Novel composite meshes to evaluate their structural property and in vivo biocompatibility for tissue repair

Composite meshes of different types have been prepared and used for tissue repair in pelvic floor disorder. An interlocking texture mesh (inter-mesh) and a membrane coated mesh (electro-mesh) have been used based on their structural property and biocompatibility. The proportion of degradation material in inter-mesh (69.6%) is found extremely higher than that of electro-mesh (3.22%), thus leading to higher product weight (65.50±2.31 g/m2) and thickness (0.500±0.025 mm). After 4 weeks of implantation in animal experiment, inter-mesh with surrounding tissues is observed to have higher breaking strength in tensile behavoir and better flexibility. Tissues on inter-mesh are found to grow faster with larger thickness (0.76±0.033 mm). The surface area loss of inter-mesh (2.49±0.25%) is much less than that of electro-mesh (7.49±0.63 %) within the first 2 weeks of implantation. However, the material’s degradation is accelerated after 2 weeks, leading to a higher shrinkage of 13.12±1.48 %

Novel composite meshes to evaluate their structural property and in vivo biocompatibility for tissue repair

404-410Composite meshes of different types have been prepared and used for tissue repair in pelvic floor disorder. An interlocking texture mesh (inter-mesh) and a membrane coated mesh (electro-mesh) have been used based on their structural property and biocompatibility. The proportion of degradation material in inter-mesh (69.6%) is found extremely higher than that of electro-mesh (3.22%), thus leading to higher product weight (65.50±2.31 g/m2) and thickness (0.500±0.025 mm). After 4 weeks of implantation in animal experiment, inter-mesh with surrounding tissues is observed to have higher breaking strength in tensile behavoir and better flexibility. Tissues on inter-mesh are found to grow faster with larger thickness (0.76±0.033 mm). The surface area loss of inter-mesh (2.49±0.25%) is much less than that of electro-mesh (7.49±0.63 %) within the first 2 weeks of implantation. However, the material’s degradation is accelerated after 2 weeks, leading to a higher shrinkage of 13.12±1.48 %

Controllable sliding transfer of wafer‐size graphene

The innovative design of sliding transfer based on a liquid substrate can succinctly transfer high‐quality, wafer‐size, and contamination‐free graphene within a few seconds. Moreover, it can be extended to transfer other 2D materials. The efficient sliding transfer approach can obtain high‐quality and large‐area graphene for fundamental research and industrial applications

TNFAIP1 contributes to the neurotoxicity induced by Aβ25–35 in Neuro2a cells

Background: Amyloid-beta (Aβ) accumulation is a hallmark of Alzheimer’s disease (AD) that can lead to neuronal dysfunction and apoptosis. Tumor necrosis factor, alpha-induced protein 1 (TNFAIP1) is an apoptotic protein that was robustly induced in the transgenic C. elegans AD brains. However, the roles of TNFAIP1 in AD have not been investigated. Results: We found TNFAIP1 protein and mRNA levels were dramatically elevated in primary mouse cortical neurons and Neuro2a (N2a) cells exposed to Aβ25–35. Knockdown and overexpression of TNFAIP1 significantly attenuated and exacerbated Aβ25–35-induced neurotoxicity in N2a cells, respectively. Further studies showed that TNFAIP1 knockdown significantly blocked Aβ25–35-induced cleaved caspase 3, whereas TNFAIP1 overexpression enhanced Aβ25–35-induced cleaved caspase 3, suggesting that TNFAIP1 plays an important role in Aβ25–35-induced neuronal apoptosis. Moreover, we observed that TNFAIP1 was capable of inhibiting the levels of phosphorylated Akt and CREB, and also anti-apoptotic protein Bcl-2. TNFAIP1 overexpression enhanced the inhibitory effect of Aβ25–35 on the levels of p-CREB and Bcl-2, while TNFAIP1 knockdown reversed Aβ25–35-induced attenuation in the levels of p-CREB and Bcl-2. Conclusion: These results suggested that TNFAIP1 contributes to Aβ25–35-induced neurotoxicity by attenuating Akt/CREB signaling pathway, and Bcl-2 expression

Identification of target genes of transcription factor activator protein 2 gamma in breast cancer cells

<p>Abstract</p> <p>Background</p> <p>Activator protein 2 gamma (AP-2γ) is a member of the transcription factor activator protein-2 (AP-2) family, which is developmentally regulated and plays a role in human neoplasia. AP-2γ has been found to be overexpressed in most breast cancers, and have a dual role to inhibit tumor initiation and promote tumor progression afterwards during mammary tumorigensis.</p> <p>Methods</p> <p>To identify the gene targets that mediate its effects, we performed chromatin immunoprecipitation (ChIP) to isolate AP-2γ binding sites on genomic DNA from human breast cancer cell line MDA-MB-453.</p> <p>Results</p> <p>20 novel DNA fragments proximal to potential AP-2γ targets were obtained. They are categorized into functional groups of carcinogenesis, metabolism and others. A combination of sequence analysis, reporter gene assays, quantitative real-time PCR, electrophoretic gel mobility shift assays and immunoblot analysis further confirmed the four AP-2γ target genes in carcinogenesis group: ErbB2, CDH2, HPSE and IGSF11. Our results were consistent with the previous reports that ErbB2 was the target gene of AP-2γ. Decreased expression and overexpression of AP-2γ in human breast cancer cells significantly altered the expression of these four genes, indicating that AP-2γ directly regulates them.</p> <p>Conclusion</p> <p>This suggested that AP-2γ can coordinate the expression of a network of genes, involving in carcinogenesis, especially in breast cancer. They could serve as therapeutic targets against breast cancers in the future.</p