Gouty arthritis is a very familiar inflammatory arthritis. Controlling inflammation is the key to preventing gouty arthritis. However, colchicine, the most highly represented drug used in clinical practice, has strict contraindications owing to some severe side effects. Curcumin (Cur), a natural anti-inflammatory drug, has demonstrated good safety and efficacy. However, the rapid degradation, poor aqueous solubility, and low bioavailability of Cur limit its therapeutic effect. To strengthen the effectiveness and bioavailability of Cur. Cur loaded tetrahedral framework nucleic acids (Cur-TFNAs) were synthesized to deliver Cur. Compared with free Cur, Cur-TFNAs exhibit a preferable drug stability, good biocompatibility (CCK-8 assay), ease of uptake (immunofluorescence), and higher tissue utilization (in vivo biodistribution). Most importantly, Cur-TFNAs present better antiinflammatory effect than free Cur both in vivo and in vitro experiments through the determination of inflammation-related cytokines expression. Therefore, we believe that Cur-TFNAs have great prospects for the prevention of gout and similar inflammatory diseases.Peer review under responsibility of KeAi Communications Co., Ltd.

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Ischemic stroke is a main cause of cognitive neurological deficits and disability worldwide due to a plethora of neuronal apoptosis. Unfortunately, numerous neuroprotectants for neurons have failed because of biological toxicity, severe side effects, and poor efficacy. Tetrahedral framework nucleic acids (tFNAs) possess excellent biocompatibility and various biological functions. Here, we tested the efficacy of a tFNA for providing neuroprotection against neuronal apoptosis in ischemic stroke. The tFNA prevented apoptosis of neurons (SHSY-5Y cells) caused by oxygen-glucose deprivation/reoxygenation through interfering with ischemia cascades (excitotoxicity and oxidative stress) in vitro. It effectively ameliorated the microenvironment of the ischemic hemisphere by upregulating expression of erythropoietin and inhibiting inflammation, which reversed neuronal loss, alleviated cell apoptosis, significantly shrank the infarction volume from 33.9% to 2.7%, and attenuated neurological deficits in transient middle cerebral artery occlusion (tMCAo) rat models in vivo. In addition, blocking the TLR2-MyD88-NF-κB signaling pathway is a potential mechanism of the neuroprotection by tFNA in ischemic stroke. These findings indicate that tFNA is a safe pleiotropic nanoneuroprotectant and a promising therapeutic strategy for ischemic stroke.

The problem of tissue vascularization is one of the obstacles that currently restricts the application of tissue engineering products to the clinic. Achieving tissue vascularization and providing adequate nutrients for tissues are an urgent problem to build complex and effective tissue-engineered tissues and organs. Therefore, the aim of this study was to investigate the effect of tetrahedral DNA nanostructures (TDNs), a novel and biocompatible nanomaterial, on angiogenesis. The results showed that TDNs can enter into endothelial cells (ECs) and promote EC proliferation, migration, tube formation, and expressions of angiogenic growth factors at the concentration of 250 nmol L −1 , which was accompanied by activation of the Notch signaling pathway. These results provided a theoretical basis for the further understanding and potential use of TDNs in tissue engineering vascularization.

Poor post‐traumatic wound healing can affect the normal function of damaged tissues and organs. For example, poor healing of corneal epithelial injuries may lead to permanent visual impairment. It is of great importance to find a therapeutic way to promote wound closure. Tetrahedral framework nucleic acids (tFNAs) are new promising nanomaterials, which can affect the biological behavior of cells. In the experiment, corneal wound healing is used as an example to explore the effect of tFNAs on wound healing. Results show that the proliferation and migration of human corneal epithelial cells are enhanced by exposure to tFNAs in vitro, possibly relevant to the activation of P38 and ERK1/2 signaling pathway. An animal model of corneal alkali burn is established to further identify the facilitation effect of tFNAs on corneal wound healing in vivo. Clinical evaluations and histological analyses show that tFNAs can improve the corneal transparency and accelerate the re‐epithelialization of wounds. Both in vitro and in vivo experiments show that tFNAs can play a positive role in corneal epithelial wound healing.

Background Although the traditional bone augmentation technology can basically meet the clinical needs at present, the effect of bone augmentation in most cases is related to the experience of the operator. Propose This study commits to providing a digital solution for precise bone augmentation in the field of oral implantology. Materials and methods After collecting the data of patients' intraoral scanning and DICOM (digital imaging and communications in medicine), the implant position is digitally designed, and the alveolar bone is digitally augmented around the ideal implant position. On the premise of ensuring that the thickness of labial bone is 2 mm, and there is sufficient alveolar bone 3 to 4 mm apically from the ideal gingival margin for implant placing, we carry out excessive augmentation of 0.5 and 1 mm on the labial bone and alveolar crest, respectively, to compensate for possible bone resorption after 6 months. After 3D printing the reconstructed alveolar bone model, the titanium mesh is trimmed and preformed on the alveolar bone model. Outcomes are reported in terms of mean values (5%‐95% percentile values). Results Thirty implant sites have accepted this novel virtually designed alveolar bone augmentation. Before the second‐stage surgery, the average vertical bone gain was 2.48 mm (0.29‐6.32), the average horizontal bone gain was 4.11 mm (1.19‐8.74), the average height of the residual alveolar bone above the implant platform was 1.44 mm (0.59‐2.92), the average thickness of the labial bone width at the implant platform was 2.00 mm (0.93‐3.64), the average thickness of the labial bone width at 2 mm apically from the implant platform was 2.74 mm (1.40‐5.46). The virtual augmentation of each tooth position was 349.41 mm3 (165.70‐482.70), while the actual augmentation of each tooth position was 352.94 mm3 (159.24‐501.78), the accuracy of the final actual augmentation reached 95.82% (range from 88.53% to 99.15%). Conclusion This case series suggests that a virtually digital guided bone regeneration (GBR) workflow is precise and controllable. The practicality, safety and effectiveness of this procedure needs to be compared to other bone augmentation procedures in randomized controlled trials.

Acute myocardial infarction, which can be extremely difficult to treat, is the worst deadly disease around the world. Reperfusion is expedient to reverse myocardial ischemia. However, during reperfusion, reactive oxygen species (ROS) produced by myocardial ischemia-reperfusion injury (MIRI) and further cell apoptosis are the most serious challenges to cardiomyocytes. Therefore, searching for reagents that can simultaneously reduce oxidative damage and MIRI-induced apoptosis is the pivotal strategy to rescue injured cardiomyocytes. Nevertheless, current cardioprotective drugs have some shortcomings, such as cardiotoxicity, inadequate intravenous administration, or immature technology. Previous studies have shown that tetrahedral DNA nanostructures (TDNs) have biological safety with promising anti-inflammatory and antioxidative potential. However, the progress that TDNs have made in the biological behavior of cardiomyocytes has not been explored. In this experiment, a cellular model of MIRI was first established. Then, confirmed by a series of experiments, our study indicates that TDNs can significantly decrease oxidative damage and apoptosis by limiting the overexpression of ROS, along with effecting the expression of apoptosis-related proteins. In addition, Western blot analysis demonstrated that TDNs could activate the Akt/Nrf2 signaling pathway to improve the myocardial injury induced by MIRI. Above all, the antioxidant and antiapoptotic capacities of TDNs make them a potential therapeutic drug for MIRI. This study provides new ideas and directions for more homogeneous diseases induced by oxidative damage.