Controlled Drug Loading and Release of a Stimuli-Responsive Lipogel Consisting of Poly(<i>N</i>‑isopropylacrylamide) Particles and Lipids

Environmentally responsive materials are attractive for advance biomedicine applications such as controlled drug delivery and gene therapies. Recently, we have introduced the fabrication of a novel type of stimuli-sensitive lipogel composite consisting of poly­(<i>N</i>-isopropylacrylamide) (pNIPAM) microgel particles and lipids. In this study, we demonstrated the temperature-triggered drug release behavior and the tunable drug loading and release capacities of the lipogel. At room temperature (22 °C), no calcein was released from the lipogel over time. At body temperature (37 °C), the release process was significantly promoted; lipids in the lipogel acted as drug holders on the pNIPAM scaffold carrier and prolonged the calcein release process from 10 min to 2 h. Furthermore, the loading and release of calcein could be effectively controlled by modulating the relative amount of lipids incorporated in the lipogel, which can be realized by the salt-induced lipid release of the lipogel

Coloration of Cotton Fibers with Anisotropic Silver Nanoparticles

Anisotropic silver nanoparticles were assembled on cotton fibers to realize the coloration of cotton. The assembly of silver nanoparticles on fibers was achieved by linking of poly­(diallyldimethylammonium chloride) (PDDA) at room temperature. The silver nanoparticle treated cotton showed different colors because of localized surface plasmon resonance (LSPR) property of silver nanoparticles. The coloration was completed through electrostatic interaction between the PDDA treated cotton surface and the anisotropic silver nanoparticles in the reaction system. Scanning electron microscopy (SEM) characterization demonstrated that the morphologies of silver nanoparticles remained unchanged during the coloration process, so the treated cotton inherited the LSPR optical features of silver nanoparticles. Moreover, the cotton colorated with silver nanoparticles showed reasonably good color fastness to washing, which will facilitate the practical application of this coloration process

Shape Evolution of Silver Nanoplates through Heating and Photoinduction

Shape conversions of silver nanoplates were realized by heating and subsequent light irradiation. The initial silver nanoprisms were transformed into silver nanodisks gradually in the process of heating, which was possibly achieved through dissolving and readsorption of silver atoms on the surface of silver nanoplates. Subsequently, under light irradiation, the heating induced silver nanodisks were reversed to silver nanoprisms in the same solution. The dissolved oxygen was found to play a pivotal role in the shape conversion from nanoprism to nanodisk. In addition to heating, deionized water could induce the shape conversion of silver nanoplates when it was added to precipitate of the initial silver nanoprisms after centrifugation. Citrate in solution is essential to the photoinduced shape conversion process. Transmission electron microscopy (TEM) and extinction spectroscopy results demonstrated that localized surface plasmon resonance (LSPR) properties of silver nanoplates were effectively tuned through shape conversion

Influence of Surface Chemistry on Particle Internalization into Giant Unilamellar Vesicles

Cellular uptake of materials plays a key role in their biomedical applications. In this work, based on the cell-mimic giant unilamellar vesicles (GUVs) and a novel type of microscale materials consisting of stimuli-responsive poly­(<i>N</i>-isopropylacrylamide) microgel particles and the incorporated lipids, the influence of particle surface chemistry, including hydrophobic/hydrophilic property and lipid decorations, on the adsorption and consequent internalization of particles into GUVs was investigated. It is found that the decoration of particle surface with lipids facilitates the adsorption of particles on GUV membrane. After that, the hydrophobic property of particle surface further triggers the internalization of particles into GUVs. These results demonstrate the importance of surface properties of particles on their interactions with lipid membranes and are helpful to the understanding of cellular uptake mechanism

Additional file 1: of Functional Application of Noble Metal Nanoparticles In Situ Synthesized on Ramie Fibers

Electronic supplementary information (ESI). The file contains supplementary Tables S1–S6 and Figures S1–S9, and NMR testing procedure. (DOC 2501 kb

Circulating CA16 strains CC045 and CC097 induce apoptosis.

<p>(A) RD cells were inoculated with CC045 and CC097 viruses at the MOI of 1.0 or DMEM as a negative control for 24 h. Cells were washed with PBS and incubated with a FITC-labeled Annexin V and stained with PI, followed by analysis via flow cytometry. Annexin V-positive/PI-negative cells were considered to be in early phase apoptosis. Annexin V-positive/PI-positive cells were considered to be in late phase apoptosis. (B) A172 cells were inoculated with CC045 or CC097 at the MOI of 1.0 for 24 h or DMEM as a negative control for Annexin-PI staining. Representative images are shown of three individual experiments (n = 3) performed for each cell line. *<i>P</i><0.05.</p

Clinical features of CC045 and CC097 strains.

<p>Clinical features of CC045 and CC097 strains.</p

Enterovirus 71 mediates cell cycle arrest in S phase through non-structural protein 3D

<p>Many viruses disrupt the host cell cycle to facilitate their own growth. We assessed the mechanism and function of enterovirus 71 (EV71), a primary causative agent for recent hand, foot, and mouth disease outbreaks, in manipulating cell cycle progression. Our results suggest that EV71 infection induces S-phase arrest in diverse cell types by preventing the cell cycle transition from the S phase into the G2/M phase. Similar results were observed for an alternate <i>picornavirus,</i> Coxsackievirus A16. Synchronization in S phase, but not G0/G1 phase or G2/M phase, promotes viral replication. Consistent with its ability to arrest cells in S phase, the expression of cyclin A2, CDK 2, cyclin E1, and cyclin B1 was regulated by EV71 through increasing transcription of cyclin E1, promoting proteasome-mediated degradation of cyclin A2 and regulating the phosphorylation of CDK 2. Finally, a non-structural protein of EV71, the RNA-dependent RNA polymerase 3D, was demonstrated to mediate S-phase cell cycle arrest. These findings suggest that EV71 induces S-phase cell cycle arrest in infected cells via non-structural protein 3D, which may provide favorable conditions for virus production.</p

Membrane changes associated with apoptosis in CA16-infected cells.

<p>(A) RD, (B) HepG2, (C) A172 and (D) SK-N-SH cells were inoculated with CA16 SHZH05 virus at the MOI of 1.0, 2.0, 1.0 and 1.0, respectively, or DMEM as a negative control for 24 h. Cells were washed with PBS, incubated with FITC-labeled Annexin V and stained with PI, followed by analysis via flow cytometry. Annexin V-positive/PI-negative cells were considered to be in early phase apoptosis. Annexin V-positive/PI-positive cells were considered to be in late phase apoptosis. Representative images are shown of three individual experiments (n = 3) performed for each cell line. *<i>P</i><0.05.</p

Nuclear fragmentation occurs in CA16-infected cells.

<p>(A) RD, (B) HepG2, (C) A172 and (D) SK-N-SH cell lines were inoculated with CA16 SHZH05 virus at the MOI of 0.2 or DMEM as a negative control. After 24 h or 48 h of infection, cells were stained with Hoechest 33258. Nuclear fragmentation was observed via fluorescence microscopy. Representative images are shown of three individual experiments (n = 3) performed for each cell line.</p