Effect of Structural Build-Up on Interlayer Bond Strength of 3D Printed Cement Mortars

Understanding the relationship between the intrinsic characteristics of materials (such as rheological properties and structural build-up) and printability and controlling intrinsic characteristics of materials through additives to achieve excellent printability is vital in digital concrete additive manufacturing. This paper aims at studying the effects of material’s structural build-up on the interlayer bond strength of 3DPC with different time gaps. Structural build-up can indirectly affect the interlayer bond strength by affecting the surface moisture of concrete. Based on the structural build-up of 3DPC, a new parameter, maximum operational time (MOT), is proposed, which can be considered as the limit of time gap to ensure high interlayer bond strength. Slump-retaining polycarboxylate superplasticizer (TS) slightly slows down the physical flocculation rate, but increases the maximum operational time of the cement paste. Nano clay significantly increases the sort-term structural build-up rate and has the function of internal curing and water retaining. Composite with nano-clay and TS can reduce the loss of surface moisture of 3D printed layers, prevent the formation of interface weak layer, and increase the interlayer bond strength between printed layers. This contribution can provide new insight into the design of 3D-printed ink with good extrudability, outstanding buildability, and excellent interlayer bond strength.     

Modeling Uniaxial Bond Stress–Slip Behavior of Reinforcing Bars Embedded in Concrete with Different Strengths

This paper aims to study the uniaxial bond stress–slip characteristics of reinforcing bars embedded in concrete with different strengths. Tests were conducted on tension–pull specimens that had a cross-sectional dimension with a reinforcing bar embedded in the center section. The experimental variable was the concrete compressive strength (20, 40, and 60 MPa). The test results show that in the specimen subjected to any fixed load, the maximum value of the concrete strain occurred around the central position, and its value increased as the compressive strength of the concrete increased. Depending on the embedded position of the steel bars, the bond stress–slip relationship was also different. In addition, the analytical results indicate that the proposed bond stress–slip constitutive relationship is very accurate in describing the true bond stress–slip relationship.     

Effect of Non-Thermal Atmospheric Plasma on Micro-Tensile Bond Strength at Adhesive/Dentin Interface: A Systematic Review

Objective: The objective of this review was to evaluate the effect of non-thermal atmospheric plasma (NTAP) on adhesives resin–dentin micro-tensile bond strength (μTBS) in previously published studies. Methods: Electronic search was conducted using the Medline, Cochrane library, and Scopus databases. The included studies were laboratory studies that investigated the effect of NTAP on adhesives μTBS to coronal dentin. Studies that evaluated the effect of NTAP on bond strength to indirect substrates, enamel or root dentin, were excluded. The methodological quality of included studies was assessed. Results: Thirteen studies were included in this systematic review. All the included studies were considered to have a medium risk of bias. NTAP significantly improved μTBS at 24 h or after short-term aging in five studies (38.5%) and both immediate and after long-term aging in 5 studies (38.5%). In two studies (15.4%), NTAP resulted in a short-term material-dependent effect that was not stable after long-term aging. Interestingly, in one study (7.7%), NTAP had a positive effect only in the etch-and-rinse (ER) mode after long-term aging. Conclusion: Within the limitations of this systematic review, NTAP application could enhance resin–dentin μTBS of ER adhesives or universal adhesives (UAs) applied in the ER mode. In the ER mode, the rewetting step after NTAP seems to be unnecessary. Because of the limited information currently available in the literature, further studies are required to evaluate the effect of the NTAP application on self-etch (SE) adhesives or UAs applied in the SE mode.     

