SW-V: modelo de streaming de software baseado em técnicas de virtualização e transporte peer-to-peer

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UNIVERSIDADE ESTADUAL PAULISTA “Júlio de Mesquita Filho” Pós-Graduação em Ciência da Computação Rafael Augusto Teixeira SW-V: Modelo de streaming de software baseado em técnicas de virtualização e transporte peer-to-peer UNESP 2010 RAFAEL AUGUSTO TEIXEIRA SW-V: Modelo de streaming de software baseado em técnicas de virtualização e transporte peer-to-peer Dissertação apresentada para obtenção do título de Mestre em Ciência da Computação, área de Arquitetura de Computadores e Sistemas Distribuídos junto ao Programa de Pós-Graduação em Ciência da Computação do Instituto de Biociências, Letras e Ciências Exatas da Universidade Estadual Paulista “Júlio de Mesquita Filho”, Campus de São José do Rio Preto. Orientador: Marcos Antônio Cavenaghi São José do Rio Preto, 26 de Março de 2010 Teixeira, Rafael Augusto. SW-V: modelo de streaming de software baseado em técnicas de virtualização e transporte peer-to-peer / Rafael Augusto Teixeira. - São José do Rio Preto : [s.n.], 2010. 90 f. : il. ; 30 cm. Orientador: Marcos Antônio Cavenaghi Dissertação (mestrado) - Universidade Estadual Paulista, Instituto de Biociências, Letras e Ciências Exatas 1. Sistemas de computação virtual. 2. Sistemas operacionais. 3. Sistemas de processamento distribuído. I. Cavenaghi, Marcos Antônio. II. Universidade Estadual Paulista, Instituto de Biociências, Letras e Ciências Exatas. III. Título. CDU – 004.75 Ficha catalográfica elaborada pela Biblioteca do IBILCE Campus de São José do Rio Preto - UNESP _______________________________Agradecimentos Em primeiro lugar, agradeço a Deus autor da maior obra científica que é a vida, todas as coisas foram criadas por Ele e sem Ele nada existiria. Agradeço por todas as vezes que iluminou minha mente e me mostrou o caminho a ser seguido, tanto na vida acadêmica quanto na vida cotidiana, pois tudo o que tenho e sou foi possível por Ele. Agradeço também ao meu orientador Prof. Dr. Marcos Antônio Cavenaghi pela confiança em mim depositada desde o momento que me aceitou como orientando, pelo acompanhamento que tive durante o trabalho, pelas correções, e pelas idéias que foram agregadas ao trabalho. Aos demais professores do programa de mestrado que com grande dedicação contribuíram para a formação das idéias deste trabalho, em especial a Prof. Dra. Roberta Spolon que acompanhou o desenvolvimento deste trabalho, ajudando sempre na organização das idéias, nas correções e submissões de artigos. Agradeço a MSTech por entender a importância do programa de mestrado e me conceder a oportunidade de conciliar os estudos e o trabalho. Aos meus amados pais Rosângela e José, que me proporcionaram desde minha infância condições para que eu nunca interrompesse os estudos, me incentivando sempre a buscar mais e nunca me acomodar. Agradeço ao carinho e amor que nunca faltou, que muitas vezes serviram de incentivo para a conclusão deste trabalho. A toda minha família que de uma forma geral foram uma base para que este trabalho se concretizasse. E por fim, agradeço a Karina, que passou de noiva a minha amada esposa durante o desenvolvimento deste trabalho, agradeço pela paciência principalmente nas horas que tive que dividir o tempo com o estudo. Agradeço pelo carinho, cuidado e amor que foram fundamentais para que esse trabalho fosse possível. Que possamos juntos, a cada dia, escrever página a página o nosso livro que nunca terá fim. Resumo Diante da constante evolução dos sistemas computacionais e seu potencial de processamento, a cada dia se torna necessário novas técnicas de aproveitamento destes recursos. Soluções que visam facilitar o gerenciamento da grande massa crescente de computadores e aplicações já se tornaram necessidades reais, não só