Chemically Recyclable Thermoplastic Polyurethane Elastomers via a Cascade Ring-Opening and Step-Growth Polymerization Strategy from Bio-renewable δ‑Caprolactone

It is highly desirable to develop chemically recyclable polymers to address the challenge in establishing a sustainable circular polymer economy. Despite the mass production and widespread applications, there are limited reported examples for the polyurethanes capable of chemical recycling to monomers with high efficiency and purity. In this contribution, we report the “living”/controlled ring-opening polymerization (ROP) of bio-renewable δ-caprolactone (δCL) at room temperature in bulk using an organobase in combination with urea as a catalyst. The telechelic PδCL diol precursor with well-defined terminal groups can be prepared using catalyst loading as low as 0.05 mol %. A one-pot strategy by cascade ROP of δCL and step-growth polymerization of PδCL diol precursors with diisocyanate under solvent-free conditions produced thermoplastic polyurethane elastomers with excellent elastic recovery, tensile strength, ultimate elongation, and low residue strain. Remarkably, the polyurethanes can be chemically recycled to recover δCL with high purity and excellent yield (∼99%) by simple thermolysis

Additional file 2 of Quantitative hypoxia mapping using a self-calibrated activatable nanoprobe

Additional file 2: Figure S2. NTR response of free Cy7-1

Additional file 1 of Quantitative hypoxia mapping using a self-calibrated activatable nanoprobe

Additional file 1: Figure S1. FTIR spectrum of Cy7/PG5-Cy5@LWHA

Additional file 3 of Quantitative hypoxia mapping using a self-calibrated activatable nanoprobe

Additional file 3: Figure S3. Cytotoxicity of (a) Cy7-1/PG5-Cy5@LWHA and (b) Cy7-1/PG5-Cy5

Data_Sheet_1_Case report: Efficacy analysis of radiofrequency catheter ablation combined with atrial appendage resection for atrial tachycardia originating from the atrial appendage in children.ZIP

ObjectiveThe aim of this study was to investigate the efficacy of radiofrequency catheter ablation (RFCA) combined with atrial appendage (AA) resection to treat atrial tachycardia (AT) originating from the AA in children.Materials and methodsUsing the Ensite three-dimensional electroanatomic mapping system, three children with AT originating from the AA were diagnosed. Clinical features and electrocardiographic (ECG) manifestations were analyzed. Ablations were performed using a cold saline-infused catheter at appendages targeting loci of AT origin under the guidance of the Ensite system. Atrial appendage resection was performed in combination with cardiac surgery, and the curative effect was evaluated.ResultsThe ages of the three patients were 3.5, 5.75, and 12.9 years. Two cases originated from the right atrial appendage (RAA) and one originated from the left atrial appendage (LAA). The ECG characteristics of AT from the RAA were as follows: (1) negative P waves in lead V1; (2) positive P waves in leads II, III, and aVF; (3) positive P wave in lead I with varying shapes in lead aVL; and (4) prolonged PR interval with no QRS wave after some P waves. The ECG of the LAA was characterized by (1) positive P waves in lead V1 with a bimodal pattern; (2) positive P waves in leads II, III, and aVF; and (3) negative P waves in leads I and aVL. Preoperative echocardiography showed cardiac enlargement and a decreased left ventricular ejection fraction (LVEF) in all three cases. One case was cured after RFCA, and the remaining two cases required AA resection after RFCA. No recurrence was detected at 1–18 months of follow-up, and the left ventricular end-diastolic diameter and LVEF returned to normal.ConclusionAtrial tachycardia originating from the AA in children showed a characteristic P-wave presentation on ECG, and sustained episodes of AT resulted in tachycardia-induced cardiomyopathy. Children who are not successfully controlled by RFCA or who have a recurrence after RFCA could benefit from AA resection.</p

