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The shielding protection given by self-prepared porous hollow silica nanoparticles (PHSN) to pesticides from degradation by UV light was investigated using avermectin as a model pesticide. It was demonstrated that PHSN carriers with a shell thickness of approximately 15 nm and a pore diameter of 4-5 nm have an encapsulation capacity of 625 g kg(-1) for avermectin using a supercritical fluid loading method. PHSN carriers exhibited remarkable UV-shielding properties for avermectin. This was affected by the intensity of UV light, the pH and the temperature of the release medium. Rises in UV intensity, pH and/or temperature reduced the UV protection of PHSN for avermectin. In addition, avermectin loaded into the inner core of the PHSN carriers was released slowly into the release medium for about 30 days following a typical sustained-release pattern. It thus appears that PHSN carriers have a promising future in applications requiring sustained pesticide release.

Porous hollow silica nanoparticles (PHSNs) with a diameter of ca 100 nm and a pore size of ca 4.5 nm were synthesized via a sol-gel route using inorganic calcium carbonate nanoparticles as templates. The synthesized PHSNs were subsequently employed as pesticide carriers to study the controlled release behaviour of avermectin. The avermectin-loaded PHSN (Av-PHSN) samples were characterized by BET, thermogravimetric analysis and IR, showing that the amount of avermectin encapsulated in the PHSN carrier could reach 58.3% w/w by a simple immersion loading method, and that most of the adsorption of avermectin on the Av-PHSN carrier might be physical. Avermectin may be loaded on the external surface, the pore channels in the wall and the inner core of the PHSN carriers, thus leading to a multi-stage sustained-release pattern from the Av-PHSN samples. Increasing pH or temperature intensified the avermectin release.

Summary Mesenchymal stem/stromal cells (MSCs) reside in the perivascular niche and modulate tissue/organ homeostasis; however, little is known about whether and how their localization and function are linked. Particularly, whether specific MSC subsets couple with and regulate specialized vessel subtypes is unclear. Here, we show that Gli1 + cells, which are a subpopulation of MSCs couple with and regulate a specialized form of vasculature. The specific capillaries, i.e . , CD31 hi EMCN hi type H vessels, are the preferable vascular subtype which Gli1 + cells are adjacent to in bone. Gli1 + cells are further identified to be phenotypically coupled with type H endothelium during bone growth and defect healing. Importantly, Gli1 + cell ablation inhibits type H vessel formation associated with suppressed bone generation and regeneration. Mechanistically, Gli1 + cells initiate angiogenesis through Gli and HIF-1α signaling. These findings suggest a morphological and functional framework of Gli1 + cells modulating coupled type H vasculature for tissue homeostasis and regenerative repair.

Mesenchymal stem cell (MSC)-based regeneration, specifically cell aggregate or cell sheet engineering, is a promising approach for tissue reconstruction. Considering the advantages of ease of harvest and lack of immune rejection, the application of autologous MSCs (i.e., patients’ own MSCs) in regenerative medicine has developed considerable interest. However, the impaired cell viability and regenerative potential following MSCs impacted by disease remain a major challenge. Resveratrol (RSV) exhibits reliable and extensive rejuvenative activities that have received increasing clinical attention. Here, we uncovered that resveratrol enhances the functionality and improves the regeneration of mesenchymal stem cell aggregates. Periodontal ligament MSCs (PDLSCs) from normal control subjects (N-PDLSCs) and periodontitis patients (P-PDLSCs) were investigated. Compared to N-PDLSCs, P-PDLSCs were less capable of forming cell aggregates, and P-PDLSC aggregates showed impaired osteogenesis and regeneration. These functional declines could be mimicked in N-PDLSCs by tumor necrosis factor alpha (TNF-α) treatment. Notably, a TNF-α-induced functional decline in N-PDLSC aggregates was rescued by RSV application. More importantly, in both N-PDLSCs and P-PDLSCs, RSV promoted cell aggregate formation and improved their osteogenic potential. Furthermore, as proven ectopically in vivo, the tissue regenerative capability of P-PDLSC aggregates was also enhanced after RSV treatment during aggregate formation in vitro. Finally, in a rat in situ regeneration model, we successfully applied both N-PDLSC aggregates and P-PDLSC aggregates to repair periodontal defects upon long-term functional improvements by RSV preconditioning. Together, our data unravel a novel methodology for using pharmacology (i.e., RSV)-based cell aggregate engineering to improve the functionality and facilitate the regeneration of MSCs from both healthy and inflammatory microenvironments, shedding light on improving the application of autologous MSC-mediated regenerative medicine.

Carbonate concretions provide unique records of ancient biogeochemical processes in marine sediments, and have the potential to reflect seawater chemistry indirectly. In fine-siliciclastic settings, they preferentially form in organicrich mudstones, owing to a significant fraction of the bicarbonate required for carbonate precipitation resulted from the decomposition of organic matter in sediments. In the Member IV of the Xiamaling Formation (ca. 1.40-1. 35 Ga), North China, however, carbonate concretions occur in organic-poor green silty shales (avg. TOC =~0.1 wt%). In order to elucidate the mechanism of the concretion formation and their environmental implications, a thorough study on the petrographic and geochemical compositions of the concretions and their host rocks was conducted. Macro-to microscopic fabrics, including deformed shale laminae surrounding the concretions, "cardhouse" structures of clay minerals and calcite geodes in the concretions, indicate that these concretions are of early diagenetic origin prior to the significant compaction of clay minerals. The carbon isotope compositions of the concretions (− 1.7‰ to + 1.5‰) are stable and close to or slightly lower than that of the contemporaneous seawater, indicating that the bicarbonates required for the concretion formation were mainly sourced from seawater by diffusion rather than produced by methanogenesis or anoxic oxidation of methane (AOM); the rare occurrence of authigenic pyrite grains in the concretions likely indicates that bacterial sulfate reduction (BSR) did not play a significant role in their formation either. Almost all the calcite in the concretions has low Mn-Fe in nuclei but high Mn-Fe in rims with average Mn/Fe ratio close to 3.3. The calcite shows positive Ce anomalies (avg. 1.43) and low Y/Ho ratios (avg. 31). This evidence suggests that Mn reduction is the dominant process responsible for the formation of calcite rims while nitrate reduction probably triggered the precipitation of calcite nuclei. Prominence of Mn reduction in the porewater likely indicates that there was sufficient oxygen to support active Mn-redox cycling in the overlying seawater.

Grand canonical Monte Carlo simulations are performed to study the adsorption of water in realistic CMK-3 and CMK-5 models at 300 K. The adsorption isotherms are characterized by negligible uptake at lower chemical potentials and complete pore filling once the threshold chemical potential is increased. Results for the isosteric heat of adsorption, radial distribution function (O-O and O-H), hydrogen bond statistics and the cluster size distribution of water molecules are presented. The snapshots of GCMC simulations in CMK-3 and CMK-5 models show that the adsorption happens via the formation of water clusters. For the CMK-3 model, it was found that the pore filling occurred via the formation of a single water cluster and a few very small clusters. The water cluster size increased with an increase in pore size of the CMK-3 model. For the CMK-5 model, it was found that the adsorption first occurred in the inner porosity (via cluster formation). There was no adsorption of water in the outer porosity during the filling of the inner porosity. After the inner porosity was completely filled, the water begins to fill the outer porosity. Snapshots from GCMC simulations of the CMK-5 model clearly show that the water adsorption in the outer porosity occurs via the formation and growth of clusters and there was no formation of layers of water in the porosity as seen for nonpolar fluids like nitrogen.