参考文献是学术论文的根系，是学术论文不可或缺的组成部分，下面是CN人才网为大家整理的最新临床医学毕业论文参考文献，欢迎参考~
篇一：最新临床医学毕业论文参考文献
[1] PORTER J R, RUCKH T T, POPAT K C. Bone tissue engineering: Areview in bone biomimetics and drug delivery strategies [J].Biotechnology progress, 2009, 25:1539-1560.
[2] KURTZ S M, ONG K L, SCHMIER J, et al. Future clinical and economicimpact of revision total hip and knee arthroplasty [J]. The Journal of boneand joint surgery. American volume, 2007, 89 Suppl 3:144-151.
[3] XU X, ZHANG K, ZHAO L, et al. Characteristics of three sizes of silicananoparticles in the osteoblastic cell line, MC3T3-E1 [J]. RSC Adv., 2014,4:46481-46487.
[4] NIE H, HO M L, WANG C K, et al. Bmp-2 plasmid loaded plga/hapcomposite scaffolds for treatment of bone defects in nude mice [J].Biomaterials, 2009, 30:892-901.
[5] KOLAR P, SCHMIDT-BLEEK K, SCHELL H, et al. The early fracturehematoma and its potential role in fracture healing [J]. Tissue engineering.Part B, Reviews, 2010, 16:427-434.
[6] ORYAN A, MOSHIRI A, MEIMANDI-PARIZI A. Implantation of anovel tissue-engineered graft in a large tendon defect initiatedinflammation, accelerated fibroplasia and improved remodeling of thenew achilles tendon: A comprehensive detailed study with new insights[J]. Cell and tissue research, 2014, 355:59-80.
[7] FERGUSON C, ALPERN E, MICLAU T, et al. Does adult fracture repairrecapitulate embryonic skeletal formation? [J]. Mechanisms ofdevelopment, 1999, 87:57-66.
[8] SIMON A M, MANIGRASSO M B, O'CONNOR J P. Cyclo-oxygenase 2function is essential for bone fracture healing [J]. Journal of bone andmineral research : the official journal of the American Society for Boneand Mineral Research, 2002, 17:963-976.
[9] DESCHASEAUX F, PONTIKOGLOU C, SENSEBE L. Boneregeneration: The stem/progenitor cells point of view [J]. Journal ofcellular and molecular medicine, 2010, 14:103-115.
[10] THOMAS M V, PULEO D A. Infection, inflammation, and boneregeneration: A paradoxical relationship [J]. Journal of dental research,2011, 90:1052-1061.
[11] OFFENBACHER S, ODLE B M, GREEN M D, et al. Inhibition ofhuman periodontal prostaglandin E2 synthesis with selected agents [J].Agents and actions, 1990, 29:232-238.
[12] OFFENBACHER S, HEASMAN P A, COLLINS J G. Modulation of hostPGE2 secretion as a determinant of periodontal disease expression [J].Journal of periodontology, 1993, 64:432-444.
[13] PRESHAW P M, HEASMAN P A. Prostaglandin E2 concentrations ingingival crevicular fluid: Observations in untreated chronic periodontitis[J]. Journal of clinical periodontology, 2002, 29:15-20.
[14] RAISZ L G. Prostaglandins and bone: Physiology and pathophysiology[J]. Osteoarthritis and cartilage / OARS, Osteoarthritis Research Society,1999, 7:419-421.
[15] WILLIAMS R C, JEFFCOAT M K, KAPLAN M L, et al. Flurbiprofen: Apotent inhibitor of alveolar bone resorption in beagles [J]. Science, 1985,227:640-642.
[16] WILLIAMS R C, JEFFCOAT M K, HOWELL T H, et al. Altering theprogression of human alveolar bone loss with the non-steroidalanti-inflammatory drug flurbiprofen [J]. Journal of periodontology, 1989,60:485-490.
[17] WEBER H P, FIORELLINI J P, PAQUETTE D W, et al. Inhibition ofperi-implant bone loss with the nonsteroidal anti-inflammatory drugflurbiprofen in beagle dogs. A preliminary study [J]. Clinical oralimplants research, 1994, 5:148-153.
[18] HARTEN R D, SVACH D J, SCHMELTZER R, et al. Salicylicacid-derived poly(anhydride-esters) inhibit bone resorption and formationin vivo [J]. Journal of biomedical materials research. Part A, 2005,72:354-362.
[19] REYNOLDS M A, PRUDENCIO A, AICHELMANN-REIDY M E, et al.Non-steroidal anti-inflammatory drug (NSAID) - derived poly(anhydride- esters) in bone and periodontal regeneration [J]. Current drug delivery,2007, 4:233-239.
[20] FULLER K, CHAMBERS T J. Effect of arachidonic acid metabolites onbone resorption by isolated rat osteoclasts [J]. Journal of bone andmineral research : the official journal of the American Society for Boneand Mineral Research, 1989, 4:209-215.
