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| 1 | Establishing proof of concept:Platelet-rich plasma and bone marrow aspirate concentrate may improve cartilage repair following surgical treatment for osteochondral lesions of the talus显示文摘Osteochondral lesions of the talus are common injuries in the athletic patient. They present a challenging clinical problem as cartilage has a poor potential for healing. Current surgical treatments consist of reparative(microfracture) or replacement(autologous osteochondral graft) strategies and demonstrate good clinical outcomes at the short and medium term follow-up. Radiological findings and second-look arthroscopy however, indicate possible poor cartilage repair with evidence of fibrous infill and fissuring of the regenerative tissue following microfracture. Longer-term follow-up echoes these findings as it demonstrates a decline in clinical outcome. The nature of the cartilage repair that occurs for an osteochondral graft to become integrated with the native surround tissue is also of concern. Studies have shown evidence of poor cartilage integration,with chondrocyte death at the periphery of the graft, possibly causing cyst formation due to synovial fluid ingress. Biological adjuncts, in the form of platelet-rich plasma(PRP) and bone marrow aspirate concentrate(BMAC), have been investigated with regard to their potential in improving cartilage repair in both in vitro and in vitro settings. The in vitro literature indicates that these biological adjuncts may increase chondrocyte proliferation as well as synthetic capability, while limiting the catabolic effects of an inflammatory joint environment. These findings have been extrapolated to in vitro animal models, with results showing that both PRP and BMAC improve cartilage repair. The basic science literature therefore establishes the proof of concept that biological adjuncts may improve cartilage repair when used in conjunction with reparative and replacement treatment strategies for osteochondral lesions of the talus. | Niall A Smyth Christopher D Murawski Amgad M Haleem Charles P Hannon Ian Savage-Elliott John G Kennedy | 2012 | World Journal of Orthopedics2012，3，7： | 8 |
| 2 | Platelet-rich plasma increases transforming growth factor-beta1 expression at graft-host interface following autologous osteochondral transplantation in a rabbit model显示文摘AIM: To explore the effect of platelet-rich plasma on protein expression patterns of transforming growth factor-beta1(TGF-β1) in cartilage following autologous osteochondral transplantation(AOT) in a rabbit knee cartilage defect model.METHODS: Twelve New Zealand white rabbits received bilateral AOT. In each rabbit, one knee was randomized to receive an autologous platelet rich plasma(PRP) injection and the contralateral knee received saline injection. Rabbits were euthanized at 3, 6 and 12 wk post-operatively. Articular cartilage sections were stained with TGF-β1 antibody. Histological regions of interest(ROI)(left, right and center of the autologous grafts interfaces) were evaluated using Meta Morph. Percentage of chondrocytes positive for TGF-β1 was then assessed.RESULTS: Percentage of chondrocytes positive for TGF-β1 was higher in PRP treated knees for selected ROIs(left; P = 0.03, center; P = 0.05) compared to control and was also higher in the PRP group at each post-operative time point(P = 6.6 × 10^(-4), 3.1 × 10^(-4) and 7.3 × 10^(-3) for 3, 6 and 12 wk, respectively). TGF-β1 expression was higher in chondrocytes of PRP-treated knees(36% ± 29% vs 15% ± 18%)(P = 1.8 × 10^(-6)) overall for each post-operative time point and ROI. CONCLUSION: Articular cartilage of rabbits treated with AOT and PRP exhibit increased TGF-β1 expression compared to those treated with AOT and saline. Our findings suggest that adjunctive PRP may increase TGF-β1 expression, which may play a role in the chondrogenic effect of PRP in vivo. | Lorraine A Boakye Keir A Ross John M Pinski Niall A Smyth Amgad M Haleem Charles P Hannon Lisa A Fortier John G Kennedy | 2015 | World Journal of Orthopedics2015，6，11： | 7 |
