Correction: Recovery of the self-cleaning property of silicon elastomers utilizing the concept of reversible coordination bonds.

Correction for 'Recovery of the self-cleaning property of silicon elastomers utilizing the concept of reversible coordination bonds' by Yuxing Shan et al., Soft Matter, 2020, 16, 8473-8481, DOI: .

Stretchable dual cross-linked silicon elastomer with a superhydrophobic surface and fast triple self-healing ability at room temperature.

Stretchable elastomers with superhydrophobic surfaces have potential applications in wearable electronics. However, various types of damage inevitably occur on these elastomers in actual application, resulting in the deterioration of the superhydrophobic properties. In this work, superhydrophobic elastomers (HB-imine-BZn-PDMS), was fabricated by employing a dual-layered structure. The bottom layer was a silicon elastomer (imine-BZn-PDMS) with an imine/coordination dual cross-linked structure and room temperature self-healing efficiency of 94%. The top layer was imine-BZn-PDMS/silica nanocomposites to provide superhydrophobic properties. The HB-imine-BZn-PDMS elastomer exhibited fast triple self-healing ability at room temperature toward surface oxidation/decomposition, ruptures, or pinholes, and high durability under abrasion and stretching. The dual dynamic bonds of imine-BZn-PDMS enabled fast recovery of superhydrophobicity in 20 min at room temperature via bond exchange, after generating pinholes across the elastomer. Following surface chemical damage, the HB-imine-BZn-PDMS elastomer also exhibited fast (40 min) room-temperature self-healing ability, which is superior to that of most current self-healing superhydrophobic materials.

Recovery of the self-cleaning property of silicon elastomers utilizing the concept of reversible coordination bonds.

Stretchable elastomers with superhydrophobic surfaces and self-cleaning abilities are fabricated for use in wearable electronics. However, scratches or ruptures are inevitable on these elastomers, thus deteriorating their self-cleaning ability. To solve this problem, in this work, we explored the ability of a self-healing silicon elastomer to recover its self-cleaning property. A cross-linked silicon elastomer (Zn-IC-PDMS) was fabricated by incorporating imidazole-zinc coordination bonds. The superhydrophobic Zn-IC-PDMS surface was synthesized by sequentially spraying polystyrene (PS) and silica particles on it to form a micro/nano complex structure. Our study shows that the surface of the elastomer exhibited a high water-contact angle (CA) (155°), low sliding angle (SA) (∼3°), and self-cleaning ability. In addition, the surface rapidly recovered its self-cleaning ability at room temperature after ruptures had been formed across the elastomer. SEM images and photographs revealed that the recovery of the self-cleaning ability was attributed to the self-healing behavior of the Zn-IC-PDMS.

Increased frequency of peripheral blood follicular helper T cells and elevated serum IL­21 levels in patients with knee osteoarthritis.

An aberrant immune response has been implicated in the pathogenesis of osteoarthritis (OA). However, the role of peripheral blood follicular helper T (TFH) cells in the pathogenesis of OA has yet to be elucidated. The purpose of the present study was to examine the role of TFH cells and serum interleukin­21 (IL­21) in the pathogenesis of OA. Frequency of peripheral blood inducible costimulator (ICOS)+, programmed death 1 (PD­1)+, and IL­21+ CXCR5+CD4+ T cells in 40 patients with OA and 13 healthy controls (HCs) were examined by flow cytometry. The disease state in individual patients was assessed using the Western Ontario and McMaster Universities Osteoarthritis Index (WOMAC). Concentrations of serum IL­21, interferon­Î³ (INF­Î³), IL­4, IL­17A, and C­reactive protein (CRP) were determined, and the erythrocyte sedimentation rate (ESR) was measured. The percentages of CXCR5+CD4+ cells, PD­1+CXCR5+CD4+, ICOS+CXCR5+CD4+ and IL­21+CXCR5+CD4+ T cells in OA patients were significantly higher than those in the HCs. Furthermore, serum IL­21, IL­17A and IFN­Î³ levels in OA patients were significantly higher than those in HCs. Expression of IL­21+TFH cells in OA patients demonstrated a positive correlation with OA disease activity, CRP levels and WOMAC. TFH cells and IL­21 appear to serve an important role in the progression of OA. IL­21+TFH cells may prove to be a marker of OA disease activity.