Aberrant calcium signaling by transglutaminase-mediated posttranslational modification of inositol 1,4,5-trisphosphate receptors

The inositol 1,4,5-trisphosphate receptor (IP₃R) in the endoplasmic reticulum mediates calcium signaling that impinges on intracellular processes. IP₃Rs are allosteric proteins comprising four subunits that form an ion channel activated by binding of IP₃ at a distance. Defective allostery in IP₃R is considered crucial to cellular dysfunction, but the specific mechanism remains unknown. Here we demonstrate that a pleiotropic enzyme transglutaminase type 2 targets the allosteric coupling domain of IP₃R type 1 (IP₃R1) and negatively regulates IP₃R1-mediated calcium signaling and autophagy by locking the subunit configurations. The control point of this regulation is the covalent posttranslational modification of the Gln2746 residue that transglutaminase type 2 tethers to the adjacent subunit. Modification of Gln2746 and IP₃R1 function was observed in Huntington disease models, suggesting a pathological role of this modification in the neurodegenerative disease. Our study reveals that cellular signaling is regulated by a new mode of posttranslational modification that chronically and enzymatically blocks allosteric changes in the ligand-gated channels that relate to disease states.Ligand-gated ion channels function by allostery that is the regulation at a distance; the allosteric coupling of ligand binding with channel gating requires reversible changes in subunit configurations and conformations (1). Inositol 1,4,5-trisphosphate receptors (IP₃Rs) are ligand-gated ion channels that release calcium ions (Ca²⁺) from the endoplasmic reticulum (ER) (2, 3). IP₃Rs are allosteric proteins comprising four subunits that assemble a calcium channel with fourfold symmetry about an axis perpendicular to the ER membrane. The subunits of three IP₃R isoforms (IP₃R1, IP₃R2, and IP₃R3) are structurally divided into three domains: the IP₃-binding domain (IBD), the regulatory domain, and the channel domain (3–6). Fitting of the IBD X-ray structures (7, 8) to a cryo-EM map (9) indicates that the IBD activates a remote Ca²⁺ channel by allostery (8); however, the current X-ray structure only spans 5% of each tetramer, such that the mechanism underlying allosteric coupling of the IBD to channel gating remains unknown.The IP₃R in the ER mediates intracellular calcium signaling that impinges on homeostatic control in various subsequent intracellular processes. Deletion of the genes encoding the type 1 IP₃R (IP₃R1) leads to perturbations in long-term potentiation/depression (3, 10, 11) and spinogenesis (12), and the human genetic disease spinocerebellar ataxia 15 is caused by haploinsufficiency of the IP₃R1 gene (13–15). Dysregulation of IP₃R1 is also implicated in neurodegenerative diseases including Huntington disease (HD) (16–18) and Alzheimer’s disease (AD) (19–22). IP₃Rs also control fundamental cellular processes—for example, mitochondrial energy production (23, 24), autophagy regulation (24–27), ER stress (28), hepatic gluconeogenesis (29), pancreatic exocytosis (30), and macrophage inflammasomes (31). On the other hand, excessive IP₃R function promotes cell death processes including apoptosis by activating mitochondrial or calpain pathways (2, 17). Considering these versatile roles of IP₃Rs, appropriate IP₃R structure and function are essential for living systems, and aberrant regulation of IP₃R closely relates to various diseases.Several factors such as cytosolic molecules, interacting proteins, and posttranslational modifications control the IP₃-induced Ca²⁺ release (IICR) through allosteric sites in IP₃Rs. Cytosolic Ca²⁺ concentrations strictly control IICR in a biphasic manner with activation at low concentrations and inhibition at higher concentrations. The critical Ca²⁺ sensor for activation is conserved among the three isoforms of IP₃ and ryanodine receptors, and this sensor is located in the regulatory domain outside the IBD and the channel domain (32). A putative ATP regulatory region is deleted in opisthotonos mice, and IICR is also regulated by this mutation in the regulatory domain (33). Various interacting proteins, such as cytochrome c, Bcl-2-family proteins, ataxin-3, huntingtin (Htt) protein, Htt-associated protein 1A (HAP1A), and G-protein–coupled receptor kinase-interacting protein 1 (GIT1), target allosteric sites in the carboxyl-terminal tail (3–5). The regulatory domain and the carboxyl-terminal tail also undergo phosphorylation by the protein kinases A/G and B/Akt and contain the apoptotic cleavage sites for the protease caspase-3 (4, 5). These factors allosterically regulate IP₃R structure and function to control cellular fates; therefore, understanding the allosteric coupling of the IBD to channel gating will elucidate the regulatory mechanism of these factors.Transglutaminase (TG) catalyses protein cross-linking between a glutamine (Gln) residue and a lysine (Lys) residue via an N^ε-(γ-glutamyl)lysine isopeptide bond (34, 35). TG type 2 (TG2) is a Ca²⁺-dependent enzyme with widespread distribution and is highly inducible by various stimulations such as oxidative stress, cytokines, growth factors, and retinoic acid (RA) (34, 35). TG2 is considered a significant disease-modifying factor in neurodegenerative diseases including HD, AD, and Parkinson’s diseases (PD) (34, 36–45) because TG2 might enzymatically stabilize aberrant aggregates of proteins implicated in these diseases—that is, mutant Htt, β-amyloid, and α-synuclein; however, the causal role of TG2 in Ca²⁺ signaling in brain pathogenesis has been unclear. Ablation of TG2 in HD mouse models is associated with increased lifespan and improved motor function (46, 47). However, TG2 knockout mice do not show impaired Htt aggregation, suggesting that TG2 may play a causal role in these disorders rather than TG2-dependent cross-links in aberrant protein aggregates (47, 48).In this study, we discovered a new mode of chronic and irreversible allosteric regulation in IP₃R1 in which covalent modification of the receptor at Gln2746 is catalyzed by TG2. We demonstrate that up-regulation of TG2 modifies IP₃R1 structure and function in HD models and propose an etiologic role of this modification in the reduction of neuronal signaling and subsequent processes during the prodromal state of the neurodegenerative disease.     