| 3 | Platelet-rich plasma for muscle injuries: A systematic review of the basic science literature显示文摘BACKGROUND Platelet-rich plasma(PRP) is an increasingly used biologic adjunct for muscle injuries, as it is thought to expedite healing. Despite its widespread use, little is known regarding the mechanisms by which PRP produces its efficacious effects in some patients.AIM To clarify the effects of PRP on muscular pathologies at the cellular and tissue levels by evaluating the basic science literature.METHODS A systematic review of PubMed/MEDLINE and EMBASE databases was performed using the Preferred Reporting Items for Systematic Reviews and MetaAnalyses(PRISMA) guidelines and checklist. Level III in vivo and in vitro studies examining PRP effects on muscles, myocytes and/or myoblasts were eligible for inclusion. Extracted data included PRP preparation methods and study results.RESULTS Twenty-three studies were included(15 in vivo, 6 in vitro, 2 in vitro/in vivo). Only one reported a complete PRP cytology(platelets, and red and white blood cell counts). Five in vitro studies reported increased cellular proliferation, four reported increased gene expression, and three reported increased cellular differentiation. Five in vivo studies reported increased gene expression, three reported superior muscle regeneration, and seven reported improved histological quality of muscular tissue.CONCLUSION The basic science literature on the use of PRP in muscle pathology demonstrates that PRP treatment confers several potentially beneficial effects on healing in comparison to controls. Future research is needed to determine optimal cytology,dosing, timing, and delivery methods of PRP for muscle pathologies. | Kyle N Kunze Charles P Hannon Jared D Fialkoff Rachel M Frank Brian J Cole | 2019 | World Journal of Orthopedics2019，10，7： | 6 |
| 4 | A new regulatory motif in cell cycle control causing specific inhibition of cyclinD/CDK4显示文摘 | Serrano M Hannon Gj Beach D | | 0，，： | 2 |
| 5 | A new regulatory motif in cell-cycle control causing specific inhibition of cyclinD/CDK4显示文摘 | Serrano M Hannon GT Beach D | 1993 | Nature1993，366，6： | 1 |
| 6 | The rest is silence显示文摘 | Bernstein E Denli A M Hannon G J | 2001 | RNA2001，7，11： | 1 |
| 7 | A new regulatory motif in cell-cycle control causing specific inhibition of cyclin D/CDK4 显示文摘 | SERRANO M HANNON G J BEACH D | 2003 | Nature2003，366，6456： | 1 |
| 8 | RNaseⅢenzymes and theinitiation of gene silencing显示文摘 | CARMELL M A HANNON G J | 2004 | Nat Struct Mol Biol2004，11，3： | 1 |
| 9 | Generalized universal Reynolds equations for variable properties fluid-film lubrification and variable geometry selfacting bearings显示文摘 | Hannon W M Braun M J Hariharan S I | 2004 | Tribology Transactions2004，47，2： | 1 |
| 10 | A new regulatory motif in cell -cycle control causing specific inhibition of cycle D/CDK4显示文摘 | Serrano M Hannon G J Beach D | 1993 | Nature1993，366，： | 1 |
| 11 | FGF-23 in fibrous dysplasia of bone and its relationship to renal phosphate wasting显示文摘 | Riminucci M Collins MT Fedarko NS Cherman N Corsi A White KE Waguespack S Gupta A Hannon T Econs MJ Bianco P Gehron Robey P | | 0，，： | 1 |
| 12 | The impact of voluntary fortification of foods on micronutrient intakes in Irish adults显示文摘 | Hannon EM Kiely M Flynn A | 2007 | BritJNutr2007，97，： | 1 |
| 13 | The rest is silence显示文摘 | Bernstein E Denli A M Hannon G J | 2001 | RNA2001，7，： | 1 |
| 14 | A new regulatory motif in cell cycle control causing specific inhibitory of cyclin DP cdk4显示文摘 | Serrano M Hannon GJ Beach D | 1993 | Nature1993，366，6456： | 1 |
| 15 | A new regulatory motif in cell-cycle control causing specific inhibition of cyclin D/CDK4 显示文摘 | Serrano M Hannon GJ Beach D | 1993 | Nature1993，366，6456： | 1 |
| 16 | Post-transcriptional gene silencing by double-stranded RNA 显示文摘 | Hammond S M Caudy A A Hannon G J | 2001 | Nat Rev Genet2001，2，： | 1 |
| 17 | Assembly of nano-scale circular supramolecular arrays through π-π aggregation of arc-shapedhelicate units 显示文摘 | Childs L J Alcock N W Hannon M J | 2001 | Angew Chem Int Ed2001，40，： | 1 |
| 18 | A new regulatory motif in cell-cy- cle control causing specific inhibition of cyclin D/CDK4 显示文摘 | Serrano M Hannon GJ Beach D | 1993 | Na- ture1993，366，： | 1 |
| 19 | Dealing with betrayal in close relationships:does commitment promote forgiveness显示文摘 | Finkel EJ Rusbult CE Kumashiro M et al. Hannon PA | | 0，，06： | 1 |
| 20 | The Value of the World's Ecosystem Services and Natural Capital显示文摘 | Costanza R d'Arge R de Groot R Farberk S Grasso M Hannon B Limburg K Naeem S O'Neill R V Paruelo J Raskin R G Suttonkk P van den Belt M | | 0，，6630： | 1 |
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