soluções focadas nas grandes corporações, mas a cada dia, novas pequenas e médias empresas e outras organizações, como por exemplo escolas, fazem parte das estatísticas do uso de computadores e aplicações. Neste contexto, focando uma ferramenta compatível neste cenário de crescimento, este trabalho desenvolve um modelo de streaming de software chamado SW-V que é baseado no estudo de técnicas de virtualização e redes peer-to-peer que elimina a necessidade da instalação e configuração do software máquina-a-máquina para que ele seja utilizado. As características principais deste modelo que o destaca das soluções atuais são: um mecanismo de seqüenciamento dos recursos que são utilizados pelo software; um mecanismo de distribuição da imagem que utiliza a própria infra-estrutura de rede eliminando a necessidade de altos investimentos em servidores; um middleware de virtualização que não requer privilégios administrativos ou de sistema para ser executado; um mecanismo peer-topeer assíncrono usado para aumentar a velocidade com que a distribuição da imagem do software ocorre para os clientes; e ainda possui suporte para que o usuário utilize as aplicações mesmo estando desconectado da rede. Durante o trabalho foram desenvolvidos pequenos módulos que vieram a comprovar que o modelo proposto pode ser adotado como base para a construção de uma solução robusta e escalável de virtualização de aplicação. Abstract In face of constant evolution of computing systems and the growing processing potential of computing, new techniques of use of these resources are necessary. Software solutions which intend make easy the management of this giant mass of computers and application are actually necessary, not only solution focused in big companies or large corporation, but each day, new small enterprises other segments like the educational organization became part of statistical of growing use of computer and software. In this scenario, this work formulate a model of software streaming based on study of virtualization techniques and peer-to-peer networks which eliminates the need of installation and configuration of determined software on each computer. The main characteristics of this model involve: a mechanism of sequencing of resources used by the software; a distribution mechanism of the software image using the available network infrastructure eliminating the need of high costs of investments and licensing; a peer-to-peer asynchronous distribution used to improve the sending of software image to the client computers; and still have off-line support where the user can execute de software even the computer is out of network and without server connection. Also some modules of mechanism proposed were developed to prove that all processes will works and all modules together can be used to build a robust and scalable framework of application virtualization. Sumário Lista de Abreviaturas e Siglas. iii Lista de Figuras. iv Lista de Tabelas. v 1 Introdução . 1 1.1 Contextualização. 1 1.2 Motivações. 2 1.3 Objetivos. 4 1.4 Estrutura da Monografia . 5 2 Virtualização . 7 2.1 No início dos mainframes . 7 2.2 A necessidade de virtualização para a arquitetura x86 . 9 2.3 Abstração e virtualização. 10 2.4 Máquinas virtuais. 14 2.5 Virtual Machine Monitor . 16 2.5.1 Propriedades do VMM . 16 2.5.2 Teorema de Popek e Goldberg . 18 2.6 Classificação das VMs. 19 2.6 Máquina virtual de aplicação . 20 2.6.1 Sistemas Multi-programados. 20 2.6.2 Emuladores e tradução binária dinâmica. 20 2.6.3 VMs de linguagem de alto-nível . 21 2.7 Máquina virtual de sistema . 22 2.8 Considerações finais . 25 3 Técnicas de Virtualização . 26 3.1 Virtualização Clássica. 26 3.2 Desafios arquiteturais do x86 . 27 3.2.1 Ring Compression . 27 3.2.2 Ring Aliasing . 28 3.2.3 Address Space Compression . 28 3.2.4 Instruções sensíveis não privilegiadas. 