Three isostructural imidazole-cation-templated metal phosphates (FJU-25) are the first examples to demonstrate that the tuning of metal cation nodes can be an efficient strategy to significantly improve the proton conductivity without changing the structure of the proton-conducting pathway.

There is a growing interest in the fact that mechanical signals may be as important as biological signals in evaluating cell viability. To investigate the alterations in biomechanics, nanomorphology and biological apoptotic signals during early apoptosis, an apoptosis model was established for cervical cancer HeLa cells induced by cytochalasin B (CB). The cellular mechanical properties, geometry, morphology and expression of key apoptotic proteins were systematically analyzed. The findings indicated a marked decline in cellular elastic modulus and volume and a considerable increase in surface roughness occurring prior to the activation of biological apoptosis signals (such as phosphatidylserine exposure or activation of CD95/Fas). Moreover, the depolymerization of filamentous actin aggravated the intracellular crowding degree, which induced the redistribution of different-sized protein molecules and protrusions across the cell membrane arising from excluded volume interactions. Statistical analysis revealed that the disassembly of the actin cytoskeleton was negatively correlated with the cellular elastic modulus and volume, but was positively correlated with surface roughness and CD95/Fas activation. The results of the present study suggest that compared with biological signals, mechanical and geometrical reconstruction is more sensitive during apoptosis and the increase in cell surface roughness arises from the redistribution of biophysical molecules. These results contribute to our in-depth understanding of the apoptosis mechanisms of cancer cells mediated by cytochalasin B.

Objective To comprehensively investigate the effects of 25 variants in 15 genes on dental caries susceptibility in a cohort of Chinese children. Methods A total of 25 variants in 15 genes were genotyped with MassARRAY iPLEX system and analyzed in 265 healthy controls and 254 children affected by dental caries with different dmft scores. The children with dental caries were stratified into “mild group” (scores from 1 to 3), “moderate group” (scores from 4 to 6), and “severe group” (scores from 7 to 14). Results The association analysis revealed that rs11362 of defensin β1 (DEFB1) was significantly associated with dental caries susceptibility (OR = 2.447, p = 1.165E−04). Furthermore, rs11362 was positively correlated with the severity of dental caries. For another selected variant of DEFB1, rs1799946 was significantly associated with dental caries susceptibility in the severe group (OR = 0.473, p = 3.70E−03) and also significant in the group consisted of moderate and severe subjects (OR = 0.623, p = .033). The results from logistic regression in additive, dominant, and recessive models also exhibited the similar patterns. Conclusion Out of 25 selected variants, only 2 of DEFB1 gene (rs11362 and rs1799946) were significantly associated with dental caries susceptibility in children.

Background The temporomandibular joint (TMJ) disc is a dense fibrocartilaginous tissue between the mandibular condyle and the temporal fossa that plays an important role during jaw movement. The central portion of the disc is avascular, has few cells, and is the site of frequent perforation [1]. Similar to cartilage, the heterogeneous TMJ disc lacks a regenerative capacity to repair itself. Tissue engineering is a promising strategy for repairing or replacing injured TMJ discs [2]. However, there are many challenges in developing an engineered TMJ disc that has the same structure, composition and mechanical

statementCellular mechanical damage is connected with the apoptosis of BMSCs, and the alterations in mechanics and nanomorphology may be a sensitive index to detect alterations in cell viability during apoptosis. AbstractStem cell apoptosis exists widely in embryonic development, tissue regeneration, repair, aging and pathophysiology of disease. The molecular mechanism of stem cell apoptosis has been extensively investigated. However, alterations in biomechanics and nanomorphology have rarely been studied.Therefore, an apoptosis model was established for bone marrow mesenchymal stem cells (BMSCs) and the reconstruction of the mechanical properties and nanomorphology of the cells were investigated in detail. Atomic force microscopy (AFM), scanning electron microscopy (SEM), laser scanning confocal microscopy (LSCM), flow cytometry and Cell Counting Kit-8 analysis were applied to assess the cellular elasticity modulus, geometry, nanomorphology, cell surface ultrastructure, biological viability and early apoptotic signal (phosphatidylserine, PS). The results indicated that the cellular elastic modulus and volume significantly decreased, whereas the cell surface roughness obviously increased during the first 3 h of cytochalasin B (CB) treatment.Moreover, these alterations preceded the exposure of biological apoptotic signal PS. These findings suggested that cellular mechanical damage is connected with the apoptosis of BMSCs, and the alterations in mechanics and nanomorphology may be a sensitive index to detect alterations in cell viability during apoptosis. The results contribute to a further understanding of the apoptosis from the perspective of cell mechanics. Biology Open • Accepted manuscript