Stretchable, wearable and highly sensitive strain sensors are vital to the development of health monitoring systems, smart robots and human machine interfaces. The recent sensor fabrication progress is respectable, but it is limited by complexity, low sensitivity and short service life. Herein we present a facile, cost-effective and scalable method for the development of high-performance composite strain sensors and stretchable conductors based on a composite film consisting of graphene platelets (GnPs) and silicon rubber. Through calculation by the tunnelling theory using experimental data, the composite film has demonstrated ideal linear and reproducible sensitivity to tensile strains, which was contributed by the superior piezoresistivity of GnPs having tunable gauge factors 27.7 -164.5. The composite sensors fabricated in different days demonstrated pretty similar performance, enabling the application as a health-monitoring device to detect various human motions from finger bending to pulse. They can be used as an electronic skin, a vibration sensor, and a human-machine interface controller. Stretchable conductors were made by coating and encapsulating GnPs with polydimethyl siloxane to create a composite; this structure allows the conductor to be readily bent and stretched with sufficient mechanical robustness and cyclability.
The scaffolding adaptor protein p62/SQSTM1 (p62) has been shown to be an autophagy receptor that acts as a link between the ubiquitination and autophagy machineries. However, the roles of autophagy and p62 in human keratinocytes are not well understood. In this study, we show that keratinocyte autophagy negatively regulates p62 expression, which is essential for the prevention of excessive inflammation and the induction of cathelicidin in human keratinocytes. Stimulation of TLR2/6 or TLR4 in primary human keratinocytes robustly activated autophagy pathways and up-regulated p62 expression through induction of NADPH oxidases 2 and 4 and the generation of reactive oxygen species. MyD88 and TNFR-associated factor 6, key signaling molecules that mediate TLR activation, played an essential role in the induction of autophagy and p62 expression. Additionally, blockade of autophagy significantly increased the generation of inflammatory cytokines and expression of p62 in primary human keratinocytes. Notably, silencing hp62 through RNA interference resulted in a significant decrease in NF-κB activation, inflammatory cytokine production, cathelicidin expression, and cell proliferation (as well as cyclin D1 expression) in keratinocytes. Epidermal expression of p62 was further found to be significantly higher in psoriatic skin than in skin affected by atopic dermatitis or from healthy controls. Collectively, our data provide new insights into the roles of autophagy and p62 in controlling cutaneous inflammation.
Hypoxia presents a two-fold challenge in the treatment of cancer, as low oxygen conditions induce biological changes that make malignant tissues simultaneously more aggressive and less susceptible to standard chemotherapy....
The first example of luminescent monosubstituted polyacetylenes (mono‐PAs) is presented, based on a contracted cis‐cisoid polyene backbone. It has an excellent circularly polarized luminescence (CPL) performance with a high dissymmetric factor (up to the order of 10−1). The luminescence stems from the helical cis‐cisoid PA backbone, which is tightly fixed by the strong intramolecular hydrogen bonds, thereby reversing the energy order of excited states and enabling an emissive energy dissipation. CPL switches are facilely achieved by the solvent and temperature through reversible conformational transition. By taking advantages of fast response and high sensitivity, the thin film of mono‐PAs could be used as a CPL‐based probe for quantitative detection of trifluoroacetic acid with a wider linear dynamic range than those of photoluminescence and circular dichroism. This work opens a new avenue to develop novel smart CPL materials through modulating conformational transition.
The purpose of the present investigation was to ascertain whether (3)IL excited states with microsecond lifetimes are universally potent for photodynamic applications, and if these long-lived states are superior to their (3)MLCT counterparts as in vitro PDT agents. A family of blue-green absorbing, Ru(II)-based transition metal complexes derived from the π-expansive dppn ligand was prepared and characterized according to its photodynamic activity against HL-60 cells, and toward DNA in cell-free media. Complexes in this series that are characterized by low-energy and long-lived (3)IL excited states photocleaved DNA with blue, green, red, and near-IR light. This panchromatic photodynamic effect translated to in vitro multiwavelength photodynamic therapy (PDT) with red-light cytotoxicities as low as 1.5 μM (EC50) for the parent complex and 400 nM for its more lipophilic counterpart. This potency is similar to that achieved with Ru(II)-based dyads containing long-lived (3)IL excitons located on appended pyrenyl units, and appears to be a general property of sufficiently long-lived excited states. Moreover, the red PDT observed for certain members of this family was almost 5 times more potent than Photofrin with therapeutic indices 30 times greater. Related Ru(II) complexes having lowest-lying (3)MLCT states of much shorter duration (≤1 μs) did not yield DNA photodamage or in vitro PDT with red or near-IR light, nor did the corresponding Os(II) complex with a submicrosecond (3)IL excited state lifetime. Therefore, metal complexes that utilize highly photosensitizing (3)IL excited states, with suitably long lifetimes (≫ 1 μs), are well-poised to elicit PDT at wavelengths even where their molar extinction coefficients are very low (<100 M(-1) cm(-1)). Herein we demonstrate that such unexpected reactivity gives rise to very effective PDT in the typical therapeutic window (600-850 nm).
Propionibacterium acne and sebaceous glands are considered to have an important role in the development of acne. Although information regarding the activation of innate immunity by P. acnes in the sebaceous gland is limited, different P. acnes phylotypes and a higher prevalence of follicular P. acnes macrocolonies/biofilms in sebaceous follicles of skin biopsies from acne compared with control skin and occasionally single P. acnes clusters in single sebaceous glands have been detected. In this study, we investigated whether P. acnes activates the inflammasome in human sebaceous glands in vivo and in vitro. We found that IL-1β expression was upregulated in sebaceous glands of acne lesions. After stimulation of human sebocytes with P. acnes, the activation of caspase-1 and secretion of IL-1β were enhanced significantly. Moreover, knocking down the expression of NLRP3 abolished P. acnes-induced IL-1β production in sebocytes. The activation of the NLRP3 inflammasome by P. acnes was dependent on protease activity and reactive oxygen species generation. Finally, we found that NALP3-deficient mice display an impaired inflammatory response to P. acnes. These results suggest that human sebocytes are important immunocompetent cells that induce the NLRP3 inflammasome, and that P. acnes-induced IL-1β activation in sebaceous glands may have a role in combating skin infections and in acne pathogenesis.
scite is a Brooklyn-based organization that helps researchers better discover and understand research articles through Smart Citations–citations that display the context of the citation and describe whether the article provides supporting or contrasting evidence. scite is used by students and researchers from around the world and is funded in part by the National Science Foundation and the National Institute on Drug Abuse of the National Institutes of Health.