糠秕马拉色菌菌丝态和酵母态基因表达差异的研究
|
摘要
背景：近年来，马拉色菌越来越引起真菌学家和临床医学家的关注，它是一类可引起多种皮肤病的嗜脂性真菌，马拉色菌除可引起花斑糠疹、马拉色菌毛囊炎外尚可引起头皮糠疹、甲真菌病、龟头包皮炎、真菌血症、皮肤脓肿等。与诱发脂溢性皮炎、特应性皮炎、头皮糠疹的免疫机制密切相关，可能与融合性网状乳头瘤病相关，并与银屑病的发病和加重相关，在严重免疫缺陷及静脉营养患者尚可引起系统性感染。但马拉色菌致病分子机制至今尚未阐明，相关基因表达比较研究亦尚未见报道。
马拉色菌最常导致的疾病为花斑糠疹，在花斑糠疹患者皮损刮取鳞屑直接镜检查见的马拉色菌大多呈菌丝态，而在健康人皮肤上则基本以酵母态形式存在，这种菌形态不同的原因目前还不清楚，推测可能与局部环境(温度、湿度、皮脂成分)不同有关。故糠秕马拉色菌在机体内外因素的作用下由酵母态转化成菌丝态很可能是临床致病的关键所在。在已公认的马拉色菌7个种中，糠秕马拉色菌较为常见，其菌丝态在试管内已被成功地诱导出，它也是目前唯一的一种可在体外培养出菌丝态的马拉色菌。通过比较糠秕马拉色菌酵母态和菌丝态的差异将对了解马拉色菌的致病机制具有重要意义。
而随着微生物基因组序列的大量测定，通过比较基因表达差异分析致病微生物的分子致病机制已成为新近微生物基因组研究的热点。近年发展起来的抑制消减杂交技术为比较同源生物的基因表达差异提供了一条新的途径。
目的：本研究试图应用抑制消减杂交技术比较糠秕马拉色菌的菌丝态和酵母态之间mRNA差异以分析糠秕马拉色菌的菌丝态和酵母态的基因表达差异，建立糠秕马拉色菌菌丝态和酵母态细胞的差异表达cDNA文库，获得其差异表达的基因片段，以了解其酵母态转化为菌丝态的相关分子机理，为进一步深入研究糠秕马拉色菌的致病机制奠定基础。
方法：首先将糠秕马拉色菌(M.furfur CBS 1878)标准株分别接种于菌丝态和酵母态液体培养基，3天后分别提取糠秕马拉色菌菌丝态和酵母态细胞的总RNA，然后从中分离出mRNA，随后逆转录生成菌丝态和酵母态细胞双链cDNA，经RsaI酶切消化后，然后运用抑制消减杂交技术进行杂交，相同的片断将被消减掉，再经过2次抑制性PCR扩增消减后片断，获得菌丝态或酵母态细胞差异表达的cDNA片段并建立差异文库。再对差异cDNA片段进行克隆及斑点杂交鉴定，最后对阳性克隆进行测序、在GenBank上进行相似性对比和利用DNA序列软件进行序列分析。
结果：1．成功培养出糠秕马拉色菌菌丝态。2．获得糠秕马拉色菌菌丝态和酵母态细胞的总RNA，并分离出其mRNA。3．建立了菌丝态及酵母态细胞差异表达的cDNA文库。4．经菌落PCR和斑点杂交鉴定差异文库，实际共得菌丝态特有片断克隆22个，酵母态特有表达片断克隆8个。5．将上述30个鉴定阳性克隆和4个可疑阳性克隆测序，用Blast程序在GeneBank中检索克隆片段基因序列的同源性，所有检索到与其他物种蛋白或序列有一定相似度的克隆可分为以下几类：①生化代谢类：A4与ATP合酶、A16与NADH脱氢酶Ⅰ、A23与细胞色素C氧化酶亚单位Ⅲ、A38与线粒体序列、A49与NADH脱氢酶Ⅱ等有一定同源度。B4与线粒体肌酸激酶有一定相似性，B7与ATP合酶的β亚基同源(A4与ATP合酶α亚基同源)，B9则与原海豹霉属的细胞色素b同源。②与转录有关：A8与剪接因子2或DNA结合蛋白相似，A13与可抑制白介素2表达的转录因子8及锌指蛋白具有高度同源，A14与核转录因子Y高度同源，与磷酸酯酶也具有一定同源性；A40与转录变体ACTN2高度同源。③与生长相关：A10与牛生长因子受体α多肽序列同源，但Blastx未找到同源蛋白。④细胞结构类：A12与细胞壁脂蛋白相关水解酶及脂蛋白具有一定同源性，A22与大肠杆菌嗜菌体衣壳蛋白有一定同源性，与米曲霉的基因组序列部分相同。⑤其他类：A15与肌联蛋白、A21与耻垢分支杆菌假设蛋白、A56与念珠棘虫属赤霉GTP结合蛋白有很高的相似度，B3与苏芸金芽胞杆菌质粒小部分序列相似，B10则有30％序列和玉蜀黍黑粉菌、绿藻门小部分序列具有相似性，B12与构巢曲霉的40S核糖体S7蛋白具有一定相似度。
6．测序的21个序列中，经过Omiga 2.0等核酸序列分析软件进行正相三个和负相三个共六个相位的ORF搜索，发现所得序列均具有起始密码子和终止密码子，即为可能的ORF，翻译后的6相位的氨基酸序列均含有大量真菌蛋白质二级结构基序。表明所获得的片断均为编码蛋白质的基因片断。
结论：采用消减杂交技术成功建立了糠秕马拉色菌的差异cDNA文库，筛选出一系列可能包含毒力相关基因的糠秕马拉色菌菌丝态和酵母态特有片段，片段部分同源则可能提示这16个片段与同源蛋白有某种功能或进化联系，分别与生化代谢酶、转录因子、生长因子、细胞结构或相关膜蛋白相似，提示这些基因片段可能与糠秕马拉色菌菌丝态和酵母态的代谢、分化、毒力或分子进化有关。这些结果对了解糠秕马拉色菌致病的分子机制提供了重要信息。
Backgrounds The genus Malassezia has received considerable attentionin recent years from mycologists and clinicial doctors. This group oflipophilic yeasts, long known to be the pathogenic agents of pityriasis (tinea)versicolor and Malassezia folliculitis, is also increasingly being associatedwith the causation of balanitis, onychomycosis, papillomatosis, and invasivehuman infections, as well as potential immunogenic triggering of atopicdermatitis, seborrheic dermatitis, and dandruff. Otherwise, Malassezia canprobably irritate and deteriorate lesions in psoriasis; and inimmunocompromised patients and those of receiving intralipid therapy theycan induce severe systemic infection. Molecular pathogenic mechanism ofMalassezia is still unclear at present. Now genome project of Malasseziaisn't broungt to consideration. Very few reports about gene experession andthe virulence-associated genes of the fungi appeared so far, which results inthe slow development in the study of pathogenic mechanism of Malassezia.
Malassezia is regularly present in its yeast phase in the skin of healthyadults, produces the clinical lesions of pityriasis versicolor when developingits mycelial phase. The conditions that induce such transformation remainunclear, although the available data at present indicate that it could be causedby changes in the local conditions (e.g. temperature, humidity, sebumcomposition) on an idiosyncratic basis. The morphological transformation ofMalassezia from a yeast phase to a mycelial phase is the key pathogenicmechanism of Malassezia that be commonly received. Malassezia furfur(M.furfur) is the only one species of Malassesia that can be induced toproduce its mycelial phase in vitro. To compare the difference of geneexpression between mycelial phase and yeast phase of M.furfur can help us toknow its molecular pathogenic mechanism.
Since 1990s, to compare the difference of gene expression betweenhomospecific microorganism has become a focus of attention inmicrobiologic society, accompanied with total genome in manymicroorganism have been sequenced. The recently developed method ofsuppression subtractive hybridization (SSH) provided a powerful new way tostudy molecular pathogenic mechanism of pathogenic microorganism bycomparison with the difference of microorganism mRNA.
Objectives To compare the difference of gene expression betweenmycelial phase of M. furfur and its yeast phase, and we try to found twodifferential cDNA libraries. To understand the molecular pathogenicmechanism of the fungi and its morphological switching mechanism from ayeast phase of growth to a mycelial phase.
Methods①To isolate the total RNA both in mycelial and yeast phase ofM. furfur, then to isolate mRNA from them severally.②Reverse them to ds-cDNA and then digest them by RsaI.③Hybridize with mycelial phase ofM.furfur as tester and its yeast phase as driver with the method of suppressionsubtractive hybridization (SSH), a reverse process also to be performed at thesame time.④The resulted PCR mixture was connected to T vector toconstruct the subtractive library.⑤Dot blot techniques were employed toindentify those positive clones.⑥That positive differential gene expressionclone to be sequenced, then search similary genes and proteins of thatacquired gene sequences by BLAST (basic local alignment search tool,BLAST) in GenBank to predict their function, and analyse them by DNAsequence analysis softwares.