28 3.2.5 Falhas silenciosas de privilégio . 29 3.2.6 Interrupt Virtualization. 29 3.3 Trap-and-emulate. 29 3.4 Virtualização completa . 30 3.5 Paravirtualização. 32 3.6 Tradução dinâmica. 33 3.7 Virtualização assistida por hardware . 34 3.8 Virtualização de memória . 35 3.9 Virtualização de dispositivo. 36 3.10 VMWare . 37 3.11 FreeBSD Jails. 39 3.12 Xen. 40 3.13 User-Mode linux . 42 3.14 QEMU. 42 3.15 JVM – Java Virtual Machine . 43 3.16 Considerações finais . 45 4 Virtualização de Aplicação . 46 4.1 Conceito de virtualização de aplicação. 46 4.2 Classificações da virtualização de aplicação . 48 i 4.3 Microsoft App-V . 50 4.4 VMWare ThinApp. 52 4.5 Citrix XenApp . 53 4.6 Considerações finais . 54 5 Redes peer-to-peer. 55 5.1 Introdução as redes peer-to-peer. 55 5.2 Características das redes peer-to-peer. 56 5.3 Classificação das redes peer-to-peer. 57 5.3.1 Classificação quanto aos índices . 58 5.3.2 Classificação quanto ao tipo de busca . 58 5.3.3 Classificação híbrida . 59 5.4 Aplicações peer-to-peer . 60 5.5 Considerações finais . 60 6 Modelo SW-V de streaming de software . 62 6.1 Introdução ao modelo SW-V . 62 6.2 Criação da imagem da aplicação. 64 6.2.1 Captura da instalação do software . 64 6.2.2 Capturando os arquivos . 65 6.2.3 Capturando as chaves de registros. 67 6.2.4 Imagem da instalação da aplicação . 69 6.3 Seqüenciamento assistido da aplicação . 69 6.4 Streaming da imagem da aplicação. 71 6.5 Middleware de virtualização. 73 6.5.1 Sistema de arquivos virtual . 75 6.5.2 Espaço virtual de registros . 76 6.5.3 Monitor de criação de subprocessos. 77 6.5.4 Interceptação de variáveis de ambiente with probable Meniere’s were selected among patients referred to the outpatient clinic of Amir-Aalam hospital between the years 2012 and 2015. Ninety-one healthy controls were selected from normal healthy subjects from the same region. The control group underwent history analysis and a physical exam to confirm their health status. We matched our control group for sex and age with both groups. Audiological, vestibular, and functional status in each patient was evaluated based on the American Academy of OtolaryngologyHead and Neck Surgery guidelines (14). The diagnosis was confirmed in all patients by ruling out the presence of anatomic lesions using magnetic resonance imaging (MRI). All the participants were requested to sign written informed consent. Patients didn’t pay for the complementary tests and their identity remained hidden throughout the study. HLA typing After taking 5cc of blood from each patient, samples were collected in EDTA tubes with anticoagulating agent stored at 20*C. The DNA was extracted using salting out method and HLA-Cw typing was performed using sequence specific primers (SSP) polymerase chain reaction [DynalAllset+TM SSP Kit] (15). Statistical analysis HLA-Cw Allele frequencies were calculated for each group and were compared using the pearson’s chi-square test and fischer exact test. The significance of association between HLA-Cw Allele and Meniere’s disease was estimated by odds ratio (OR) and 95% confidence intervals (95% CI) using the stata software (version8). P values less than 0.05 were considered to be statistically significant. 262 Iranian Journal of Otorhinolaryngology, Vol.28(4), Serial No.87, Jul 2016 HLA-CW Alleles in Meniere disease Results The clinical features of the patients are shown in table 1. HLA-Cw allele frequencies were determined in all patients. The distributions of HLA-Cw frequencies were compared among Table1: Clinical characteristics of the patients. Sex (M/F) Mean age Onset time (Years) Unilateral/bilateral Level of Mild hearing Moderate Severe Total number of patients *Meniere’s Disease Definite MD* 13/10 34.96±13.047 (13-71) 3.74±3.107 (1-12) 21/1 13 8 2 23 different groups. There was a statistically significant difference in the frequency