern Ocean. Our observations reveal that anticyclonic (cyclonic) eddies are responsible for nearly half of the subsurface high (low)-temperature extremes detected, although only 10% of the profiles are located in eddy interiors. Over the past decade (2006 to 2019), both mean and extreme temperature anomalies within eddies in the Antarctic Circumpolar Current increased significantly, promoting the rise in subsurface ocean temperature variability. This enhanced role of eddies is likely a result of enhanced eddy pumping due to the increase in eddy intensity and ocean stratification caused by ocean warming. Our analysis underscores the crucial role of eddies in amplifying ocean temperature variability and extremes, with their effects expected to be even more pronounced as global warming persists.

A grooved conduit combined with decellularized tissues for peripheral nerve regeneration.

Peripheral nerve injury (PNI) is a common and severe clinical disease worldwide, which leads to a poor prognosis because of the complicated treatments and high morbidity. Autologous nerve grafting as the gold standard still cannot meet the needs of clinical nerve transplantation because of its low availability and limited size. The development of artificial nerve conduits was led to a novel direction for PNI treatment, while most of the currently developed artificial nerve conduits was lack biochemical cues to promote nerve regeneration. In this study, we designed a novel composite neural conduit by inserting decellularized the rat sciatic nerve or kidney in a poly (lactic-co-glycolic acid) (PLGA) grooved conduit. The nerve regeneration effect of all samples was analyzed using rat sciatic nerve defect model, where decellularized tissues and grooved PLGA conduit alone were used as controls. The degree of nerve regeneration was evaluated using the motor function, gastrocnemius recovery, and morphological and histological assessments suggested that the combination of a grooved conduit with decellularized tissues significantly promoted nerve regeneration compared with decellularized tissues and PLGA conduit alone. It is worth to note that the grooved conduits containing decellularized nerves have a promotive effect similar to that of autologous nerve grafting, suggesting that it could be an artificial nerve conduit used for clinical practice in the future.

The role of RhoA/ROCK pathway in the ischemic stroke-induced neuroinflammation.

It is widely known that ischemic stroke is the prominent cause of death and disability. To date, neuroinflammation following ischemic stroke represents a complex event, which is an essential process and affects the prognosis of both experimental stroke animals and stroke patients. Intense neuroinflammation occurring during the acute phase of stroke contributes to neuronal injury, BBB breakdown, and worse neurological outcomes. Inhibition of neuroinflammation may be a promising target in the development of new therapeutic strategies. RhoA is a small GTPase protein that activates a downstream effector, ROCK. The up-regulation of RhoA/ROCK pathway possesses important roles in promoting the neuroinflammation and mediating brain injury. In addition, nuclear factor-kappa B (NF-κB) is another vital regulator of ischemic stroke-induced neuroinflammation through regulating the functions of microglial cells and astrocytes. After stroke onset, the microglial cells and astrocytes are activated and undergo the morphological and functional changes, thereby deeply participate in a complicated neuroinflammation cascade. In this review, we focused on the relationship among RhoA/ROCK pathway, NF-κB and glial cells in the neuroinflammation following ischemic stroke to reveal new strategies for preventing the intense neuroinflammation.

Protection of H2S against Hypoxia/Reoxygenation Injury in Rat Hippocampal Neurons through Inhibiting Phosphorylation of ROCK2 at Thr436 and Ser575.

