Nitric oxide(NO) induces apoptosis in human osteoblasts. Treatment with exogenous NO donors, SNAP (S-Nitroso-N-acetylpenicillamine) and SNP (sodium nitroprusside), to MG-63 osteoblasts resulted in apoptotic morphological changes, as shown by a bright blue-fluorescent condensed nuclei and chromatin fragmentation by fluorescence microscope of Hoechst 33258-staining. The activities of caspase-9 and the subsequent caspase-3-like cysteine proteases were increased during NO-induced cell death. Pretreatment with Z-VAD-FMK (a pan-caspase inhibitor) or Ac-DEVD-CHO (a specific caspase-3 inhibitor) abrogated the NO-induced cell death. The NO donor markedly activated JNK, a stress-activated protein kinase in the human osteoblasts. This study showed that the inhibition of the JNK pathway markedly reduced NO-induced cell death. But neither PD98059 (MEK inhibitor) nor SB203580 (p38 MAPK inhibitor) had any effect on NO-induced death. Taken together, these results suggest that JNK/SAPK may be related to NO-induced apoptosis in MG-63 human osteoblasts.
Apolipophorin‐III is a hemolymph protein whose function is to facilitate lipid transport in an aqueous medium. Recently, apolipophorin‐III in Galleria mellonella larvae showed to play an unexpected role in insect immune activation. We identified the cDNA sequence of Hyphantria cunea apolipophorin‐III by oligonucleotide‐primed amplification, and 5′‐ and 3′‐RACE PCR. Since H. cunea has an unusually low level of apolipophorin‐III in the hemolymph, a recombinant apolipophorin‐III was overexpressed using a baculovirus expression system to investigate its biological activity. Recombinant apolipophorin‐III and E. coli were injected into the hemocoel of last instar larvae, and the changes in apolipophorin‐III in hemolymph was determined by Western blot. Injection of apolipophorin‐III induced a slight increase of apolipophorin‐III in the recipients'hemolymph. While E. coli injection led to remarkably increased concentration of apolipophorin‐III in hemolymph. To investigate the induction of antimicrobial peptide by the injection of recombinant apoLp‐III and E. coli, Northern blot was performed. Apolipophorin‐III injection as well as bacterial injection into the larvae showed the induction on the expression of lysozyme gene. Apolipophorin‐III is apparently related to the immune response through an unknown mechanism. The role of apolipophorin‐III in insect immunity should be related to the activation of transcription factor of antimicrobial peptide.
Background: The use of three-dimensional printing (3D) application technology continues to shine in oral and maxillofacial surgery. Current applications of in maxillofacial surgery include trauma surgery, pathology induced defects, tissue engineering, complex temporomandibular joint reconstruction and correction of complicated facial asymmetry. Objective: The aims of this study were to review the current methods of 3D printing in the literature and explore their application in oral and maxillofacial surgery. Methods: A PubMed search was performed to review current methods of 3D printing within surgery and to look at their merits and pitfalls. Their use within facial surgery was then noted. Findings: We found there were three types of technology mainly used in surgical 3D printing. The main use within facial surgery included 3D reconstruction planning, custom implants and novel tissue engineering. Conclusion: 3D printing technology in surgery has advanced greatly since its infancy in 1994. Its use within maxillofacial surgery continues to show growth and exciting prospect.
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