Immobilizing c(RGDfc) on the surface of metal-phenolic networks by thiol-click reaction for accelerating osteointegration of implant.

The limited osteointegration often leads to the failure of implant, which can be improved by fixing bioactive molecules onto the surface, such as arginyl-glycyl-aspartic acid (RGD): a cell adhesion motif. Metal-Phenolic Networks (MPNs) have garnered increasing attention from different disciplines in recent years due to their simple and rapid process for depositing on various substrates or particles with different shapes. However, the lack of cellular binding sites on MPNs greatly blocks its application in tissue engineering. In this study, we present a facile and efficient approach for producing PC/Fe@c(RGDfc) composite coatings through the conjugation of c(RGDfc) peptides onto the surface of PC/Fe-MPNs utilizing thiol-click reaction. By combined various techniques (ellipsometry, X-ray photoelectron spectroscopy, Liquid Chromatography-Mass Spectrometry, water contact angle, scanning electronic microscopy, atomic force microscopy) the physicochemical properties (composition, coating mechanism and process, modulus and hydrophilicity) of PC/Fe@c(RGDfc) surface were characterized in detail. In addition, the PC/Fe@c(RGDfc) coating exhibits the remarkable ability to positively modulate cellular attachment, proliferation, migration and promoted bone-implant integration in vivo, maintaining the inherent features of MPNs: anti-inflammatory, anti-oxidative properties, as well as multiple substrate deposition. This work contributes to engineering MPNs-based coatings with bioactive molecules by a facile and efficient thiol-click reaction, as an innovative perspective for future development of surface modification of implant materials.

Engineering tunable dual peptide hybrid coatings promote osseointegration of implants.

Utilizing complementary bioactive peptides is a promising surface engineering strategy for bone regeneration on osteogenesis. In this study, we designed block peptides, (Lysine)6-capped RGD (K6-(linker-RGD)3) and OGP (K6-linker-(YGFGG)2), which were mildly grafted onto PC/Fe-MPNs through supramolecular interactions between K6 and PC residues on the MPNs surface to form a dual peptide coating, named PC/Fe@K6-RGD/OGP. The properties of the block peptides coating, including mechanics, hydrophilicity, chemical composition, etc., were detailly characterized by various techniques (ellipsometry, quartz crystal microbalance, X-ray photoelectron spectroscopy, water contact angle, scanning electronic microscopy and atomic force microscopy). Importantly, the RGD/OGP ratio can be well adjusted, which allowed optimizing the RGD/OGP ratio to endow significantly enhanced osteogenic activity of MC3T3-E1 cells through the Wnt/ß-catenin pathway, while also promoting cell adhesion, immune regulation, inhibiting osteoclast differentiation and oxidative stress reduction. In vivo, the optimized RGD/OGP coatings promoted bone regeneration and osseointegration around implants in rats with bone defects. In conclusion, rationally designed PC/Fe@K6-RGD/OGP coating integrated RGD and OGP bioactivities, providing a convenient approach to enhance bioinert implant surfaces for bone regeneration.

Using deep learning for the automated identification of cone and rod photoreceptors from adaptive optics imaging of the human retina.

Adaptive optics imaging has enabled the enhanced in vivo retinal visualization of individual cone and rod photoreceptors. Effective analysis of such high-resolution, feature rich images requires automated, robust algorithms. This paper describes RC-UPerNet, a novel deep learning algorithm, for identifying both types of photoreceptors, and was evaluated on images from central and peripheral retina extending out to 30° from the fovea in the nasal and temporal directions. Precision, recall and Dice scores were 0.928, 0.917 and 0.922 respectively for cones, and 0.876, 0.867 and 0.870 for rods. Scores agree well with human graders and are better than previously reported AI-based approaches.

A Dual-Mode Optical Thermometer with High Sensitivity Based on BaAl12O19:Sm2+/SrAl12O19:Sm3+ Solid Solution Phosphors.

A series of BaAl12O19:Sm2+/SrAl12O19:Sm3+ mixed-phase phosphors were produced in one step using the traditional high-temperature solid-phase process. Because Sm is divalent in BaAl12O19 and trivalent in SrAl12O19, the coexistence of Sm2+ and Sm3+ is realized in the mixed-phase host. Since the temperature sensitivity of Sm2+ and Sm3+ in the solid solution host is significantly different, this makes it possible for the sample to measure temperature based on the fluorescence intensity ratio (FIR). The crystal model, ion emission spectrum, and temperature sensitivity of these phosphors are studied in detail. Under the co-excitation of a 410 nm excitation source, this sample has excellent temperature measurement performance in the range of 313-513 K. Based on the FIR method, the maximum absolute temperature sensitivity (Sa) is 0.55 K-1 at 513 K, and the maximum relative temperature sensitivity (Sr) is 2.47%K-1 at 453 K. Moreover, based on the photoluminescence lifetime temperature measurement mode, the largest value of Sa at 413 K is 0.046 K-1, and the maximum value of Sr at 473 K is 3.10%K-1. In short, the BaAl12O19:Sm2+/SrAl12O19:Sm3+ solid solution is a kind of phosphor with nice temperature measurement ability, and it has very strong potential in the application of noncontact optical thermometers.