篇二：最新临床医学毕业论文参考文献
[1] ZUANY-AMORIM C, HASTEWELL J, WALKER C. Toll-like receptors aspotential therapeutic targets for multiple diseases [J]. Nat Rev Drug Discov,2002, 1(10): 797-807.
[2] KAWAI T, AKIRA S. The roles of TLRs, RLRs and NLRs in pathogenrecognition [J]. International immunology, 2009, 21(4): 317-37.
[3] CULLEN T W, GILES D K, WOLF L N, et al. Helicobacter pylori versus thehost: remodeling of the bacterial outer membrane is required for survival in thegastric mucosa [J]. PLoS pathogens, 2011, 7(12): e1002454.
[4] JIN M S, KIM S E, HEO J Y, et al. Crystal structure of the TLR1-TLR2heterodimer induced by binding of a tri-acylated lipopeptide [J]. Cell, 2007,130(6): 1071-82.
[5] KANG J Y, NAN X, JIN M S, et al. Recognition of lipopeptide patterns byToll-like receptor 2-Toll-like receptor 6 heterodimer [J]. Immunity, 2009, 31(6):873-84.
[6] TRIANTAFILOU M, GAMPER F G, LEPPER P M, et al. Lipopolysaccharidesfrom atherosclerosis-associated bacteria antagonize TLR4, induce formation ofTLR2/1/CD36 complexes in lipid rafts and trigger TLR2-induced inflammatoryresponses in human vascular endothelial cells [J]. Cellular microbiology, 2007,9(8): 2030-9.
[7] HAYASHI F, SMITH K D, OZINSKY A, et al. The innate immune response tobacterial flagellin is mediated by Toll-like receptor 5 [J]. Nature, 2001,410(6832): 1099-103.
[8] LUND J, SATO A, AKIRA S, et al. Toll-like receptor 9-mediated recognition ofHerpes simplex virus-2 by plasmacytoid dendritic cells [J]. The Journal ofexperimental medicine, 2003, 198(3): 513-20.
[9] DIEBOLD S S, KAISHO T, HEMMI H, et al. Innate antiviral responses bymeans of TLR7-mediated recognition of single-stranded RNA [J]. Science,2004, 303(5663): 1529-31.
[10] VAN BERGENHENEGOUWEN J, PLANTINGA T S, JOOSTEN L A, et al.TLR2 & Co: a critical analysis of the complex interactions between TLR2 andcoreceptors [J]. J Leukoc Biol, 2013, 94(5): 885-902.
[11] MEDVEDEV A E. Toll-like receptor polymorphisms, inflammatory andinfectious diseases, allergies, and cancer [J]. Journal of interferon & cytokineresearch : the official journal of the International Society for Interferon andCytokine Research, 2013, 33(9): 467-84.
[12] LI J, WANG X, ZHANG F, et al. Toll-like receptors as therapeutic targets forautoimmune connective tissue diseases [J]. Pharmacology & therapeutics, 2013,138(3): 441-51.
[13] VAZ J, AKBARSHAHI H, ANDERSSON R. Controversial role of toll-likereceptors in acute pancreatitis [J]. World journal of gastroenterology : WJG,2013, 19(5): 616-30.
[14] HACKAM D J, GOOD M, SODHI C P. Mechanisms of gut barrier failure inthe pathogenesis of necrotizing enterocolitis: Toll-like receptors throw theswitch [J]. Seminars in pediatric surgery, 2013, 22(2): 76-82.
[15] FALCK-HANSEN M, KASSITERIDI C, MONACO C. Toll-like receptors inatherosclerosis [J]. International journal of molecular sciences, 2013, 14(7):14008-23.
[16] ROH Y S, SEKI E. Toll-like receptors in alcoholic liver disease, non-alcoholicsteatohepatitis and carcinogenesis [J]. J Gastroenterol Hepatol, 2013, 28 Suppl1(38-42.
[17] PRADA P O, COELHO M S, ZECCHIN H G, et al. Low salt intake modulatesinsulin signaling, JNK activity and IRS-1ser307 phosphorylation in rat tissues[J]. The Journal of endocrinology, 2005, 185(3): 429-37.
[18] NIEDZIELSKA I, NIEDZIELSKI Z, TKACZ M, et al. Toll-like receptors andthe tendency of normal mucous membrane to transform to polyp or colorectalcancer [J]. Journal of physiology and pharmacology : an official journal of thePolish Physiological Society, 2009, 60 Suppl 1(65-71.
[19] BELMONT L, RABBE N, ANTOINE M, et al. Expression of TLR9 intumor-infiltrating mononuclear cells enhances angiogenesis and is associatedwith a worse survival in lung cancer [J]. International journal of cancer Journalinternational du cancer, 2014, 134(4): 765-77.
[20] PODDA G, NYIRENDA M, CROOKS J, et al. Innate immune responses in theCNS: role of toll-like receptors, mechanisms, and therapeutic opportunities inmultiple sclerosis [J]. Journal of neuroimmune pharmacology : the officialjournal of the Society on NeuroImmune Pharmacology, 2013, 8(4): 791-806.