Results 1. Succeed in culturing mycelial phase of M. furfur. 2. Succeed ingaining total RNA both in mycelial and yeast phase of M. furfur and isolatingtheir mRNA. 3. Two differential cDNA libraries had been found with M.furfur in mycelial phase and its yeast phase. 4. Twenty-two positive cloneswere acquired by subtraction in positive direction. Eight positive clones wereacquired by subtraction in reverse direction. Positive clones in both directionsand four suspicious positive clones were sent to sequencing. 5. Thirty-fourfragments were compared through BLASTn and BLASTx in GenBank.Thirteen fragments were either repeated or belonging to vector sequences;fifteen fragments acquired by subtraction in positive direction and sixfragments from reverse direction weren't repeated and also not belonging tovector sequences. 6. All of these 21 clones have more or less homologywith genes or proteins from other biological species. Sum up homologousgenes and proteins of these fragments, they can be clarified into fivecategories:①Fragments homologize to biochemical metabolic enzyme: A4,A16, A23, A38, A49, B4, B7, and B9.②Fragments homologize to transcription associated protein: A8, A13, A14, A40, and B 12.③Fragmentshomologize to growth factor: A10.④Fragments homologize to cell structureproteins: A12 and A22.⑤Others: A15, A21, B3, and B10.7. Open readingframeworks and lots of fungi motifs have been found existing in all of 21fragments by sequence analysis software. Initiation codons and terminationcodons exist in all of them too.
Conclusions Succeed in founding two differential cDNA library with M.furfur in mycelial phase and yeast phase by suppressive subtractivehybridization techniques, and a series of fragments which possibly containedgenes related to virulence of M. furfur have been screened. These sequenceshomologize to genes of fungal virulence or molecular evolution such asmembrane protein, metabolic enzyme and cell structure, et cetra.
马拉色菌最常导致的疾病为花斑糠疹，在花斑糠疹患者皮损刮取鳞屑直接镜检查见的马拉色菌大多呈菌丝态，而在健康人皮肤上则基本以酵母态形式存在，这种菌形态不同的原因目前还不清楚，推测可能与局部环境(温度、湿度、皮脂成分)不同有关。故糠秕马拉色菌在机体内外因素的作用下由酵母态转化成菌丝态很可能是临床致病的关键所在。在已公认的马拉色菌7个种中，糠秕马拉色菌较为常见，其菌丝态在试管内已被成功地诱导出，它也是目前唯一的一种可在体外培养出菌丝态的马拉色菌。通过比较糠秕马拉色菌酵母态和菌丝态的差异将对了解马拉色菌的致病机制具有重要意义。
而随着微生物基因组序列的大量测定，通过比较基因表达差异分析致病微生物的分子致病机制已成为新近微生物基因组研究的热点。近年发展起来的抑制消减杂交技术为比较同源生物的基因表达差异提供了一条新的途径。
目的：本研究试图应用抑制消减杂交技术比较糠秕马拉色菌的菌丝态和酵母态之间mRNA差异以分析糠秕马拉色菌的菌丝态和酵母态的基因表达差异，建立糠秕马拉色菌菌丝态和酵母态细胞的差异表达cDNA文库，获得其差异表达的基因片段，以了解其酵母态转化为菌丝态的相关分子机理，为进一步深入研究糠秕马拉色菌的致病机制奠定基础。
方法：首先将糠秕马拉色菌(M.furfur CBS 1878)标准株分别接种于菌丝态和酵母态液体培养基，3天后分别提取糠秕马拉色菌菌丝态和酵母态细胞的总RNA，然后从中分离出mRNA，随后逆转录生成菌丝态和酵母态细胞双链cDNA，经RsaI酶切消化后，然后运用抑制消减杂交技术进行杂交，相同的片断将被消减掉，再经过2次抑制性PCR扩增消减后片断，获得菌丝态或酵母态细胞差异表达的cDNA片段并建立差异文库。再对差异cDNA片段进行克隆及斑点杂交鉴定，最后对阳性克隆进行测序、在GenBank上进行相似性对比和利用DNA序列软件进行序列分析。
结果：1．成功培养出糠秕马拉色菌菌丝态。2．获得糠秕马拉色菌菌丝态和酵母态细胞的总RNA，并分离出其mRNA。3．建立了菌丝态及酵母态细胞差异表达的cDNA文库。4．经菌落PCR和斑点杂交鉴定差异文库，实际共得菌丝态特有片断克隆22个，酵母态特有表达片断克隆8个。5．将上述30个鉴定阳性克隆和4个可疑阳性克隆测序，用Blast程序在GeneBank中检索克隆片段基因序列的同源性，所有检索到与其他物种蛋白或序列有一定相似度的克隆可分为以下几类：①生化代谢类：A4与ATP合酶、A16与NADH脱氢酶Ⅰ、A23与细胞色素C氧化酶亚单位Ⅲ、A38与线粒体序列、A49与NADH脱氢酶Ⅱ等有一定同源度。B4与线粒体肌酸激酶有一定相似性，B7与ATP合酶的β亚基同源(A4与ATP合酶α亚基同源)，B9则与原海豹霉属的细胞色素b同源。②与转录有关：A8与剪接因子2或DNA结合蛋白相似，A13与可抑制白介素2表达的转录因子8及锌指蛋白具有高度同源，A14与核转录因子Y高度同源，与磷酸酯酶也具有一定同源性；A40与转录变体ACTN2高度同源。③与生长相关：A10与牛生长因子受体α多肽序列同源，但Blastx未找到同源蛋白。④细胞结构类：A12与细胞壁脂蛋白相关水解酶及脂蛋白具有一定同源性，A22与大肠杆菌嗜菌体衣壳蛋白有一定同源性，与米曲霉的基因组序列部分相同。⑤其他类：A15与肌联蛋白、A21与耻垢分支杆菌假设蛋白、A56与念珠棘虫属赤霉GTP结合蛋白有很高的相似度，B3与苏芸金芽胞杆菌质粒小部分序列相似，B10则有30％序列和玉蜀黍黑粉菌、绿藻门小部分序列具有相似性，B12与构巢曲霉的40S核糖体S7蛋白具有一定相似度。
6．测序的21个序列中，经过Omiga 2.0等核酸序列分析软件进行正相三个和负相三个共六个相位的ORF搜索，发现所得序列均具有起始密码子和终止密码子，即为可能的ORF，翻译后的6相位的氨基酸序列均含有大量真菌蛋白质二级结构基序。表明所获得的片断均为编码蛋白质的基因片断。
结论：采用消减杂交技术成功建立了糠秕马拉色菌的差异cDNA文库，筛选出一系列可能包含毒力相关基因的糠秕马拉色菌菌丝态和酵母态特有片段，片段部分同源则可能提示这16个片段与同源蛋白有某种功能或进化联系，分别与生化代谢酶、转录因子、生长因子、细胞结构或相关膜蛋白相似，提示这些基因片段可能与糠秕马拉色菌菌丝态和酵母态的代谢、分化、毒力或分子进化有关。这些结果对了解糠秕马拉色菌致病的分子机制提供了重要信息。
Backgrounds The genus Malassezia has received considerable attentionin recent years from mycologists and clinicial doctors. This group oflipophilic yeasts, long known to be the pathogenic agents of pityriasis (tinea)versicolor and Malassezia folliculitis, is also increasingly being associatedwith the causation of balanitis, onychomycosis, papillomatosis, and invasivehuman infections, as well as potential immunogenic triggering of atopicdermatitis, seborrheic dermatitis, and dandruff. Otherwise, Malassezia canprobably irritate and deteriorate lesions in psoriasis; and inimmunocompromised patients and those of receiving intralipid therapy theycan induce severe systemic infection. Molecular pathogenic mechanism ofMalassezia is still unclear at present. Now genome project of Malasseziaisn't broungt to consideration. Very few reports about gene experession andthe virulence-associated genes of the fungi appeared so far, which results inthe slow development in the study of pathogenic mechanism of Malassezia.
Malassezia is regularly present in its yeast phase in the skin of healthyadults, produces the clinical lesions of pityriasis versicolor when developingits mycelial phase. The conditions that induce such transformation remainunclear, although the available data at present indicate that it could be causedby changes in the local conditions (e.g. temperature, humidity, sebumcomposition) on an idiosyncratic basis. The morphological transformation ofMalassezia from a yeast phase to a mycelial phase is the key pathogenicmechanism of Malassezia that be commonly received. Malassezia furfur(M.furfur) is the only one species of Malassesia that can be induced toproduce its mycelial phase in vitro. To compare the difference of geneexpression between mycelial phase and yeast phase of M.furfur can help us toknow its molecular pathogenic mechanism.
Since 1990s, to compare the difference of gene expression betweenhomospecific microorganism has become a focus of attention inmicrobiologic society, accompanied with total genome in manymicroorganism have been sequenced. The recently developed method ofsuppression subtractive hybridization (SSH) provided a powerful new way tostudy molecular pathogenic mechanism of pathogenic microorganism bycomparison with the difference of microorganism mRNA.
Objectives To compare the difference of gene expression betweenmycelial phase of M. furfur and its yeast phase, and we try to found twodifferential cDNA libraries. To understand the molecular pathogenicmechanism of the fungi and its morphological switching mechanism from ayeast phase of growth to a mycelial phase.
Methods①To isolate the total RNA both in mycelial and yeast phase ofM. furfur, then to isolate mRNA from them severally.②Reverse them to ds-cDNA and then digest them by RsaI.③Hybridize with mycelial phase ofM.furfur as tester and its yeast phase as driver with the method of suppressionsubtractive hybridization (SSH), a reverse process also to be performed at thesame time.④The resulted PCR mixture was connected to T vector toconstruct the subtractive library.⑤Dot blot techniques were employed toindentify those positive clones.⑥That positive differential gene expressionclone to be sequenced, then search similary genes and proteins of thatacquired gene sequences by BLAST (basic local alignment search tool,BLAST) in GenBank to predict their function, and analyse them by DNAsequence analysis softwares.
