Synthesis and properties of free-standing monolayer amorphous carbon.

Bulk amorphous materials have been studied extensively and are widely used, yet their atomic arrangement remains an open issue. Although they are generally believed to be Zachariasen continuous random networks1, recent experimental evidence favours the competing crystallite model in the case of amorphous silicon2-4. In two-dimensional materials, however,  the corresponding questions remain unanswered. Here we report the synthesis, by laser-assisted chemical vapour deposition5, of centimetre-scale, free-standing, continuous and stable monolayer amorphous carbon, topologically distinct from disordered graphene. Unlike in bulk materials, the structure of monolayer amorphous carbon can be determined by atomic-resolution imaging. Extensive characterization by Raman and X-ray spectroscopy and transmission electron microscopy reveals the complete absence of long-range periodicity and a threefold-coordinated structure with a wide distribution of bond lengths, bond angles, and five-, six-, seven- and eight-member rings. The ring distribution is not a Zachariasen continuous random network, but resembles the competing (nano)crystallite model6. We construct a corresponding model that enables density-functional-theory calculations of the properties of monolayer amorphous carbon, in accordance with observations. Direct measurements confirm that it is insulating, with resistivity values similar to those of boron nitride grown by chemical vapour deposition. Free-standing monolayer amorphous carbon is surprisingly stable and deforms to a high breaking strength, without crack propagation from the point of fracture. The excellent physical properties of this stable, free-standing monolayer amorphous carbon could prove useful for permeation and diffusion barriers in applications such as magnetic recording devices and flexible electronics.

Physical exercise in liver diseases.

Liver diseases contribute to ~2 million deaths each year and account for 4% of all deaths globally. Despite various treatment options, the management of liver diseases remains challenging. Physical exercise is a promising nonpharmacological approach to maintain and restore homeostasis and effectively prevent and mitigate liver diseases. In this review, we delve into the mechanisms of physical exercise in preventing and treating liver diseases, highlighting its effects on improving insulin sensitivity, regulating lipid homeostasis, and modulating immune function. In addition, we evaluate the impact of physical exercise on various liver diseases, including liver ischemia/reperfusion injury, cardiogenic liver disease, metabolic dysfunction-associated steatotic liver disease, portal hypertension, cirrhosis, and liver cancer. In conclusion, the review underscores the effectiveness of physical exercise as a beneficial intervention in combating liver diseases.

Neutrophil extracellular traps promote MASH fibrosis by metabolic reprogramming of HSC.

BACKGROUND AND AIMS: Metabolic dysfunction-associated steatohepatitis (MASH) fibrosis is a reversible stage of liver disease accompanied by inflammatory cell infiltration. Neutrophils extrude a meshwork of chromatin fibers to establish neutrophil extracellular traps (NETs), which play important roles in inflammatory response regulation. Our previous work demonstrated that NETs promote HCC in MASH. However, it is still unknown if NETs play a role in the molecular mechanisms of liver fibrosis. APPROACH AND RESULTS: Following 12 weeks of Western diet/carbon tetrachloride, MASH fibrosis was identified in C57BL/6 mice with increased NET formation. However, NET depletion using DNase I treatment or mice knocked out for peptidyl arginine deaminase type IV significantly attenuated the development of MASH fibrosis. NETs were demonstrated to induce HSCs activation, proliferation, and migration through augmented mitochondrial and aerobic glycolysis to provide additional bioenergetic and biosynthetic supplies. Metabolomic analysis revealed markedly an altered metabolic profile upon NET stimulation of HSCs that were dependent on arachidonic acid metabolism. Mechanistically, NET stimulation of toll-like receptor 3 induced cyclooxygenase-2 activation and prostaglandin E2 production with subsequent HSC activation and liver fibrosis. Inhibiting cyclooxygenase-2 with celecoxib reduced fibrosis in our MASH model. CONCLUSIONS: Our findings implicate NETs playing a critical role in the development of MASH hepatic fibrosis by inducing metabolic reprogramming of HSCs through the toll-like receptor 3/cyclooxygenase-2/cyclooxygenase-2 pathway. Therefore, NET inhibition may represent an attractive treatment target for MASH liver fibrosis.

Surgery-mediated tumor-promoting effects on the immune microenvironment.

