基因硕士论文参考文献格式一
[1] 李剑欣,张绪梅,徐琪寿.色氨酸的生理生化及其应用[J].氨基酸和生物资源,2005,27 (3) : 58-62[2] 沈同,王镜岩.生物化学[M].北京:高等教育出版社, 1990.
[3] 周骏山.实用氨基酸手册[M].上海:上海中医学院出版社, 1992.
[4] 韦平和,吴梧桐.色氨酸生物工程研究进展[J].药物生物技术,1998,5(3):180.
[5] 王大慧,韦萍,欧阳平凯.D-色氨酸研究进展[J].化工进展,2002, 21( 2): 103~ 106
[6] 宋文霞, 王瑞明. L-色氨酸的研究[J]. 农产品加工学刊, 2005, 3: 18-20.
[7] 左祖帧,黄钦耿,吴伟斌等.L-色氨酸研究进展[J]. 安徽农学通报,2010,16(7): 38-40.
[8] 葛权松,郁宝平.必需氨基酸-色氨酸营养的研究[J].畜牧与兽医, 1995,27,228-230
[9] 崔芹,崔山.色氨酸营养研究进展[J]中国饲料,2003,15,20—23
[10] Snyder H, MacDonald J. A Synthesis of Tryptophan and Tryptophan Analogs [J]. J Am Chem Soc, 1955,77(5):1257-1259.
[11] Nakazawa H,Enei H,Okumura S,et al.Synthesis of L-tryptophan from pyruvate ammonia andindole[J].Agricultural and Biological Chemistry,1972,36:2523-2528
[12] 张素珍,刘英昊.用北京鼓棒杆菌细胞转化生产 L-色氨酸[J].微生物学报, 1993, 33(1):69-73.
[13] 陈俊峰,苏丽娜,王璋等. 从土壤中分离 L-色氨酸生产菌株及其高产诱变选育的研究[J].食品与发酵工业,2007,33(7): 37-41.
[14] Pittard A J,Neidhardt F C,CurtissIII R,et al. Escherichia coli and Salmonella, cellular and molecular biology[M]. Washington DC: Am Soc Microbiol,1996. 458-484.
[15] Azuma S, Tsunekawa H, Okabe M, et al.Hyper-production of L-trytophan via fermentation withcrystallization[J]. Appl Microbiol Biotechnol, 1993, 39(4):471-476.
[16] Berry A. Improving production of aromatic compounds in Escherichia coli by metabolic engineering[J].Trends Biotechnol, 1996, 14: 250-256.
[17] Ikeda M, Katsumata R. Hyperproduction of tryptophan by Corynebacterium glutamicum with the modifiedpentose phosphate pathway[J]. Appl Environ Microbiol, 1999,65 (6):2497-2502.
[18] 赵志军.L-色氨酸生产菌株构建及代谢调控研究[D].江苏:江南大学, 2011.
[19] 李永辉,刘云,王世春等. 大肠杆菌 ppsA 和 tktA 基因的串联表达 [J].生物工程学报,2003,9(3):301-306.
[20] 王静, 于金龙, 张婷等. 大肠杆菌生物合成中心代谢途径的改造及其对工程菌色氨酸产量的影响 [J].中国医药生物技术, 2008, 3(2): 93-97.
[21] Bongaerts J, Kramer M, Muller U, et al. Metabolic engineering for microbial production of aromatic aminoacids and derived compounds[J]. Metab Eng, 2001, (3):289-300.
[22] Hagino H , Nakayama K. DAHP synthetase and its control in Corynebacterium glutamicum[J]. Agric. Biol.Chem, 1974, 38: 2125–2134.
[23] Wehrmann A, Morakkabati S, Kramer R, et al. Functional analysis of sequences adjacent to dapE ofCorynebacterium glutamicum reveals the presence of aroP, which encodes the aromatic amino acidtransporter[J]. Bacteriol, 1995, 177: 5991–5993.