Table_5_Comprehensive Expression Profile Analysis of Neutrophil Extracellular Trap-Affected Genes in Gastric Cancer Cells and the Clinical Significance of lncRNA NEAT1-Related Signaling.xlsx

BackgroundGastric cancer (GC) is the fifth most common malignant tumor and the third leading cause of cancer-related deaths worldwide. Neutrophil extracellular traps (NETs) can enhance the invasion of GC cells and are associated with poor prognosis in patients. However, its mechanism of action is not completely understood.MethodsThe content of NETs in the peripheral blood of patients with GC was detected by enzyme-linked immunosorbent assay. GC AGS cells were treated with or without NETs for 24 h. High-throughput RNA sequencing was performed to screen differentially expressed long non-coding RNAs (lncRNAs), microRNAs (miRNAs), and messenger RNAs (mRNAs). Real-time polymerase chain reaction (PCR) was used to verify gene expression. A competing endogenous RNA (ceRNA) regulatory network was constructed. Modules were screened using the molecular complex detection (MCODE) plug-in. Gene Ontology and Kyoto Encyclopedia of Genes and Genomes enrichment analyses were performed using the genes in the network. The role and clinical significance of the lncRNA NEAT1-related signaling pathway were validated.ResultsThe content of NETs in the patients with GC was significantly higher than that in healthy controls and was also higher in patients with high-grade (stages III and IV) GC. NETs promoted the invasion of AGS cells. A total of 1,340 lncRNAs, 315 miRNAs, and 1,083 mRNAs were differentially expressed after NET treatment. The expression of five genes was validated using real-time PCR, which were in accordance with the RNA sequencing results. A ceRNA regulatory network was constructed with 1,239 lncRNAs, 310 miRNAs, and 1,009 mRNAs. Four genes (RAB3B, EPB41L4B, ABCB11, and CCDC88A) in the ceRNA network were associated with patient prognosis, with RAB3B being the most prominent and with signaling among the lncRNA NEAT1, the miRNA miR-3158-5p, and RAB3B. NEAT1 was upregulated in AGS cells after NET treatment. RNA interference of NEAT1 inhibited the invasion of AGS cells induced by NETs, inhibited miR-3158-5p expression, and promoted RAB3B expression. NEAT1 and RAB3B expression were positively correlated in patients with GC. Furthermore, RAB3B was upregulated and miR-3158-5p was downregulated in GC tissues compared with adjacent normal tissues, which was also associated with cancer stage.ConclusionThis study provides a comprehensive analysis of differentially expressed genes in NET-treated GC cells and validated the clinical significance of NEAT1-related signaling.</p

Table_3_Comprehensive Expression Profile Analysis of Neutrophil Extracellular Trap-Affected Genes in Gastric Cancer Cells and the Clinical Significance of lncRNA NEAT1-Related Signaling.xls