BACKGROUND: H2S (hydrogen sulfide) protects cerebral vasodilatation and endothelial cells against oxygen-glucose deprivation/reoxygenation injury via the inhibition of the RhoA-ROCK pathway and ROCK2 expression. However, the inhibitory mechanism of H2S on ROCK2 expression is still unclear. The study aimed to investigate the target and mechanism of H2S in inhibition of ROCK2. METHODS: His-ROCK2wild protein was constructed, expressed, and was used for phosphorylation assay in vitro. Liquid chromatography-tandem mass spectrometry (LC-MS/MS) was used to determine the potential phosphorylation sites of ROCK2. Recombinant ROCK2wild-pEGFP-N1, ROCK2T436A-pEGFP-N1, and ROCK2S575F-pEGFP-N1 plasmids were constructed and transfected into rat hippocampal neurons (RHNs). ROCK2 expression, cell viability, the release of lactate dehydrogenase (LDH), nerve-specific enolase (NSE), and Ca2+ were detected to evaluate the neuroprotective mechanism of H2S. RESULTS: Phosphorylation at Thr436 and Ser575 of ROCK2 was observed by mass spectrometry when Polo-like kinase 1 (PLK1) and protein kinase A (PKA) were added in vitro, and NaHS significantly inhibited phosphorylation at Thr436 and Ser575. Additionally, NaHS significantly inhibited the expression of ROCK2 and recombinant proteins GFP-ROCK2, GFP-ROCK2T436A, and GFP-ROCK2S575F in transfected RHNs. Compared with empty plasmid, GFP-ROCK2T436A, and GFP-ROCK2S575F groups, NaHS significantly inhibited the release of LDH, NSE, and Ca2+ and promoted ROCK2 activity in the GFP-ROCK2wild group. Thr436 and Ser575 may be dominant sites that mediate NaHS inhibition of ROCK2 protein activity in RHNs. Compared with the empty plasmid, GFP-ROCK2T436A, and the GFP-ROCK2S575F group, NaHS had more significant inhibitory effects on hypoxia/reoxygenation (H/R) injury-induced cell viability reduction and increased LDH and NSE release in the GFP-ROCK2wild group. CONCLUSION: Exogenous H2S protected the RHNs against H/R injury via Thr436 and Ser575 of ROCK2. These findings suggested that Thr436 and Ser575 may be the dominant sites that mediated the effect of NaHS on protecting RHNs against H/R injury.

A clustering-optimized segmentation algorithm and application on food quality detection.

For solving the problem of quality detection in the production and processing of stuffed food, this paper suggests a small neighborhood clustering algorithm to segment the frozen dumpling image on the conveyor belt, which can effectively improve the qualified rate of food quality. This method builds feature vectors by obtaining the image's attribute parameters. The image is segmented by a distance function between categories using a small neighborhood clustering algorithm based on sample feature vectors to calculate the cluster centers. Moreover, this paper gives the selection of optimal segmentation points and sampling rate, calculates the optimal sampling rate, suggests a search method for optimal sampling rate, as well as a validity judgment function for segmentation. Optimized small neighborhood clustering (OSNC) algorithm uses the fast frozen dumpling image as a sample for continuous image target segmentation experiments. The experimental results show the accuracy of defect detection of OSNC algorithm is 95.9%. Compared with other existing segmentation algorithms, OSNC algorithm has stronger anti-interference ability, faster segmentation speed as well as more efficiently saves key information ability. It can effectively improve some disadvantages of other segmentation algorithms.

Antifreezing, Adhesive, and Ultra-Stretchable Ionogel for AI-Enabled Motion Tracking and Recognition in Winter Sports.

Motion tracking and recognition are gaining increasing attention in athletes' training for winter sports due to their importance in posture correction and injury prevention. Electronic skin serves as a better candidate compared to vision-based methods. However, the challenges of its application include sensing materials with good stretchability, softness, anti-freeze, non-volatility, and adhesion, and data processing techniques of high intelligence and efficiency. Here, we propose an antifreezing, adhesive, and ultra-stretchable organic ionogel (OIG). Maximum elongation of over 6500% has been obtained for the OIG of the double network, and the mechanical stretchability is retained at temperatures ranging from -50 to 50 °C. Importantly, the multi-sensor system could realize motion "recognition" rather than "perception" with the help of a convolutional neural network.

Hydrogen sulfide inhibits lipopolysaccharide-based neuroinflammation-induced astrocyte polarization after cerebral ischemia/reperfusion injury.

