Bandwidth-tunable THz absorber based on diagonally distributed double-sized VO2 disks.

Terahertz absorbers combined with phase-changing VO2 are a class of stealth materials with adjustable absorptance. However, such absorbers still suffer from insufficient absorption bandwidth. We propose a three-layer terahertz (THz) absorber, consisting of an array of diagonally distributed double-sized VO2 disks on a silica-coated gold film. We find this structure can generate the superposition of three resonant absorption peaks to broaden the absorption band. The finite element simulation (FES) results show that the absorption bandwidth can be adjusted from 2.63 to 5.04 THz by simply changing the sizes of the VO2 disks. In addition, the peak absorptance can be continuously regulated from 9.8% to 96% by varying the conductivity of VO2. Finally, the absorber is polarization-insensitive and has wide-angle absorption. The wide absorption band and adjustable bandwidth of the absorbers have important applications potentially for intelligent stealth materials.

Potential In Vitro Tissue-Engineered Anterior Cruciate Ligament by Copolymerization of Polyvinyl Alcohol and Collagen.

BACKGROUND AND PURPOSE: Suitable tissue-engineered scaffolds to replace human anterior cruciate ligament (ACL) are well developed clinically as the development of tissue engineering. As water-soluble polymer compound, polyvinyl alcohol (PVA) has been wildly used as the materials to replace ACL. The aim of this study was to explore the feasibility of constructing tissue-engineered ACL by the copolymerization of PVA and collagen (PVA/COL). METHODS: PVA and COL were copolymerized at a mass ratio of 3:1. The pore size and porosity of the scaffold were observed by electron microscope. The maximum tensile strength of the scaffold was determined by electronic tension machine. The cytotoxicity of the scaffold was evaluated by MTT assay. The morphology of ACL cells cultured on the surface of the scaffold was observed by inverted microscope. The degradation of the scaffold was recorded in the rabbit model. RESULTS: The average pore size of the polymer scaffold was 100 to 150 µm and the porosity was about 90%. The maximum tensile strength of the scaffold material was 8.10 ±â€Š0.28 MPa. PVA/COL could promote the proliferation ability of 3T3 cells. ACL cells were successfully cultured on the surface of PVA/COL scaffold, with natural growth rate, differentiation, and proliferation. Twenty-four weeks after the plantation of scaffold, obvious degradations were observed in vivo. CONCLUSION: The model of in-vitro tissue-engineered ACL was successfully established by PVA/COL scaffolds.

Modified Blair ankle fusion for ankle arthritis.

OBJECTIVE: To investigate the clinical outcome of modified Blair ankle fusion for ankle arthritis. METHODS: Between November 2009 and June 2012, 28 patients with ankle arthritis were treated, among whom 11 had obvious foot varus deformity, and 17 were almost normal in appearance. There were 13 males and 15 females with an average age of 49.4 years (range, 23-67 years). The main symptoms included swelling, pain, and a limited range of motion of the ankles. The ankle joints functions were assessed by American Orthopedic Foot and Ankle Society (AOFAS) ankle and hindfoot score and visual analog scale (VAS) preoperatively and at 1 year follow-up. RESULTS: Twenty-eight patients were followed up for 19.8 months on average (range, 1-2 years). Superficial wound infection occurred in 3 cases, and was cured after debridement; the other incisions healed by first intention without complications. All ankles were fused at 1 year follow-up after operation. The symptom was relieved completely in all patients at last follow-up without complication of implant failure, or nonunion. The postoperative AOFAS ankle and hindfoot score was 83.13±3.76, showing significant difference when compared with the preoperative score (45.38±3.21, P<0.01). VAS was significantly decreased from 8.01±0.63 to 2.31±1.05 at 1 year follow-up (P<0.05). CONCLUSION: Modified Blair ankle fusion has the advantages of high feasiblity, less cost and rigid fixation. It shows high reliability in pain relief and may obtain a good clinical effectiveness.

Long non-coding RNA MEG3 regulates the progress of osteoarthritis by regulating the miR-34a/Klotho axis.