[24] Yanofsky C, Horn V, Gollnick P. Physiological studies of tryptophan transport and tryptophanase operoninduction in Escherichia coli[J]. J Bacteriol, 1991;173:6009
[25] Katsumata R, Ikeda M. Hyperproduction of tryptophan in Corynebacterium glutamicum by pathwayengineering [J]. Nat Biotechnol, 1993, 11(8):921-925.
[26] Ikeda,M, Nakanishi,K, Kino,K, and Katsumata,R. Fermentative production of tryptophan by a stablerecombinant strain of Corynebacterium glutanicum with a modified serine-biosynthetic pathway[J]. BiosciBiotechnol Biochem,1994,58,674-678.
[27] Ray J M,Yanofsky C,Bauerle R. Mutational analysis of the catalytic and feedback sites of thetryptophan-sensitive 3-deoxy-D-arabino-heptulosonate-7-phosphatesynthase of Escherichia coli [J]. Journalof Bacteriology,1988,170(12): 5500-5506.
[28] Kikuchi,Tsujimoto Y K,Kurahashi O. Mutational analysis of the feedback sites of phenylalanine–sensitive3-deoxy-D-arabino-heptulosonate-7-phosphate synthase of Escherichia coli [J]. Applied and EnvironmentalMicrobiology,1997,63(2): 761-762.
[29] Liao H F,Lin L L,Chien H R,et al. Serine 187 is a crucial residue for allosteric regulation ofCorynebacterium glutamicum 3–deoxy-D-arabino–heptulosonate–7–phosphatesynthase[J].FEMSMicrobiology Letter,2001,194(1): 59-64.
[30] Jossek R, Bongaerts J, Sprenger G. Characterization of a new feedback-resistant 3-deoxy-D-arabino–heptulosonate-7-phosphate synthase AroF of Escherichia coli [J].FEMS microbiol letter, 2001,202(1):145-148.
[31]Weaver, L. M., and Herrmann, K. M. (1990). Cloning of an aroF allele encoding a tyrosine-insensitive3-deoxy-d-arabino-heptusonolate-7-phosphate synthase. J. Bacteriol. 172, 6581–6584.
[32] Edwards, R. M., Taylor, P. P., Hunter, M. G., and Fotheringham, I. G.(1987). Composite plasmids for aminoacid synthesis. WO 87/00202.
[33] 李剑欣, 郭长江, 刘云, 等. 大肠杆菌邻氨基苯甲酸合成酶编码基因 trpED 的克隆与表达[J]. 生物技术通讯, 2007, 18(2):183-185.
[34] Caligiuri MG, Bauerle R. Identification of amino acid residues involved in feedback regulation of theanthranilate synthase complex from Salmonella typhimurium. Evidence for an amino-terminal regulatorysite. J Biol Chem. 1991 May 5;266(13):8328–8335.
[35] Zhao,Z,J,Zou,C,Zhu,Chen,J(2011) Development of L-tryptophan production strain by defined geneticmodification in Escherichia coli. J in Microbiol Biotechnol.
[36] Yanofsky C, Horn V, Gollnick P. Physiological studies of tryptophan transport and tryptophanase operoninduction in Escherichia coli[J]. J Bacteriol, 1991;173:6009
[37] 刘红全,戴继勋. 基因打靶技术的研究进展[J].遗传, 2002,24(6):707-711.
[38] MurphyKC, CampelloneKG, PoteeteAR. PCR-mediated gene replacement in Escherichia coli [J]. Gene,2000, 246 (1/2):321-330.
[39] Yu D , Ellis H M ,Lee E C ,Jenkins N A. An efficient recombination system for chromosome engineering inEscherichia coli[J]. Proc Natl Acad Sci USA,2000, 97(11): 5678～5983.
[40] Copeland N G ,Jenkins N A ,Court D L . Recombineering : a powerful new tool for mouse functionalgenomics[J]. NatRev Genet, 2001, 2(10):769～779.