Circulating T helper 9 cells and increased serum interleukin-9 levels in patients with knee osteoarthritis.

The purpose of this study was to examine the roles of T helper 9 (Th9) cells and the serum interleukin (IL)-9 level in the pathogenesis of osteoarthritis (OA). The numbers of IL-9(+) CD4(+) CD8(-) T cells, interferon (IFN)-γ+ CD4(+) CD8(-) T cells, IL-4(+) CD4(+) CD8(-) T cells, and IL-17A(+) CD4(+) CD8(-) T cells in 25 OA patients and 13 healthy controls (HC) were examined by flow cytometry. The serum concentrations of IL-9, IL-4, IL-17A, and IFN-γ were also determined. The numbers of CD4(+) CD45RO(+) T cells, Th9 cells, Th1 cells, and Th17 cells in OA patients were significantly higher than those in HCs. Furthermore, serum IL-9, IL-17A, and IFN-γ levels in OA patients were higher than those in HCs. The number of Th9 cells was positively correlated with the number of Th17 cells in OA patients. Furthermore, greater numbers of Th9 cells were positively associated with elevated C-reactive protein, and both Th9 cells and IL-9 levels were positively correlated with the Western Ontario and McMaster Universities Osteoarthritis index in OA patients. Th9 cell numbers and IL-9 levels are correlated with OA patient symptoms and joint functionality and may be a marker of disease activity.

Higher frequency of peripheral blood follicular regulatory T cells in patients with new onset ankylosing spondylitis.

Follicular helper T (TFH) cells and B cells are linked to the pathogenesis of ankylosing spondylitis (AS). Follicular regulatory T (TFR) cells suppress TFH cell and germinal center B cell numbers in vivo. The role of TFR cells in AS is unknown. The frequency of peripheral blood inducible FOXP3+CXCR5+CD4+TFR cells and CXCR5+CD4+TFH cells were taken from 20 onset AS patients and 10 healthy controls, and were examined by flow cytometry, their disease activity were measured by the Bath Ankylosing Spondylitis Disease Activity Index. The concentrations of serum interleukin (IL)-21, immunoglobulin G, immunoglobulin A, immunoglobulin M and C-reactive protein were examined, and the values of erythrocyte sedimentation rate were measured. The frequency of peripheral blood FOXP3+CXCR5+CD4+TFR cells, CXCR5+CD4+TFH cells, the ratio of FOXP3+CXCR5+CD4+TFR/CXCR5+CD4+TFH cells and the concentration of serum IL-21 in the AS patients were significantly higher than those in the healthy controls (P < 0.0001, P = 0.0027, P < 0.0001, P = 0.0039, respectively). The frequency of FOXP3+CXCR5+CD4+TFR cells and the ratio of FOXP3+CXCR5+CD4+TFR/CXCR5+CD4+TFH cells still significantly rose in those patients after standard treatment (P = 0.0006, P < 0.0001), the concentration of serum IL-21 decreased after treatment (P = 0.0049), accompanied by significantly minimized disease activities. Furthermore, the TFR cells were negatively correlated with serum immunoglobulin A in those patients before treatment (r = -0.582, P = 0.0071), and the frequency of TFR cells was negatively correlated with that of TFH cells and the concentration of serum IL-21 after treatment (r = -0.550, P = 0.046; r = -0.581, P = 0.0371). TFR cells might participate in the pathogenesis of AS, and might be responsible for controlling the autoantibodies, the frequency and function of TFH cells to inhibit the development of AS.