Myricetin induces apoptosis in HepG2 cells through Akt/p70S6K/bad signaling and mitochondrial apoptotic pathway.

The present investigation was undertaken to gain insight into the molecular mechanism by which myricetin induces apoptosis in human hepatocarcinoma HepG2 cells. Myricetin caused the disruption of mitochondrial membrane potential in a dose-dependent manner. Moreover, myricetin triggered translocation of the pro-apoptotic protein Bax to the mitochondria, downregulation of anti-apoptotic Bcl-2 expression and upregulated the expression of pro-apoptotic protein Bad in the mitochondria. The present study also showed that myricetin promoted the release of cytochrome C from mitochondria into the cytosol followed by an increase in the proteolytic activation of caspase-3 and the concomitant degradation of PARP protein. Additionally, western blot analysis showed that the Akt/p70s6k1 pathway was inhibited in myricetin-treated HepG2 cells, accordingly the phosphorylation of Bad at Ser136 was downregulated. Collectively, these findings indicate that myricetin induced apoptosis in HepG2 cell through mitochondria apoptotic pathway and Akt/p70s6k1/Bad signaling. Present results provide new information on the possible mechanisms for the anti-cancer activity of myricetin.

Myricetin induces G2/M phase arrest in HepG2 cells by inhibiting the activity of the cyclin B/Cdc2 complex.

Myricetin, a naturally occurring flavonol, has been shown to inhibit the proliferation of human hepatoma HepG2 cells and to induce G2/M phase arrest. However, the underlying mechanisms of Myricetin activity have yet to be revealed. The aim of the present study was to clarify the molecular mechanisms of cell cycle arrest induced by myricetin in HepG2 cells. The MTT assay confirmed that exposure of HepG2 cells to myricetin triggered G2/M phase arrest. Western blot analysis showed that myricetin increased the protein levels of the p53/p21 cascade, and markedly decreased Cdc2 and cyclin B1 protein levels in HepG2 cells. Additionally, myricetin treatment resulted in the up-regulation of Thr14/Tyr15 phosphorylated (inactive) Cdc2 and p27, and the down-regulation of CDK7 kinase protein, as well as CDK7-mediated Thr161 phosphorylated (active) Cdc2. These data indicate that a decrease in cyclin B/Cdc2 complex activity mediated G2/M phase arrest induced by myricetin in HepG2 cells. This novel finding provides insight into the potential applications of myricetin in the treatment of hepatocellular carcinoma.

[Effect of pregnancy rats supplemented with docosahexaenoic acid on carnitine palmitoyl transferase-I gene expression in offspring].

OBJECTIVE: To investigate the effect on lipid metabolic and carnitine palmitoyl transferase-I (CPT-I) gene expression of offspring when their maternal rats supplemented with docosahexaenoic acid (DHA) during pregnancy. METHOD: Female SD rats were randomly divided into A, B, C groups. Group A was fed with basic diet, group B was supplemented with low dose of DHA, and group C supplemented with high dose of DHA during pregnancy. All the male offspring were suckled by maternal rats in group A. Offspring were fed with basic diet from weaning (week 3) to week 8. Body weight, body fat, triglycerides (TG), total cholesterol (TC), high density lipoprotein (HDL-C) and CPT- I mRNA level were observed in eight rats of every group. RESULTS: The birth body weights in three groups of offspring of rats were no significantly difference(P > 0.05). At the end of 8 weeks, the body weights in group C was significantly lower than that of the group A/P < 0.05), then the body fat, TG in B and C were significantly lower than those of group A (P < 0.05), but HDL-C in C were significantly higher than those of group A (P < 0.05), but the TC was no significant difference in three groups. The CPT-I mRNA levels in B and C were persistently higher than those of group A during experiment. CONCLUSION: Supplementation with DHA during pregnancy mediate fatty acid oxidation and decrease blood lipid in offspring that could persistently increase CPT-I gene expression. But excess DHA consumption during pregnancy could cause adverse health effects in offspring.