Bioinspired Liquid Metal based Soft Humanoid Robots.

The pursuit of constructing humanoid robots to replicate the anatomical structures and capabilities of human beings has been a long-standing significant undertaking and especially garnered tremendous attention in recent years. However, despite the progress made over recent decades, humanoid robots have predominantly been confined to those rigid metallic structures, which however starkly contrast with the inherent flexibility observed in biological systems. To better innovate this area, the present article systematically explores the value and potential of liquid metals and their derivatives in facilitating a crucial transition towards soft humanoid robots. Through a comprehensive interpretation of bionics, we present an overview of liquid metals' multifaceted roles as essential components in constructing advanced humanoid robots - functioning as soft actuators, sensors, power sources, logical devices, circuit systems, and even transformable skeletal structures. We conceived that the integration of these components with flexible structures, facilitated by the unique properties of liquid metals, can create unexpected versatile functionalities and behaviors to better fulfill human needs. Finally, we envision a revolution in humanoid robots, transitioning from metallic frameworks to hybrid soft-rigid structures resembling that of biological tissues. This article is expected to provide fundamental guidance for the coming research, thereby advancing the area. This article is protected by copyright. All rights reserved.

Shaping active matter from crystalline solids to active turbulence.

Active matter drives its constituent agents to move autonomously by harnessing free energy, leading to diverse emergent states with relevance to both biological processes and inanimate functionalities. Achieving maximum reconfigurability of active materials with minimal control remains a desirable yet challenging goal. Here, we employ large-scale, agent-resolved simulations to demonstrate that modulating the activity of a wet phoretic medium alone can govern its solid-liquid-gas phase transitions and, subsequently, laminar-turbulent transitions in fluid phases, thereby shaping its emergent pattern. These two progressively emerging transitions, hitherto unreported, bring us closer to perceiving the parallels between active matter and traditional matter. Our work reproduces and reconciles seemingly conflicting experimental observations on chemically active systems, presenting a unified landscape of phoretic collective dynamics. These findings enhance the understanding of long-range, many-body interactions among phoretic agents, offer new insights into their non-equilibrium collective behaviors, and provide potential guidelines for designing reconfigurable materials.

Inhibitory effect of CUL1 on atherosclerosis through the p53 pathway.

Background: Atherosclerosis (AS) is a serious chronic condition associated with cardiovascular and cerebrovascular diseases. Research on AS is currently lacking, and there is a need to increase research to improve the diagnosis, treatment, and prognosis of AS. Therefore, the aim of the present study was to explore the molecular mechanism and identify potential biomarkers in AS. Methods: First, we downloaded the GSE28829 dataset and screened differentially expressed genes (DEGs). Then, DEGs were analyzed by functional enrichment analysis and protein-protein interaction (PPI) networks to determine hub genes. The key gene for AS was identified following the expression analysis of AS, clinical correlation with immune factors, the gene set enrichment analysis (GSEA) enrichment pathway, and receiver-operating characteristic curve analysis. In functional experiments, correlations between cullin 1 (CUL1), cytokines, and downstream targets in AS were investigated. Results: We identified 595 upregulated and 391 downregulated DEGs enriched in neutrophil degranulation, the B-cell receptor signaling pathway, cell-matrix adhesion, and fatty acid degradation. Through PPI, we identified 7 hub genes for the expression analysis, immunoassay, and GSEA. Finally, CUL1 was identified as the inhibitory gene in AS associated with immune factors, and was found to have a strong prognostic prediction ability. The results indicated that CUL1 upregulated interleukin (IL)-6, IL-1ß, and tumor necrosis factor-α concentrations, and weakened the cell proliferation of AS. It was also found that CUL1 exerted its inhibitory function in AS by the p53 pathway. Conclusions: The findings of the present study indicate that CUL1 is a suppressing gene in AS, and has the potential to be a therapeutic and prognostic biomarker for AS.

Expression and predictive value of NLRP3 in patients with atrial fibrillation and stroke.