Background: Osteoarthritis (OA) is one of the most common chronic diseases today, and its prevalence and incidence are expected to increase as life expectancy increases. By investigating the inhibition of long non-coding RNA maternally expressed gene 3 (lncRNA MEG3) in OA, we hope to provide some new insights into the treatment of osteoarthritis. Methods: By constructing an osteoarthritis model, the knee joint tissue of the model was observed using hematoxylin and eosin staining (HE) and computed tomography (CT). Detection of miR-34a and Klotho expression by fluorescent quantitative polymerase chain reaction (PCR) and Western blot. The lncRNA MEG3 overexpression vector was constructed and transfected into C28/I2 cells. Reverse transcription quantitative polymerase chain reaction (RT-qPCR) was used to detect the results of lncRNA MEG3 and miR-34a expression in each group of cells, and Western blot was used to detect the results of Klotho, recombinant fibroblast growth factor 23 (FGF23), B-cell lymphoma-2 (Bcl-2), BCL2-associated X (Bax), Transforming growth factor beta 1 (TGF-ß1), cysteinyl aspartate specific proteinase 3 (Caspase3) and cysteinyl aspartate specific proteinase 8 (Caspase8) protein expression. Results: Compared with the control group, HE and CT results showed significant pathological changes in the knee joint of the osteoarthritis model mice. and Klotho expression was significantly decreased and miR-34a expression was significantly increased in the model group (P<0.05). Compared with those in the control group, the expression levels of lncRNA MEG3, Klotho, FGF23, and Bcl-2 decreased significantly and the expression levels of microRNA-34a (miR-34a), Bax, TGF-ß1, Caspase 3, and Caspase 8 increased sharply (P<0.05) in the lipopolysaccharides (LPS) group. Meanwhile, lncRNA MEG3 overexpression upregulated the expression of miR-34a, Bax, TGF-ß1, Caspase3 and Caspase8, and downregulated the expression of Klotho, FGF23 and Bcl-2. Conclusions: lncRNA MEG3 regulated the expression of FGF23, Bcl-2, Bax, TGF-ß1, Caspase 3, and Caspase 8 by regulating the miR-34a/Klotho axis, thereby affecting the progress of OA.

LncRNA MEG3 promotes osteogenesis of hBMSCs by regulating miR-21-5p / SOD3 axis.

BACKGROUND: This study aimed to investigate the role of long non-coding (Lnc) RNA MEG3 on the osteogenesis of human bone marrow mesenchymal stem cells (hBMSCs). MATERIALS AND METHODS: The binding of miR-21-5p to LncRNA MEG3 and SOD3 was determined using luciferase reporter assay; fluorescence quantitative PCR was used to detect the expression of LncRNA MEG3 at different induction times. hBMSCs were transfected with LncRNA MEG3 overexpression vector and induced for osteoblasts for 14 days. Alkaline phosphatase (ALP) staining, and alizarin red staining were used to detect bone differentiation, immunofluorescence assays were used to detect the expression of SOD3 and COL2A1. RESULTS: Luciferase reporter assay revealed that miR-21-5p bond to LncRNA MEG3 and SOD3. Flow cytometry analysis showed that hBMSCs were highly pure. After osteogenic induction for 14 days, compared with the control group, the overexpression of LncRNA MEG3 significantly increased the activity of ALP and enhanced the formation of calcium nodules in hBMSCs. The overexpression also increased the expression of COL2A1 and SOD3 significantly (P<0.05). CONCLUSIONS: LncRNA MEG3 can promote the osteogenesis and bone regeneration of hBMSCs and increasing the expression of SOD3 and COL2A1 via targeting the miR-21-5p/SOD3 axis.

Bcl-xL expression following articular cartilage injury and its effects on the biological function of chondrocytes.