Increased interleukin 21 and follicular helper T-like cells and reduced interleukin 10+ B cells in patients with new-onset systemic lupus erythematosus.

OBJECTIVE: To elucidate the potential role of follicular helper T cells (TFH) and interleukin 10 (IL-10)+ B cells in the development of systemic lupus erythematosus (SLE). METHODS: The numbers of peripheral blood CD27+, CD38+, CD86+, CD95+, IL-10+ B cells, and inducible T cell costimulator (ICOS)+, programmed death-1 (PD-1)+, IL-21+, CXCR5+CD4+ TFH-like cells were examined in 23 patients with new onset SLE and 20 healthy controls (HC). RESULTS: In comparison with HC, significantly reduced numbers of CD19+ and IL-10+ B cells, but increased numbers of CD27(high), CD86+, CD95+ B cells, CXCR5+CD4+, ICOS+, PD-1+, and IL-21+ TFH-like cells were detected, which were accompanied by higher levels of serum IL-21, but lower levels of IL-10 in the patients. Treatment with anti-SLE therapy modulated the imbalance of different subsets of B and TFH-like cells. The levels of serum IL-21 and IL-10 were positively correlated with the numbers of CD4+CXCR5+ TFH-like and CD19+CD5+CD1d+ B cells in the patients, respectively. The numbers of CD27(high) B cells were correlated positively with IL-21+ TFH-like cells, but negatively with IL-10+ B cells. The values of SLE Disease Activity Index, C3, and erythrocyte sedimentation rate were correlated positively with serum IL-21, but negatively with IL-10 in those patients. CONCLUSION: Our data indicate that the imbalance of IL-21+ TFH-like, CD27(high), and IL-10+ B cells may be associated with the pathogenesis of SLE, and levels of serum IL-21 and IL-10 may be valuable for evaluating disease activity in SLE.

Plasma levels of IL-37 and correlation with TNF-α, IL-17A, and disease activity during DMARD treatment of rheumatoid arthritis.

The aim of this study was to assess the change of IL-37 concentrations in rheumatoid arthritis (RA) patients under Disease-modifying anti-rheumatic drug (DMARD) therapy, and to establish a correlation between Interleukin-37 and pro-inflammatory cytokines in plasma and disease activity. The plasma level of IL-37 was determined using ELISA in 50 newly diagnosed RA patients and 30 healthy controls (HC). Plasma levels of IL-17A, IL-6 and TNF-α were measured using flow a cytometric bead array assay. We found that the concentrations of IL-37, as well as IL-17A, IL-6 and TNF-α, were higher in plasma of RA patients compared to HCs. Compared to patients who did not respond to DMARD treatment, treatment of patients responsive to DMARDs resulted in down-regulation of IL-17A, IL-6 and TNF-α expression. The plasma level of the anti-inflammatory cytokine IL-37 was also decreased in drug responders after DMARD treatment. The plasma level of IL-37 in RA patients was positively correlated with pro-inflammatory cytokines (IL-17A, TNF-α) and disease activity (CRP, DAS28) in RA patients. IL-37 expression in RA and during DMARD treatment appears to be controlled by the level of pro-inflammatory cytokines. This results in a strong correlation between plasma levels of IL-37 and disease activity in RA patients.

A higher frequency of peripheral blood activated B cells in patients with non-traumatic osteonecrosis of the femoral head.