Results 1. Succeed in culturing mycelial phase of M. furfur. 2. Succeed ingaining total RNA both in mycelial and yeast phase of M. furfur and isolatingtheir mRNA. 3. Two differential cDNA libraries had been found with M.furfur in mycelial phase and its yeast phase. 4. Twenty-two positive cloneswere acquired by subtraction in positive direction. Eight positive clones wereacquired by subtraction in reverse direction. Positive clones in both directionsand four suspicious positive clones were sent to sequencing. 5. Thirty-fourfragments were compared through BLASTn and BLASTx in GenBank.Thirteen fragments were either repeated or belonging to vector sequences;fifteen fragments acquired by subtraction in positive direction and sixfragments from reverse direction weren't repeated and also not belonging tovector sequences. 6. All of these 21 clones have more or less homologywith genes or proteins from other biological species. Sum up homologousgenes and proteins of these fragments, they can be clarified into fivecategories:①Fragments homologize to biochemical metabolic enzyme: A4,A16, A23, A38, A49, B4, B7, and B9.②Fragments homologize to transcription associated protein: A8, A13, A14, A40, and B 12.③Fragmentshomologize to growth factor: A10.④Fragments homologize to cell structureproteins: A12 and A22.⑤Others: A15, A21, B3, and B10.7. Open readingframeworks and lots of fungi motifs have been found existing in all of 21fragments by sequence analysis software. Initiation codons and terminationcodons exist in all of them too.
Conclusions Succeed in founding two differential cDNA library with M.furfur in mycelial phase and yeast phase by suppressive subtractivehybridization techniques, and a series of fragments which possibly containedgenes related to virulence of M. furfur have been screened. These sequenceshomologize to genes of fungal virulence or molecular evolution such asmembrane protein, metabolic enzyme and cell structure, et cetra.
引文
1. Guillot G, Gueho E, Lesourd M, et al. Identification of Malassezia species: a practical approach. J Mycol Med, 1996, 6: 103-110.
2. Sugita TM, Takashima T, Shinoda H, et al. New yeast species, Malassezia dermatis, isolated from patients with atopic dermatitis. J Clin Microbiol, 2002, 40: 1363-1367.
3. Nell A, James SA, Bond CJ, et al. Identification and distribution of a novel Malassezia species yeast on normal equine skin. Vet Rec, 2002, 150: 395-398.
4. Gaitanis G, Robert V, Velegraki A. Verifiable single nucleotide polymorphisms of the internal transcribed spacer 2 region for the identification of 11 Malassezia species. J Dermatol Sci, 2006, 43(3): 214-217.
5. Mirhendi H, Makimura K, Zomorodian K, et al. A simple PCR-RFLP method for identification and differentiation of 11 Malassezia species. J Microbiol Methods, 2005, 61(2): 281-284.
6. Hirai A, Kano R, Makimura K, et al. Malassezia nana sp. nov., a novel lipid-dependent yeast species isolated from animals. Int J Syst Evol Microbiol, 2004, 54(Pt2): 623-627.
7. Cabanes FJ, Theelen B, Castella G, et al. Two new lipid-dependent Malassezia species from domestic animals. FEMS Yeast Res, 2007, 16: [Epub ahead of print]
8. Cabanes FJ, Hernandez JJ, Castella G. Molecular analysis of Malassezia sympodialis: related strains from domestic animals. J Clin Microbiol, 2005, 43: 277-283.
9. Gupta AK, Boekhout T, Theelen B, et al. Identification and typing of Malassezia species by amplified fragment length polymorphism and sequence analyses of the internal transcribed spacer and large-subunit regions of ribosomal DNA. J Clin Microbiol, 2004, 42(9): 4253-4260.
10. Gupta AK, Batra R, Bluhm R, et al. Skin diseases associated with Malassezia species. J Am Acad Dermatol, 2004, 51(5): 785-798.
11. Gueho E, Boekhout T, Ashbee HR, et al. The role of Malassezia species in the ecology of human skin and as pathogens. Med Mycol, 1998, 36 Suppl 1: 220-229.
12．王群，吴勤学，靳培英，等．嗜脂性马拉色菌与银屑病发病相关关系初探．中国麻风皮肤病杂志，2001，17(4)：231-233．
13. Redline RW, Redline SS, Boxerbaum B, et al. Systemic Malassezia furfur infections in patients receiving intralipid therapy. Hum Pathol, 1985, 16(8): 815-822.
14．李薇．糠秕马拉色菌的系统感染．国外医学皮肤性病学分册，1997，23：263-265．
15. Masure O, Leostic C, Abalain ML, et al. Malasseziafurfur septicaemia in a child with leukaemia. J Infect, 1991, 23(3): 335-336.
16. Dixon DM, McNeil MM, Cohen ML, et al. Fungal infections: a growing threat. Public Health Rep, 1996, 111 (3): 226-235.
17. Faergemann J. A new model for growth and filament production of Pityrosporum ovale (orbiculare) on human stratum corneum in vitro. J Invest Derrnatol, 1989, 92: 117-119.
18. Ran Y, Yoshiike T, Ogawa H. Lipase of Malassezia furfur: some properties and their relationship to cell growth. J Meal Vet Mycol, 1993, 31(1): 77-85.
19. Riciputo RM, Oliveri S, Micali G, et al. Phospholipase activity in Malassezia furfur pathogenic strains. Mycoses, 1996, 39(5-6): 233-235.
20．冉玉平，周光平，坪井良治，等．糠秕孢子菌与培养人角朊细胞的相互作用．中华皮肤科杂志，1997，30：294-298．
21. Diatchenko L, Lau YF, Campbell AP, et al, Suppression subtractive hybridization: a method for generating differentially regulated or tissue-specific cDNA probes and libraries. Proc Natl Acad Sci USA, 1996: 6025-6030.
22. Siebert PD, Chenchik A, Kellogg DE, et al. An improved PCR method for walking in uncloned genomic DNA. Nucleic Acids Res, 1995, 23(6): 1087-1088.
23. Akopyants NS, Fradkov A, Diatchenko L, et al. PCR-based subtractive hybridization and differences in gene content among strains of Helicobacter pylori. Proc Natl Acad Sci U S A, 1998, 95(22): 13108-13113.
24. Bogush ML, Velikodvorskaya TV, Lebedev YB, et al. Identificatiori and localization of differences between Escherichia coli and Salmonella typhimurium genomes by suppressive subtractive hybridization. Mol Gen Genet, 1999, 262(4-5): 721-729.
25．鲍朗，胡昌华，李学敏，等．利用抑制消减杂交技术研究钩端螺旋体致病相关基因．中华微生物学和免疫学杂志2001，21(5)：574-577．
26. Goswami RS, Xu JR, Trail F, et al. Genomic analysis of host-pathogen interaction between Fusarium graminearum and wheat during early stages of disease development. Microbiology, 2006, 152(Pt 6): 1877-1890.
27．冉玉平，罗汉超，李志玉．含菜子油培养基对花斑癣致病真菌的培养研究．中华皮肤科杂志，1987，20(1)：4-7．
28．梁作辉，冉玉平，代亚玲，等．马拉色菌菌丝态培养研究．华西医学，2005，20(1)：36-37．
29. Odds EC. Switch of phenotype as an escape mechanism of the intruder. Mycoses, 1997, 40(Suppl 2): 9-12.
30. Gow NA. Growth and guidance of the fungal hypha. Microbiology, 1994, 140 (Pt 12): 3193-3205.
31. Saadatzadeh MR, Ashbee HR, Cunliffe W J, et al. Cell-mediated immunity to the mycelial phase of Malassezia spp. In patients with pityriasis versicolor and controls. Br J Dermatol, 2001,144 (1): 77-84.
32. Prohic A, Ozegovic L. Malassezia species isolated from lesional and non-lesional skin in patients with pityriasis versicolor. Mycoses, 2007, 50(1): 58-63.
33. Miranda KC. de Araujo CR, Soares A J, et al. Identification of Malassezia species in patients with pityriasis versicolor in Goiania-GO. Rev Soc Bras Med Trop, 2006, 39(6): 582-583.
34. Lamar EE, Palmer E. Y-encoded, species-specific DNA in mice: evidence that the Y chromosome exists in two polymorphic forms in inbred strains. Cell, 1984, 37(1): 171-177.
35. Watson JB, Margulies JE. Diferential cDNA screening strategies to identify novel stage-specific proteins in the developing mammalian brain. Developmental Neuroscience, 1994,15: 77-86.
36. Liang P, Pardee AB. Diferential display of eukaryonic messenger RNA by means of the polymerase chain reaction. Science, 1992, 257: 967-971.
37. Poirier GMC, Pyati J, Wan JS, et al. Screening of diferentially expressed cDNA clones by diferential display using amplified RNA. Nucleic Acids Res, 1997, 25: 913-914.
38. Soares MB. Identification and cloning of diferentially expressed genes. Curr Opin Biotechnol, 1997, 8: 542-546.
39. Wadhwa R. Duncan E, Kaul SC, et al. An efective elimination of false positives isolated from diferential display of mRNAs. Mol Biotechnol, 1996, 6(2): 213-217.
40. Geng M, Wallrapp C, Muller-Pillasch F, et al. Isolation of diferentially expressed genes by combining representational diference analysis (RDA) and cDNA library arrays. Biotechniques, 1998, 25(3): 434-438.
41. Lawson ND, Berliner N. Representational diference analysis of a commited myeloid progenitor cell line reveals evidence for bilineage potential. Proc Natl Acad Sci USA, 1998, 95(17): 10129-10133.
42. Adams MD, Kerlavage AR, Fields C, et al. 3400 new expressed sequence tags identify a diversity of transcripts in human brain. Nature Genet, 1993,4: 256-267.
43. Adams MD, Kerlavage AR, Fleischmann RD, et al. Initial assessment of human gene diversity and expression paterns based upon 83 million nucleotides of cDNA sequence. Nature, 1995,377 (suppl): 3-174.
