A bone scaffold material (nano-HA/ collagen/PLA composite) was developed by biomimetic synthesis. It shows some features of natural bone both in main composition and hierarchical microstructure. Nano-hydroxyapatite and collagen assembled into mineralized fibril. The three-dimensional porous scaffold materials mimic the microstructure of cancellous bone. Cell culture and animal model tests showed that the composite material is bioactive. The osteoblasts were separated from the neonatal rat calvaria. Osteoblasts adhered, spread, and proliferated throughout the pores of the scaffold material within a week. A 15-mm segmental defect model in the radius of the rabbit was used to evaluate the bone-remodeling ability of the composite. Combined with 0.5 mg rhBMP-2, the material block was implanted into the defect. The segmental defect was integrated 12 weeks after surgery, and the implanted composite was partially substituted by new bone tissue. This scaffold composite has promise for the clinical repair of large bony defects according to the principles of bone tissue engineering.
A designed hierarchical structure was made by self-assembly of nano-fibrils of mineralized collagen resembling extracellular matrix. The collagen fibrils were formed by self-assembly of collagen triple helices. Hydroxyapatite (HA) crystals grew on the surface of these fibrils in such a way that their c-axes were oriented along the longitudinal axes of the fibrils. The mineralized collagen fibrils aligned parallel to each other to form mineralized collagen fibers. For the first time, the new hierarchical self-assembly structure of collagen−hydroxyapatite composite was verified by conventional and high-resolution transmission electron microscopy.
APOBEC3G (also known as CEM15) is an innate intracellular antiretroviral factor that is counteracted by the Vif protein of lentiviruses. While APOBEC3G orthologues from several species are active against a broad range of retroviruses, given Vif proteins have a narrow spectrum of activity. For instance, HIV-1 Vif efficiently blocks APOBEC3G from human but not African green monkey (AGM), whereas the reverse is observed with SIV AGM Vif. Here, we demonstrate that a single amino acid at position 128 of human and AGM APOBEC3G governs the virus-specific sensitivity of these proteins to Vif-mediated inhibition. Furthermore, we show that this phenotype correlates with the ability of Vif to bind APOBEC3G and interfere with its incorporation into virions. These results shed light on an important determinant of the tropism of primate lentiviruses.The replication of a virus within its host and its spread to a new species require that innate lines of defense be overcome. APOBEC3G 1 is a cytidine deaminase that confers broad protection against retroviruses and limits the cross-species transmission of these pathogens (1-5). Packaged during viral assembly, APOBEC3G associates with the retroviral reverse transcription complex, where it deaminates cytosine residues to uracil in the growing minus-strand viral DNA (4 -7). These U-rich transcripts are either degraded or yield proviruses that are largely non-functional due to G-to-A hypermutation. APOBEC3G is counteracted by the Vif (virion infectivity factor) protein of lentiviruses, which associates with the enzyme to prevent its virion incorporation and trigger its proteasomal degradation (5, 8 -12). In the absence of Vif, human APOBEC3G is active against a broad spectrum of retroelements, as it can inhibit the replication of lentiviruses such as human and simian immunodeficiency virus (HIV and SIV, respectively) and equine infectious anemia virus (EIAV), of the gammaretrovirus murine leukemia virus (MLV) (4, 7), and of the hepadnavirus hepatitis B virus (13). APOBEC3G orthologues are also effective against several of these viruses. Vifdefective HIV-1, for instance, is blocked by APOBEC3G from human, rhesus macaque, African green monkey, and mouse (5). In contrast, a far greater degree of specificity is noted in the Vif sensitivity of these antiviral factors. As an example, the Vif protein of HIV-1 can only counter human and chimpanzee APOBEC3G, but is ineffective against the rhesus macaque, AGM, and mouse orthologues of the enzyme. Conversely, Vif from SIV AGM is active against AGM but not human APOBEC3G (5). Here, we took advantage of these speciesspecific differences to explore further the mechanism of Vif action. EXPERIMENTAL PROCEDURESExpression Vectors-Wild type and vif-defective HIV-1 proviral clones were described previously (14). To permit its trans-expression, a His-tagged form of HIV-1 Vif was inserted into the pEF1/Myc-His plasmid (Invitrogen), yielding the pEF1-VifHis plasmid. The plasmids expressing the HA-tagged form of huAPOBEC3G (3) and the SIV AGM.TAN Vif (pgVif/...
Nanofibers exist widely in human tissue with different patterns. Electrospinning nanotechnology has recently gained a new impetus due to the introduction of the concept of biomimetic nanofibers for tissue regeneration. The advanced electrospinning technique is a promising method to fabricate a controllable continuous nanofiber scaffold similar to the natural extracellular matrix. Thus, the biomedical field has become a significant possible application field of electrospun fibers. Although electrospinning has developed rapidly over the past few years, electrospun nanofibers are still at a premature research stage. Further comprehensive and deep studies on electrospun nanofibers are essential for promoting their biomedical applications. Current electrospun fiber materials include natural polymers, synthetic polymers and inorganic substances. This review briefly describes several typically electrospun nanofiber materials or composites that have great potential for tissue regeneration, and describes their fabrication, advantages, drawbacks and future prospects.
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