Surgical resection continues to be the mainstay treatment for solid cancers even though chemotherapy and immunotherapy have significantly improved patient overall survival and progression-free survival. Numerous studies have shown that surgery induces the dissemination of circulating tumor cells (CTCs) and that the resultant inflammatory response promotes occult tumor growth and the metastatic process by forming a supportive tumor microenvironment (TME). Surgery-induced platelet activation is one of the initial responses to a wound and the formation of fibrin clots can provide the scaffold for recruited inflammatory cells. Activated platelets can also shield CTCs to protect them from blood shear forces and promote CTCs evasion of immune destruction. Similarly, neutrophils are recruited to the fibrin clot and enhance cancer metastatic dissemination and progression by forming neutrophil extracellular traps (NETs). Activated macrophages are also recruited to surgical sites to facilitate the metastatic spread. More importantly, the body's response to surgical insult results in the recruitment and expansion of immunosuppressive cell populations (i.e. myeloid-derived suppressor cells and regulatory T cells) and in the suppression of natural killer (NK) cells that contribute to postoperative cancer recurrence and metastasis. In this review, we seek to provide an overview of the pro-tumorigenic mechanisms resulting from surgery's impact on these cells in the TME. Further understanding of these events will allow for the development of perioperative therapeutic strategies to prevent surgery-associated metastasis.

A monocarboxylic acid induction strategy to prepare tough and thermo-reversible poly(vinyl alcohol) physical gels with high transparency.

To date, poly(vinyl alcohol) (PVA) gels attract tremendous attention because of their potential applications in a wide variety of fields. Here, a novel monocarboxylic acid induction strategy was developed to fabricate tough and thermo-reversible PVA physical gels by introducing monocarboxylic acids into the PVA/dimethyl sulfoxide (DMSO) system. The obtained PVA gels exhibited appropriate crystalline architectures, leading to superior mechanical properties and high transparency. Furthermore, the role of monocarboxylic acids in the formation of PVA physical gels and the effects of alkyl chain length, concentration, and the induction time of monocarboxylic acids on the properties of PVA physical gels were also investigated.

Thermal- and pH-responsive triple-shape memory hydrogel based on a single reversible switch.

Here we provide a novel method for fabricating a pH- and thermal-responsive triple-shape memory hydrogel based on a single reversible switch phase. A high-density quadruple hydrogen-bonding ureido-pyrimidinone (UPy) system was introduced into the hydrogel network, which can occur to varied degrees of dissociation under different pH and temperature conditions. Different degrees of dissociation and reassociation can be viewed as different subsets of memory elements to freeze and unfreeze the temporary shapes. Although this class of hydrogels contains only a single transition phase, they feature a large dissociative differential in response to varied external stimuli to provide multiple windows for programming different temporary shapes.

Effective Mean Square Differences: A Matching Algorithm for Highly Similar Sheet Metal Parts.

The accurate identification of highly similar sheet metal parts remains a challenging issue in sheet metal production. To solve this problem, this paper proposes an effective mean square differences (EMSD) algorithm that can effectively distinguish highly similar parts with high accuracy. First, multi-level downsampling and rotation searching are adopted to construct an image pyramid. Then, non-maximum suppression is utilised to determine the optimal rotation for each layer. In the matching, by re-evaluating the contribution of the difference between the corresponding pixels, the matching weight is determined according to the correlation between the grey value information of the matching pixels, and then the effective matching coefficient is determined. Finally, the proposed effective matching coefficient is adopted to obtain the final matching result. The results illustrate that this algorithm exhibits a strong discriminative ability for highly similar parts, with an accuracy of 97.1%, which is 11.5% higher than that of the traditional methods. It has excellent potential for application and can significantly improve sheet metal production efficiency.

PRDM16 expression and function in mammalian cochlear development.

BACKGROUND: PR domain containing 16 (PRDM16) is a key transcriptional regulator in the development of craniofacial, adipose, and neural tissues. Our lab identified PRDM16 expression in the epithelial cells of the Kölliker's organ (KO) that starts at ~E13.5 and is maintained until KO disappearance. A transgenic mouse model that carries a gene trap null allele of Prdm16 (Prdm16cGT ) was used to characterize the impact of Prdm16 loss on cochlear development. RESULTS: At P0 Prdm16cGT null cochlea exhibited hypoplastic KO, shortened cochlear duct, increased density of hair cells (HCs) and supporting cells (SCs) in the apical turn as well as multiple isolated ectopic HCs within the KO domain. KO epithelial cells proliferation rate was reduced in the apical turn of the developing Prdm16cGT null cochlea vs controls. Bulk RNA sequencing of cochlear duct cells at E14.5 followed by quantitative real time PCR and mRNA Fluorescence in-situ hybridization (FISH) validation identified differentially expressed genes in Prdm16cGT null vs littermate control cochleae. Upregulated genes at E14.5 included Fgf20, as well as several Notch pathway genes (Lfng, Hes1, and Jag1). CONCLUSIONS: This study characterizes Prdm16 expression during cochlear development and establishes its requirement for KO development.