OBJECTIVE: To investigate the expression and prognostic value of NLRP3 in non-valvular atrial fibrillation (NVAF) patients with ischemic stroke (IS). METHODS: A retrospective analysis from January 2019 to December 2021 was conducted in 105 patients with NVAF who were treated in our hospital and were divided into the simple NVAF group (simple group) and combined IS group (consolidation group) according to the occurrence of IS. The relative expression of NLRP3 in serum was tested via qRT-PCR. The serum TNF-α, IL-6, and CRP levels were measured by double antibody sandwich enzyme-linked immunosorbent assay (DAS-ELISA), and the correlation between the expression of NLRP3, TNF-α, IL-6, CRP and non-valvular atrial fibrillation stroke risk score (CHA2DS2-VASc score) was analyzed by Pearson method. The independent predictors of NVAF combined with IS were analyzed by regression equation. Meanwhile, the predictive value of the factors was assessed by receiver operating characteristic (ROC) curve. RESULTS: The scores of NLRP3, TNF-α, IL-6, CRP and CHA2DS2-VASc in the consolidation group were obviously higher than those in the simple group. Pearson analysis revealed that the NLRP3, TNF-α, IL-6, and CRP levels in IS patients were positively correlated with CHA2DS2-VASc score. Logistic analysis revealed that NLRP3, IL-6, CRP and CHA2DS2-VASc could be used as potential factors to predict the merging of NVAF with IS. ROC showed that combined detection of NLRP3, IL-6, CRP and CHA2DS2-VASc in predicting NVAF complicated with IS exhibited an area under the curve of more than 0.9. CONCLUSION: NLRP3 is highly expressed in peripheral blood of patients with NVAF complicated with IS, which is a potential indicator for predicting NVAF complicated with IS.

The Identification of Key Genes and Biological Pathways in Heart Failure by Integrated Bioinformatics Analysis.

PURPOSE: Heart failure (HF) is a clinical syndrome caused by ventricular insufficiency. In order to further explore the biomarkers related to HF, we apply the high-throughput database. MATERIALS AND METHODS: The GSE21610 was applied for the differentially expressed gene (DEG) analysis. The Database for Annotation, Visualization, and Integrated Discovery (DAVID) was performed to assess Gene ontology (GO) and the Kyoto Encyclopedia of Genes and Genomes (KEGG) analyses. The Gene Set Enrichment Analysis (GSEA) was used for gene expression profile GSE21610. The Protein-Protein Interaction (PPI) network and modules were also constructed for research. These hub gene function pathways were estimated in HF progression. RESULT: We have identified 434 DEGs in total, including 304 downregulated DEGs and 130 upregulated DEGs. GO and KEGG illustrated that DEGs in HF were significantly enriched in G protein-coupled receptor binding, peroxisome, and cAMP signaling pathway. GSEA results showed gene set GSE21610 was gathered in lipid digestion, defense response to fungus, and intestinal lipid absorption. Finally, through analyzing the PPI network, we screened hub genes CDH1, TFRC, CCL2, BUB1B, and CD19 by the Cytoscape software. CONCLUSION: This study uses a series of bioinformatics technologies to obtain hug genes and key pathways related to HF. These analysis results provide us with new ideas for finding biomarkers and treatment methods for HF.

The Identification of Candidate Biomarkers and Pathways in Atherosclerosis by Integrated Bioinformatics Analysis.

BACKGROUND: Atherosclerosis (AS) is a type of yellow substance containing cholesterol in the intima of large and middle arteries, which is mostly caused by fat metabolism disorders and neurovascular dysfunction. MATERIALS AND METHODS: The GSE100927 data got analyzed to find out the differentially expressed genes (DEGs) using the limma package in R software. Gene Ontology (GO) and the Kyoto Encyclopedia of Genes and Genomes (KEGG) analyses of the DEGs were assessed by the Database for Annotation, Visualization, and Integrated Discovery (DAVID). The Search Tool for the Retrieval of Interacting Genes (STRING) visualized the Protein-Protein Interaction (PPI) network of the aggregated DEGs. GSEA software was used to verify the biological process. RESULT: We screened 1574 DEGs from 69 groups of atherosclerotic carotid artery and 35 groups of control carotid artery, including 1033 upregulated DEGs and 541 downregulated DEGs. DEGs of AS were chiefly related to immune response, Epstein-Barr virus infection, vascular smooth muscle contraction, and cGMP-PKG signaling pathway. Through PPI networks, we found that the hub genes of AS were PTAFR, VAMP8, RNF19A, VPRBP, RNF217, KLHL42, NEDD4, SH3RF1, UBE2N, PJA2, RNF115, ITCH, SKP1, FBXW4, and UBE2H. GSEA analysis showed that GSE100927 was concentrated in RIPK1-mediated regulated necrosis, FC epsilon receptor fceri signaling, Fceri-mediated NF KB activation, TBC rabgaps, TRAF6-mediated induction of TAK1 complex within TLR4 complex, and RAB regulation of trafficking. CONCLUSION: Our analysis reveals that immune response, Epstein-Barr virus infection, and so on were major signatures of AS. PTAFR, VAMP8, VPRBP, RNF217, KLHL42, and NEDD4 might facilitate the AS tumorigenesis, which could be new biomarkers for diagnosis and therapy of AS.

BK Channel Deficiency in Osteoblasts Reduces Bone Formation via the Wnt/ß-Catenin Pathway.

