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Bacterial cellulose (BC) nanofiber-supported polyaniline (PANI) nanocomposites have been synthesized via in situ polymerization of aniline onto BC nanofibers scalfold. Optimized preparation conditions were employed to achieve higher conductivity. The resultant BC/PANI nanocomposites were fully characterized in terms of structure, morphology, and thermal stability. The flake-like morphology of BC/PANI nanocomposites was observed using a field-emission gun scanning electron microscope. By manipulating the ordered flake-type nanostructure, BC/PANI nanocomposites achieved outstanding electrical conductivity as high as 5.1 S/cm. The as-prepared BC/PANI nanocomposites demonstrated a mass-specific capacitance of 273 F/g at 0.2 A.g −1 current density in supercapacitor application, the highest value reported so far for polymer-supported PANI composites.

Core-sheath structured conductive nanocomposites were prepared by wrapping a homogenous layer of polypyrrole (PPy) around bacterial cellulose (BC) nanofibers via in situ polymerization of self-assembled pyrrole. By manipulating the ordered core-sheath nanostructure, BC/PPy nanocomposites were achieved and outstanding electrical conductivity as high as 77 S cm À1 was obtained with the optimized reaction protocols, i.e., feeding mass ratio of BC/Py 1 : 10, molar ratio of FeCl 3 /Py 0.5 : 1, molar ratio of HCl/Py 1.2 : 1, volume ratio of DMF-H 2 O 1 : 2, reaction temperature 0 C, and reaction time 6 h. The BC/PPy nanocomposites demonstrated promising potential for supercapacitors, with a highest mass specific capacitance hitting 316 F g À1 at 0.2 A g À1 current density. The whole-optimized protocol in preparing highly conductive PPy/BC composites may be readily extended to the preparation of new conductive materials based on core-sheath structured BC nanocomposites for various technological applications.

The evolutionarily conserved serine/threonine kinase mTOR (mechanistic target of rapamycin) forms the distinct protein complexes mTORC1 and mTORC2 and integrates signals from the environment to coordinate downstream signaling events and various cellular processes. T cells rely on mTOR activity for their development and to establish their homeostasis and functional fitness. Here, we review recent progress in our understanding of the upstream signaling and downstream targets of mTOR. We also provide an updated overview of the roles of mTOR in T‐cell development, homeostasis, activation, and effector‐cell fate decisions, as well as its important impacts on the suppressive activity of regulatory T cells. Moreover, we summarize the emerging roles of mTOR in T‐cell exhaustion and transdifferentiation. A better understanding of the contribution of mTOR to T‐cell fate decisions will ultimately aid in the therapeutic targeting of mTOR in human disease.

This paper concerns the problem of exponential synchronization for a class of general delayed dynamical networks with hybrid coupling via pinning periodically intermittent control. Both the internal delay and coupling delay are taken into account in the network model. Meanwhile, the transmission delay and self-feedback delay are involved in the delayed coupling term. By establishing a new differential inequality, several simple and useful exponential synchronization criteria are derived analytically. It is shown that the controlled synchronization state can vary in comparison with the conventional synchronized solution, and the degree of the node and the inner delayed coupling matrix play important roles in the controlled synchronization state. By choosing different inner delayed coupling matrices and the degrees of the node, different controlled synchronization states can be obtained. Furthermore, the detail pinning schemes deciding what nodes should be chosen as pinned candidates and how many nodes are needed to be pinned for a fixed coupling strength are provided. The simple procedures illuminating how to design suitable intermittent controllers in real application are also given. Numerical simulations, including an undirected scale-free network and a directed small-world network, are finally presented to demonstrate the effectiveness of the theoretical results.

Background: MLL5 protein regulates cell cycle progression. Results: MLL5 regulates the expression of E2F1-target genes through an association with HCF-1. Conclusion: MLL5 stimulates H3K4 trimethylation at E2F1 responsive promoters and cause transcriptional activation of E2F1 target genes to facilitate the G 1 to S phase transition. Significance: Our results reveal a novel molecular mechanism of MLL5 protein in the regulation of cell cycle progression.

Cleidocranial dysplasia (CCD) is characterized by the runt-related transcription factor 2 (RUNX2) mutation, which results in delayed tooth eruption due to disturbed functions of dental follicle. Accumulating evidence has revealed a key regulatory circuit, including RUNX2, miR-31, and special AT-rich binding protein 2 (SATB2) acting in concert in mesenchymal stem cell homeostasis and functions. However, whether such a regulatory loop works in dental follicle cells (DFCs) remains unknown. Herein, we investigated the roles of RUNX2-miR-31-SATB2 in DFCs from patients with CCD (DFCs-CCD) to advance our understanding regarding physical tooth eruption. We identified a novel mutation on exon 5 (c.634T>G, p.T212P) in RUNX2 via exome sequencing in the CCD patient with typical clinical presentations. Compared with DFCs from healthy donors, DFCs-CCD displayed significantly lower osteogenic, osteoclast-inductive, and matrix-degrading capacities and had lower RUNX2 (a transcriptional inhibitor of miR-31), higher miR-31, and downregulated SATB2. Lower ratios of RANKL/OPG and RANKL/RANK, as well as decreased expression of matrix metalloproteinase 9 (MMP9) and matrix metalloproteinase 2 (MMP2), would lead to inactivation of osteoclasts and suppression of bone matrix remodeling in DFCs-CCD. Furthermore, the roles of the RUNX2-miR-31-SATB2 loop in DFCs-CCD were revealed by endogenous miR-31 knockdown, which resulted in increased SATB2 and RUNX2, as well as osteoclast-inductive and matrix degradation capacities. Conversely, SATB2, RUNX2, MMP9, MMP2, and osteoclast-inductive factors expression declined upon ectopic miR-31 overexpression in normal DFCs. Importantly, neonatal mice with in vivo siRUNX2 delivery exhibited less activated osteoclasts around dental follicles and delayed tooth eruption. Together, these results suggest that RUNX2 mutation/haploinsufficiency disturbs osteoclast-inductive signaling in DFCs, which may be responsible for delayed tooth eruption in CCD patients. Manipulation of the RUNX2-miR-31-SATB2 loop may be a potential way to facilitate tooth eruption in CCD patients.

Bacteria cellulose (BC) nanofibers supported palladium(0) nanocomposites were prepared and fully characterized in terms of morphology, crystallinity, composition, and thermal stability. The as-prepared catalyst was further successfully explored in Heck coupling reaction between aryl halide and styrene or acrylates, with a yield over 86–96% for the first coupling reaction. With coupling yields decreased less than 10% for the fifth reaction cycle, Pd/BC catalyst exhibits great potential as recyclable catalyst for Heck coupling.