The effect of lipopolysaccharide (LPS)-based neuroinflammation following cerebral ischemia/reperfusion (I/R) on the genotypic transformation of reactive astrocytes and its relationship with endogenous hydrogen sulfide (H2S) were investigated in present study. We found that LPS promoted the cerebral I/R-induced A1 astrocytes proliferation in mouse hippocampal tissues and deteriorated the reduction of hydrogen sulfide (H2S) content in mouse sera, H2S donor NaHS could inhibit A1 astrocytes proliferation. Similarly, knockout of cystathionine γ-lyase (CSE), one of endogenous H2S synthases, likewise up-regulated the cerebral I/R-induced A1 astrocytes proliferation, which could also be blocked by NaHS. Besides, supplement with H2S promoted the A2 astrocytes proliferation in hippocampal tissues of CSE knockout (CSE KO) mice or LPS-treated mice following cerebral I/R. In the oxygen glucose deprivation/reoxygenation (OGD/R) model of astrocytes, H2S also promoted the transformation of astrocytes into A2 subtype. Moreover, we found that H2S could up-regulate the expression of α-subunit of large-conductance Ca2+-activated K+ (BKCa) channels in astrocytes, and the channel opener BMS-191011 likewise promoted the transformation of astrocyte into A2 subtype. In conclusion, H2S inhibits the proliferation of A1 astrocytes induced by LPS-based neuroinflammation following cerebral I/R and promotes the transformation of astrocytes into A2 subtype, which may be related to up-regulation of BKCa channels.

Total flavones of Rhododendron induce the transformation of A1/A2 astrocytes via promoting the release of CBS-produced H2S.

BACKGROUND: We previously found that total flavones of Rhododendron (TFR) protected against the cerebral ischemia/reperfusion (I/R) injury. But the detailed mechanism is not clear. Recent research revealed that reactive astrocytes were divided into A1 and A2 phenotypes for their morphological and functional remodeling and neurotoxic- vs-neuroprotective effect on the injury of the central nervous system (CNS). PURPOSE: The present study was undertaken to explore the role and mechanism of TFR on the phenotypic change of astrocytes following cerebral I/R in vivo and oxygen glucose deprivation/re-oxygenation (OGD/R) in vitro. STUDY DESIGN AND METHODS: We tested the expression of astrocytes marker glial fibrillary acidic protein (GFAP), A1 astrocytes marker C3 protein and A2 astrocytes marker S100a10, as well as the BrdU/GFAP-positive cells, GFAP/S100a10-positive cells and GFAP/C3-positive cells in mice hippocampal tissues to evaluate the phenotypic change of astrocytes. Besides, we assessed the change of astrocyte phenotypes following OGD/R in vitro. RESULTS: We found that mice cerebral I/R promoted the astrocytes proliferation of both A1 and A2 phenotypes in hippocampal tissues. While treatment with TFR could promote the proliferation of A2 astrocytes but inhibit the A1 astrocytes proliferation in mice hippocampal tissues, suggesting that TFR could accelerate the astrocytes transformation into A2 subtype following cerebral I/R. Whereas, in OGD/R model of astrocytes, we found that TFR inhibited the proliferation of both A1 and A2 astrocytes. Besides, we found that TFR could up-regulate the release of cystathionine ß-synthase (CBS)-produced hydrogen sulfide (H2S) and inhibit RhoA/Rho kinase pathway, and revealed that the inhibitory effect of TFR on astrocytes proliferation could be blocked by aminooxyacetic acid (AOAA), an CBS inhibitor. Furthermore, TFR could ameliorate the mice cerebral I/R injury and the OGD/R-induced astrocytic damage. CONCLUSION: These findings suggested that TFR could affect the transformation of astrocytes subtypes following cerebral I/R, which may be related to up-regulation of CBS-produced H2S and subsequent inhibition of RhoA/ROCK pathway.

Piezoelectric-enhanced photocatalytic performance of porous carbon nitride nanosheets.