A photothermally triggered one-component shape memory polymer material prepared by cross-linking porphyrin-based amphiphilic copolymer self-assemblies.

Photothermally triggered shape memory polymer materials are usually prepared by dispersing photothermally responsive fillers or compounds into shape memory polymer matrixes through physical blending, while the migration and non-biodegradability of the fillers limit their potential applications (e.g., in the biomedical field). Here, we synthesized a new type of porphyrin-based amphiphilic random copolymer bearing a reactive moiety of carbonyl group by co-polymerizing methyl methacrylate (MMA), butyl acrylate (BA), diacetone acrylamide (DAAM), acrylic acid (AA) and double-bonded vinyl porphyrin monomers, followed by induced self-assembly in aqueous solution to give rise to amphiphilic random copolymer nanoparticles. The nanoparticles were further crosslinked by means of adipic dihydrazide (ADH) to fabricate the photothermally triggered one-component shape memory polymer material. Compared with the most-studied multi-phase/multi-component shape memory polymer materials, the porphyrin moiety, playing the role of a photo-to-heat converter, covalently bonded into the polymer structure would certainly make it more homogeneous and more stable in principle.

Regulatory T-cell and neutrophil extracellular trap interaction contributes to carcinogenesis in non-alcoholic steatohepatitis.

BACKGROUND & AIMS: Regulatory T-cells (Tregs) impair cancer immunosurveillance by creating an immunosuppressive environment that fosters tumor cell survival. Our previous findings demonstrated that neutrophil extracellular traps (NETs), which are involved both in innate and adaptive immunity, are abundant in livers affected by non-alcoholic steatohepatitis (NASH). However, how NETs interact with Tregs in the development of NASH-associated hepatocellular carcinoma (NASH-HCC) is not known. METHODS: A choline-deficient, high-fat diet+diethylnitrosamine mouse model and the stelic animal model were utilized for NASH-HCC and a western diet mouse model was used for NASH development. Treg depletion was achieved using FoxP3-DTR mice. RNA sequencing was used to explore the mechanism by which NETs could regulate Treg differentiation. Bioenergetic analyses of naïve CD4+ T-cells were assessed by Seahorse. RESULTS: Although the absolute number of CD4+ T-cells is lower in NASH livers, the Treg subpopulation is selectively increased. Depleting Tregs dramatically inhibits HCC initiation and progression in NASH. There is a positive correlation between increased NET and hepatic Treg levels. RNA sequencing data reveals that NETs impact gene expression profiles in naïve CD4+ T-cells, with the most differentially expressed genes being those involved in mitochondrial oxidative phosphorylation. By facilitating mitochondrial respiration, NETs can promote Treg differentiation. Metabolic reprogramming of naïve CD4+ T-cells by NETs requires toll-like receptor 4. Blockade of NETs in vivo using Pad4-/- mice or DNase I treatment reduces the activity of Tregs. CONCLUSIONS: Tregs can suppress immunosurveillance in the premalignant stages of NASH. NETs facilitate the crosstalk between innate and adaptive immunity in NASH by promoting Treg activity through metabolic reprogramming. Therapies targeting NETs and Treg interactions could offer a potential strategy for preventing HCC in patients with NASH. LAY SUMMARY: Regulatory T-cells (Tregs) can promote tumor development by suppressing cancer immunosurveillance, but their role in carcinogenesis during non-alcoholic steatohepatitis (NASH) progression is unknown. Herein, we discovered that selectively increased intrahepatic Tregs can promote an immunosuppressive environment in NASH livers. Neutrophil extracellular traps (NETs) link innate and adaptive immunity by promoting Treg differentiation via metabolic reprogramming of naïve CD4+ T-cells. This mechanism could be targeted to prevent liver cancer in patients with NASH.

Liquid Crystalline Hydrogel with Thermally Induced Reversible Shape Change and Water-Triggered Shape Memory.

