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Drawing inspiration from cohesive integration of skeletal muscles and sensory skins in vertebrate animals, we present a design strategy of soft robots, primarily consisting of an electronic skin (e-skin) and an artificial muscle. These robots integrate multifunctional sensing and on-demand actuation into a biocompatible platform using an in-situ solution-based method. They feature biomimetic designs that enable adaptive motions and stress-free contact with tissues, supported by a battery-free wireless module for untethered operation. Demonstrations range from a robotic cuff for detecting blood pressure, to a robotic gripper for tracking bladder volume, an ingestible robot for pH sensing and on-site drug delivery, and a robotic patch for quantifying cardiac function and delivering electrotherapy, highlighting the application versatilities and potentials of the bio-inspired soft robots. Our designs establish a universal strategy with a broad range of sensing and responsive materials, to form integrated soft robots for medical technology and beyond. Integrating sensing and actuation capabilities in soft robots is crucial for advancements in medical diagnostics and targeted therapies. Zhang et al. developed bio-inspired sensory robots with multifunctionality for minimally invasive medical procedures.

Background Green tea and black tea have shown beneficial effects on cardiovascular health, and they are recommended for the prevention of cardiovascular disease (CVD) events. However, the impact of herbal tea on cardiovascular health remains unclear. This study aims to evaluate the potential benefits of herbal tea consumption in reducing the risk of incident CVD events in the general population. Methods Data for this study were derived from the Multi-Ethnic Study of Atherosclerosis (MESA). The primary outcome was incident CVD events, while secondary outcomes included all-cause and cardiovascular mortality. Cox proportional hazards regression models were used to examine the relationship between herbal tea consumption and the risk of incident CVD events. Kaplan-Meier survival curves were employed to assess the timing of incident CVD events, all-cause mortality and cardiovascular mortality. Results A total of 4711 participants were included in the analysis, with 1834 (38.9%) in the herbal tea group and 2877 (61.1%) in the control group. Over a median follow-up of 14.1 years, 547 participants (11.61%) experienced new-onset CVD events. The herbal tea group had a significantly lower incidence of new-onset CVD events (9.0% vs. 13.3%, p  < 0.001), all-cause mortality (5.1% vs. 8.8%, p  < 0.001), and cardiovascular mortality (1.4% vs. 2.5%, p  = 0.01) compared to the control group. Multivariate Cox regression analysis revealed that herbal tea consumption was independently associated with a lower risk of incident CVD events [HR 0.83, 95% CI (0.69–0.997), p  = 0.046] and all-cause mortality [HR 0.76, 95% CI (0.60–0.97), p  = 0.03]. Kaplan-Meier analysis confirmed that participants in the herbal tea group had a significantly lower risk of incident CVD events, as well as lower all-cause and cardiovascular mortality. Secondary analyses indicated that moderate frequency herbal tea consumption (2 cups/month to 2 cups/week) and consistent consumption were associated with the most pronounced cardiovascular benefits. Conclusions This study demonstrated that herbal tea consumption was associated with a lower risk of incident CVD events, as well as reduced all-cause and cardiovascular mortality. These benefits were especially evident among individuals who consumed herbal tea at a moderate frequency and maintained consistent intake over time.

Background Inflammation and the nervous system play pivotal roles in cardiac remodeling after myocardial infarction (MI). Recent study showed renal denervation (RDN) could reduce cardiac inflammation, however, the specific mechanism remains unclear. Methods We firstly reanalyzed the previous heart single-cell RNA sequencing (scRNA-seq) and spatial transcriptomics to examine the alterations in immune cell subsets following MI. Subsequently, we carried out diverse denervation procedures to explore the relationship between the nerve axis and the inflammatory response. Finally, we performed bulk RNA-seq and neurotransmitter analysis to explore the molecular mechanisms implicated in the migration of splenic myeloid cells after MI. Results Myeloid cells manifested the most substantial changes following MI and accumulated in the vicinity of the infarct area. The afferent renal nerve - splenic nerve axis regulates the migratory capacities of splenic myeloid cells after MI. RDN decreased the norepinephrine (NE) levels in the spleen after MI and attenuated the expression of ITGA9 on splenic myeloid cells, which impaired their interaction with VCAM-1 on cardiac endothelial cells and thereby reduced their migration to the heart. Conclusions Our study highlights the crucial role of the afferent renal nerve-splenic nerve axis in regulating cardiac inflammation and provides a interventional target for improving cardiac function after myocardial ischemic injury.

