RESUMEN
Greenhouse cover pollution with green shading composed of dust, microalgae and bacteria is a severe problem in tropical areas. The shading results in lower greenhouse indoor light intensity reducing the yield and quality of protected horticulture crops. However, few studies have focused on environmentally efficient ways to remove green shading to increase greenhouse production. In this study, five purified microalgae were isolated from the green shading of three greenhouse roofs and were identified using morphological and molecular assessments. The effects of Ultraviolet-C irradiation (UV-C, 254 nm) at doses of 100, 200 and 300 mJ cm-2 on the growth of GLY-1 microalgae were investigated. The results indicated that five purified microalgae all appeared to belong to the genus of Jaagichlorella. The purified microalgae cell density and chlorophyll content decreased respectively by 26.89-74.44 % and 42.02-77.31 % at 1-3 d after UV-C treatment with doses ranging from 100 to 300 mJ cm-2. The inhibition of the growth rate of microalgae was significantly positively correlated with the UV-C irradiation dose and significantly negatively correlated with treatment time. In summary, UV-C irradiation treatment at 300 mJ cm-2 and 3 d could substantially inhibit microalgae growth in green shading on greenhouse covers. UV-C irradiation could be an effective method for solving the problem of greenhouse cover pollution with microalgae.
Asunto(s)
Microalgas , Rayos Ultravioleta , Clorofila , Polvo , LuzRESUMEN
Macrophages and osteoclasts are both derived from monocyte/macrophage lineage, which plays as the osteoclastic part of bone metabolism. Although they are regulated by bone implant surface nanoarchitecture and involved in osseointegration, the beneath mechanism has not been simultaneously analyzed in a given surface model and their communication with osteoblasts is also blurring. Here, the effect of implant surface topography on monocyte/macrophage lineage osteoclastogenesis and the subsequent effect on osteogenesis are systematically investigated. The nanoporous surface is fabricated on titanium implant by etching and anodizing to get the nanotubes structure. The early bone formation around implant is significantly accelerated by the nanoporous surface in vivo. Meanwhile, the macrophage recruitment and osteoclast formation are increased and decreased respectively. Mechanistically, the integrin mediated FAK phosphorylation and its downstream MAPK pathway (p-p38) are significantly downregulated by the nanoporous surface, which account for the inhibition of osteoclastogenesis. In addition, the nanoporous surface can alleviate the inhibition of osteoclasts on osteogenesis by changing the secretion of clastokines, and accelerate bone regeneration by macrophage cytokine profiles. In conclusion, these data indicate that physical topography of implant surface is a critical factor modulating monocyte/macrophage lineage commitment, which provides theoretical guidance and mechanism basis for promoting osseointegration by coupling the osteogenesis and osteoclastogenesis.
RESUMEN
The injectable hydrogel is an ideal reservoir for drug delivery. In this study, a new injectable DNA hydrogel was fabricated. Firstly, the DNA pre-gel was obtained by heat-cool treatments to induce cross-linkage through base-paring. Then, the pre-gel was cross-linked with chitosan (CS) through electrostatic interaction, which was confirmed by ATR-FTIR and XPS analysis. The DNA-CS hybrid gel showed finely tunable various properties such as porosity and viscosity. To simulate the biomedical application, the dexamethasone (Dex) was loaded into the gel and coated onto titanium implant surface to induce macrophages M2 polarization. Due to the excellent biocompatibility and Dex delivery, the decorated implant surface was favorable for RAW264.7 cells growth and showed powerful effects of inducing M2 polarization both in vitro and in vivo. In conclusion, it is the first report of DNA hydrogel synthesis via CS cross-linkage and the injectable DNA-CS hybrid gel was superb for therapeutic delivery.