Global knockout of the BK channel has been proven to affect bone formation; however, whether it directly affects osteoblast differentiation and the mechanism are elusive. In the current study, we further investigated the role of BK channels in bone development and explored whether BK channels impacted the differentiation and proliferation of osteoblasts via the canonical Wnt signaling pathway. Our findings demonstrated that knockout of Kcnma1 disrupted the osteogenesis of osteoblasts and inhibited the stabilization of ß-catenin. Western blot analysis showed that the protein levels of Axin1 and USP7 increased when Kcnma1 was deficient. Together, this study confirmed that BK ablation decreased bone mass via the Wnt/ß-catenin signaling pathway. Our findings also showed that USP7 might have the ability to stabilize the activity of Axin1, which would increase the degradation of ß-catenin in osteoblasts.

Consistency and applicability of different brief screen instrument of cognitive function in elderly population.

BACKGROUND: Screening for cognitive impairment (CI) is often hampered by lack of consensus as to which screening instrument to use. The aim is to assess the consistence and applicability of different CI screening tools. METHOD: In a cross-sectional study from October 2017 to September 2018 in 7 communities in Shanghai, China, elder (≧60) residential volunteers with no history of major cardiovascular diseases, cancers and other comorbidities known to affect cognitive functions were recruited. The participants underwent tests with 7 cognitive function screening instruments. Multivariate linear regressions were performed to test correlations between demographic characteristics, including gender, age, education, and marital status, with cognitive test scores. Mini-Mental State Examination (MMSE) score adjusted according to the correlation coefficients was used to detect CI with a cutoff of 24. Other cognitive function scores were compared between participants with and without CI. In addition, Pearson's correlation test was used to detect association between different test scores. RESULTS: 172 participants with relatively low education levels were included. Age and education showed significant association with cognitive test scores. Using adjusted MMSE, 39.6% of participants were identified with CI, while the percentage was 87.2% when adjusted Montreal Cognitive Assessment (MoCA) with cutoff of 26 was used. Analysis of "abnormal" test scores showed that MMSE had the highest percentage of valid data (98.8%). MoCA and Isaacs test of Verbal Fluency (VF) score had correlation with most the other scores, while MMSE only significantly associated with VF and MoCA. CONCLUSIONS: MMSE may still present the most applicable tools for quick screen of cognitive functions, especially when environmental conditions may interfere with participants' attention.

Homocysteine level is positively and independently associated with serum creatinine and urea nitrogen levels in old male patients with hypertension.

A cross-sectional study to show whether and how serum fasting homocysteine levels are associated with renal function changes in patients with hypertension. Homocysteine levels were associated with serum creatinine and blood urea nitrogen (BUN) levels with coefficients of 2.04 and 0.07, respectively, only in males and independent of confounders. In addition, low density lipoprotein cholesterol (LDL-C) levels were positively and left ventricular ejection fraction (LVEF) was negatively associated with serum creatinine level in males; age was positively associated with serum creatinine levels in females. Age was a common risk factor positively associated with BUN levels in both sexes, while total cholesterol (TC) levels and glycemic control were independent risk factors that were positively associated with BUN levels only in males. LDL-C levels and LVEF were negatively associated with BUN levels in females. Body mass index (BMI) was positively associated and hemoglobin A1c (HbA1c) levels, high density lipoprotein cholesterol (HDL-C) levels and the presence of stroke were negatively associated with serum uric acid levels in male patients. In contrast, only LVEF was positively associated with uric acid levels in females. In conclusion, homocysteine level is an independent risk factor associated with serum creatinine and BUN levels in male patients with hypertension.

Identification of the Key Genes Involved in the Effect of Folic Acid on Endothelial Progenitor Cell Transcriptome of Patients with Type 1 Diabetes.

Type 1 diabetes (T1D) is one of the most common autoimmune diseases in children. Previous studies have suggested that endothelial progenitor cells (EPCs) might be engaged in the regulating of the biological processes in T1D and folic acid (FA) might be engaged in regulating EPC function. The present study has identified 716 downregulated genes and 617 upregulated genes in T1D EPC cases after treated with FA. Bioinformatics analysis has shown that these DEGs were engaged in regulating metabolic processes, cell proliferation-related processes, bone marrow development, cell adhesion, platelet degranulation, and cellular response to growth factor stimulus. Furthermore, we have conducted and identified hub PPI networks. Importantly, we have identified 6 upregulated genes (POLR2A, BDNF, CDC27, LTN1, RAB1A, and CUL2) and 8 downregulated genes (SHC1, GRIN2B, TTN, GNAL, GNB2, PTK2, TF, and TLR9) as key regulators involved in the effect of FA on endothelial progenitor cell transcriptome of patients with T1D. We think that this study could provide novel information to understand the roles of FA in regulating EPCs of T1D patients.