BackgroundGastric cancer (GC) is the fifth most common malignant tumor and the third leading cause of cancer-related deaths worldwide. Neutrophil extracellular traps (NETs) can enhance the invasion of GC cells and are associated with poor prognosis in patients. However, its mechanism of action is not completely understood.MethodsThe content of NETs in the peripheral blood of patients with GC was detected by enzyme-linked immunosorbent assay. GC AGS cells were treated with or without NETs for 24 h. High-throughput RNA sequencing was performed to screen differentially expressed long non-coding RNAs (lncRNAs), microRNAs (miRNAs), and messenger RNAs (mRNAs). Real-time polymerase chain reaction (PCR) was used to verify gene expression. A competing endogenous RNA (ceRNA) regulatory network was constructed. Modules were screened using the molecular complex detection (MCODE) plug-in. Gene Ontology and Kyoto Encyclopedia of Genes and Genomes enrichment analyses were performed using the genes in the network. The role and clinical significance of the lncRNA NEAT1-related signaling pathway were validated.ResultsThe content of NETs in the patients with GC was significantly higher than that in healthy controls and was also higher in patients with high-grade (stages III and IV) GC. NETs promoted the invasion of AGS cells. A total of 1,340 lncRNAs, 315 miRNAs, and 1,083 mRNAs were differentially expressed after NET treatment. The expression of five genes was validated using real-time PCR, which were in accordance with the RNA sequencing results. A ceRNA regulatory network was constructed with 1,239 lncRNAs, 310 miRNAs, and 1,009 mRNAs. Four genes (RAB3B, EPB41L4B, ABCB11, and CCDC88A) in the ceRNA network were associated with patient prognosis, with RAB3B being the most prominent and with signaling among the lncRNA NEAT1, the miRNA miR-3158-5p, and RAB3B. NEAT1 was upregulated in AGS cells after NET treatment. RNA interference of NEAT1 inhibited the invasion of AGS cells induced by NETs, inhibited miR-3158-5p expression, and promoted RAB3B expression. NEAT1 and RAB3B expression were positively correlated in patients with GC. Furthermore, RAB3B was upregulated and miR-3158-5p was downregulated in GC tissues compared with adjacent normal tissues, which was also associated with cancer stage.ConclusionThis study provides a comprehensive analysis of differentially expressed genes in NET-treated GC cells and validated the clinical significance of NEAT1-related signaling.</p

The effects of gold nanoparticles on the human blood functions

<p>The gold nanoparticles (AuNPs) have been widely used as drug delivery systems at several biomedical fields. However, the effect of AuNPs on the components of human blood is not well characterized. AuNPs firstly interacted with blood when using AuNPs as the drug delivery carries. Therefore, it is urgent to investigate the effect of AuNPs (including the ligands of AuNPs) on human blood, especially its components. In this study, we investigated the possible effects of polyethylene glycol-coated AuNPs (PEG@AuNPs) and citric acid-coated AuNPs (CT-AuNPs) on the blood cell function and distribution of those nanoparticles in blood components including erythrocytes, leukocytes, platelets (PLTs) cells and plasma. We found that the amount of CT-AuNPs engulfed by leukocytes was four folds more compared to PEG@AuNPs, indicating that PEGylation might have the ability to escape the immune system. We found that each individual leukocyte uptaked more AuNPs particles than individual platelet. However, there are more PLTs than leukocytes in the blood. The total amount of AuNPs including PEG@AuNPs and CT-AuNPs accumulation in PLTs were more than in leukocytes. Moreover, we found that both CT-AuNPs and PEG@AuNPs-induced PLTs activation at high concentration. We therefore concluded that the interactions between nanodrug delivery systems (AuNPs) and human blood components, especially the PLTs should be careful evaluated prior to their clinical applications.</p

Table_1_Comprehensive Expression Profile Analysis of Neutrophil Extracellular Trap-Affected Genes in Gastric Cancer Cells and the Clinical Significance of lncRNA NEAT1-Related Signaling.xls