of HLA-Cw*04 in patients with definite or probable Meniere’s disease (18%) and healthy controls (1%) (P=0.001) (Table.2). Probable MD 17/7 41.04±16.815 (15-76) 7.63±7.033 (1-24) 19/5 9 5 9 24 Control 51/40 38.53±10.513(14-78) N/A N/A N/A N/A N/A 91 Table 2: Distribution of HLA-Cw Alleles in patients and controls. HLA-C MD* patients (n=47) (%) # Control group (n=91) (%) # P value allele OR (CI 95%) Cw*01 Cw*02 Cw*03 Cw*04 Cw*06 Cw*07 Cw*08 Cw*12 Cw*13 Cw*14 Cw*15 Cw*16 Cw*17 Cw*18 Total *Meniere’s disease 2 (2.1%) 0 (0%) 2 (2.1%) 17 (18.1%) 10 (10.6%) 13 (13.8%) 4(4.3%) 8(19.1%) 0 (0%) 7(7.4%) 1(1.1%) 17(18.1%) 3(3.2%) 0(0%) 94(100%) 7 (3.8%) 7 (3.8%) 9 (4.9%) 2 (1.1%) 33 (18.1%) 25 (13.7%) 4(2.2%) 43(23.6%) 3(1.6%) 17(9.3%) 0(0%) 9(4.9%) 7(3.8%) 16(8.8%) 182(100%) 0.72 0.09 0.34 <0.0001 0.10 0.98 0.45 0.39 0.55 0.59 0.34 <0.0001 1.00 0.002 0.543(0.111-2.669) 0.418(0.88-1.975) 19.870(4.481-88.101) 0.538(0.252-1.145) 1.008(0.490-2.074) 1.978(0.483-8.092) 0.766(0.413-1.419) 0.781(0.312-1.955) 4.244(1.811-9.943) 0.824(0.208-3.263) HLA-Cw*16 allele frequency was also significantly higher in patients with definite or probable Meniere’s disease compared to the controls. [p: 0.0001, OR: 4.244, 95% CI(1.81-9.94)] (Table.2). On the other hand, HLA-Cw *18 allele frequency was significantly decreased in patients compared to the control group (P=0.002) (Table. 2). Frequencies of HLA-Cw alleles showed significant differences between probable Meniere’s disease and definite Meniere’s disease group. There was an increase in the frequency of HLA-Cw*12 in probable Meniere’s disease group compared to definite Meniere’s disease group (P=0.046, OR; 0.328, 95% CI (0.107- 1.012)] (Table. 3). Iranian Journal of Otorhinolaryngology, Vol.28(4), Serial No.87, Jul 2016 263 Dabiri S, et al Table 3: Distribution of HLA-Cw Alleles in definite MD, probable MD patients, and controls. HLA-C allele Definite MD* patients (n=23) (%)# Probable MD* patients (n=24) (%)# Control group (n=91) (%) # P value (Definite vs. probable) P value (Definit vs. Control) P value (probable vs. Control) Cw*01 Cw*02 Cw*03 Cw*04 2 (4.3%) 0(0%) 1 (2.2%) 8(17.4%) 0(0%) 0(0%) 1(2.1%) 9(18.8%) 7 (3.8%) 7 (3.8%) 9 (4.9%) 2 (1.1%) 0.23 N/A >0.99ǂ 0.86 >0.99 0.35ǂ 0.69ǂ 10-4 0.35 0.35 0.69ǂ 10-4 Cw*06 7(15.2%) 3(6.3%) 33 (18.1%) 0.15 0.64 0.46 Cw*07 Cw*08 8(17.4%) 0(0%) 5(10.4%) 4(8.3%) 25 (13.7%) 4(2.2%) 0.32 0.11ǂ 0.52 0.58ǂ 0.54 0.06ǂ Cw*12 Cw*13 5(10.9%) 0(0%) 13(27.1%) 0(0%) 43(23.6%) 3(1.6%) 0.04 N/A 0.05 >0.99ǂ 0.62 >0.99ǂ Cw*14 Cw*15 3(6.5%) 1(2.2%) 4(8.3%) 0(0%) 17(9.3%) 0(0%) >0.99 0.48ǂ 0.77 0.48ǂ >0.99 N/A Cw*16 Cw*17 Cw*18 9(19.6%) 2(4.3%) 0(0%) 8(16.7%) 1(2.1%) 0(0%) 9(4.9%) 7(3.8%) 16(8.8%) 0.71 0.61ǂ N/A 0.001 >0.99ǂ 0.04ǂ >0.99 0.02ǂ 0.06ǂ Total #46(100%) #48(100%) #182(100%) *Meniere’s Disease, ǂ analyzed with fisher exact test, others are analyzed using chi square #The number of alleles is twice the number of patients, as each person has two alleles—one maternal and one paternal. Frequencies of HLA-Cw*04 (P<0.001) and HLA-Cw*16 (P=0.001) were found to be significantly higher in definite Meniere’s disease patients compared to the control subjects. Though, the allele frequency of HLA-Cw*18 was significantly lower in definite Meniere’s disease compared to the controls (P= 0.047) (Table. 