44. Velculescu VE, Zhang L, Vogelstein B. Serial analysis of gene expression. Science, 1995, 270(5235): 484-487.
45. Powell J. Enhanced concatemer cloning-a modification to the SAGE (Serial Analysis of Gene Expression) technique. Nucleic Acids Res, 1998, 26(14): 3445.3446.
46. Hibi K, Liu Q, Beaudry GA, et al. Serial analysis of gene expression in nonsmall cell lung cancer. Cancer Res, 1998, 58 (24): 5690-5694.
47. de Waard V, van den Berg BMM, Veken J, et al. Serial analysis of gene expression to assess the endothelial cell response to an atherogenic stimulus. Gene, 1999, 226(1): 1-8.
48. Schena M, Shalon D, Davis RW, et al. Quantitative monitoring of gene expression patterns with a complementary DNA microarray. Science, 1995, 270(5235): 467-470.
49. DeRisi JL, Iyer VR. Brown PO. Exploring the metabolic and genetic control of gene expression on a genomic scale. Science, 1997, 278: 680-686.
50. Jones DA. Fitzpatrick. Genomics and the discovery of new drug targets. Curr Opin Chem Biol, 1999, 3(1): 71-76.
51. Aitman TJ, Glazier AM, Wallace CA. Identification of CD36 (Fat) as an insulin-resistance gene causing defective fatty acid and glucose metabolism in hypertensive rats. Nat Genet, 1999, 21 (1): 76-83.
52. Harakava R, Gabriel DW. Genetic differences between two strains of Xylella fastidiosa revealed by suppression subtractive hybridization. Appl Environ Microbiol, 2003,69(2): 1315-1319.
53. Petroziello J, Yamane A, Westendorf L, et al. Suppression subtractive hybridization and expression profiling identifies a unique set of genes overexpressed in non-small-cell lung cancer. Oncogene, 2004, 23(46): 7734-7745.
54. Srivastava AK, Venkatachalam P, Raghothama KG, et al. Identification of lead-regulated genes by suppression subtractive hybridization in the heavy metal accumulator Sesbania drummondii. Planta, 2007, 225(6): 1353-1365.
55. Jesnowski R, Zubakov D, Faissner R, et al. Genes and proteins differentially expressed during in vitro malignant transformation of bovine pancreatic duct cells. Neoplasia, 2007, 9(2): 136-146.
56. Rosok O, Sioud M. Discovery of differentially expressed genes: technical considerations. Methods Mol Biol, 2007, 360:115-129.
57. Von Stein OD, Hies WG, Hofmann M. A high throughput screening for rarely transcribed diferentially expressed genes. Nucleic Acids Res, 1997, 25(13): 2598-2602.
58. Yoshimi M, Miyaishi O, Nakamura S, et al. Identification of genes preferentially expressed in articular cartilage by suppression subtractive hybridization. J Med Dent Sci, 2005, 52(4): 203-211.
59. Zhang YL, Ong CT, Leung KY. Molecular analysis of genetic differences between virulent and avirulent strains of Aeromonas hydrophila isolated from diseased fish. Microbiology, 2000, 146 (Pt 4): 999-1009.
60. Lee SH, Lee S, Choi D, et al. Identification of the down-regulated genes in a mat1-2-deleted strain of Gibberella zeae, using cDNA subtraction and microarray analysis. Fungal Genet Biol, 2006, 43(4): 295-310.
61. Bernier SP, Sokol PA. Use of suppression-subtractive hybridization to identify genes in the Burkholderia cepacia complex that are unique to Burkholderia cenocepacia. J Bacteriol, 2005, 187(15): 5278-5291.
62. Tosti A, Villardita S, Fazzini ML. The parasitic colonization of the horny layer in tinea versicolor. J Invest Dermatol, 1972, 59 (3): 233-237.
63. Salkin IF, Gordon MA. Polymorphism of Malassezia furfur. Can J Microbiol, 1977, 23 (4): 471-475.
64. Nazzaro-Porro M, Passi S, Caprilli F, et al. Induction of hyphae in culture of Pityrosporum by cholesterol and cholesterol esters. J Invest Dermatol, 1977, 69: 531-534.
65. Dorn M. Roehnert K. Dimorphism ofPityrosporum orbiculare in a defined culture medium. J Invest Dermatol, 1977, 69: 244-248.
66. Faergemarm J, Aly R, Howard I, et al. Growth and filament production of Pityrosporum orbiculare and Pityrosporum ovale on human stratum comeum in vitro. Acta Dermatol Venereol, 1983, 63: 388-392.
67. Bhattacharyya T, Richardson MD, Cordery CS. Morphological transition in Pityrosporum ovale In: The 26th Annual Meeting of the European Society for Dermatological Research (ESDR) Amsterdam, 1996, poster No. 21, 28th. Amsterdam, Holland.
68．王效义，秦珑，戴二黑，等．应用抑制消减杂交技术研究鼠疫菌与假结核菌基因组之间的差异．军事医学科学院院刊，2005，29：18-24．
69．郭应禄，张志文，艾军魁，等．肾癌抑制性消减杂交文库的构建及意义．中华泌尿外科杂志，2002(9)：517-520．
70. Porkka KP, Visakorpi T. Detection of differentially expressed genes in prostate cancer by combining suppression subtractive hybridization and cDNA library array. J Pathol, 2001, 193(1): 73-79.
71．林莉，潘亚萍，李琛，等．牙龈卟啉单胞菌不同毒力株基因差异的比较研究．中华口腔医学杂志，2006，41：734-738．
72. Alphey L. DNA sequencing: from experimental methods to bioinformatics. BIOS Scientifc Publishers Limited, 1997: 1-9.
73. Ivanov AS, Veselovsky AV, Dubanov AV, et al. Bioinformatics platform development: from gene to lead compound. Methods Mol Biol, 2006, 316: 389-431.
74. Calderone RA, Braun PC. Adherence and receptor relationships of Candida albicans. Microbiol Rev, 1991, 55(1): 1-20.
75. Louie A, Dixon DM, el-Maghrabi EA, et al. Relationship between Candida albicans epidermolytic proteinase activity and virulence in mice. J Med Vet Mycol, 1994, 32(1): 59-64.
76. Sundstrom P. Adhesins in Candida albicans. Curr Opin Microbiol, 1999, 2(4): 353-357.
77. Gilbert W. Towards a paradigm shift in biology. Nature, 1991, 349(6305): 99.
78. Gilbert W. DNA sequencing, today and tomorrow. Hosp Pract (Off Ed), 1991, 26(10): 165-169, 172, 174.
79. Cherry JM, Adler C, Ball C, et al. SGD: Saccharomyces Genome Database. Nucleic Acids Res, 1998, 26(1): 73-79.
80. Botstein D. Of genes and genomes. Ann N Y Acad Sci, 1999, 882: 32-41; discussion 56-65.
81. Li X, Wang J, Manley JL. Loss of splicing factor ASF/SF2 induces G2 cell cycle arrest and apoptosis, but inhibits intemucleosomal DNA fragmentation. Genes Dev, 2005, 19(22): 2705-2714.
82. Williams TM, Moolten D, Burlein J, et al. Identification of a zinc finger protein that inhibits IL-2 gene expression. Science, 1991, 254(5039): 1791-1794.
83. Sagaram US, Butchko RA, Shim WB. The putative monomeric G-protein GBP1 is negatively associated with fumonisin Bl production in Fusarium verticillioides. Mol Plant Pathol, 2006, 7(5): 381-389.
1. Gueho E, Boekhout T, Ashbee HR, et al. The role of Malassezia species in the ecology of human skin and as pathogens. Med Mycol, 1998, 36(supp 11): 220-229.
2. Saadatzadeh MR, Ashbee HR, Cunliffe W J, et al. Cell-mediated immunity to the mycelial phase of Malassezia spp. In patients with pityriasis versicolor and controls. Br J Dermatol, 2001, 144 (1): 77-84.
3. Gupta AK, Bluhm R, Summerbell R. Pityriasis versicolor. J Eur Acad Dermatol Venereol, 2002, 16 (1): 19-33.
4. Gaitanis G, Velegraki A, Frangoulis E, et al. Identification of Malassezia species from patient skin scales by PCR-RELP. Clin Microbiol Infect, 2002, 8 (3): 162-173.
5. Aspiroz C, Moreno LA, Rezusta A, et al. Differentiation of thee biotypes of Malassezia species on human normal skin. Correspondence with M.globosa, M.sympodialis and M.restricta. Mycopathologia, 1999, 145 (2): 69-74.
6. Guillot G, Gueho E, Lesourd M, et al. Identification of Malassezia species: a practical approach. J Mycol Med, 1996, 6: 103-110.
7. Sugita TM, Takashima T, Shinoda H, et al. New yeast species, Malassezia dermatis, isolated from patients with atopic dermatitis. J Clin Microbiol, 2002, 40: 1363-1367.
8. Nell A, James SA, Bond C J, et al. Identification and distribution of a novel Malassezia species yeast on normal equine skin. Vet Rec,2002, 150: 395-398.
9. Hirai A, Kano R, Makimura K, et al. Malassezia nana sp. nov., a novel lipid-dependent yeast species isolated from animals. Int J Syst Evol Microbiol. 2004, 54(Pt 2): 623-7.
10. Cabanes FJ, Theelen B, Castella G, et al. Two new lipid-dependent Malassezia species from domestic animals. FEMS Yeast Res,2007,16: [Epub ahead of print]
11. Cabanes FJ, Hemandez JJ, Castella G. Molecular analysis of Malassezia sympodialis: related strains from domestic animals. J Clin Microbiol 2005, 43: 277-283.