Asunto(s)
Quitosano , ADN , Sistemas de Liberación de Medicamentos , Hidrogeles , Electricidad EstáticaRESUMEN
The aquaporins (AQPs) are a family of integral membrane proteins which play critical roles in controlling transcellular water movement in various tissues throughout the body. AQP1 helps mediate the cellular response to osmotic stress and tissue water permeability. However, the mechanism by which AQP1 mediates changes in cell volume is not completely clear. Here, we investigated how AQP1 responds to and controls cell volume upon osmotic stimuli during the early phase after the immediate response. Cells overexpressing AQP1 were exposed to hypotonic or hypertonic medium in the presence or absence of staurosporine or W-7 hydrochloride, and fluorescence imaging was performed at 0, 5, 10, and 15 min later. Osmotic stimuli induced redistribution of AQP1 into the cell membrane, hypotonic stimuli caused cell enlargement, and hypertonic stimuli induced a reduction in cell size, which was blocked by T157A/T239A mutations. Changes in cell size induced by osmotic stimuli were blocked by an antagonist of calmodulin kinase, W-7 hydrochloride, but not by the PKC inhibitor staurosporine. These results suggest that calmodulin kinase regulates AQP1 activity during the early response to osmotic stimuli.
Asunto(s)
Acuaporina 1/metabolismo , Calmodulina/metabolismo , Acuaporina 1/genética , Proteínas Quinasas Dependientes de Calcio-Calmodulina/antagonistas & inhibidores , Proteínas Quinasas Dependientes de Calcio-Calmodulina/metabolismo , Calmodulina/antagonistas & inhibidores , Membrana Celular/metabolismo , Tamaño de la Célula/efectos de los fármacos , Medios de Cultivo/farmacología , Células Endoteliales de la Vena Umbilical Humana , Humanos , Mutación , Ósmosis/fisiología , Proteína Quinasa C/antagonistas & inhibidores , Proteína Quinasa C/metabolismo , Estaurosporina/farmacología , Sulfonamidas/farmacologíaRESUMEN
Mesoporous silica thin film has been widely used in various fields, particularly the medical implant coating for drug delivery. However, some drawbacks remain with the films produced by traditional method (evaporation-induced self-assembly, EISA), such as the poor permeability caused by their horizontal aligned mesochannels. In this study, the vertical aligned mesoporous silica thin film (VMSTF) is uniformly grown alongside the walls of titania nanotubes array via a biphase stratification growth method, resulting in a hierarchical two-layered nanotubular structure. Due to the exposure of opened mesopores, VMSTF exhibits more appealing performances, including rapid degradation, efficient small-molecular drug (dexamethasone) loading and release, enhanced early adhesion and osteogenic differentiation of MC3T3-E1 cells. This is the first time successfully depositing VMSTF on nanoporous substrate and our findings suggest that the VMSTF may be a promising candidate for bone implant surface coating to obtain bioactive performances.
RESUMEN
The inflammatory response is the first and inevitable event after implant surgery in vivo, in which the macrophages M1 polarization is mediated. Numerous publications indicate that the physical properties of implant surface nanostructure can influence macrophages M1 polarization status, whereas the regulation mechanisms have not been elucidated yet. Unlike the conventional biochemical factors that can directly bind to the cellular surface receptors or be transported into cytoplasm, the physical information of implant surface nanostructure can only be sensed by direct contact with cells. Therefore, we infer that the implant surface nanostructure may have unique regulation mechanisms. In this study, we compared the influences of the titanium implant surface coated with titania nanotubes on the surface (â¼100â¯nm diameter, NT-100) and the standard IFN-γ/LPS stimulation on the macrophages M1 polarization. Both the NT-100 surface and IFN-γ/LPS stimulation could induce macrophages M1 polarization, indicated by significant upregulation of M1-specific molecules including CD86, iNOS, CCR7 and IL-1ß, without affecting the M2-specific molecules including CD206, Arg1 and IL-10. However, we found that the IFN-γ/LPS induced macrophages M1 polarization was mediated by RBP-J-IRF8 pathway, whereas the NT-100 surface was more related to FAK-MAPKs pathway, particularly the JNK and ERK1/2 signaling. Our study demonstrated that the implant surface nanostructure has great potential to trigger the host inflammatory response through distinct pathways from conventional biochemical factors, which may remind us to re-consider the unique regulation mechanisms of nano surface on cell functions. Our finding offers a theoretical basis for titanium implant modification to benefit tissue integration.