3). Discussion The frequency of HLA-Cw alleles in 3 groups of definite Meniere’s disease patients, probable Meniere’s disease patients, and healthy controls has been appraised in this study. A significant association between HLA-Cw*04 and HLA-Cw*16 alleles with both probable and definite Meniere’s disease was observed in our patients. This was in agreement with the study of Koyama and colleagues in which they found significant association between HLA-Cw4 and HLADRB1*1602 in a Japanese sample. (16) Khorsandi et al. also found that HLA-Cw4 is found more in Iranian definite Meniere’s disease patients (13). The frequency of HLA-Cw*18 allele was significantly higher in the control group. HLA-Cw*12 allele frequency was significantly higher in probable Meniere’s disease group compared to the patients with definite Meniere’s. The observed association of HLA-Cw alleles in our patients suggested an autoimmune mechanism in both definite and probable Meniere’s disease. This is in agreement with Greco’s study who discussed Meniere’s autoimmunity in literature (4). A mechanism based approach to the disease diagnosis and treatment warrants more accurate diagnostic methods and more straightforward and powerful treatment approaches. Earlier studies have identified an association between the HLA-Cw7 antigen and Meniere’s disease in a British population (17). A significant increase in the frequency of HLA-Cw7 alleles in patients with Meniere’s disease was observed compared to other inner ear diseases and healthy subjects (18). Some studies have found an association between HLA-DRB1 alleles and Meniere’s disease. However the results had not been repeated in other populations (19,20). Yeo et al. have found that frequency of HLA-Cw*0303 and HLA-Cw*0602 alleles 264 Iranian Journal of Otorhinolaryngology, Vol.28(4), Serial No.87, Jul 2016 HLA-CW Alleles in Meniere disease were significantly increased in Korean patients with MD compared to healthy controls; on the other hand, HLA-B44 and HLA-Cw*0102 were significantly decreased in their patients (19). This can support the idea of the association between probable Meniere’s disease and the HLA Alleles. In another study on 80 Mediterranean patients with bilateral Meniere’s disease, an association between HLA-DRB1 *1101 and bilateral Meniere’s disease was observed; but there was no association between HLACw and bilateral Meniere’s disease (20). The number of patients with bilateral Meniere’s disease was very low in our studied population. The discrepancies in results are probably due to the ethnic or geographic background or also might be as a result of differences in phenotypic or clinical manifestations of patients in different studies which require careful interpretation. To the best of our knowledge, this is the first study which compares HLA-Cw allele frequencies in definite Meniere’s disease and probable Meniere’s disease patients in an Iranian sample. Some HLA loci are inherited as haplotype blocks. Therefore the association found between HLA-Cw and Meniere’s disease in our study might be due to an association with another unknown gene in linkage with the 75–85. 4. Bachmann F (1994) Molecular aspects of plasminogen, plasminogen activators and plasmin. In: Bloom AL, Forbes CD, Thomas DP, Tuddenham EGD, eds. Haemostasis and thrombosis. U.K.: Chuchill Livingston. pp 525–600. 5. Castellino FJ, Powell JR (1981) Human plasminogen. Methods Enzymol 80 Pt C: 365–378. 6. Estelles A, Aznar J, Gilabert J (1980) A qualitative study of soluble fibrin monomer complexes in normal labour and abruptio placentae. Thromb Res 18: 513–519. 7. Aznar J, Gilabert J, Estelles A, Parrilla JJ (1980) Evaluation of plasminogen and other fibrinolytic parameters in the amniotic fluid. Thromb Haemost 43: 182. 8. Gonias SL, Hembrough TA, Sankovic M (2001) Cytokeratin 8 functions as a major plasminogen receptor in select epithelial and carcinoma cells. Front Biosci 6: D1403–D1411. 9. Dano K, Behrendt N, Hoyer-Hansen G, Johnsen M, Lund LR, Ploug M, Romer J (2005) Plasminogen activation and cancer. Thromb Haemost 93: 676–681. 10. Pancholi V, Fischetti VA (1998) a-enolase, a novel strong plasmin(ogen) binding protein on the surface of pathogenic streptococci. J Biol Chem 273: 14503–14515. 11. Bergmann S, Rohde M, Preissner KT, Hammerschmidt S (2005) The nine residue plasminogen-binding motif of the pneumococcal enolase is the major cofactor of plasmin-mediated degradation of extracellular matrix, dissolution of fibrin and transmigration. Thromb Haemost 94: 304–311. 