12．陈征，冉玉平，熊琳，等．马拉色菌在新生儿皮肤定植的研究．中华皮肤科杂志，2006，39：371-373．
13. Iskit S, Ilkit M, Turc-Bicer A, et al. Effect of circumcision on genital colonization of Malassezia spp. in a pediatric population. Medical Mycology. 2006, 44(2): 113-7.
14. Chowdhary A, Randhawa HS, Sharma S, et al. Malassezia furfur in a case of onychomycosis: colonizer or etiologic agent?. Med Mycol, 2005, 43(1): 87-90
15．王群，吴勤学，靳培英，等．嗜脂性马拉色菌与银屑病发病相关关系初探．中国麻风皮肤病杂志，2001，17(4)：231-233．
16. Redline RW, Redline SS, Boxerbaum B, et al. Systemic Malassezia furfur infections in patients receiving intralipid therapy. Hum Pathol, 1985, 16(8): 815-822.
17．李薇．糠秕马拉色菌的系统感染．国外医学皮肤性病学分册，1997，23：263-265．
18. Masure O, Leostic C, Abalain ML, et al. Malassezia furfur septicaemia in a child with leukaemia. J Infect, 1991, 23(3): 335-336.
19. Dixon DM, McNeil MM, Cohen ML, et al. Fungal infections: a growing threat. Public Health Rep, 1996, 111(3): 226-235.
20. Wroblewski N, Bar S, Mayser P. Missing granulocytic infiltrate in pityriasis versicolor-indication of specific anti-inflammatory activity of the pathogen. Mycoses, 2005, 48(Suppl 1): 66-71.
21. DeAngelis YM, Gemmer CM, Kaczvinsky JR, et al. Three etiologic facets of dandruff and seborrheic dermatitis: Malassezia fungi, sebaceous lipids, and individual sensitivity. J Invest Dermatol (Symposium Proceedings), 2005, 10(3): 295-297
22. Gaitanis G, Chasapi V, Velegraki A. Novel application of the masson-fontana stain for demonstrating Malassezia species melanin-like pigment production in vitro and in clinical specimens. J Clin Microbiol, 2005,43(8): 4147-4151
23. Casagrande BF, Fluckiger S, Linder MT, et al. Sensitization to the yeast malassezia sympodialis is specific for extrinsic and intrinsic atopic eczema. J Invest Dermatol, 2006,126(11): 2551.
24. Baroni A, Paoletti I, Ruocco E, et al. Possible role of Malassezia furfur in psoriasis: modulation of TGF-betal, integrin, and HSP70 expression in human keratinocytes and in the skin of psoriasis-affected patients. J Cutan Pathol, 2004, 31(1): 35-42..
25. Crespo Erchiga V, Ojeda Marto A, Vera Casano A, et al. Malassezia globosa as the causative agent of pityriasis versicolor. Br J Dermatol, 2000, 143 (4): 799-803.
26. Crespo-Erchiga V, Florencio VD. Malassezia yeasts and pityriasis versicolor. Curr Opin Infect Dis, 2006, 19(2): 139-147
27. Nakabayashi A, Sei Y, Guiot J. Identification of Malassezia species isolated from patients with seborrhoeic dermatitis, atopic dermatitis, pityriasis versicolor and normal subjects. Med Mycol, 2000,38(5): 337-341.
28. Miranda KC, de Araujo CR, Soares A J, et al. Identification of Malassezia species in patients with pityriasis versicolor in Goiania-GO.Rev Soc Bras Med Trop, 2006, 39(6): 582-583.
29. Ashbee. HR, Ingham E, Holland KT, et al. The carriage of Malassezia furfur serovars A, B and C in patients with pityriasis versicolor, seborrhoeic dermatitis and controls. Br J Dermatol, 1993, 129(5): 533-540.
30. Gupta AK, Kohli Y, Faergemann J, et al. Epidemiology of Malassezia yeasts associated with pityriasis versicolor in Ontario, Canada. Med Mycol, 2001, 39 (2): 199-206.
31. Gupta AK, Kohli Y, Summerbell RC, et al. Quantitative culture of Malassezia species from different body sites of individuals with or without dermatoses. Med Mycol, 2001, 39 (3): 243-251.
32．李志瑜，冉玉平，熊琳，等．从花斑癣患者皮损区及非皮损区分离和鉴定马拉色菌．中华皮肤科杂志，2003，36(8)：430-432．
33. Saadatzadeh MR, Ashbee HR, Holland KT. Production of the mycelial phase of Malassezia in vitro. Med Mycol, 2001, 39: 487-493.
34．梁作辉，冉玉平，代亚玲，等．马拉色菌菌丝相培养研究．华西医学，2005，20(1)：36-37．
35. Prohic A, Ozegovic L. Malassezia species isolated from lesional and non-lesional skin in patients with pityriasis versicolor. Mycoses, 2007, 50(1): 58-63.
36. Selander C, Zargari A, Mollby R, et al. Higher pH level, corresponding to that on the skin of patients with atopic eczema, stimulates the release of Malassezia sympodialis allergens. Allergy, 2006, 61(8): 1002-1008.
37. Andersson A, Rasool O, Schmidt M, et al. Cloning, expression and characterization of two new IgE-binding proteins from the yeast Malassezia sympodialis with sequence similarities to heat shock proteins and manganese superoxide dismutase. Eur J Biochem, 2004, 271(10): 1885-94.
38. Vilhelmsson M, Johansson C, Jacobsson-Ekman G, et al. The Malassezia Sympodialis Allergen Mala s 11 Induces Human Dendritic Cell Maturation, in Contrast to Its Human Homologue Manganese Superoxide Dismutase. Int Arch Allergy Immunol, 2007, 143(2): 155-162.
39. Sohnle PG, Collins-Lech C. Cell-mediated immunity to Pityrosporum orbiculare in tinea versicolor. J Clin Invest, 1978, 62 (1): 45-53.
40. Scheynius A, Faergemann J, Forsum U, et al. Phenotypic characterization in situ of inflammatory cells in pityriasis (tinea) versicolor. Acta Derm Venereol, 1984, 64 (6): 473-479.
41. Bergbrant IM, Andersson B, Faergemann J. Cell-mediated immunity to Malassezia furfur in patients with seborrhoeic dermatitis and pityriasis versicolor. Clin Exp Dermatol, 1999,24 (5): 402-406.
42. Sohnle PG. Collins-Lech C. Analysis of the lymphocyte transformation response to Pityrosporum orbiculare in patients with tinea versicolor. Clin Exp Immunol, 1982, 49 (3): 559-564.
43. Freire-Ruano A, Crespo-Leiro MG, Muniz J, et al. Dermatologic complications after heart transplantation: incidence and prognosis. Med Clin (Barc), 2000, 115 (6): 208-210.
44. Virgili A, Zampino MR, La Malfa V, et al Prevalence of superficial dermatomycoses in 73 renal transplant recipients. Dermatology, 1999, 199 (1): 31-34.
45. Hashim FA, Elhassan AM. Tinea versicolor and visceral leishaniasis. Int J Dermatol, 1994, 33 (4): 258-259.
46. Faergemann. J. Antibodies to Pityrosporum orbiculare in patients with tinea versicolor and controls of various ages. J Invest Dermatol, 1983, 80 (2): 133-135.
47. Silva V, Fischman O, de Camargo ZP. Humoral immune response to Malassezia furfur in patients with pityriasis versicolor and seborrheic dermatitis. Mycopathologia, 1997, 139 (2): 79-85.
48. Ishibashi Y, Sugita T, Nishikawa A. Cytokine secretion profile of human keratinocytes exposed to Malassezia yeasts. FEMS Immuno Med Microbiol, 2006, 48(3): 400-9.
49. Ran YP, Yoshiket T, Ogawa H. Lipase of Malassezia furfur, some properties and their relationship to cell growth. J Med Vet Mycol, 1993, 31: 77-85.
50．冉玉平，周光平，坪井良治，等．糠秕孢子菌与培养人角阮细胞的相互作用．中华皮肤科杂志，1997，30：294-298．
51．罗东辉，王侠生，何芳德．糠秕孢子菌对培养角质形成细胞产生细胞因子的影响及电镜观察．临床皮肤科杂志，2000，29：1-3．
52. Christina E, Walter E, Ingham E, et al. In vitro modulation of keratino-cytederived interleukin-1(IL-1a) and peripheral blood mononuclear cell-drived IL-1β response to cutaneous commensal mcroorganisms. Infect Immuni, 1995, 63 (4): 1223-1228.
53. Kesavan S, Walters CE, Holland KT, et al. The effects of Malassezia on pro-inflammatory cytokine production by human peripheral blood mono-nuclear cells in vitro. Med Mycol, 1998, 36 (2): 97-106.
54. Kesavan S, Holland KT, Ingam E. The effects of lipid extraction on the immunomodulatory activity of Malassezia species in vitro. Med Mycol, 2000, 38 (3): 239-247.
55. Watanabe S, Kano R, Sato H, et al. The effects of Malassezia yeasts on cytokine production by human keratinocytes. J Invest Dermatol, 2001, 116 (5): 769-773.
56. Tosti A, Villardita S, Fazzini ML. The parasitic colonization of the horny layer in tinea versicolor. J Invest Dermatol, 1972, 59 (3): 233-237.
57. Salkin IF, Gordon MA. Polymorphism of Malasseziafurfur. Can J Microbiol, 1977, 23 (4): 471-475.
58. Nazzaro-Porro M, Passi S, Caprilli F, et al. Induction of hyphae in culture of Pityrosporum by cholesterol and cholesterol esters. J Invest Dermatol, 1977, 69: 531-534.
59. Dorn M, Roehnert K. Dimorphism of Pityrosporum orbiculare in a defined culture medium. J Invest Dermatol, 1977, 69: 244-248.