基因硕士论文参考文献格式二
[1] Orza n Z, Murgia A. Connexin 26 deafness is not always congenital [J].International Journal of Pediatric Otorhinolaryngology,2007,71:501.
[2]Salvinelli F, Casale M, D′Ascanio L,et al. Hearing loss associated with 35delGmutation in connexin-26(GJB2) gene :Audiogram analysis[J].The Journal ofLaryngology & Otology,2004,118:8.
[3] Murgia A ,Orzan E, Polli R,et al. Cx26 deafness: mutation analysis and clinicalvariability [J] . J Med Genet, 1999, 36:829.
[4] Iliadou V, Eleftheriades N, Metaxas AS, et al. Audiological profile of the prevalentgenetic form of childhood sensorineural hearing loss due to GJB2 mutations innorthern Greece [J]. EurArch Otorhinolaryngol,2004,261:259.
[5] Xue ZL, Arti P, Simon A,et al. Audiological features of GJB2 (connexin26)deafness [J] . Ear & Hea ring,2005 ,26 : 361.
[6] Tomohiro O, Akihiro O, Shigenari H,et al. Clinical features of patients with GJB2(connexin26) mutations: Severity of hearing loss is correlated with genotypes andprotein expression patterns [J]. J Hum Genet,2005,50:76 .
[7] Rikkert LS, Patrick LMH, Delphine F,et al. GJB2 mutations and degree of hearingloss:Amulticenter study [J] .Am J Hum Genet,2005,77:945.
[8] Toth T, Kupka S, Haack B,et al. GJB2 mutations in patients with non-syndromichearing loss from Northeastern Hungary[J]. Human Mutation,2004,23:631.
[9] Anderson S, Bankier AT, Barrell BG, et al. Sequence and organization of thehuman mitochondrial genome [J]. Nature, 1981, 290(5806): 457-465.
[10] Oilveira CA, Macie1-Guerra A T, Sartorato EL. Deafness resulting frommutations in the GJB2 (connexin26) gene in BraziLian patients [J].ClinGenet,2002,61:354.
[11] Walsh T, Abu Rayan A, Abu Sa’ed J, et al. Genomic analysis of a heterogeneousMendelian phenotype:Multiple novel alleles for inherited hearing loss in thePalestinian population [J].Human Genomics,2006,2:203.
[12] 于飞, 韩东一, 戴朴，等. 1190 例非综合征性耳聋患者 GJB2 基因突变序列.解放军医学院博士学位论文分析. 中华医学杂志, 2007, 87(40):2814-2819.
[13] Ballana E, Ventayol M, Rabionet R, et al. Connexins and deafness Homepage[EB/OL]. [2014-1-5].
[14] 于飞. 非综合征型耳聋患者 GJB2 基因突变筛查和全频谱突变图谱绘制[D].中国人民解放军军医进修学院, 2006, 博士学位论文:45-122.
[15] 徐志勇, 高国凤, 刘畅，等. 耳聋患者及正常人 GJB2 基因的突变筛查. 中华医学遗传学杂志, 2009, 26(2):144-146.
[16] Norris VW, Arnos KS, Hanks WD,et al. Does universal new-born hearingscreening identify all children with GJB2 (Connexin 26) deafness? Penetranceof GJB2 deafness [J]. Ear&Hearing,2006,27:732.
[17] Liu XZ, Pandya A, Angeli S. Audiological Features of GJB2 (Connexin 26)Deafness. Ear & Hearing. 2005,26(3): 361–9.
[18] Lim.LHY, Bradshaw JK, Guo Yingshi,et al. Genotypic and PhenotypicCorrelations of DFNB1-Related Hearing Impairment in the Midwestern UnitedStates.Arch Otolaryngol Head Neck Surg. 2003;129:836-840.
[19] Kenna,MA. Feldman.HA.Neault, MW, et al.Audiologic Phenotype andProgression in GJB2(Connexin 26) Hearing Loss. Arch Otolaryngol Head NeckSurg. 2010;136(1):81-87.