Background Brominated Flame Retardants (BFRs) have attracted widespread concern due to their environmental persistence and potential toxicity. This study aims to examine the association between BFRs exposure and hypertension. Methods We used data from the National Health and Nutrition Examination Survey (NHANES) spanning 2005 to 2016 for the cross-sectional analysis. To evaluate the individual and combined impacts of BFRs exposure on hypertension, we utilized multivariate models, including generalized additive models, weighted quantile sum (WQS) regression, and Bayesian kernel machine regression (BKMR) models. Results 9882 individuals (48% male) aged ≥ 20 were included in the final analysis, of whom 4114 had hypertension. After controlling for potential covariates, higher serum concentrations of PBDE100 (OR: 1.26; 95% CI: 1.01, 1.57) and PBDE153 (OR: 1.50; 95% CI: 1.18, 1.88) were significantly associated with hypertension. A nonlinear relationship between PBDE28 and hypertension was observed ( P  = 0.03). Moreover, BFRs mixture were positively associated with the prevalence of hypertension in both the WQS (β:1.09; 95% CI: 1.02, 1.17; P  = 0.02) and BKMR models. Conclusion Our study suggested that BFRs exposure is positively associated with hypertension in the general population. To confirm this association and elucidate the mechanisms, further research is required.

Background Arrhythmogenic cardiomyopathy (ACM) is an inherited cardiomyopathy characterized with progressive cardiac fibrosis and heart failure. However, the exact mechanism driving the progression of cardiac fibrosis and heart failure in ACM remains elusive. This study aims to investigate the underlying mechanisms of progressive cardiac fibrosis in ACM caused by newly identified Desmoglein-2 (DSG2) variation. Methods We identified homozygous DSG2 F531C variant in a family with 8 ACM patients using whole-exome sequencing and generated Dsg2 F536C knock-in mice. Neonatal and adult mouse ventricular myocytes isolated from Dsg2 F536C knock-in mice were used. We performed functional, transcriptomic and mass spectrometry analyses to evaluate the mechanisms of ACM caused by DSG2 F531C variant. Results All eight patients with ACM were homozygous for DSG2 F531C variant. Dsg2 F536C/F536C mice displayed cardiac enlargement, dysfunction, and progressive cardiac fibrosis in both ventricles. Mechanistic investigations revealed that the variant DSG2-F536C protein underwent misfolding, leading to its recognition by BiP within the endoplasmic reticulum, which triggered endoplasmic reticulum stress, activated the PERK-ATF4 signaling pathway and increased ATF4 levels in cardiomyocytes. Increased ATF4 facilitated the expression of TGF-β1 in cardiomyocytes, thereby activating cardiac fibroblasts through paracrine signaling and ultimately promoting cardiac fibrosis in Dsg2 F536C/F536C mice. Notably, inhibition of the PERK-ATF4 signaling attenuated progressive cardiac fibrosis and cardiac systolic dysfunction in Dsg2 F536C/F536C mice. Conclusions Hyperactivation of the ATF4/TGF-β1 signaling in cardiomyocytes emerges as a novel mechanism underlying progressive cardiac fibrosis in ACM. Targeting the ATF4/TGF-β1 signaling may be a novel therapeutic target for managing ACM.