60. Faergemann J, Aly R, Howard I, et al. Growth and filament production of Pityrosporum orbiculare and Pityrosporum ovale on human stratum corneum in vitro. Acta Dermatol Venereol, 1983, 63: 388-392.
61. Faergemann J. A new model for growth and filament production of Pityrosporum ovale (orbiculare) on human stratum corneum in vitro. J Invest Dermatol, 1989, 92: 117-119.
62. Bhattacharyya T, Richardson MD, Cordery CS. Morphological transition in Pityrosporum ovale In: The 26th Annual Meeting of the European Society for Dermatological Research (ESDR) Amsterdam. 1996, poster No.21, 28th. Amsterdam, Holland.
63. Sunenshine PJ, Schwartz RA, Janniger CK. Tinea versicolor. Int J Dermatol, 1998, 37 (9): 648-655.
2. Sugita TM, Takashima T, Shinoda H, et al. New yeast species, Malassezia dermatis, isolated from patients with atopic dermatitis. J Clin Microbiol, 2002, 40: 1363-1367.
3. Nell A, James SA, Bond CJ, et al. Identification and distribution of a novel Malassezia species yeast on normal equine skin. Vet Rec, 2002, 150: 395-398.
4. Gaitanis G, Robert V, Velegraki A. Verifiable single nucleotide polymorphisms of the internal transcribed spacer 2 region for the identification of 11 Malassezia species. J Dermatol Sci, 2006, 43(3): 214-217.
5. Mirhendi H, Makimura K, Zomorodian K, et al. A simple PCR-RFLP method for identification and differentiation of 11 Malassezia species. J Microbiol Methods, 2005, 61(2): 281-284.
6. Hirai A, Kano R, Makimura K, et al. Malassezia nana sp. nov., a novel lipid-dependent yeast species isolated from animals. Int J Syst Evol Microbiol, 2004, 54(Pt2): 623-627.
7. Cabanes FJ, Theelen B, Castella G, et al. Two new lipid-dependent Malassezia species from domestic animals. FEMS Yeast Res, 2007, 16: [Epub ahead of print]
8. Cabanes FJ, Hernandez JJ, Castella G. Molecular analysis of Malassezia sympodialis: related strains from domestic animals. J Clin Microbiol, 2005, 43: 277-283.
9. Gupta AK, Boekhout T, Theelen B, et al. Identification and typing of Malassezia species by amplified fragment length polymorphism and sequence analyses of the internal transcribed spacer and large-subunit regions of ribosomal DNA. J Clin Microbiol, 2004, 42(9): 4253-4260.
10. Gupta AK, Batra R, Bluhm R, et al. Skin diseases associated with Malassezia species. J Am Acad Dermatol, 2004, 51(5): 785-798.
11. Gueho E, Boekhout T, Ashbee HR, et al. The role of Malassezia species in the ecology of human skin and as pathogens. Med Mycol, 1998, 36 Suppl 1: 220-229.
12．王群，吴勤学，靳培英，等．嗜脂性马拉色菌与银屑病发病相关关系初探．中国麻风皮肤病杂志，2001，17(4)：231-233．
13. Redline RW, Redline SS, Boxerbaum B, et al. Systemic Malassezia furfur infections in patients receiving intralipid therapy. Hum Pathol, 1985, 16(8): 815-822.
14．李薇．糠秕马拉色菌的系统感染．国外医学皮肤性病学分册，1997，23：263-265．
15. Masure O, Leostic C, Abalain ML, et al. Malasseziafurfur septicaemia in a child with leukaemia. J Infect, 1991, 23(3): 335-336.
16. Dixon DM, McNeil MM, Cohen ML, et al. Fungal infections: a growing threat. Public Health Rep, 1996, 111 (3): 226-235.
17. Faergemann J. A new model for growth and filament production of Pityrosporum ovale (orbiculare) on human stratum corneum in vitro. J Invest Derrnatol, 1989, 92: 117-119.
18. Ran Y, Yoshiike T, Ogawa H. Lipase of Malassezia furfur: some properties and their relationship to cell growth. J Meal Vet Mycol, 1993, 31(1): 77-85.
19. Riciputo RM, Oliveri S, Micali G, et al. Phospholipase activity in Malassezia furfur pathogenic strains. Mycoses, 1996, 39(5-6): 233-235.
20．冉玉平，周光平，坪井良治，等．糠秕孢子菌与培养人角朊细胞的相互作用．中华皮肤科杂志，1997，30：294-298．
21. Diatchenko L, Lau YF, Campbell AP, et al, Suppression subtractive hybridization: a method for generating differentially regulated or tissue-specific cDNA probes and libraries. Proc Natl Acad Sci USA, 1996: 6025-6030.
22. Siebert PD, Chenchik A, Kellogg DE, et al. An improved PCR method for walking in uncloned genomic DNA. Nucleic Acids Res, 1995, 23(6): 1087-1088.
23. Akopyants NS, Fradkov A, Diatchenko L, et al. PCR-based subtractive hybridization and differences in gene content among strains of Helicobacter pylori. Proc Natl Acad Sci U S A, 1998, 95(22): 13108-13113.
24. Bogush ML, Velikodvorskaya TV, Lebedev YB, et al. Identificatiori and localization of differences between Escherichia coli and Salmonella typhimurium genomes by suppressive subtractive hybridization. Mol Gen Genet, 1999, 262(4-5): 721-729.
25．鲍朗，胡昌华，李学敏，等．利用抑制消减杂交技术研究钩端螺旋体致病相关基因．中华微生物学和免疫学杂志2001，21(5)：574-577．
26. Goswami RS, Xu JR, Trail F, et al. Genomic analysis of host-pathogen interaction between Fusarium graminearum and wheat during early stages of disease development. Microbiology, 2006, 152(Pt 6): 1877-1890.
27．冉玉平，罗汉超，李志玉．含菜子油培养基对花斑癣致病真菌的培养研究．中华皮肤科杂志，1987，20(1)：4-7．
28．梁作辉，冉玉平，代亚玲，等．马拉色菌菌丝态培养研究．华西医学，2005，20(1)：36-37．
29. Odds EC. Switch of phenotype as an escape mechanism of the intruder. Mycoses, 1997, 40(Suppl 2): 9-12.
30. Gow NA. Growth and guidance of the fungal hypha. Microbiology, 1994, 140 (Pt 12): 3193-3205.
31. Saadatzadeh MR, Ashbee HR, Cunliffe W J, et al. Cell-mediated immunity to the mycelial phase of Malassezia spp. In patients with pityriasis versicolor and controls. Br J Dermatol, 2001,144 (1): 77-84.
32. Prohic A, Ozegovic L. Malassezia species isolated from lesional and non-lesional skin in patients with pityriasis versicolor. Mycoses, 2007, 50(1): 58-63.
33. Miranda KC. de Araujo CR, Soares A J, et al. Identification of Malassezia species in patients with pityriasis versicolor in Goiania-GO. Rev Soc Bras Med Trop, 2006, 39(6): 582-583.
34. Lamar EE, Palmer E. Y-encoded, species-specific DNA in mice: evidence that the Y chromosome exists in two polymorphic forms in inbred strains. Cell, 1984, 37(1): 171-177.
35. Watson JB, Margulies JE. Diferential cDNA screening strategies to identify novel stage-specific proteins in the developing mammalian brain. Developmental Neuroscience, 1994,15: 77-86.
36. Liang P, Pardee AB. Diferential display of eukaryonic messenger RNA by means of the polymerase chain reaction. Science, 1992, 257: 967-971.
37. Poirier GMC, Pyati J, Wan JS, et al. Screening of diferentially expressed cDNA clones by diferential display using amplified RNA. Nucleic Acids Res, 1997, 25: 913-914.
38. Soares MB. Identification and cloning of diferentially expressed genes. Curr Opin Biotechnol, 1997, 8: 542-546.
39. Wadhwa R. Duncan E, Kaul SC, et al. An efective elimination of false positives isolated from diferential display of mRNAs. Mol Biotechnol, 1996, 6(2): 213-217.
40. Geng M, Wallrapp C, Muller-Pillasch F, et al. Isolation of diferentially expressed genes by combining representational diference analysis (RDA) and cDNA library arrays. Biotechniques, 1998, 25(3): 434-438.
41. Lawson ND, Berliner N. Representational diference analysis of a commited myeloid progenitor cell line reveals evidence for bilineage potential. Proc Natl Acad Sci USA, 1998, 95(17): 10129-10133.
42. Adams MD, Kerlavage AR, Fields C, et al. 3400 new expressed sequence tags identify a diversity of transcripts in human brain. Nature Genet, 1993,4: 256-267.
43. Adams MD, Kerlavage AR, Fleischmann RD, et al. Initial assessment of human gene diversity and expression paterns based upon 83 million nucleotides of cDNA sequence. Nature, 1995,377 (suppl): 3-174.
44. Velculescu VE, Zhang L, Vogelstein B. Serial analysis of gene expression. Science, 1995, 270(5235): 484-487.
45. Powell J. Enhanced concatemer cloning-a modification to the SAGE (Serial Analysis of Gene Expression) technique. Nucleic Acids Res, 1998, 26(14): 3445.3446.
46. Hibi K, Liu Q, Beaudry GA, et al. Serial analysis of gene expression in nonsmall cell lung cancer. Cancer Res, 1998, 58 (24): 5690-5694.
47. de Waard V, van den Berg BMM, Veken J, et al. Serial analysis of gene expression to assess the endothelial cell response to an atherogenic stimulus. Gene, 1999, 226(1): 1-8.
48. Schena M, Shalon D, Davis RW, et al. Quantitative monitoring of gene expression patterns with a complementary DNA microarray. Science, 1995, 270(5235): 467-470.
