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3D printing has attracted a lot of attention in recent years. Over the past three decades, various 3D printing technologies have been developed including photopolymerization-based, materials extrusion-based, sheet lamination-based, binder jetting-based, power bed fusion-based and direct energy deposition-based processes. 3D printing offers unparalleled flexibility and simplicity in the fabrication of highly complex 3D objects. Tactile sensors that emulate human tactile perceptions are used to translate mechanical signals such as force, pressure, strain, shear, torsion, bend, vibration, etc. into electrical signals and play a crucial role toward the realization of wearable electronics and electronic skin. To date, many types of 3D printing technologies have been applied in the manufacturing of various types of tactile sensors including piezoresistive, capacitive and piezoelectric sensors. This review attempts to summarize the current state-of-the-art 3D printing technologies and their applications in tactile sensors for wearable electronics and electronic skin. The applications are categorized into five aspects: 3D-printed molds for microstructuring substrate, electrodes and sensing element; 3D-printed flexible sensor substrate and sensor body for tactile sensors; 3D-printed sensing element; 3D-printed flexible and stretchable electrodes for tactile sensors; and fully 3D-printed tactile sensors. Latest advances in the fabrication of tactile sensors by 3D printing are reviewed and the advantages and limitations of various 3D printing technologies and printable materials are discussed. Finally, future development of 3D-printed tactile sensors is discussed.

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MXene, as a novel 2D crystal material, possessing tunable bandgap, low optical attenuation and broadband nonlinear optical responses that may promote the fabrications of advanced electro-photonics devices has gathered remarkable attention recently. However, current investigations of 2D crystals for photonics devices suffer from the limitations of reproducibility, scalability, and compatibility. Inkjet printing is one of the powerful additive manufacturers that facilitate well-controlled, low-cost, scalable and small-footprint electrophotonics devices on myriad substrates. Herein, we directly inkjet printed MXene nanosheets in laser resonators with both fiber and free-space geometrics, and achieved extensive spectral band ultrafast laser operations from near-to the mid-infrared regime with pulse duration going to 100 femtoseconds. The demonstrations of versatile inkjet-printed devices based on MXene, while forthputting its distinct electro-optical properties, may allow the realizations of advanced MXene enable photonics devices shortly.

Background and objectives Indoxyl sulfate, a protein-bound uremic toxin, may be associated with cardiovascular events and mortality in patients with CKD. This study aimed to investigate the relationship between indoxyl sulfate and heart failure in patients on hemodialysis.Design, setting, participants, & measurements Patients on hemodialysis for .6 months were enrolled within 6 months. Patients with congestive heart failure, angina pectoris, acute myocardial infarction, cerebral infarction, or cerebral hemorrhage within 3 months before the study or those ,18 years old were excluded. The primary end point was first heart failure event during follow-up. ResultsIn total, 258 patients (145 men) with a mean age of 57.0614.6 years old were enrolled. Median plasma indoxyl sulfate level was used to categorize patients into two groups: the low-indoxyl sulfate group (indoxyl sulfate #32.35 mg/ml) and the high-indoxyl sulfate group (indoxyl sulfate .32.35 mg/ml). Then, patients were prospectively followed up for a median of 48.0 (interquartile range: 33.5-48.0) months. During follow-up, 68 patients experienced episodes of first heart failure. Kaplan-Meier analysis revealed the incidence of first heart failure event in the high-indoxyl sulfate group was significantly higher than in the low-indoxyl sulfate group (log rank P,0.001). Cox regression analysis showed indoxyl sulfate was significantly associated with first heart failure event (indoxyl sulfate as the continuous variable: hazard ratio, 1.02; 95% confidence interval [95% CI], 1.01 to 1.03; P=0.001; indoxyl sulfate as the dichotomous variable: hazard ratio, 3.49; 95% CI, 1.97 to 6.20; P,0.001). After adjustment for other confounding factors, the results remained significant (indoxyl sulfate as the continuous variable: hazard ratio, 1.04; 95% CI, 1.02 to 1.06; P,0.001; indoxyl sulfate as the dichotomous variable: hazard ratio, 5.31; 95% CI, 2.43 to 11.58; P,0.001).Conclusions Plasma indoxyl sulfate was associated with first heart failure event in patients on hemodialysis. Whether indoxyl sulfate is only a biomarker or involved in the pathogenesis of heart failure in hemodialysis warrants additional study.

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Coronary microembolization (CME), a common reason for periprocedural myocardial infarction (PMI), bears very important prognostic implications. However, the molecular mechanisms related to CME remain largely elusive. Statins have been shown to prevent PMI, but the underlying mechanism has not been identified. Here, we examine whether the NLRP3 inflammasome contributes to CME-induced cardiac injury and investigate the effects of statin therapy on CME. In vivo study, mice with CME were treated with 40 mg/kg/d rosuvastatin (RVS) orally or a selective NLRP3 inflammasome inhibitor MCC950 intraperitoneally (20 mg/kg/d). Mice treated with MCC950 and RVS showed improved cardiac contractile function and morphological changes, diminished fibrosis and microinfarct size, and reduced serum lactate dehydrogenase (LDH) level. Mechanistically, RVS decreased the expression of NLRP3, caspase-1, interleukin-1β, and Gasdermin D N-terminal domains. Proteomics analysis revealed that RVS restored the energy metabolism and oxidative phosphorylation in CME. Furthermore, reduced reactive oxygen species (ROS) level and alleviated mitochondrial damage were observed in RVS-treated mice. In vitro study, RVS inhibited the activation of NLRP3 inflammasome induced by tumor necrosis factor α plus hypoxia in H9c2 cells. Meanwhile, the pyroptosis was also suppressed by RVS, indicated by the increased cell viability, decreased LDH and propidium iodide uptake in H9c2 cells. RVS also reduced the level of mitochondrial ROS generation in vitro. Our results indicate the NLRP3 inflammasome-dependent cardiac pyroptosis plays an important role in CME-induced cardiac injury and its inhibitor exerts cardioprotective effect following CME. We also uncover the anti-pyroptosis role of RVS in CME, which is associated with regulating mitochondrial ROS.