Liquid crystalline hydrogel (LCH) is synthesized through simultaneous polymerization of hydrophobic and hydrophilic monomers in an oil-in-water emulsion, resulting in phase-separated liquid crystalline network (LCN) embedded in a hydrogel matrix. This material features some properties and functions of both LCN and hydrogel, displaying stable LC phase over repeated hydration and dehydration cycles of the hydrogel matrix. Using mechanically stretched and photocrosslinked LCH, the thermally induced LC-isotropic phase transition in LCN domains can be translated into reversible macroscopic deformation of the LCH. Moreover, the LCH exhibits water absorption-controlled shape memory effect.

Neutrophil Elastase and Neutrophil Extracellular Traps in the Tumor Microenvironment.

Tumor-associated neutrophils (TANs) play a major role during cancer development and progression in the tumor microenvironment. Neutrophil elastase (NE) is a serine protease normally expressed in neutrophil primary granules. Formation of neutrophil extracellular traps (NETs), a mechanism used by neutrophils, has been traditionally associated with the capture and killing of bacteria. However, there are recent discoveries suggesting that NE secretion and NETs formation are also involved in the tumor microenvironment. Here, we focus on how NE and NETs play a key regulatory function in the tumor microenvironment, such as tumor proliferation, distant metastasis, tumor-associated thrombosis, and antitumor activity. Additionally, the potential use of NETs, NE, or associated molecules as potential disease activity biomarkers or therapeutic targets will be introduced.

Photon Counting Imaging with Low Noise and a Wide Dynamic Range for Aurora Observations.

The radiation intensity of observed auroras in the far-ultraviolet (FUV) band varies dramatically with location for aerospace applications, requiring a photon counting imaging apparatus with a wide dynamic range. However, combining high spatial resolution imaging with high event rates is technically challenging. We developed an FUV photon counting imaging system for aurora observation. Our system mainly consists of a microchannel plate (MCP) stack readout using a wedge strip anode (WSA) with charge induction and high-speed electronics, such as a charge sensitive amplifier (CSA) and pulse shaper. Moreover, we constructed an anode readout model and a time response model for readout circuits to investigate the counting error in high counting rate applications. This system supports global rates of 500 kilo counts, 0.610 dark counts s-1 cm-2 at an ambient temperature of 300 K and 111 µm spatial resolution at 400 kilo counts s-1 (kcps). We demonstrate an obvious photon count loss at incident intensities close to the counting capacity of the system. To preserve image quality, the response time should be improved and some noise performance may be sacrificed. Finally, we also describe the correlation between counting rate and imaging resolution, which further guides the design of space observation instruments.

Genome-Wide Identification, Expression Profile and Evolution Analysis of Karyopherin ß Gene Family in Solanum tuberosum Group Phureja DM1-3 Reveals Its Roles in Abiotic Stresses.

In eukaryotic cells, nucleocytoplasmic trafficking of macromolecules is largely mediated by Karyopherin ß/Importin (KPNß or Impß) nuclear transport factors, and they import and export cargo proteins or RNAs via the nuclear pores across the nuclear envelope, consequently effecting the cellular signal cascades in response to pathogen attack and environmental cues. Although achievements on understanding the roles of several KPNßs have been obtained from model plant Arabidopsis thaliana, comprehensive analysis of potato KPNß gene family is yet to be elucidated. In our genome-wide identifications, a total of 13 StKPNß (Solanum tuberosum KPNß) genes were found in the genome of the doubled monoploid S. tuberosum Group Phureja DM1-3. Sequence alignment and conserved domain analysis suggested the presence of importin-ß N-terminal domain (IBN_N, PF08310) or Exporin1-like domain (XpoI, PF08389) at N-terminus and HEAT motif at the C-terminal portion in most StKPNßs. Phylogenetic analysis indicated that members of StKPNß could be classified into 16 subgroups in accordance with their homology to human KPNßs, which was also supported by exon-intron structure, consensus motifs, and domain compositions. RNA-Seq analysis and quantitative real-time PCR experiments revealed that, except StKPNß3d and StKPNß4, almost all StKPNßs were ubiquitously expressed in all tissues analyzed, whereas transcriptional levels of several StKPNßs were increased upon biotic/abiotic stress or phytohormone treatments, reflecting their potential roles in plant growth, development or stress responses. Furthermore, we demonstrated that silencing of StKPNß3a, a SA- and H2O2-inducible KPNß genes led to increased susceptibility to environmental challenges, implying its crucial roles in plant adaption to abiotic stresses. Overall, our results provide molecular insights into StKPNß gene family, which will serve as a strong foundation for further functional characterization and will facilitate potato breeding programs.