49. DeRisi JL, Iyer VR. Brown PO. Exploring the metabolic and genetic control of gene expression on a genomic scale. Science, 1997, 278: 680-686.
50. Jones DA. Fitzpatrick. Genomics and the discovery of new drug targets. Curr Opin Chem Biol, 1999, 3(1): 71-76.
51. Aitman TJ, Glazier AM, Wallace CA. Identification of CD36 (Fat) as an insulin-resistance gene causing defective fatty acid and glucose metabolism in hypertensive rats. Nat Genet, 1999, 21 (1): 76-83.
52. Harakava R, Gabriel DW. Genetic differences between two strains of Xylella fastidiosa revealed by suppression subtractive hybridization. Appl Environ Microbiol, 2003,69(2): 1315-1319.
53. Petroziello J, Yamane A, Westendorf L, et al. Suppression subtractive hybridization and expression profiling identifies a unique set of genes overexpressed in non-small-cell lung cancer. Oncogene, 2004, 23(46): 7734-7745.
54. Srivastava AK, Venkatachalam P, Raghothama KG, et al. Identification of lead-regulated genes by suppression subtractive hybridization in the heavy metal accumulator Sesbania drummondii. Planta, 2007, 225(6): 1353-1365.
55. Jesnowski R, Zubakov D, Faissner R, et al. Genes and proteins differentially expressed during in vitro malignant transformation of bovine pancreatic duct cells. Neoplasia, 2007, 9(2): 136-146.
56. Rosok O, Sioud M. Discovery of differentially expressed genes: technical considerations. Methods Mol Biol, 2007, 360:115-129.
57. Von Stein OD, Hies WG, Hofmann M. A high throughput screening for rarely transcribed diferentially expressed genes. Nucleic Acids Res, 1997, 25(13): 2598-2602.
58. Yoshimi M, Miyaishi O, Nakamura S, et al. Identification of genes preferentially expressed in articular cartilage by suppression subtractive hybridization. J Med Dent Sci, 2005, 52(4): 203-211.
59. Zhang YL, Ong CT, Leung KY. Molecular analysis of genetic differences between virulent and avirulent strains of Aeromonas hydrophila isolated from diseased fish. Microbiology, 2000, 146 (Pt 4): 999-1009.
60. Lee SH, Lee S, Choi D, et al. Identification of the down-regulated genes in a mat1-2-deleted strain of Gibberella zeae, using cDNA subtraction and microarray analysis. Fungal Genet Biol, 2006, 43(4): 295-310.
61. Bernier SP, Sokol PA. Use of suppression-subtractive hybridization to identify genes in the Burkholderia cepacia complex that are unique to Burkholderia cenocepacia. J Bacteriol, 2005, 187(15): 5278-5291.
62. Tosti A, Villardita S, Fazzini ML. The parasitic colonization of the horny layer in tinea versicolor. J Invest Dermatol, 1972, 59 (3): 233-237.
63. Salkin IF, Gordon MA. Polymorphism of Malassezia furfur. Can J Microbiol, 1977, 23 (4): 471-475.
64. Nazzaro-Porro M, Passi S, Caprilli F, et al. Induction of hyphae in culture of Pityrosporum by cholesterol and cholesterol esters. J Invest Dermatol, 1977, 69: 531-534.
65. Dorn M. Roehnert K. Dimorphism ofPityrosporum orbiculare in a defined culture medium. J Invest Dermatol, 1977, 69: 244-248.
66. Faergemarm J, Aly R, Howard I, et al. Growth and filament production of Pityrosporum orbiculare and Pityrosporum ovale on human stratum comeum in vitro. Acta Dermatol Venereol, 1983, 63: 388-392.
67. Bhattacharyya T, Richardson MD, Cordery CS. Morphological transition in Pityrosporum ovale In: The 26th Annual Meeting of the European Society for Dermatological Research (ESDR) Amsterdam, 1996, poster No. 21, 28th. Amsterdam, Holland.
68．王效义，秦珑，戴二黑，等．应用抑制消减杂交技术研究鼠疫菌与假结核菌基因组之间的差异．军事医学科学院院刊，2005，29：18-24．
69．郭应禄，张志文，艾军魁，等．肾癌抑制性消减杂交文库的构建及意义．中华泌尿外科杂志，2002(9)：517-520．
70. Porkka KP, Visakorpi T. Detection of differentially expressed genes in prostate cancer by combining suppression subtractive hybridization and cDNA library array. J Pathol, 2001, 193(1): 73-79.
71．林莉，潘亚萍，李琛，等．牙龈卟啉单胞菌不同毒力株基因差异的比较研究．中华口腔医学杂志，2006，41：734-738．
72. Alphey L. DNA sequencing: from experimental methods to bioinformatics. BIOS Scientifc Publishers Limited, 1997: 1-9.
73. Ivanov AS, Veselovsky AV, Dubanov AV, et al. Bioinformatics platform development: from gene to lead compound. Methods Mol Biol, 2006, 316: 389-431.
74. Calderone RA, Braun PC. Adherence and receptor relationships of Candida albicans. Microbiol Rev, 1991, 55(1): 1-20.
75. Louie A, Dixon DM, el-Maghrabi EA, et al. Relationship between Candida albicans epidermolytic proteinase activity and virulence in mice. J Med Vet Mycol, 1994, 32(1): 59-64.
76. Sundstrom P. Adhesins in Candida albicans. Curr Opin Microbiol, 1999, 2(4): 353-357.
77. Gilbert W. Towards a paradigm shift in biology. Nature, 1991, 349(6305): 99.
78. Gilbert W. DNA sequencing, today and tomorrow. Hosp Pract (Off Ed), 1991, 26(10): 165-169, 172, 174.
79. Cherry JM, Adler C, Ball C, et al. SGD: Saccharomyces Genome Database. Nucleic Acids Res, 1998, 26(1): 73-79.
80. Botstein D. Of genes and genomes. Ann N Y Acad Sci, 1999, 882: 32-41; discussion 56-65.
81. Li X, Wang J, Manley JL. Loss of splicing factor ASF/SF2 induces G2 cell cycle arrest and apoptosis, but inhibits intemucleosomal DNA fragmentation. Genes Dev, 2005, 19(22): 2705-2714.
82. Williams TM, Moolten D, Burlein J, et al. Identification of a zinc finger protein that inhibits IL-2 gene expression. Science, 1991, 254(5039): 1791-1794.
83. Sagaram US, Butchko RA, Shim WB. The putative monomeric G-protein GBP1 is negatively associated with fumonisin Bl production in Fusarium verticillioides. Mol Plant Pathol, 2006, 7(5): 381-389.
1. Gueho E, Boekhout T, Ashbee HR, et al. The role of Malassezia species in the ecology of human skin and as pathogens. Med Mycol, 1998, 36(supp 11): 220-229.
2. Saadatzadeh MR, Ashbee HR, Cunliffe W J, et al. Cell-mediated immunity to the mycelial phase of Malassezia spp. In patients with pityriasis versicolor and controls. Br J Dermatol, 2001, 144 (1): 77-84.
3. Gupta AK, Bluhm R, Summerbell R. Pityriasis versicolor. J Eur Acad Dermatol Venereol, 2002, 16 (1): 19-33.
4. Gaitanis G, Velegraki A, Frangoulis E, et al. Identification of Malassezia species from patient skin scales by PCR-RELP. Clin Microbiol Infect, 2002, 8 (3): 162-173.
5. Aspiroz C, Moreno LA, Rezusta A, et al. Differentiation of thee biotypes of Malassezia species on human normal skin. Correspondence with M.globosa, M.sympodialis and M.restricta. Mycopathologia, 1999, 145 (2): 69-74.
6. Guillot G, Gueho E, Lesourd M, et al. Identification of Malassezia species: a practical approach. J Mycol Med, 1996, 6: 103-110.
7. Sugita TM, Takashima T, Shinoda H, et al. New yeast species, Malassezia dermatis, isolated from patients with atopic dermatitis. J Clin Microbiol, 2002, 40: 1363-1367.
8. Nell A, James SA, Bond C J, et al. Identification and distribution of a novel Malassezia species yeast on normal equine skin. Vet Rec,2002, 150: 395-398.
9. Hirai A, Kano R, Makimura K, et al. Malassezia nana sp. nov., a novel lipid-dependent yeast species isolated from animals. Int J Syst Evol Microbiol. 2004, 54(Pt 2): 623-7.
10. Cabanes FJ, Theelen B, Castella G, et al. Two new lipid-dependent Malassezia species from domestic animals. FEMS Yeast Res,2007,16: [Epub ahead of print]
11. Cabanes FJ, Hemandez JJ, Castella G. Molecular analysis of Malassezia sympodialis: related strains from domestic animals. J Clin Microbiol 2005, 43: 277-283.
12．陈征，冉玉平，熊琳，等．马拉色菌在新生儿皮肤定植的研究．中华皮肤科杂志，2006，39：371-373．
13. Iskit S, Ilkit M, Turc-Bicer A, et al. Effect of circumcision on genital colonization of Malassezia spp. in a pediatric population. Medical Mycology. 2006, 44(2): 113-7.
14. Chowdhary A, Randhawa HS, Sharma S, et al. Malassezia furfur in a case of onychomycosis: colonizer or etiologic agent?. Med Mycol, 2005, 43(1): 87-90
15．王群，吴勤学，靳培英，等．嗜脂性马拉色菌与银屑病发病相关关系初探．中国麻风皮肤病杂志，2001，17(4)：231-233．
16. Redline RW, Redline SS, Boxerbaum B, et al. Systemic Malassezia furfur infections in patients receiving intralipid therapy. Hum Pathol, 1985, 16(8): 815-822.