[20] Liu XZ, Pandya A, Angeli S. Audiological Features of GJB2 (Connexin 26)Deafness. Ear & Hearing. 2005,26(3): 361–9.
[21]Wilcox SA, Saunders K, Osborne AH, et al. High frequency hearing lossassociated with mutations in the GJB2 gene.Hum Genet. 2000;106:399-405.
[22] Mcguirt WT, Prasad SD, Cucci RA, et al. Clinical presentation of DFNB1[J].Adv Otorhinolaryngol, 2002,61:113-119.
[23] 孙宝春. 感音神经性耳聋中内耳畸形的分类以及与 SLC26A4、GJB2 基因关系的研究. 中国人民解放军军医进修学院博士学位论文, 2011.
[24] Propst EJ, Bleaser S, Stockley TL ， et al. Temporal bone imaging in GJB2deafness [J]. Laryngoscope,2006,116:2178-2186.
[25] Kenna MA, Wu BL, Cotanche DA, et al. Connexin 26 studies in patients withsensorineaural hearing loss[J]. Arch Otolaryngol Head NeckSurg,2001,127:1037-1042.
[26] Preciado DA, Lim LH，Cohen AP, et al. A diagnostic paradigm for childhoodidiopathic sensorineural hearing loss[J]. Otolaryngol Head NeckSurg,2004,131:804-809.
[27] Snoeckx RL, Huygen PL, Feldmann D, et al. GJB2 mutations and degree ofhearing loss: a multicenter study.Am J Hum Genet, 2005, 77(6):945-957.
[28] Azaiez H, Chamberlin GP, Fischer SM, et al. GJB2: the spectrum ofdeafness-causing allele variants and their phenotype. Hum Mutat,2004,24(4):305-311.
[29] Cryns K, Orzan E, Murgia A, et al. A genotype-phenotype correlation for GJB2(connexin 26) deafness. J Med Genet, 2004, 41(3):147-154.
[30] Li L,Lu J, Tao Z, et al. The p.V37I exclusive genotype of GJB2: a geneticrisk-indicator of postnatal permanent childhood hearing impairment. PloS,2012,7(5),e36612.
[31] Hwa HL,Ko TM, Hsu CJ, et al. Mutation spectrum of the connexin 26(GJB2)gene in Taiwanese patients with prelingual deafness. Genetics in medicine:official Journal Of the American College of Medicine Genetics,2013,5(3),161-165.
[32] Wattanasirichaigoon D, Limwaongse C, Jariengprasert C, et al. High prevalenceof V37I genetic variant in the connexin-26(GJB2) gene among non-syndromichearing-impaired and control Thai inpiduals, Clinical genetics,2004,66(5),452-460.
[33] Jara O, Acuna R, Garcia IE,et al. Critical role of the first transmembrane domainof Cx26 in regulating oligomerization and function. Molecular Biology of theCell. 2012,23(17), 3299-3311.
[34] Kelly PM, Harris DJ, Comer BC, et al. Novel mutations in the connexin 26 gene(GJB2) that cause autosomal recessive (DFNB1) hearing loss. Amerian Journalof Human genetics.1998,62(4),792-799.
[35] Abe S, Usami S, Shinkawa H, et al.K. Prevalent connexin 26 gene (GJB2)mutations in Japanese[J]. J Med Genet,2000,37:41-43.
[36] Rabionet R, Zelante L, Lopez-BigasN,et al. Molecular basis of childhooddeafness resulting from mutations in the GIB2 (connexin26) gene[J].HumGenet,2000,106:40-44.
[37] Bruzzone R, Veronesi V, Gomes D, et al. Loss of function and residual channelactivity of connexin 26 mutations associated with non 一 syndromic deafness[Jl.FEBS Letters.2003,533:79-88.