Neutrophil extracellular traps promote inflammation and development of hepatocellular carcinoma in nonalcoholic steatohepatitis.

Nonalcoholic steatohepatitis (NASH) is a progressive, inflammatory form of fatty liver disease. It is the most rapidly rising risk factor for the development of hepatocellular carcinoma (HCC), which can arise in NASH with or without cirrhosis. The inflammatory signals promoting the progression of NASH to HCC remain largely unknown. The propensity of neutrophils to expel decondensed chromatin embedded with inflammatory proteins, known as neutrophil extracellular traps (NETs), has been shown to be important in chronic inflammatory conditions and in cancer progression. In this study, we asked whether NET formation occurs in NASH and contributes to the progression of HCC. We found elevated levels of a NET marker in serum of patients with NASH. In livers from STAM mice (NASH induced by neonatal streptozotocin and high-fat diet), early neutrophil infiltration and NET formation were seen, followed by an influx of monocyte-derived macrophages, production of inflammatory cytokines, and progression of HCC. Inhibiting NET formation, through treatment with deoxyribonuclease (DNase) or using mice knocked out for peptidyl arginine deaminase type IV (PAD4-/- ), did not affect the development of a fatty liver but altered the consequent pattern of liver inflammation, which ultimately resulted in decreased tumor growth. Mechanistically, we found that commonly elevated free fatty acids stimulate NET formation in vitro. CONCLUSION: Our findings implicate NETs in the protumorigenic inflammatory environment in NASH, suggesting that their elimination may reduce the progression of liver cancer in NASH. (Hepatology 2018).

Injectable and Near-Infrared-Responsive Hydrogels Encapsulating Dopamine-Stabilized Gold Nanorods with Long Photothermal Activity Controlled for Tumor Therapy.

Gold nanorods (AuNRs) are confirmed to have excellent and repeated photothermal properties under near-infrared (NIR)-light irradiation above 780 nm. However, AuNRs easily leaked out from local pathological tissues and circulated in the body, reducing photothermal therapy (PTT) efficacy. By complexing AuNRs with a scaffold via interactions, AuNRs might be dispersed in the scaffold and fixed in the tumor site. Thus, based on the mussel-mimetic adhesion concept, AuNRs were designed to be coated with polydopamine (PDA), and then the prepared polydopamine-coated AuNRs (AuNR-PDA) were incorporated into a thermosensitive injectable hydrogel composed of ß-glycerophosphate-bound chitosan (CGP) and dopamine-modified alginate (Alg-DA) efficiently. Due to the strong interactions between PDA and polymers, AuNR-PDA could be immobilized stably and evenly into the obtained CGP/Alg-DA/AuNR composite hydrogel, which can avoid overheating locally or leaking out. The sol-gel transition temperature of the composite hydrogel was adjusted to the body temperature at around 37 °C to be conveniently injectable in vivo. With NIR irradiation at 808 nm of wavelength, the composite hydrogel was locally heated quickly to over 50 °C depending on controlling the irradiation powers and times. Moreover, the in vitro cytotoxicity test of the composite hydrogel showed good biocompatibility to normal cells but obvious suppression to tumor cells' growth under multiple times of photothermal therapy. Furthermore, the in vivo antitumor test demonstrated the obvious suppression to tumor growth of the CGP/Alg-DA/AuNR composite hydrogel under multiple PTTs. Therefore, the injectable CGP/Alg-DA/AuNR hydrogel could be a promising candidate for the long-term repeated photothermal treatment of tumors.

The Effects of Physical Exercise on Fatty Liver Disease.

The increasing prevalence of obesity has made nonalcoholic fatty liver disease (NAFLD) the most common chronic liver disease. As a consequence, NAFLD and especially its inflammatory form nonalcoholic steatohepatitis (NASH) are the fastest increasing etiology of end-stage liver disease and hepatocellular carcinoma. Physical inactivity is related to the severity of fatty liver disease irrespective of body weight, supporting the hypothesis that increasing physical activity through exercise can improve fatty liver disease. This review summarizes the evidence for the effects of physical exercise on NAFLD and NASH. Several clinical trials have shown that both aerobic and resistance exercise reduce the hepatic fat content. From clinical and basic scientific studies, it is evident that exercise affects fatty liver disease through various pathways. Improved peripheral insulin resistance reduces the excess delivery of free fatty acids and glucose for free fatty acid synthesis to the liver. In the liver, exercise increases fatty acid oxidation, decreases fatty acid synthesis, and prevents mitochondrial and hepatocellular damage through a reduction of the release of damage-associated molecular patterns. In conclusion, physical exercise is a proven therapeutic strategy to improve fatty liver disease.

