Modified TIG Welding Joint Process: An Approach to Improve Microstructure and Fracto-Mechanical Behavior by MWCNTs Inducement in Al-Mg-Si Alloy.

This work provides a comprehensive investigation of multi-walled carbon nanotubes (MWCNTs) inducement in weldment and their apparent effect on the microstructure, %elongation and ultimate fracture behavior of Al-Mg-Si alloy referring modified tungsten inert gas (TIG) welding joints. Serious experimental work is carried out at 1 wt%, 1.5 wt%, and 2 wt% of MWCNTs to provide a gradually increasing heterogeneous nucleation. The behavior of grain morphology showed the pure field of epitaxial growth without MWCNTs, and the forestry type morphology for 1 wt% MWCNTs at low welding currents (160 A), though there was a noticeable conversion into equiaxed (EQZ) grains filled with inter-dendritic particles at high welding currents (180 A and 200 A) for 1.5 wt% and 2 wt% of MWCNTs. Moreover, the formation of a cellular type network above the fusion line predominated initially at all parameters. Conversely, fine EQZ grains were formed as they moved upward into the welded zone (WZ) explicitly at a high heat input. A conceptual pictorial model is presented in the study which summarized the behavior of morphological changes at the utilized parameters. The welded joints have demonstrated an increasing trend of strength and %elongation in contrast to joints without added MWCNTs. Comparative results have shown an exceptional increment of 71 to 76% and 67 to 75% of elongation up to ultimate tensile strength (UTS), and a fracture point that was clinched for 1 wt% and 1.5 wt% MWCNTs at 180A. From macro to micro-examination of the fracture surfaces, pure ductile modes constituting elliptical cup and cone type isotropic flow was evident in all specimens. Detailed confirmation of the pull-out fracture mode of MWCNTs has highlighted in the scanning electron microscope (SEM) images that intimated a methodical contribution in load-transfer from matrix to the fiber under axial load. Overall, a concise en-route for MWCNTs inducement is well-appointed through tube fillers along with an activating facilitator (TiO2) in contrast to stereotype fillers for improved behavior termed as modified TIG welding joint process in study.

Poly(lactide-co-glycolide)/fibrin gel construct as a 3D model to evaluate gene therapy of cartilage in vivo.

Combination of gene therapy with tissue engineering can enhance the interplay between cells and matrix, leading to better restoration and regeneration of tissues and organs in vivo. In this study the PLGA/fibrin gel hybrids were employed to load lipofectamine/pDNA-TGF-ß1 complexes and mesenchymal stem cells (MSCs) (experimental group), acting as a cartilage-mimetic tissue platform. The gene complexes distributed more evenly in the hybrid scaffolds, whereas they adhered onto the pore walls of the PLGA sponges. The filled fibrin gel rendered gene release in a slower manner, too. Moreover, the fibrin gel entrapped MSCs and contributed to a higher cell loading density in the hybrid constructs. In vivo assay showed that in the defects implanted with the experimental constructs both gene and protein expression levels of TGF-ß1 were significantly higher than those of the fibrin-free group at weeks 1, 3, and 6 after surgery. The full articular cartilage defects repaired by the experimental group for 12 w were resurfaced by neo-tissues with a similar thickness, cell arrangement, and color to the normal neighboring cartilage and abundant glycosaminoglycans.

Influence of the molecular weight of poly(lactide-co-glycolide) on the in vivo cartilage repair by a construct of poly(lactide-co-glycolide)/fibrin gel/mesenchymal stem cells/transforming growth factor-ß1.

The poly(lactide-co-glycolide) (PLGA, LA/GA 75/25) sponges with different weight average molecular weights (Mw 52, 122, and 177 kDa) were fabricated and were used to build the constructs of PLGA/fibrin gel/mesenchymal stem cells (MSCs)/transforming growth factor-ß1 (TGF-ß1). The PLGA 177 with the highest Mw (177 kDa) had the fastest degradation rate at the initial stage, whereas the PLGA 122 had the moderate degradation rate and smallest mass loss. After implantation in rabbit knees for 12 weeks, the full-thickness defects (both cartilage and subchondral bone were destroyed with a diameter and depth of 4 mm) repaired by the PLGA 122 group had formed a hyaline cartilage-like tissue with abundant glycosaminoglycans on the top layer and subchondral bone on the bottom layer. The group also achieved the best macroscopic (11.3 ± 0.8) and histological scoring (Wakitani, 0.5 ± 0.6). To unveil the mechanism of the cartilage repair outcome and the PLGA degradation behaviors, the chondrogenesis-related genes, inflammatory cytokines, and matrix metalloproteinase (MMP) activity were analyzed by quantitative reverse transcription-polymerase chain reaction at week 1, 3, and 6 postsurgery. At each time point, the regenerated tissues by the PLGA 122 group had the highest mRNA expression of SOX9 and collagen type II, but the smallest mRNA expression of interleukin-1ß and tumor necrosis factor α, and MMP-13 and MMP-3. In summary, as a scaffolding matrix, the PLGA with different Mw shows a huge difference in cartilage regeneration in vivo. The one with a moderate Mw (122 kDa) causes the weakest inflammatory response and results in the best cartilage regeneration.