17．李薇．糠秕马拉色菌的系统感染．国外医学皮肤性病学分册，1997，23：263-265．
18. Masure O, Leostic C, Abalain ML, et al. Malassezia furfur septicaemia in a child with leukaemia. J Infect, 1991, 23(3): 335-336.
19. Dixon DM, McNeil MM, Cohen ML, et al. Fungal infections: a growing threat. Public Health Rep, 1996, 111(3): 226-235.
20. Wroblewski N, Bar S, Mayser P. Missing granulocytic infiltrate in pityriasis versicolor-indication of specific anti-inflammatory activity of the pathogen. Mycoses, 2005, 48(Suppl 1): 66-71.
21. DeAngelis YM, Gemmer CM, Kaczvinsky JR, et al. Three etiologic facets of dandruff and seborrheic dermatitis: Malassezia fungi, sebaceous lipids, and individual sensitivity. J Invest Dermatol (Symposium Proceedings), 2005, 10(3): 295-297
22. Gaitanis G, Chasapi V, Velegraki A. Novel application of the masson-fontana stain for demonstrating Malassezia species melanin-like pigment production in vitro and in clinical specimens. J Clin Microbiol, 2005,43(8): 4147-4151
23. Casagrande BF, Fluckiger S, Linder MT, et al. Sensitization to the yeast malassezia sympodialis is specific for extrinsic and intrinsic atopic eczema. J Invest Dermatol, 2006,126(11): 2551.
24. Baroni A, Paoletti I, Ruocco E, et al. Possible role of Malassezia furfur in psoriasis: modulation of TGF-betal, integrin, and HSP70 expression in human keratinocytes and in the skin of psoriasis-affected patients. J Cutan Pathol, 2004, 31(1): 35-42..
25. Crespo Erchiga V, Ojeda Marto A, Vera Casano A, et al. Malassezia globosa as the causative agent of pityriasis versicolor. Br J Dermatol, 2000, 143 (4): 799-803.
26. Crespo-Erchiga V, Florencio VD. Malassezia yeasts and pityriasis versicolor. Curr Opin Infect Dis, 2006, 19(2): 139-147
27. Nakabayashi A, Sei Y, Guiot J. Identification of Malassezia species isolated from patients with seborrhoeic dermatitis, atopic dermatitis, pityriasis versicolor and normal subjects. Med Mycol, 2000,38(5): 337-341.
28. Miranda KC, de Araujo CR, Soares A J, et al. Identification of Malassezia species in patients with pityriasis versicolor in Goiania-GO.Rev Soc Bras Med Trop, 2006, 39(6): 582-583.
29. Ashbee. HR, Ingham E, Holland KT, et al. The carriage of Malassezia furfur serovars A, B and C in patients with pityriasis versicolor, seborrhoeic dermatitis and controls. Br J Dermatol, 1993, 129(5): 533-540.
30. Gupta AK, Kohli Y, Faergemann J, et al. Epidemiology of Malassezia yeasts associated with pityriasis versicolor in Ontario, Canada. Med Mycol, 2001, 39 (2): 199-206.
31. Gupta AK, Kohli Y, Summerbell RC, et al. Quantitative culture of Malassezia species from different body sites of individuals with or without dermatoses. Med Mycol, 2001, 39 (3): 243-251.
32．李志瑜，冉玉平，熊琳，等．从花斑癣患者皮损区及非皮损区分离和鉴定马拉色菌．中华皮肤科杂志，2003，36(8)：430-432．
33. Saadatzadeh MR, Ashbee HR, Holland KT. Production of the mycelial phase of Malassezia in vitro. Med Mycol, 2001, 39: 487-493.
34．梁作辉，冉玉平，代亚玲，等．马拉色菌菌丝相培养研究．华西医学，2005，20(1)：36-37．
35. Prohic A, Ozegovic L. Malassezia species isolated from lesional and non-lesional skin in patients with pityriasis versicolor. Mycoses, 2007, 50(1): 58-63.
36. Selander C, Zargari A, Mollby R, et al. Higher pH level, corresponding to that on the skin of patients with atopic eczema, stimulates the release of Malassezia sympodialis allergens. Allergy, 2006, 61(8): 1002-1008.
37. Andersson A, Rasool O, Schmidt M, et al. Cloning, expression and characterization of two new IgE-binding proteins from the yeast Malassezia sympodialis with sequence similarities to heat shock proteins and manganese superoxide dismutase. Eur J Biochem, 2004, 271(10): 1885-94.
38. Vilhelmsson M, Johansson C, Jacobsson-Ekman G, et al. The Malassezia Sympodialis Allergen Mala s 11 Induces Human Dendritic Cell Maturation, in Contrast to Its Human Homologue Manganese Superoxide Dismutase. Int Arch Allergy Immunol, 2007, 143(2): 155-162.
39. Sohnle PG, Collins-Lech C. Cell-mediated immunity to Pityrosporum orbiculare in tinea versicolor. J Clin Invest, 1978, 62 (1): 45-53.
40. Scheynius A, Faergemann J, Forsum U, et al. Phenotypic characterization in situ of inflammatory cells in pityriasis (tinea) versicolor. Acta Derm Venereol, 1984, 64 (6): 473-479.
41. Bergbrant IM, Andersson B, Faergemann J. Cell-mediated immunity to Malassezia furfur in patients with seborrhoeic dermatitis and pityriasis versicolor. Clin Exp Dermatol, 1999,24 (5): 402-406.
42. Sohnle PG. Collins-Lech C. Analysis of the lymphocyte transformation response to Pityrosporum orbiculare in patients with tinea versicolor. Clin Exp Immunol, 1982, 49 (3): 559-564.
43. Freire-Ruano A, Crespo-Leiro MG, Muniz J, et al. Dermatologic complications after heart transplantation: incidence and prognosis. Med Clin (Barc), 2000, 115 (6): 208-210.
44. Virgili A, Zampino MR, La Malfa V, et al Prevalence of superficial dermatomycoses in 73 renal transplant recipients. Dermatology, 1999, 199 (1): 31-34.
45. Hashim FA, Elhassan AM. Tinea versicolor and visceral leishaniasis. Int J Dermatol, 1994, 33 (4): 258-259.
46. Faergemann. J. Antibodies to Pityrosporum orbiculare in patients with tinea versicolor and controls of various ages. J Invest Dermatol, 1983, 80 (2): 133-135.
47. Silva V, Fischman O, de Camargo ZP. Humoral immune response to Malassezia furfur in patients with pityriasis versicolor and seborrheic dermatitis. Mycopathologia, 1997, 139 (2): 79-85.
48. Ishibashi Y, Sugita T, Nishikawa A. Cytokine secretion profile of human keratinocytes exposed to Malassezia yeasts. FEMS Immuno Med Microbiol, 2006, 48(3): 400-9.
49. Ran YP, Yoshiket T, Ogawa H. Lipase of Malassezia furfur, some properties and their relationship to cell growth. J Med Vet Mycol, 1993, 31: 77-85.
50．冉玉平，周光平，坪井良治，等．糠秕孢子菌与培养人角阮细胞的相互作用．中华皮肤科杂志，1997，30：294-298．
51．罗东辉，王侠生，何芳德．糠秕孢子菌对培养角质形成细胞产生细胞因子的影响及电镜观察．临床皮肤科杂志，2000，29：1-3．
52. Christina E, Walter E, Ingham E, et al. In vitro modulation of keratino-cytederived interleukin-1(IL-1a) and peripheral blood mononuclear cell-drived IL-1β response to cutaneous commensal mcroorganisms. Infect Immuni, 1995, 63 (4): 1223-1228.
53. Kesavan S, Walters CE, Holland KT, et al. The effects of Malassezia on pro-inflammatory cytokine production by human peripheral blood mono-nuclear cells in vitro. Med Mycol, 1998, 36 (2): 97-106.
54. Kesavan S, Holland KT, Ingam E. The effects of lipid extraction on the immunomodulatory activity of Malassezia species in vitro. Med Mycol, 2000, 38 (3): 239-247.
55. Watanabe S, Kano R, Sato H, et al. The effects of Malassezia yeasts on cytokine production by human keratinocytes. J Invest Dermatol, 2001, 116 (5): 769-773.
56. Tosti A, Villardita S, Fazzini ML. The parasitic colonization of the horny layer in tinea versicolor. J Invest Dermatol, 1972, 59 (3): 233-237.
57. Salkin IF, Gordon MA. Polymorphism of Malasseziafurfur. Can J Microbiol, 1977, 23 (4): 471-475.
58. Nazzaro-Porro M, Passi S, Caprilli F, et al. Induction of hyphae in culture of Pityrosporum by cholesterol and cholesterol esters. J Invest Dermatol, 1977, 69: 531-534.
59. Dorn M, Roehnert K. Dimorphism of Pityrosporum orbiculare in a defined culture medium. J Invest Dermatol, 1977, 69: 244-248.
60. Faergemann J, Aly R, Howard I, et al. Growth and filament production of Pityrosporum orbiculare and Pityrosporum ovale on human stratum corneum in vitro. Acta Dermatol Venereol, 1983, 63: 388-392.
61. Faergemann J. A new model for growth and filament production of Pityrosporum ovale (orbiculare) on human stratum corneum in vitro. J Invest Dermatol, 1989, 92: 117-119.
62. Bhattacharyya T, Richardson MD, Cordery CS. Morphological transition in Pityrosporum ovale In: The 26th Annual Meeting of the European Society for Dermatological Research (ESDR) Amsterdam. 1996, poster No.21, 28th. Amsterdam, Holland.
63. Sunenshine PJ, Schwartz RA, Janniger CK. Tinea versicolor. Int J Dermatol, 1998, 37 (9): 648-655.