12. Sun H, Ringdahl U, Homeister JW, Fay WP, Engleberg NC, Yang AY, Rozek LS, Wang X, Sjobring U, Ginsburg D (2004) Plasminogen is a critical host pathogenicity factor for group A streptococcal infection. Science 305: 1283–1286. 13. Epple G, Schleuning WD, Kettelgerdes G, Kottgen E, Gessner R, Praus M (2004) Prion protein stimulates tissue-type plasminogen activator-mediated plasmin generation via a lysine-binding site on kringle 2. Journal of Thrombosis and Haemostasis 2: 962–968. 14. Praus M, Kettelgerdes G, Baier M, Holzhutter HG, Jungblut PR, Maissen M, Epple G, Schleuning WD, Kottgen E, Aguzzi A, Gessner R (2003) Stimulation of plasminogen activation by recombinant cellular prion protein is conserved in the NH2-terminal fragment PrP23-110. Thromb Haemost 89: 812–819. 15. Salmona M, Capobianco R, Colombo L, De LA, Rossi G, Mangieri M, Giaccone G, Quaglio E, Chiesa R, Donati MB, Tagliavini F, Forloni G (2005) Role of plasminogen in propagation of scrapie. J Virol 79: 11225–11230. 16. Wiman B, Wallen P (1975) Proceedings: On the primary structure of human plasminogen and plasmin, cyanogen bromide fragments. Thromb Diath Haemorrh 34: 350. 17. Wiman B, Wallen P (1975) On the primary structure of human plasminogen and plasmin. Purification and characterization of cyanogen-bromide fragments. Eur J Biochem 57: 387–394. 18. McClintock DK, Bell PH (1971) The mechanism of activation of human plasminogen by streptokinase. Biochem Biophys Res Commun 43: 694–702. 19. Reddy KN, Markus G (1972) Mechanism of activation of human plasminogen by streptokinase. Presence of active center in streptokinase-plasminogen complex. J Biol Chem 247: 1683–1691. 20. Schick LA, Castellino FJ (1974) Direct evidence for the generation of an active site in the plasminogen moiety of the streptokinase-human plasminogen activator complex. Biochem Biophys Res Commun 57: 47–54. 21. Miles LA, Castellino FJ, Gong Y (2003) Critical role for conversion of gluplasminogen to lys-plasminogen for optimal stimulation of plasminogen activation on cell surfaces. Trends Cardiovasc Med 13: 21–30. 22. Horrevoets AJG, Pannekoek H, Nesheim ME (1996) A Steady-state Template Model That Describes the Kinetics of Fibrin- stimulated [Glu1]- and [Lys78]Plasminogen Activation by Native tissue- type Plasminogen Activator the past [34]. SDS-PAGE, on the precipitated plasminogen, was carried out as previously described [46,47] using 7% gels. The supernates were quite dilute (%0.2 mg/mL) and were not monitored on gels. Author Contributions Conceived and designed the experiments: JAK. Performed the experiments: JAK. Analyzed the data: JAK. Contributed reagents/materials/ analysis tools: JAK. Wrote the paper: JAK. and Variants That Lack Either the Finger or Kringle-2 Domain. J Biol Chem 272: 2183–2191. 23. Carter DM, Kornblatt JA (2005) Interactions between canine plasminogen and 8-anilino-1-naphthalene sulfonate: structural insights from a fluorescent probe. Cell Mol Biol (Noisy. -le-grand) 51 Suppl: OL755–OL765. 24. Alkjaersig N, Fletcher AP, Sherry S (1959) vi-Aminocaproic acid: an inhibitor of plasminogen activation. J Biol Chem 234: 832–837. 25. Marshall JM, Brown AJ, Ponting CP (1994) Conformational studies of human plasminogen and plasminogen fragments: evidence for a novel third conformation of plasminogen. Biochemistry 33: 3599–3606. 26. Kornblatt JA, Schuck P (2005) Influence of temperature on the conformation of canine plasminogen: an analytical ultracentrifugation and dynamic light scattering study. Biochemistry 44: 13122–13131. 27. Olivari S, Molinari M (2007) Glycoprotein folding and the role of EDEM1, EDEM2 and EDEM3 in degradation of folding-defective glycoproteins. FEBS Lett 581: 3658–3664. 