[21] BURDELYA L G, BRACKETT C M, KOJOUHAROV B, et al. Central role ofliver in anticancer and radioprotective activities of Toll-like receptor 5 agonist[J]. Proceedings of the National Academy of Sciences of the United States ofAmerica, 2013, 110(20): E1857-66.
[22] LUCAS K, MAES M. Role of the Toll Like receptor (TLR) radical cycle inchronic inflammation: possible treatments targeting the TLR4 pathway [J].Molecular neurobiology, 2013, 48(1): 190-204.
[23] RAJPUT S, VOLK-DRAPER L D, RAN S. TLR4 Is a Novel Determinant ofthe Response to Paclitaxel in Breast Cancer [J]. Molecular cancer therapeutics,2013, 12(8): 1676-87.
[24] LIN Y T, VERMA A, HODGKINSON C P. Toll-Like Receptors and HumanDisease: Lessons from Single Nucleotide Polymorphisms [J]. Curr Genomics,2012, 13(8): 633-45.
[25] SOMMARIVA M, DE CECCO L, DE CESARE M, et al. TLR9 AgonistsOppositely Modulate DNA Repair Genes in Tumor versus Immune Cells andEnhance Chemotherapy Effects [J]. Cancer Res, 2011, 71(20): 6382-90.
[26] KAWAI T, AKIRA S. Toll-like receptors and their crosstalk with other innatereceptors in infection and immunity [J]. Immunity, 2011, 34(5): 637-50.
[27] MIYAKE K. Innate recognition of lipopolysaccharide by CD14 and toll-likereceptor 4-MD-2: unique roles for MD-2 [J]. Internationalimmunopharmacology, 2003, 3(1): 119-28.
[28] CULINA S, BOITARD C, MALLONE R. Antigen-based immune therapeutics 72for type 1 diabetes: magic bullets or ordinary blanks? [J]. Clinical &developmental immunology, 2011, 2011(286248.
[29] LEHUEN A, DIANA J, ZACCONE P, et al. Immune cell crosstalk in type 1diabetes [J]. Nat Rev Immunol, 2010, 10(7): 501-13.
[30] PATTERSON C C, DAHLQUIST G G, GYURUS E, et al. Incidence trends forchildhood type 1 diabetes in Europe during 1989-2003 and predicted new cases2005-20: a multicentre prospective registration study [J]. Lancet, 2009,373(9680): 2027-33.
[31] BACH J F, CHATENOUD L. The hygiene hypothesis: an explanation for theincreased frequency of insulin-dependent diabetes [J]. Cold Spring Harborperspectives in medicine, 2012, 2(2): a007799.
[32] BLUESTONE J A, HEROLD K, EISENBARTH G. Genetics, pathogenesis andclinical interventions in type 1 diabetes [J]. Nature, 2010, 464(7293): 1293-300.
[33] LI M, SONG L, GAO X, et al. Toll-like receptor 4 on islet beta cells sensesexpression changes in high-mobility group box 1 and contributes to theinitiation of type 1 diabetes [J]. Experimental & molecular medicine, 2012,44(4): 260-7.
[34] DEVARAJ S, TOBIAS P, JIALAL I. Knockout of toll-like receptor-4 attenuatesthe pro-inflammatory state of diabetes [J]. Cytokine, 2011, 55(3): 441-5.
[35] DEVARAJ S, DASU M R, PARK S H, et al. Increased levels of ligands ofToll-like receptors 2 and 4 in type 1 diabetes [J]. Diabetologia, 2009, 52(8):1665-8.
[36] ALKANANI A K, REWERS M, DONG F, et al. Dysregulated Toll-likereceptor-induced interleukin-1beta and interleukin-6 responses in subjects atrisk for the development of type 1 diabetes [J]. Diabetes, 2012, 61(10):2525-33.
[37] SADELAIN M W, QIN H Y, LAUZON J, et al. Prevention of type I diabetes inNOD mice by adjuvant immunotherapy [J]. Diabetes, 1990, 39(5): 583-9.
[38] TIAN B, HAO J, ZHANG Y, et al. Upregulating CD4+CD25+FOXP3+regulatory T cells in pancreatic lymph nodes in diabetic NOD mice by adjuvantimmunotherapy [J]. Transplantation, 2009, 87(2): 198-206.
[39] CARAMALHO I, RODRIGUES-DUARTE L, PEREZ A, et al. Regulatory Tcells contribute to diabetes protection in lipopolysaccharide-treated non-obesediabetic mice [J]. Scand J Immunol, 2011, 74(6): 585-95.
[40] GULDEN E, IHIRA M, OHASHI A, et al. Toll-like receptor 4 deficiencyaccelerates the development of insulin-deficient diabetes in non-obese diabeticmice [J]. Plos One, 2013, 8(9): e75385.