Mesenchymal stem cells protect against obstruction-induced renal fibrosis by decreasing STAT3 activation and STAT3-dependent MMP-9 production.

STAT3 is a transcription factor implicated in renal fibrotic injury, but the role of STAT3 in mesenchymal stem cell (MSC)-induced renoprotection during renal fibrosis remains unknown. We hypothesized that MSCs protect against obstruction-induced renal fibrosis by downregulating STAT3 activation and STAT3-induced matrix metalloproteinase-9 (MMP-9) expression. Male Sprague-Dawley rats underwent renal arterial injection of vehicle or MSCs (1 × 106/rat) immediately before sham operation or induction of unilateral ureteral obstruction (UUO). The kidneys were harvested after 4 wk and analyzed for collagen I and III gene expression, collagen deposition (Masson's trichrome), fibronectin, α-smooth muscle actin, active STAT3 (p-STAT3), MMP-9, and tissue inhibitor of matrix metalloproteinases 1 (TIMP-1) expression. In a separate arm, the STAT3 inhibitor S3I-201 (10 mg/kg) vs. vehicle was administered to rats intraperitoneally just after induction of UUO and daily for 14 days thereafter. The kidneys were harvested after 2 wk and analyzed for p-STAT3 and MMP-9 expression, and collagen and fibronectin deposition. Renal obstruction induced a significant increase in collagen, fibronectin, α-SMA, p-STAT3, MMP-9, and TIMP-1 expression while exogenously administered MSCs significantly reduced these indicators of obstruction-induced renal fibrosis. STAT3 inhibition with S3I-201 significantly reduced obstruction-induced MMP-9 expression and tubulointerstitial fibrosis. These results demonstrate that MSCs protect against obstruction-induced renal fibrosis, in part, by decreasing STAT3 activation and STAT3-dependent MMP-9 production.

Microarray Analysis Gene Expression Profiles in Laryngeal Muscle After Recurrent Laryngeal Nerve Injury.

OBJECTIVES: The pathophysiology of recurrent laryngeal nerve (RLN) transection injury is rare in that it is characteristically followed by a high degree of spontaneous reinnervation, with reinnervation of the laryngeal adductor complex (AC) preceding that of the abducting posterior cricoarytenoid (PCA) muscle. Here, we aim to elucidate the differentially expressed myogenic factors following RLN injury that may be at least partially responsible for the spontaneous reinnervation. METHODS: F344 male rats underwent RLN injury (n = 12) or sham surgery (n = 12). One week after RLN injury, larynges were harvested following euthanasia. The mRNA was extracted from PCA and AC muscles bilaterally, and microarray analysis was performed using a full rat genome array. RESULTS: Microarray analysis of denervated AC and PCA muscles demonstrated dramatic differences in gene expression profiles, with 205 individual probes that were differentially expressed between the denervated AC and PCA muscles and only 14 genes with similar expression patterns. CONCLUSIONS: The differential expression patterns of the AC and PCA suggest different mechanisms of reinnervation. The PCA showed the gene patterns of Wallerian degeneration, while the AC expressed the gene patterns of reinnervation by adjacent axonal sprouting. This finding may reveal important therapeutic targets applicable to RLN and other peripheral nerve injuries.

Poly(vinyl alcohol)-Poly(ethylene glycol) Double-Network Hydrogel: A General Approach to Shape Memory and Self-Healing Functionalities.

A double-network polymer hydrogel composed of chemically cross-linked poly(ethylene glycol) (PEG) and physically cross-linked poly(vinyl alcohol) (PVA) was prepared. When the hydrogel (70 wt % of water) is subjected to freezing/thawing treatment under strain, the enhanced physical network as a result of crystallization of PVA chains can stabilize the hydrogel deformation after removal of the external force at room temperature. Subsequent disruption of the physical network of PVA by heating allows for the recovery of the initial shape of the hydrogel. Moreover, the double-network hydrogel exhibits self-healing capability stemming from the physical network of PVA by virtue of the extensive interchain hydrogen bonding between the hydroxyl side groups. This study thus demonstrates a general approach to imparting both the shape memory and self-healing properties to chemically cross-linked hydrogels that otherwise do not have such functionalities. Moreover, by making use of the fixed hydrogel elongation, the effect of anisotropy arising from chain orientation on the self-healing was also observed.