OBJECTIVES: B cells play important roles in inflammatory diseases. This study was aimed at examining the frequency of different subsets of B cells in patients with non-traumatic osteonecrosis of the femoral head (NONFH). METHODS: The percentages of the different subsets of circulating B cells in 28 patients with steroid-related, alcohol-related, or idiopathic NONFH and 10 healthy controls (HC) were examined by flow cytometry. The concentrations of serum C-reactive protein (CRP), fibrinogen (FIB), immunoglobulins, cytokines and blood erythrocyte sedimentation rate (ESR) were measured. RESULTS: In comparison with those in the HC, significantly higher percentages of CD27-, CD86+, CD95+, and CD27+CD95+CD19+ but lower CD27+CD19+ B cells were detected in the patients. The percentages of CD86+, CD95+, and CD27+CD95+CD19+ B cells in each group of the patients were significantly higher than those in the HC. The levels of serum IL-17A and IFN-γ in steroid group and serum TNF-α in alcoholic group were significantly higher than those in the HC. The percentages of CD86+CD19+ B cells were positively associated with the degrees of femoral head collapse in both steroid and alcoholic groups of patients and the levels of serum TNF-α were positively associated with the degrees of femoral head collapse in the alcoholic NONFH patients. CONCLUSIONS: These data suggest a higher frequency of CD86+CD19+ activated B cells and elevated levels of serum TNF-α may be associated with the development of NONFH.

Higher frequency of peripheral blood interleukin 21 positive follicular helper T cells in patients with ankylosing spondylitis.

OBJECTIVE: The role of follicular Th (TFH) cells remains unclear in the pathogenesis of ankylosing spondylitis (AS). Our study examined the frequency of different subsets of circulating CXCR5+CD4+ T cells in patients with AS before and after receiving therapy. METHODS: Percentages of peripheral blood inducible costimulator (ICOS)+, programmed death 1 (PD-1)+, and interleukin 21 (IL-21)+ CXCR5+CD4+ T cells in 26 patients with AS and 12 healthy controls (HC) were examined by flow cytometry, and the disease activity of individual patients was measured by Bath AS Disease Activity Index (BASDAI). The concentrations of serum IL-21, IgG, IgA, IgM, and C-reactive protein (CRP) were examined and the values of erythrocyte sedimentation rate (ESR) were measured. The potential association among these measures was analyzed. RESULTS: In comparison with that in HC, significantly increased percentages of CXCR5+CD4+, CXCR5+CD4+PD-1+, and CXCR5+CD4+IL-21+, but not CXCR5+CD4+ICOS+ and PD-1+ICOS+CXCR5+CD4+ T cells, and elevated concentrations of serum IL-21 were detected in patients with AS (p = 0.001, p = 0.012, p < 0.001, p = 0.233, p = 0.216, p < 0.001, respectively). Treatment with meloxicam, thalidomide, and etanercept for 1 month significantly reduced percentages of IL-21+CXCR5+CD4+ T cells and concentrations of serum IL-21 (p < 0.001, p < 0.001, respectively), accompanied by significantly minimized disease activity in drug responders, but not in the drug nonresponders. Further, percentages of IL-21+CXCR5+CD4+ T cells were positively correlated with BASDAI in patients (r = 0.6, p = 0.0012) and in the drug-responders 1 month after treatment (r = 0.68, p = 0.005), while the percentages of PD-1+CXCR5+CD4+ T cells were negatively correlated with BASDAI (r = -0.58, p = 0.0018). CONCLUSION: These data suggest that IL-21+CXCR5+CD4+ T cells may be associated with development of AS and that the frequency of IL-21+CXCR5+CD4+ T cells may be a biomarker for evaluation of disease activity and drug responses in patients with AS, particularly in drug-responding patients.

Peripheral B-cell activation and exhaustion markers in patients with ankylosing spondylitis.