28. Sawyer JT, Lukaczyk T, Yilla M (1994) Dithiothreitol treatment induces heterotypic aggregation of newly synthesized secretory proteins in HepG2 cells. J Biol Chem 269: 22440–22445. 29. Yilla M, Doyle D, Sawyer JT (1992) Early disulfide bond formation prevents heterotypic aggregation of membrane proteins in a cell-free translation system. J Cell Biol 118: 245–252. 30. Ptitsyn OB (1995) How the molten globule became. Trends Biochem Sci 20: 376–379. 31. Stryer L (1965) The interaction of a naphthalene dye with apomyoglobin and apohemoglobin. A fluorescent probe of non-polar binding sites. J Mol Biol 13: 482–495. 32. Daniel E, Weber G (1966) Cooperative effects in binding by bovine serum albumin. I. The binding of 1-anilino-8-naphthalenesulfonate. Fluorimetric titrations. Biochemistry 5: 1893–1900. 33. Weber G, Daniel E (1966) Cooperative effects in binding by bovine serum albumin. II. The binding of 1-anilino-8-naphthalenesulfonate. Polarization of the ligand fluorescence and quenching of the protein fluorescence. Biochemistry 5: 1900–1907. 34. Kornblatt JA, Rajotte I, Heitz F (2001) Reaction of canine plasminogen with 6-aminohexanoate: a thermodynamic study combining fluorescence, circular dichroism, and isothermal titration calorimetry. Biochemistry 40: 3639–3647. 35. Kahn PC (1979) The interpretation of near-ultraviolet circular dichroism. Methods Enzymol 61: 339–378. 36. Okamoto S, Oshiba S, Mihara H, Okamoto U (1968) Synthetic inhibitors of fibrinolysis: in vitro and in vivo mode of action. Ann N Y Acad Sci 146: 414–429. 37. Castellino FJ, Brockway WJ, Thomas JK, Liano HT, Rawitch AB (1973) Rotational diffusion analysis of the conformational alterations produced in plasminogen by certain antifibrinolytic amino acids. Biochemistry 12: 2787–2791. 38. Kornblatt JA (2000) Understanding the fluorescence changes of human plasminogen when it binds the ligand, 6-aminohexanoate: a synthesis. Biochim Biophys Acta 1481: 1–10. 39. Cockell CS, Marshall JM, Dawson KM, Cederholm-Williams SA, Ponting CP (1998) Evidence that the conformation of unliganded human plasminogen is maintained via an intramolecular interaction between the lysine-binding site of kringle 5 and the N-terminal peptide. Biochem J 333(Pt 1): 99–105. 40. Abad MC, Arni RK, Grella DK, Castellino FJ, Tulinsky A, Geiger JH (2002) The X-ray crystallographic structure of the angiogenesis inhibitor angiostatin. J Mol Biol 318: 1009–1017. 41. Chang Y, Mochalkin I, McCance SG, Cheng B, Tulinsky A, Castellino FJ (1998) Structure and ligand binding determinants of the recombinant kringle 5 domain of human plasminogen. Biochemistry 37: 3258–3271. 42. Mulichak AM, Tulinsky A, Ravichandran KG (1991) Crystal and molecular structure of human plasminogen kringle 4 refined at 1.9-A resolution. Biochemistry 30: 10576–10588. 43. Wang X, Terzyan S, Tang J, Loy JA, Lin X, Zhang XC (2000) Human plasminogen catalytic domain undergoes an unusual conformational change upon activation. J Mol Biol 295: 903–914. PLoS ONE | www.plosone.org 7 July 2009 | Volume 4 | Issue 7 | e6196 Reduction of Plasminogen 44. Getz EB, Xiao M, Chakrabarty T, Cooke R, Selvin PR (1999) A comparison between the sulfhydryl reductants tris(2-carboxyethyl)phosphine and dithiothreitol for use in protein biochemistry. Anal Biochem 273: 73–80. 45. Cleland WW (1964) Dithiothreitol, A New protective reagent for SH Groups. Biochemistry 3: 480–482. 46. Kornblatt JA, Marchal S, Rezaei H, Kornblatt MJ, Balny C, Lange R, Debey MP, Hui Bon HG, Marden MC, Grosclaude J (2003) The fate of the prion protein in the prion/plasminogen complex. Biochem Biophys Res Commun 305: 518–522. 47. Laemmli UK (1970) Cleavage of structural proteins during the assembly of the head of bacteriophage T4. Nature 227: 680–685. PLoS ONE | www.plosone.org 8 July 2009 | Volume 4 | Issue 7 | e6196
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