States of Water in Hydrogels Containing with Glyceryl Methacrylate

Hydrogel materials were prepared by thermopolymerization with different content of glyceryl methacrylate and hydroxyethyl methacrylate. The different states of water in swelling hydrogels were described and studied by differential scanning calorimetry （DSC）. It was found that the hydrophilicity of GMA was stronger than HEMA, the water content and bound water of GMA hydrogel are higher than HEMA hydrogel. With the increase of GMA content, the content of free water in hydrogel increased. When GMA content was lower than 50%, the increase of GMA content also increased the content of bound water; but when GMA content was higher than 50%, the increase of GMA content decreased the content of bound water, which was caused by the chain hydrogen bond formed on the GMA chain with hydroxyl group each other.     

Effects of surface treatment and artificial aging on the shear bond strength of orthodontic brackets bonded to four different provisional restorations

Objective:To evaluate the combined effects of material type, surface treatment, and thermocycling on the bond strength of orthodontic brackets to materials used for the fabrication of provisional crowns.Materials and Methods:Four materials were included in this study (ProTemp, Trim Plus, Trim II, and Superpont C+B). Sixty cylindrical specimens (1 × 3 cm) were prepared from each material and equally divided into three groups. The first group was ground with silica carbide paper, the second was polished with pumice, and the last group was sandblasted with 50-µm aluminum oxide particles. Stainless-steel maxillary central incisor brackets (Victory Series, 3M) were bonded to the provisional material specimens with Transbond XT light-cured composite resin, and half of the specimens from each group were thermocycled 500 times in 5°C and 55°C water baths. Then the brackets were debonded with shear testing, and the results were statistically analyzed by three-way analysis of variance and Tukey''s multiple-comparison tests at α  =  0.05. Adhesive Remnant Index (ARI) was also identified.Results:Before and after thermocycling, ProTemp materials showed the highest shear bond strength with orthodontic brackets (10.3 and 13.1 MPa, respectively). The statistical analysis indicated an interaction among the three independent variables (P < .05) and statistically significant differences in bond strength among provisional materials (P < .001), surface treatments (P < .001), and thermocycling (P < .05). According to the ARI, most groups demonstrated adhesive failure.Conclusions:The provisional material type, surface treatment, and artificial aging have a significant effect on bond strength. Sandblasting treatment exerts a beneficial effect on shear bond strength.