AIMS: Ankylosing spondylitis (AS) is an autoimmune disease and is associated with abnormal B cell function. However, the roles of different B cell subsets are less clear. This study aimed to examine the frequency of different subsets of B cells in AS patients following standard therapies. MAIN METHODS: Eighteen newly diagnosed AS patients and 10 healthy controls (HC) were recruited in this study. The expression of CD27, CD38, CD86, CD95 and IgD on CD19(+) B cells was examined by flow cytometry. The disease activity was scored according to the Bath Ankylosing Spondylitis Disease Activity Index (BASDAI). Serum levels of C-reactive protein (CRP), rheumatoid factor (RF), IgG, IgA and IgM, and the erythrocyte sedimentation rate (ESR) were measured. KEY FINDINGS: The frequency of CD27(+) B cells was decreased in AS patients compared with HC (p=0.018), while CD86(+) and CD27(-)CD95(+) B cell subsets increased in AS patients (p<0.001). Meanwhile, the frequencies of CD38(+) and CD95(+) B cell positively correlated with BASDAI (r=0.6505, p=0.0035; r=0.6854, p=0.0017, respectively), while CD38(-)CD86(+) B cell negatively correlated with BASDAI (r=-0.7329, p<0.001). We also found that CD27(-) and CD95(+) B cell negatively correlated with RF levels (r=-0.5141, p=0.0290; r=-0.4944, p=0.0370, respectively), while CD27(+) B cell positively correlated with IgG levels (p=0.0148, r=0.5640). Moreover, CD86(+) and CD27(-)CD95(+) B cell subsets increased following treatment with Meloxicam and Etanercept for one month (p<0.001; p<0.001). SIGNIFICANCE: These findings suggest that CD27(-)CD95(+)CD19(+) and CD86(+)CD19(+) B cells may be reasonable cellular targets for the therapeutic intervention of AS.

Downregulation and altered function of natural killer cells in hepatitis B virus patients treated with entecavir.

The aim of the present study was to investigate the natural killer (NK) cell phenotype and function in chronic hepatitis B virus (HBV) patients and to study the effects of entecavir therapy (10 mg/day, p.o.) on these responses. Peripheral blood NK cells were collected from 18 chronic HBV patients and 14 healthy controls. The effect of entecavir therapy on the phenotype and function of NK cells in chronic HBV patients was characterized by flow cytometry analysis. Concentrations of alanine aminotransferase (ALT) and aspartate aminotransferase (AST), HBV viral loads in both groups and potential associations between the frequency of peripheral NK cell subsets and clinical measures were determined. There was a significant reduction in the number of CD3(-)CD56(+) NK cells in chronic HBV patients compared with healthy controls. Furthermore, there were significant increases in the percentage of CD3(-)CD56(+)NKG2D(+) and CD3(-)CD56(+)NKP30(+) NK activating receptors in chronic HBV patients compared with healthy individuals, who exhibited downregulated expression following entecavir treatment. Spearman's correlation analysis revealed that there was a significant positive correlation between the percentage of NKG2D(+) and NKP30(+) NK cells and serum ALT levels. Characterization of NK cell degranulation indicated that the frequency of CD107a(+) NK cells in HBV patients (in response to K562 stimulation) was significantly greater than in healthy controls but decreased following entecavir treatment. Entecavir treatment of hepatitis B e antigen-positive chronic HBV-infected patients not only led to a reduction in HBV DNA loads and normalization of ALT and AST levels, but also resulted in the recovery of NK cell-mediated immunity.

Ionizing radiation stimulates secretion of pro-inflammatory cytokines: dose-response relationship, mechanisms and implications.

In previous studies we showed a marked increase in secretion of inflammatory cytokines TNFalpha and interleukin (IL)-1beta by mouse macrophages in response to different doses of ionizing radiation (IR). Here we show the stimulation of IL-12 and IL-18 secretion by mouse peritoneal macrophages after whole-body irradiation with exploration of the possible mechanisms and implications in cancer radiotherapy. Both low (0.075 Gy) and high (2 Gy) doses of IR were found to cause sustained stimulation of IL-12 and IL-18 secretion by mouse macrophages; this paralleled the activation of NF-kappaB as well as up-regulated expression of CD14 and TLR4-MD2 on the macrophage surface and MyD88 in the cytoplasm. The expression of CD14, TLR4-MD2 and MyD88 increased in a dose-dependent manner from radiation doses between 0.05 and 2 Gy. The secretion of IL-12 and IL-18 showed a dose-dependent increase from doses between 0.05 and 4 Gy. It is concluded that IR can stimulate the secretion of IL-12 and IL-18 presumably via activation of the Toll signaling pathway in macrophages. The potential harmful effect of repeated doses of radiation used in radiotherapy for certain cancers is discussed.