[38] Huculak C, Bruyere H, Nelson TN, et al. V37I connexin 26 allele in patients withsensorineural hearing loss: evidence of its pathogenicity. American Journal ofMedical Genetics Part A. 2006,140(22): 2394-2400.
[39] Choi SY, Lee KY, Kim HJ, et al. Functional evaluation of GJB2 variants innonsyndromic hearing loss. Mol Med, 2011, 17(5-6):550-556.
基因硕士论文参考文献格式三
[1] Wolford LM. Idiopathic condylar resorption of the temporomandibular joint inteenage girls (cheerleaders syndrome)[J]. Proc Bayl Univ Med Cent 2001，14:246-52.
[2] Richette P, Corvol M, Bardin T. Estrogens, cartilage,and osteoarthritis[J]. JointBone Spine 2003;70(4):257-62.
[3] Wluka AE, Cicuttini FM, Spector TD. Menopause,oestrogens and arthritis[J].Maturitas 2000;35(3):183-99
[4] Nekora-Azak A. Temporomandibular disorders in relation to female reproductivehormones: A literature review[J]. Prosthet Dent 2004;91:491–493.
[5] Hayes WC, Bodine AJ. Flow- independent viscoelastic properties of articularcartilage matrix [J]. J Biomech,1978, 11(8- 9): 407- 419
[6] Knudson CB ， Knudson W ． Cartilage proteoglycans semin[J] ． Cell DevBiol ,2001,12：69-78．
[7] McAlindon T. Glucosanune and chondroitin for osteoarthrit is [ J ] . Bull RheumDis, 2001, 50( 7) : 1-4.
[8] Bank RA,Bayliss MT,Lafeber FP,et al.Ageing and zonal variation in posttransla-tional modification of Clagen in normal human articular cartilage[ J ].Biochem,1998,330(Pt1):345-351.
[9] Ringsholt M, H gdall EV, Johansen JS, et al.YKL-40 protein expression in normaladult human tissues – an immunohistochemical study[J].J Mol Histol, 2007,38:33– 43.
[10] Huang K, Wu LD. YKL-40: a Potential Biomarker for Osteoarthritis[J].Int MedRes,2009,37(1):18-24.
[11] Guerassimov A，Zhang Y，Cartman A，et a1．Immune responses to cartilage linkprotein an d the G1 domain of proteoglyean aggreean in patients withostearthritis[J]．Arthris Rheum，1999，42(3)：527-533.
[12] Maehara, Hideaki 1; Suzuki,et al. G1-G2 Aggrecan Product that can beGenerated by M-calpain on Truncation at Ala709-Ala710 is Present Abundantlyin Human Articular Cartilage [J]. Biochem ,2007,141 (4): 469-477.
[13] Kraetsch HG,Unger C,Wernhof P,et al.Cartilage specific autoimmunity inrheumatoid arthritis：characterization of a triple helical B cellepitope in theintegrin bindingdomain of Clagen type II[J]．Eur J Immunol，2001，31(6)：171—173.
[14] Moret FM, Hack CE, van der Wurff-Jacobs KM, et al.Intra-articularCD1c-expressing myeloid dendritic cells from rheumatoid arthritis patientsexpress a unique set of T cellattracting chemokines and spontaneously induceTh1, Th17 and Th2 cellactivity[J]. Arthritis Res Ther, 2013, 15:R155.
[15] Synovial fluid CD1c+ myeloid dendritic cells – the inflammatory pictureemerges [J]. Arthritis Research & Therapy,2013, 15:128.
[16] Susan Kovats. Estrogen receptors regulate an inflammatory pathway of dendriticcell differentiation: mechanisms and implications for immunity[J]. Horm Behav,2012 August ; 62(3): 254–262.
[17] Fernandes JC, Martel-Pelletier J, Pelletier JP et al. The role of cytokines inosteoarthritis pathophysiology[J]. Biorheology,2002,39(1-2):237-246.
[18] Bezerra MC, Carvalho JF, Prokopowitsch AS,et al. RANK, RANKL andosteoprotegerin in arthritic bone loss[J]. Braz J Med Biol Res,2005,38(2):161-170.