Two-dimensional (2D) piezoelectric semiconductor materials are garnering significant attention in applications such as intelligent sensing and energy harvesting due to their exceptional physical and chemical properties. Among these, molybdenum disulfide (MoS2), a 2D wide-bandgap semiconductor, exhibits piezoelectricity in odd-layered structures due to the absence of an inversion symmetry center. In this study, we present a straightforward chemical vapor deposition (CVD) technique to synthesize monolayer MoS2 on a Si/SiO2 substrate, achieving a lateral size of approximately 50 µm. Second-harmonic generation (SHG) characterization confirms the non-centrosymmetric crystal structure of the wide-bandgap MoS2, indicative of its piezoelectric properties. We successfully transferred the triangular MoS2 to a polyethylene terephthalate (PET) flexible substrate using a wet-transfer method and developed a wide-bandgap MoS2-based micro-displacement sensor employing maskless lithography and hot evaporation techniques. Our testing revealed a piezoelectric response current of 5.12 nA in the sensor under a strain of 0.003% along the armchair direction of the monolayer MoS2. Furthermore, the sensor exhibited a near-linear relationship between the piezoelectric response current and the strain within a displacement range of 40–100 µm, with a calculated response sensitivity of 1.154 µA/%. This research introduces a novel micro-displacement sensor, offering potential for advanced surface texture sensing in various applications.

Transient receptor potential vanilloid family member 1 (TRPV1) has been revealed as a therapeutic target of osteoarthritis (OA), the most common deteriorating whole joint disease, by impeding macrophagic inflammation and chondrocytes ferroptosis. However, the clinical application for capsaicin as the TRPV1 agonist is largely limited by its chronic toxicity. To address this issue, we developed a bifunctional controllable magnetothermal switch targeting TRPV1 for the alleviation of OA progression by coupling of magnetic nanoparticles (MNPs) to TRPV1 monoclonal antibodies (MNPs-TRPV1). Under the alternating magnetic field (AMF) stimulation, MNPs-TRPV1 locally dissipated heat, which was sufficient to trigger the opening and activation of TRPV1, and effectively impeded macrophagic inflammation and chondrocyte ferroptosis. This magnetothermal modulation of TRPV1 simultaneously attenuated synovitis and cartilage degeneration in mice incurred by destabilization of medial meniscus surgery, indicating the delayed OA progression. Furthermore, MNPs-TRPV1 with AMF exposure remarkably reduced knee pain sensitivity, alleviated the crippled gait, and improved spontaneous ambulatory activity performance in the mice OA model. Overall, this work provides a potential pathogenesis-based precise OA therapy with temporally and spatially magnetothermal modulation of TRPV1 in a controllable manner.

Background Catheter ablation is recommended in patients with frequent and symptomatic ventricular arrhythmias (VAs) in an otherwise normal heart. Right or left outflow tract (OT) are the most common origins, and catheter ablation is highly effective with low complication rates. However, outcome of catheter ablation of VAs other than the OT (non-OTVAs) is limited. The aim of this single-center study was to assess the safety and mid-term outcome of catheter ablation for non-OTVAs. Method and Results From 2013 to 2018, 251 patients who underwent catheter ablation for idiopathic non-OTVAs were enrolled and grouped according to the origins including His-Purkinje system (HPS, n = 108), papillary muscle / moderator band (PM/MB, n = 47), tricuspid annulus (TA, n = 70), and mitral annulus (MA, n = 26), 244 (97.2%) had acute elimination of VAs. The time of VAs recurrence of the single procedure was 1.69 (0.12,9.72) months, with 66% occurring within the first 3 months. The recurrence rate was significantly higher in the PM/MB group than in the TA ( p  = 0.025) and MA groups ( p  = 0.023). The single procedure success rate in all patients was 70.1%, in which 66.7%, 59.6%, 80%, and 76.9% were achieved in the HPS, PM/MB, TA, and MA groups, respectively ( p  = 0.284). After multiple procedures, the total success rate was 76.5% at the follow-up of 4.38 ± 2.42 years. The rate was significantly lower in the PM/MB group than in the TA group ( p  = 0.035). In subgroup analysis, no significant difference was observed in the recurrence rate of single procedure in patients with different VA origins within the PM/MB (log-rank test, p  = 0.546). Conclusion Despite a certain percentage of recurrences observed in the mid-term follow-up, catheter ablation remained feasible and effective for idiopathic non-OTVAs.