Through the utilisation of mechanical energy, piezocatalysis and piezophotocatalysis have emerged as promising strategies to tackle the current energy and environmental issues. In this work, porous graphitic carbon nitride (g-C3N4) nanosheets were synthesised via a novel self-templating process followed by ultrasonic exfoliation to produce materials with a thickness of 1.5-2 nm and a high specific surface area of 59.48 m2/g. Piezo-response force microscopy (PFM) indicated that the as-prepared porous g-C3N4 nanosheets show excellent piezoelectric response. Moreover, the porous g-C3N4 nanosheets exhibit remarkable piezophotocatalytic degradation of Rhodamine B (RhB), showing an optimal first-order rate constant (k = 0.301 min-1) under visible light and ultrasonic co-excitation, which was 2.3 times the value under visible light irradiation alone and 9.7 times the value under only ultrasonic excitation. A piezoelectric field generated by ultrasonic excitation drove photogenerated electrons and holes in opposite directions to migrate towards the surface of the nanosheets, resulting in the generation of more reactive radicals and thereby accelerating RhB degradation. By highlighting the potential of porous g-C3N4 nanosheets as a piezo-semiconductor for environmental remediation applications, this study paves the way for developing a new method for converting solar and mechanical energy via a piezo-mediation photocatalytic reaction.

Thermal Nociception of Ionic Skin: TRPV1 Ion Channel-Inspired Heat-Activated Dynamic Ionic Liquid.

The artificial reproduction of the tactile sensory function of natural skin is crucial for intelligent sensing, human-computer interaction, and medical health. Thermal nociception is an essential human tactile function to avoid noxious thermal stimuli, which depends on the specific heat-activation of the TRPV1 ion channel. Inspired by the TRPV1, a dynamic ionic liquid with heat-activation characteristics is designed and prepared, which can be activated at 45 °C, which is near the physiological noxious temperature, accompanied by a steep rise in electrical response signals. Its electrical behavior can be deemed to be the extreme version of temperature sensation similar to the natural thermal nociceptor. The heat-activation mechanism is confirmed as a feasible strategy to regulate the thermal response behavior of ions, and this reported dynamic ionic liquid has an unprecedented intrinsic temperature response sensitivity of up to 156.79%/°C. In consideration of the similarity between the heat-activated dynamic ionic liquid and the TRPV1 ion channel in terms of heat-activation characteristics, electrical output signal, and ultrathermal sensitivity, an all-liquid ionic skin with the ability of thermal nociception is further fabricated, which shows considerable potential to assist patients with tactile desensitization to avoid noxious thermal stimuli.

In vitro study of decellularized rat tissues for nerve regeneration.

Peripheral nerve injuries cause an absence or destruction of nerves. Decellularized nerves, acting as a replacement for autografts, have been investigated in the promotion of nerve repair and regeneration, always being incorporated with stem cells or growth factors. However, such a strategy is limited by size availability. The potential application in heterotopic transplantation of other decellularized tissues needs to be further explored. In this study, rat decellularized kidney (dK) was selected to be compared with decellularized peripheral nerve (dN), since dK has aboundant ECM components and growth factors. The PC-12 cells were cultured on dK and dN scaffolds, as shown in the similar behaviors of cell metabolism and viability, but have a more regular arrangement on dN compared to dK, indicating that the natural structure plays an important role in guiding cell extension. However, we found significant upregulation of axon-growth-associated genes and proteins of PC-12 cells in the dK group compared to the dN group by qRT-PCR, immunofluorescence, and western blotting. Furthermore, various neurotrophic factors and growth factors of acellular kidney and nerve were evaluated by ELISA assay. The lower expression of neurotrophic factors but higher expression of growth factors such as VEGF and HGF from dK suggests that axon growth and extension for PC-12 cells may be partially mediated by VEGF and HGF expression from decellularized kidney, which further points to a potential application in nerve repair and regeneration.