[19] Wang P,Zhu F,Konstantopoulos K.Prostaglandin E2induces interleukin-6expression in human chondrocytes via cAMP/protein kinaseA andphosphatidylinositol 3 -kinase dependent NF -kappaB activation[J].Am J PhysiolCell Physiol,2010,298: C1445-C1456．
[20] Cuzzocrea S,Mazzon E,Dugo L, et al.Inducible nitric oxide synthase mediatesbone loss in ovariectomized mice[J].Endocrinology,2003 ,44(3):1098-1107.
[21] Ge X, Ma X, Meng J,et al. Role of Wnt-5A in interleukin-1beta-induced matrixmetalloproteinase expression in rabbit temporomandibular joint condylarchondrocytes [J].Arthritis Rheum,2009,60(9):2714-2722.
[22] Ge XP, Gan YH, Zhang CG ,et al.Requirement of the NF-κB pathway forinduction of Wnt-5A by interleukin-1β in condylar chondrocytes of thetemporomandibular joint: functional crosstalk between the Wnt-5A and NF-κBsignaling pathways[J].Osteoarthritis Cartilage,2011 ,19(1):111-117.
[23] Brouillette MJ, Ramakrishnan PS, Wagner VM,et al. Strain-dependent oxidantrelease in articular cartilage originates from mitochondria[J].Biomech ModelMechanobiol,2013,13(3):565-72.
[24] Yu SM, Kim SJ. Thymoquinone-induced reactive oxygen species causesapoptosis of chondrocytes via PI3K/Akt and p38kinase pathway[J].ExpBiol Med,2013,238(7):811-20.
[25] Liu X, Xu Y, Chen S,et al. Rescue of proinflammatory cytokine-inhibitedchondrogenesis by the antiarthritic effect of melatonin in synoviummesenchymal stem cells via suppression of reactive oxygen species and matrixmetalloproteinases[J]. Free Radic Biol Med,2014,3(68):234-46
[26] 方泽强,马绪臣.颞下颌关节骨关节病髁突软骨细胞雌激素受体 β 差异表达的研究[J].华西口腔医学杂志,2006,24(5):469-472.
[27] Chen JQ1, Cammarata PR, Baines CP,et al. Regulation of mitochondrialrespiratory chain biogenesis by estrogens/estrogen receptors and physiological,path- ological and pharmaCogical implications[J].Biochim Biophys Acta,2009 ,1793 (10):1540-70
[28] Carolyn M. Klinge.Estrogenic Control of Mitochondrial Function and Biogen-esis[J]. Cell Biochem, 2008 ,105(6): 1342–1351.
[29] Horst Claassen,Michael Schünke,Bodo Kurz.Estradiol protects cultured articularchondrocytes from oxygen-radical-induced damage[J]. Cell Tissue Res ,2005,(319): 439–445.
[30] Claassen H, Steffen R, Hassenpflug J,et al. 17β-estradiol reduces expression ofMMP-1, -3, and -13 in human primary articular chondrocytes from femalepatients cultured in a three dimensional alginate system[J].Cell Tissue Res,2010,342 (2):283 -293 .
[31] Lee YJ, Lee EB, Kwon YE et al. Effect of estrogen on the expression of matrixmetalloproteinase (MMP)-1, MMP-3, and MMP-13 and tissue inhibitor ofmetalloproternase-1 inosteoarthritis chondrocytes[J].Rheumatol Int,2003,23(6):282-288.
[32] 谷志远,傅开元,张震康.颞下颌关节紊乱病[M].北京市非台区方庄芳群园 3 区3 号楼:人民卫生出版社,2008,57.
[33] Kou XX, Wu YW, Ding Y,et al.17β-estradiol aggravates temporomandibular jointinflammation through the NF-κB pathway in ovariectomized rats[J].ArthritisRheum,2011,63(7):1888-1897.