Labeling of human insulin-like growth factor-I eukaryotic expression vector with green fluorescent protein.

OBJECTIVE: To label human insulin-like growth factor-I (hIGF-I) eukaryotic expression vector with green fluorescent protein (GFP) for the repair of articular cartilage defects. METHODS: GFP cDNA was inserted into pcDNA(3.1)-hIGF-1 to construct the co-expression vector with two multiple cloning sites mammalian expression vector under two cytomegalovirus promoters/enhancers respectively. Recombinant pcGI was transfected into NIH 3T3 cells with the help of lipofectamine. RESULTS: Enzyme digestion and agarose gel electrophoresis analysis revealed that pcGI vector contained correct GFP and hIGF-I cDNA. Expression of hIGF-1 and GFP was confirmed in transfected NIH 3T3 cells by immunocytochemical analysis and fluorescence microscopy. CONCLUSIONS: hIGF-I eukaryotic expression vector has been successfully labeled with GFP.

[Influence of different mechanical environments on repair of cartilage defect with rabbit marrow mesenchymal stem cells].

OBJECTIVE: To study the influence of different mechanical environments on repair cartilage defect with marrow mesenchymal stem cells as seed cells. METHODS: The rabbit marrow mesenchymal stem cells were isolated and cultured. The cartilage defects were repaired by autologous tissue engineered cartilage with the marrow mesenchymal stem cells as seed cells. Fifteen rabbits with cartilage defect were divided into 3 groups: dislocation group with cell-free scaffold (control group), dislocation group with cartilaginous construct and normal mechanical environment group with cartilaginous construct. The repaired tissue was harvested and examined 6 weeks postoperatively. RESULTS: The repair tissue in normal mechanical environment group with cartilaginous construct showed cartilage-like tissue in superficial layer and subchondral bone tissue in deep layer 6 weeks postoperatively. The defect was filled with bone tissue in dislocation group with cartilaginous construct 6 weeks postoperatively. The surrounding normal cartilage tissue showed vascular invasion from subchondral area and the concomitant thinning of the normal cartilage layer. The cartilaginous construct left in the femoral trochlea groove formed hyaline cartilage-like tissue. The defect was repaired by fibrous tissue in control group. CONCLUSION: The repaired tissue by tissue engineered cartilage with marrow mesenchymal stem cells as seed cells showed the best result in normal mechanical environment group, which indicates that it will be essential for the formation and maintenance of tissue engineered cartilage to keep the normal mechanical stress stimulus.

Radiographic verification of pedicle screw pilot hole placement in thoracic spine using Kirschner wires versus spiral wires.

OBJECTIVE: To evaluate the feasibility of the pedicle screw pilot holes placement in thoracic spine using the spiral wires as the guide pin. METHODS: The pedicle screw pilot holes were drilled within the center of the pedicle and the lateral and medial pedicle walls were violated in 9 human dried thoracic vertebrae. Kirschner wires or spiral wires were separately placed in the holes, and then the posteroanterior and lateral radiographs were taken. The radiographs were evaluated by 3 experienced spine surgeons and 3 young orthopedists. After radiographs were shown to these observers, they combined the posteroanterior and lateral radiographs in each place and determined whether the pedicle screw pilot hole violated the pedicle cortex or not. The results were analyzed by a statistical software. RESULTS: Sensitivity, specificity and accuracy of the method using spiral wires to detect pedicle pilot hole placement were significantly higher than those of using Kirschner wires. With a true posteroanterior radiograph, the sensitivity, specificity and accuracy of the method using spiral wires approximated or attained 100%. CONCLUSIONS: The method of intrapedicular pilot hole placement verification using spiral wires is effective for guiding the accurate placement of pedicle screws.