This study aimed to investigate the expression of B-cell lymphoma-extra large (Bcl-xL) in cartilage tissues following articular cartilage injury and to determine its effects on the biological function of chondrocytes. A total of 25 necrotic cartilage tissue samples and 25 normal tissue samples were collected from patients diagnosed with osteoarthritis at our hospital from December 2015 to December 2018. The mRNA expression levels of Bcl-xL, caspase-3, and matrix metalloproteinase-3 (MMP-3) in the normal and necrotic tissues were examined via quantitative polymerase chain reaction, and their protein expression levels were detected via western blotting. The expression levels of Bcl-xL, insulin-like growth factor-1 (IGF-1), and bone morphogenetic protein (BMP) were significantly lower but those of caspase-3, MMP-3, interleukin-1ß (IL-1ß), and chemokine-like factor 1 (CKLF1) levels were markedly higher in necrotic cartilage tissues than in normal tissues. Following cell transfection, the expression levels of Bcl-xL, IGF-1, and BMP were remarkably higher but those of caspase-3, MMP-3, IL-1ß, and CKLF1 were notably lower in the Si-Bcl-xL group than in the NC group. The Si-Bcl-xL group showed significantly lower cell growth and noticeably higher apoptosis rate than the NC group (normal control group). The expression of Bcl-xL is reduced following articular cartilage injury, and this reduction promotes the proliferation and inhibits the apoptosis of chondrocytes. Therefore, Bcl-xL could serve as a relevant molecular target in the clinical practice of osteoarthritis and other diseases causing cartilage damage.

The reassuring CT scan with a lethal diagnosis.

We discuss an interesting case of a patient who presented with symptoms of abdominal and worsening chronic back pain with a known history of abdominal aortic aneurysm.

[The methods of shorting proximal femoral and total hip arthroplasty for Crowe IV dysplastic hip of adults].

OBJECTIVES: To discuss the methods and outcome of shorting proximal femoral and total hip arthroplasty for Crowe IV dysplastic hip of adults. METHODS: From July 2000 to February 2006, 13 cases of osteoarthritis secondary to severe development dysplastic hip were treated by total hip replacement and the shorting proximal femoral. RESULTS: The duration of follow-up ranged from 4 months to 55 months. The average score increased from 36.9 to 84.1 points after the surgery according to Harris. All the patients could walk independently. Their paces were improved obviously and the function of their hips was satisfactory. CONCLUSIONS: The treatment by total hip arthroplasty and the shorting of posterior femoral is effective and efficient for osteoarthritis secondary to Crowe IV development dysplastic hip in adults. The long-term followup is necessary for further study.

DNA-functionalized gold nanoparticle-based fluorescence polarization for the sensitive detection of silver ions.

Despite their practical applications, Ag+ ions are environmental pollutants and affect human health. So the effective detection methods of Ag+ ions are imperative. Herein, we developed a simple, sensitive, selective, and cost-effective fluorescence polarization sensor for Ag+ detection in aqueous solution using thiol-DNA-functionalized gold nanoparticles (AuNPs). In this sensing strategy, Ag+ ions can specifically interact with a cytosine-cytosine (CC) mismatch in DNA duplexes and form stable metal-mediated cytosine-Ag+-cytosine (C-Ag+-C) base pairs. The formation of the C-Ag+-C complex results in evident changes in the molecular volume and fluorescence polarization signal. To achieve our aims, we prepared two complementary DNA strands containing C-base mismatches (probe A: 5'-SH-A10-TACCACTCCTCAC-3' and probe B: 5'-TCCTCACCAGTCCTA-FAM-3'). The stable hybridization between probe A and probe B occurs with the formation of the C-Ag+-C complex in the presence of Ag+ ions, leading to obvious fluorescence quenching in comparison to the system without AuNP enhancement. The assay can be used to identify nanomolar levels of Ag+ within 6 min at room temperature, and has extremely high specificity for Ag+, even in the presence of higher concentrations of interfering metal ions. Furthermore, the sensor was successfully applied to the detection of Ag+ ions in environmental water samples and showed excellent selectivity and high sensitivity, implying its promising application in the future.

Bcl-xL expression improves the therapeutic effect of human umbilical cord stem cell transplantation on articular cartilage injury in rabbit.

