Interfacial Hydrogen Bond-Reinforced Adhesion and Cohesion Enabling an Ultrastretchable and Wet Adhesive Hydrogel Strain Sensor.

Historically, research on silicotungstic-acid-based hydrogels has primarily focused on their adhesive properties, often at the expense of mechanical strength (cohesion). In this study, we present a novel approach to fabricate a polysaccharide hydrogel that harmoniously balances both adhesion and cohesion via interfacial hydrogen bonds. This hydrogel, composed of carboxymethyl cellulose (CMC), polyacrylamide (PAM), silicotungstic acid (SiW), and lithium chloride (LiCl), showcases a unique combination of properties: strain-responsive ionic conductivity, superior transparency, remarkable stretchability, and robust adhesion. Contrary to conventional PAM hydrogels, our PAM-SiW networked hydrogel addresses the common challenge of achieving good adhesion without compromising on cohesion. Specifically, our hydrogel demonstrates a maximum toughness of 20.3 MJ/m3 and a strain of 4079%, an accomplishment rarely observed in other adhesive hydrogel. Furthermore, the hydrogel's adhesion is both reversible and versatile, adhering effectively to a variety of wet and dry substrates. This makes it a promising candidate for advanced healthcare applications, particularly as a mechanically reinforced underwater adhesive with unparalleled stability. We also provide insights into the role of LiCl in the hydrogel matrix, emphasizing its influence on electrostatic interactions without affecting the hydrogen bonds. This study serves as a testament to the potential of harmonizing adhesive and cohesive properties in hydrogels, paving the way for future innovations in the field.

Effects of increasing sensitizing doses of ovalbumin on airway hyperresponsiveness in asthmatic mice.

BACKGROUND: The dosage of ovalbumin (OVA) during the sensitization stage is considered a crucial factor in the development of airway hyperresponsiveness (AHR). However, the inconsistent dosages of sensitizing OVA used in current studies and the lack of research on their impact on AHR are notable limitations. METHODS: We examined the impact of increasing sensitizing doses of OVA in a murine asthma model, which entailed initial sensitization with OVA followed by repeated exposure to OVA aerosols. BALB/c mice were primed with doses of OVA (0, 10, 20, 50, and 100 µg) plus 1 mg Alum on Days 0 and 7, and were challenged with OVA aerosols (10 mg/mL for 30 min) between Days 14 and 17. Antigen-induced AHR to methacholine (MCh), as well as histological changes, eosinophilic infiltration, and epithelial injury were assessed. RESULTS: The result indicated that there are striking OVA dose-related differences in antigen-induced AHR to MCh. The most intense antigen-induced AHR to MCh was observed with sensitization at 50 µg, while weaker responses were seen at 10, 20, and 100 µg. Meanwhile, there was a significant increase in eosinophil count with sensitization at 50 µg. The changes of AHR were correlated with total cells count, lymphocytes count, eosinophils count, and basophils count in bronchoalveolar lavage fluid; however, it did not correlate with histological changes such as cellular infiltration into bronchovascular bundles and goblet cell hyperplasia of the bronchial epithelium. CONCLUSION: Overall, this study demonstrated that sensitization with 50 µg of OVA resulted in the most significant AHR compared to other dosages. These findings may offer valuable insights for future research on mouse asthma modeling protocols.

Inhibition of GSK3ß and RIP1K Attenuates Glial Scar Formation Induced by Ischemic Stroke via Reduction of Inflammatory Cytokine Production.

In the chronic phase following ischemic stroke, glial scars can prevent axonal regeneration and the intensification of inflammation. The protective effect of inhibition of glycogen synthase kinase-3ß (GSK3ß) or receptor-interacting protein 1 kinase (RIP1K) on ischemic stroke has been previously reported. The current study examined the effects of RIP1K and GSK3ß on ischemic stroke-induced glial scar formation. To investigate this, we used an in vivo model of ischemic stroke based on middle cerebral artery occlusion for 90 min followed by reperfusion for 7 d, and an in vitro model in primary cultured astrocytes involving oxygen and glucose deprivation for 6 h followed by reoxygenation for 24 h. Both in vivo and in vitro, we found that SB216763, a GSK3ß inhibitor, and necrostatin-1 (Nec-1), a RIP1K inhibitor, decreased levels of glial scar markers, including glial fibrillary acidic protein (GFAP), neurocan, and phosphacan. SB216763 and Nec-1 also decreased levels of inflammatory related cytokines, including interleukin-6 (IL-6), interleukin-1 ß (IL-1ß), and tumor necrosis factor-α (TNF-α). However, only Nec-1 increased the level of interleukin-1 receptor antagonist. Concurrent neutralization of TNF-α, IL-1ß, and IL-6 with their antibodies provided better reduction in oxygen and glucose deprivation-induced increases in scar markers than obtained with separate use of each antibody. Further investigations showed that SB216763 reduced the levels of necroptosis-related proteins, including RIP1K, p-RIP1K, RIP3K, p-RIP3K, mixed lineage kinase domain-like protein (MLKL), and p-MLKL, while Nec-1 decreased the expression of p-GSK3ß. Compared with Nec-1 (10 µM) and SB216763 (1 µM) alone, Nec-1 and SB216763 in combination reduced levels of GFAP, neurocan, and inflammatory-related cytokines. In conclusion, inhibition of GSK3ß or RIP1K reduced glial scar formation induced by ischemic stroke. The underlying mechanisms might be at least, partially related to reducing levels of inflammatory-related cytokines and to blocking an interaction between GSK3ß- and RIP1K-mediated pathways.

Layered assembly of graphene oxide and Co-Al layered double hydroxide nanosheets as electrode materials for supercapacitors.

An innovative strategy of fabricating electrode material by layered assembling two kinds of one-atom-thick sheets, carboxylated graphene oxide (GO) and Co-Al layered double hydroxide nanosheet (Co-Al LDH-NS) for the application as a pseudocapacitor is reported. The Co-Al LDH-NS/GO composite exhibits good energy storage properties.

Role of Neurotrophin 3 in spinal neuroplasticity in rats subjected to cord transection.

That neuroplasticity occurs in mammalian spinal cord is well known, though the underlying mechanism still awaits elucidation. This study evaluated the role of endogenous Neurotrophin-3 (NT-3) in the spinal neuroplasticity. Following cord transection at the junction between T9 and T10, the hindlimb locomotor functions of rats showed gradual but significant improvement from 7 to 28 days post-operation. Corresponding to this was a significant increase in the level of NT-3 in the cord segments caudal to injury site. Significantly, after NT-3-antibody administration, the spinal transected rats displayed poor hindlimb locomotor functions and a decrease in the number of neurons in spinal laminae VIII-IX. Whether NT-3-antibody was administered, corticospinal tract regeneration and somatosensory evoked potentials could not be detected. Our findings suggested that endogenous NT-3 could play an important role in spinal plasticity in adult spinal cords subjected to transection, possibly through a regulation of neuronal activity in the local circuitry.