The role of adaptive immunity in myocardial recovery post myocardial infarction (MI), particularly the immune response by B lymphocytes, remains elusive. Bone marrow immune microenvironment in response to MI is remotely regulated by the hypothalamic pituitary adrenal (HPA) axis. We utilized the cardioprotective actions of SGLT2 inhibitor to identify and characterize bone marrow B cell subsets that respond to myocardial injury. Initially, we preformed ligation of left anterior descendant (LAD) coronary artery in male C57BL/6J mice to monitor the dynamic changes of immune cells across tissues. Mechanistic insights from mouse models demonstrated arrest of bone marrow B cell maturation and function 24 h post MI. A secondary MI model (twice MIs) in mice was established for the first time to evaluate the dosage-dependent cardioprotection of empagliflozin (EMPA). Single-cell RNA-Seq further demonstrated that EMPA restored bone marrow naïve B cell (B220+CD19+CD43−IgM+IgD+) counts and function. Additionally, we recruited 14 acute MI patients with single LAD disease, and profiled B cells post percutaneous coronary intervention (PCI) (compared to 18 matched no-MI controls). We revealed a positive correlation of increased B cell counts with enhanced ejection fraction in MI patients with PCI while lymphopenia was associated with patients with heart failure. Mechanistically, MI triggers the release of glucocorticoids from neuroendocrine system, inducing NHE1-mediated autophagic death of bone marrow B cells while repressing B cell progenitor proliferation and differentiation. Infusion of B cells derived from bone marrow significantly improved cardiac function and diminished infarct size post MI. These findings provide new mechanistic insights into regulation of adaptive immune response post MI, and support targeting bone marrow B cell development for improved ventricular remodeling and reduced heart failure after MI.

Background As an indicator of cardiac autonomic nervous activity, heart rate variability (HRV) is closely linked to premature ventricular complexes (PVCs). However, its role in patients with frequent PVCs originating from the ventricular outflow tract remains unclear. Hypothesis Here, we hypothesize that there may be alterations in HRV among patients with frequent PVCs originating from the ventricular outflow tract, which could play significant roles in the management of such patients. Methods A retrospective study was conducted, including 106 patients with frequent outflow tract PVCs and 106 healthy participants as controls. HRV was assessed based on the 24‐hour Holter recording. The originating foci of PVCs were identified during radiofrequency catheter ablation. Results Patients with frequent outflow tract PVCs exhibited decreased levels of high frequency (HF), standard deviation of all NN intervals, and standard deviation of the average NN intervals, but increased ratios of low frequency to HF (LF/HF ratio), even after propensity score‐matched analysis. Further investigation revealed that patients with PVCs originating from right ventricular outflow tract (RVOT) had much higher LF/HF ratios. Multivariate logistic regression analysis demonstrated that the LF/HF ratio was independently associated with PVCs originating from RVOT. Receiver operating characteristics curve indicated that the LF/HF ratio effectively determined the origin of PVCs (the area under the curve = 0.75, p < .001). Conclusions Patients with frequent outflow tract PVCs exhibited impaired HRV. Additionally, the LF/HF ratio played a significant role in determining the origin of outflow tract PVCs. A total of 106 frequent outflow tract premature ventricular complexes (OT‐PVCs) patients undergoing radiofrequency catheter ablation and 106 healthy participants were included in the study to examine the significance of heart rate variability (HRV) in patients with frequent OT‐PVCs. Patients with OT‐PVCs showed impaired HRV, while those with RVOT‐PVCs exhibited higher low frequency to high frequency ratios compared to patients with LVOT‐PVCs.