BACKGROUND: To investigate the therapeutic effect of transplantation of B-cell lymphoma-extra large (Bcl-xL) gene modified human umbilical cord blood stem cells (HUCSCs) on rabbit articular cartilage injury. MATERIALS AND METHODS: HUCSCs were isolated and identified. Lentiviral encoding Bcl-xL was applied to modify HUCSCs. The effects of Bcl-xL overexpression on apoptosis and related gene expression after differentiation induction of HUCSCs were detected. Additionally, the efficiency of transplantation of Bcl-xL gene modified HUCSCs on articular cartilage injury were evaluated. RESULTS: HUCSCs could differentiate into chondrocytes after induction. Compared with control group, the apoptosis after induction was significantly elevated, but reduced by Bcl-xL gene overexpression. The differentiation of HUCSCs into chondrocytes was displayed by expression of type II collagen (CII), but accompanying with expression of caspase-3 and matrix metalloproteinase-3 (MMP-3). By contrast, Bcl-xL gene overexpression reduced caspase-3 and MMP-3 expression, but further increased CII expression. Pathological staining showed that Bcl-xL gene modified HUCSCs could obviously repair cartilage injury. Compared with sham control group, the expression of caspase-3 and MMP-3 in model group was significantly up-regulated, while the expression of CII was significantly down-regulated. Transplantation of HUCSCs could ameliorate the injury, while Bcl-xL modification could improve the therapeutic effect of transplantation of HUCSCs. Moreover, Bcl-xL modification could further decrease cartilage injury-induced expression of caspase-3 and MMP-3, and improve the expression of CII compared with transplantation of normal HUCSCs. CONCLUSIONS: Bcl-xL gene modification decreases cell differentiation-induced apoptosis and improves the efficiency of HUCSCs transplantation in the repairing of cartilage injury.

Exploring the interaction of silver nanoparticles with lysozyme: Binding behaviors and kinetics.

The role of nanoparticle interaction with biomolecules to form a biocorona is the key to nanoparticle behavior and its consequences in the physiological environment. Since the adsorbed biocorona decides the fate of a nanomaterials in vivo, and thus a comprehensive understanding of the dynamic interactions of the proteins with the nanoparticle is imperative. Herein we investigate the interaction of a model protein, lysozyme with silver nanoparticles (AgNPs) using fluorescence, synchronous fluorescence, UV-vis absorption spectrum and circular dichroism (CD) techniques under the physiological conditions. The results indicated that the binding of AgNPs to lysozyme may be a static quenching mechanism. With the analysis of the fluorescence spectral data, the binding constants and the thermodynamic parameters were determined, which suggests that the binding of AgNPs to lysozyme is a spontaneous process. Moreover, it was demonstrated that the main acting forces between AgNPs and lysozyme may be hydrophobic interactions. At the same time, the conformational change of lysozyme induced by AgNPs was investigated with synchronous fluorescence spectroscopy and CD techniques. The results of kinetic studies reveal that the adsorption of lysozyme on AgNPs surface tends to follow pseudo-second-order kinetic characteristic with obvious hysteresis effect.

Inhibition of microRNA-21 decreases the invasiveness of fibroblast-like synoviocytes in rheumatoid arthritis via TGFß/Smads signaling pathway.

OBJECTIVES: MicroRNA-21 (miR21) is aberrantly elevated in rheumatoid arthritis (RA) patients, the significance of this microRNA in RA pathogenesis and treatment, however, has not been investigated. In this study, by using RA-derived fibroblast-like synoviocyte (FLS) cells as a model, we investigated the effect and corresponding mechanism of miR21 inhibition on FLSs invasion. MATERIALS AND METHODS: miR21 expression in synovial tissue and FLSs in RA patients and non-RA controls were determined by stem-loop RT-PCR. The effect of miR21 on FLSs viability and invasiveness were evaluated using miR21 inhibition. Cell viability was evaluated by MTT assay and the expression of genes at mRNA and protein levels was determined by RT-PCR and Western blot, respectively. RESULTS: Our results showed that miR21 expression was highly increased in synovial tissue and FLSs in RA patients. Also, we reported that miR21 inhibitor treatment could significantly suppress the invasiveness of FLSs without affecting cell viability. The decreased FLSs invasion by miR21 inhibition was associated with down-regulated expression of matrix metalloproteinase (MMP)-1, MMP3, and MMP13. Further analysis revealed that miR21 inhibition could suppress the expression of TGFß1 and Smad4, but promote that of Smad7. Moreover, suppression of FLS invasion and MMPs expression by miR21 treatment could be counteracted by additional TGFß1 treatment. CONCLUSION: Our results indicated that miR21 inhibition can down-regulate the expression of MMP1, MMP3, and MMP13 and consequently suppress the invasiveness of FLS, which is achieved through TGFß1/Smad4/7 signaling pathway. The findings of this study could offer a novel approach for RA treatment.