BackgroundGastric cancer (GC) is the fifth most common malignant tumor and the third leading cause of cancer-related deaths worldwide. Neutrophil extracellular traps (NETs) can enhance the invasion of GC cells and are associated with poor prognosis in patients. However, its mechanism of action is not completely understood.MethodsThe content of NETs in the peripheral blood of patients with GC was detected by enzyme-linked immunosorbent assay. GC AGS cells were treated with or without NETs for 24 h. High-throughput RNA sequencing was performed to screen differentially expressed long non-coding RNAs (lncRNAs), microRNAs (miRNAs), and messenger RNAs (mRNAs). Real-time polymerase chain reaction (PCR) was used to verify gene expression. A competing endogenous RNA (ceRNA) regulatory network was constructed. Modules were screened using the molecular complex detection (MCODE) plug-in. Gene Ontology and Kyoto Encyclopedia of Genes and Genomes enrichment analyses were performed using the genes in the network. The role and clinical significance of the lncRNA NEAT1-related signaling pathway were validated.ResultsThe content of NETs in the patients with GC was significantly higher than that in healthy controls and was also higher in patients with high-grade (stages III and IV) GC. NETs promoted the invasion of AGS cells. A total of 1,340 lncRNAs, 315 miRNAs, and 1,083 mRNAs were differentially expressed after NET treatment. The expression of five genes was validated using real-time PCR, which were in accordance with the RNA sequencing results. A ceRNA regulatory network was constructed with 1,239 lncRNAs, 310 miRNAs, and 1,009 mRNAs. Four genes (RAB3B, EPB41L4B, ABCB11, and CCDC88A) in the ceRNA network were associated with patient prognosis, with RAB3B being the most prominent and with signaling among the lncRNA NEAT1, the miRNA miR-3158-5p, and RAB3B. NEAT1 was upregulated in AGS cells after NET treatment. RNA interference of NEAT1 inhibited the invasion of AGS cells induced by NETs, inhibited miR-3158-5p expression, and promoted RAB3B expression. NEAT1 and RAB3B expression were positively correlated in patients with GC. Furthermore, RAB3B was upregulated and miR-3158-5p was downregulated in GC tissues compared with adjacent normal tissues, which was also associated with cancer stage.ConclusionThis study provides a comprehensive analysis of differentially expressed genes in NET-treated GC cells and validated the clinical significance of NEAT1-related signaling.</p

Table_2_Comprehensive Expression Profile Analysis of Neutrophil Extracellular Trap-Affected Genes in Gastric Cancer Cells and the Clinical Significance of lncRNA NEAT1-Related Signaling.xls

BackgroundGastric cancer (GC) is the fifth most common malignant tumor and the third leading cause of cancer-related deaths worldwide. Neutrophil extracellular traps (NETs) can enhance the invasion of GC cells and are associated with poor prognosis in patients. However, its mechanism of action is not completely understood.MethodsThe content of NETs in the peripheral blood of patients with GC was detected by enzyme-linked immunosorbent assay. GC AGS cells were treated with or without NETs for 24 h. High-throughput RNA sequencing was performed to screen differentially expressed long non-coding RNAs (lncRNAs), microRNAs (miRNAs), and messenger RNAs (mRNAs). Real-time polymerase chain reaction (PCR) was used to verify gene expression. A competing endogenous RNA (ceRNA) regulatory network was constructed. Modules were screened using the molecular complex detection (MCODE) plug-in. Gene Ontology and Kyoto Encyclopedia of Genes and Genomes enrichment analyses were performed using the genes in the network. The role and clinical significance of the lncRNA NEAT1-related signaling pathway were validated.ResultsThe content of NETs in the patients with GC was significantly higher than that in healthy controls and was also higher in patients with high-grade (stages III and IV) GC. NETs promoted the invasion of AGS cells. A total of 1,340 lncRNAs, 315 miRNAs, and 1,083 mRNAs were differentially expressed after NET treatment. The expression of five genes was validated using real-time PCR, which were in accordance with the RNA sequencing results. A ceRNA regulatory network was constructed with 1,239 lncRNAs, 310 miRNAs, and 1,009 mRNAs. Four genes (RAB3B, EPB41L4B, ABCB11, and CCDC88A) in the ceRNA network were associated with patient prognosis, with RAB3B being the most prominent and with signaling among the lncRNA NEAT1, the miRNA miR-3158-5p, and RAB3B. NEAT1 was upregulated in AGS cells after NET treatment. RNA interference of NEAT1 inhibited the invasion of AGS cells induced by NETs, inhibited miR-3158-5p expression, and promoted RAB3B expression. NEAT1 and RAB3B expression were positively correlated in patients with GC. Furthermore, RAB3B was upregulated and miR-3158-5p was downregulated in GC tissues compared with adjacent normal tissues, which was also associated with cancer stage.ConclusionThis study provides a comprehensive analysis of differentially expressed genes in NET-treated GC cells and validated the clinical significance of NEAT1-related signaling.</p