Fabrication of poly(lactide-co-glycolide) scaffold filled with fibrin gel, mesenchymal stem cells, and poly(ethylene oxide)-b-poly(L-lysine)/TGF-ß1 plasmid DNA complexes for cartilage restoration in vivo.

A poly (lactide-co-glycolide) (PLGA) scaffold filled with fibrin gel, mesenchymal stem cells (MSCs) and poly(ethylene oxide)-b-poly (L-lysine) (PEO-b-PLL)/pDNA-TGF-ß1 complexes was fabricated and applied in vivo for synchronized regeneration of cartilage and subchondral bone. The PEO-b-PLL/pDNA-TGF-ß1 complexes could transfect MSCs in vitro to produce TGF-ß1 in situ and up regulate the expression of chondrogenesis-related genes in the construct. The expression of heterogeneous TGF-ß1 in vivo declined along with the prolongation of implantation time, and lasted for 3 and 6 weeks in the mRNA and protein levels, respectively. The constructs (Experimental group) of PLGA/fibrin gel/MSCs/(PEO-b-PLL/pDNA-TGF-ß1 complexes) were implanted into the osteochondral defects of rabbits to restore the functional cartilages, with gene-absent constructs as the Control. After 12 weeks, the Experimental group regenerated the neo-cartilage and subchondral bone with abundant deposition of glycosaminoglycans (GAGs) and type II collagen. The regenerated tissues had good integration with the host tissues too. By contrast, the defects were only partially repaired by the Control constructs. qRT-PCR results demonstrated that expression of the chondrogenesis-marker genes in the Experimental group was significantly higher than that of the Control group, and was very close to that of the normal cartilage tissue.

The restoration of full-thickness cartilage defects with BMSCs and TGF-beta 1 loaded PLGA/fibrin gel constructs.

Poly(lactide-co-glycolide) (PLGA) sponge was filled with fibrin gel, bone marrow mesenchymal stem cells (BMSCs) and transforming growth factor-ß1 (TGF-ß1) to obtain a construct for cartilage restoration in vivo. The PLGA sponge lost its weight steadily in vitro, but degraded much faster in the construct of PLGA/fibrin gel/BMSCs implanted in the full-thickness cartilage defects. The in vivo degradation of the fibrin gel inside the construct was prolonged to 12 wk too. The CM-DiI labeled allogenic BMSCs were detectable after transplantation (implantation) into the defects for 12 wk by small animal in vivo fluorescence imaging and confocal laser scanning microscopy. In vivo repair experiments were firstly performed by implantation of the PLGA/fibrin gel/BMSCs and PLGA/BMSCs constructs into full-thickness cartilage defects (3 mm in diameter and 4 mm in depth) of New Zealand white rabbits for 12 wk. The defects implanted with the PLGA/fibrin gel/BMSCs constructs were filled with cartilage-like tissue containing collagen type II and glycosaminoglycans (GAGs), while those by the PLGA/BMSCs constructs were filled with fibrous-like tissues. To repair the defects of larger size (4 mm in diameter), addition of growth factors was mandatory as exemplified here by further loading of TGF-ß1. Implantation of the PLGA/fibrin gel/BMSCs/TGF-ß1 constructs into the full-thickness cartilage defects for 12 wk resulted in full restoration of the osteochondral tissue. The neo-cartilage integrated well with its surrounding cartilage and subchondral bone. Immunohistochemical and GAGs staining confirmed the similar distribution of collagen type II and GAGs in the regenerated cartilage as that of hyaline cartilage. The quantitative reverse transcription-polymerase chain reaction (qRT-PCR) revealed that the cartilage special genes were significantly up-regulated compared with those of the TGF-ß1 absent constructs.