The synthesis mechanism of anionic surfactant-templated mesoporous silica (AMS) is described. A family of highly ordered mesoporous silica structures have been synthesized via an approach based on the self-assembly of anionic surfactants and inorganic precursors by using aminopropylsiloxane or quaternized aminopropylsiloxane as the co-structure-directing agent (CSDA), which is a different route from previous pathways. Mesophases with differing surface curvatures, varying from cage type (tetragonal P42/mnm; cubic Pm3̄n with modulations; cubic Fd3̄m) to cylindrical (two-dimensional hexagonal p6mm), bicontinuous (cubic Ia3̄d and Pn3̄m), and lamellar have been obtained by controlling the charge density of the micelle surfaces by varying the degree of ionization of the carboxylate surfactants. Changing the degree of ionization of the surfactant results in changes of the surfactant packing parameter g, which leads to different mesostructures. Furthermore, variation of the charge density of positively charged amino groups of the CSDA also gives rise to different values of g. Mesoporous silicas, functionalized with amino and quaternary ammonium groups and with the various structures given above, have been obtained by extraction of the surfactant. This report leads to a deeper understanding of the interactions between the surfactant anions and the CSDA and provides a feasible and facile approach to the mesophase design of AMS materials.

Gastrulation in amniotes begins with extensive re-arrangements of cells in the epiblast resulting in the formation of the primitive streak. We have developed a transfection method that enables us to transfect randomly distributed epiblast cells in the Stage XI-XIII chick blastoderms with GFP fusion proteins. This allows us to use time-lapse microscopy for detailed analysis of the movements and proliferation of epiblast cells during streak formation. Cells in the posterior two thirds of the embryo move in two striking counter-rotating flows that meet at the site of streak formation at the posterior end of the embryo. Cells divide during this rotational movement with a cell cycle time of 6-7 h. Daughter cells remain together, forming small clusters and as result of the flow patterns line up in the streak. Expression of the cyclin-dependent kinase inhibitor, P21/Waf inhibits cell division and severely limits embryo growth, but does not inhibit streak formation or associated flows. To investigate the role off cell-cell intercalation in streak formation we have inhibited the Wnt planar-polarity signalling pathway by expression of a dominant negative Wnt11 and a Dishevelled mutant Xdd1. Both treatments do not result in an inhibition of streak formation, but both severely affect extension of the embryo in later development. Likewise inhibition of myosin II which as been shown to drive cell-cell intercalation during Drosophila germ band extension, has no effect on streak formation, but also effectively blocks elongation after regression has started. These experiments make it unlikely that streak formation involves known cell-cell intercalation mechanisms. Expression of a dominant negative FGFR1c receptor construct as well as the soluble extracellular domain of the FGFR1c receptor both effectively block the cell movements associated with streak formation and mesoderm differentiation, showing the importance of FGF signalling in these processes.

Induced pluripotent stem cells (iPSCs) have the potential to revolutionise cell therapy; however, it remains unclear whether iPSCs can be generated from human osteoarthritic chondrocytes (OCs) and subsequently induced to differentiate into chondrocytes. In the present study, we investigated the differentiation potential of OCs into iPSCs using defined transcription factors and explored the possibility of using these OC-derived iPSCs for chondrogenesis. Our study demonstrates that iPSCs can be generated from OCs and that these iPSCs are indistinguishable from human embryonic stem cells (hESCs). To promote chondrogenic differentiation, we used lentivirus to transduce iPSCs seeded in alginate matrix with transforming growth factor-β1 (TGF-β1) and then in vitro co-cultured these iPSCs with chondrocytes. Gene expression analysis showed that this combinational strategy promotes the differentiation of the established iPSCs into chondrocytes in alginate matrix. Increased expression of cartilage-related genes, including collagen II, aggrecan, and cartilage oligomeric matrix protein (COMP), and decreased gene expression of the degenerative cartilage marker, vascular endothelial growth factor (VEGF), were observed. The histological results revealed a dense sulphated extracellular matrix in the co-culture of TGF-β1-transfected iPSCs with chondrocytes in alginate matrix. Additionally, in vivo chondroinductive activity was also evaluated. Histological examination revealed that more new cartilage was formed in the co-culture of TGF-β1-transfected iPSCs with chondrocytes in alginate matrix. Taken together, our data indicate that iPSCs can be generated from OCs by defi ned factors and the combinational strategy results in significantly improved chondrogenesis of OC-derived iPSCs. This work adds to our understanding of potential solutions to osteoarthritic cell replacement problem.

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Abstract:In the past decades, much attention has been paid to toxicity assessment of nanoparticles prior to clinical and biological applications. While in vitro studies have been increasing constantly, in vivo studies of nanoparticles have not established a unified system until now. Predictive models and validated standard methods are imperative. This review summarizes the current progress in approaches assessing nanotoxicity in main systems, including the hepatic and renal, gastrointestinal, pulmonary, cardiovascular, nervous, and immune systems. Histopathological studies and specific functional examinations in each system are elucidated. Related injury mechanisms are also discussed.

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