Relevant bibliographies by topics / Bernardo Bini

Academic literature on the topic 'Bernardo Bini'

Author: Grafiati
Published: 10 March 2023

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Journal articles on the topic "Bernardo Bini"

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Ben-Amos, Ilana Krausman. "Bernard Capp. The Ties That Bind: Siblings, Family, and Society in Early Modern England." American Historical Review 125, no. 1 (February 1, 2020): 303–4. http://dx.doi.org/10.1093/ahr/rhz809.

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Kenny, Dermot, Ólafur G. Jónsson, Patricia A. Morateck, and Robert R. Montgomery. "Naturally Occurring Mutations in Glycoprotein Ibα That Result in Defective Ligand Binding and Synthesis of a Truncated Protein." Blood 92, no. 1 (July 1, 1998): 175–83. http://dx.doi.org/10.1182/blood.v92.1.175.413a36_175_183.

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The platelet GPIb-V-IX complex is the receptor for the initial binding of von Willebrand factor (vWF) mediating platelet adhesion. The complex is composed of four membrane-spanning glycoproteins (GP): GPIbα, GPIbβ, GPIX, and GPV. Bernard-Soulier syndrome results from a qualitative or quantitative defect in one or more components of the platelet membrane GPIb-V-IX complex. We describe the molecular basis of a novel Bernard-Soulier syndrome variant in two siblings in whom GPIbα was not detected on the platelet surface but that was present in a soluble form in plasma. DNA sequence analysis showed that the affected individuals were compound heterozygotes for two mutations. One, inherited from a maternal allele, a T777 → C point mutation in GPIbα converting Cys65 → Arg within the second leucine rich repeat, the other, a single nucleotide substitution (G2078 → A) for the tryptophan codon (TGG) causing a nonsense codon (TGA) at residue 498 within the transmembrane region of GPIbα, inherited from a mutant paternal allele. The Bernard-Soulier phenotype was observed in siblings who were compound heterozygotes for these two mutations. Although GPIbα was not detected on the surface of the patient's platelets, soluble GPIbα could be immunoprecipitated from plasma. When plasmids encoding GPIbα containing the Cys65 → Arg mutation were transiently transfected into Chinese hamster ovary (CHO) cells stably expressing the GPβ-IX complex (CHOβIX), the expression of GPIbα was similar to the wild-type (WT) GPIbα, but did not bind vWF. When plasmids encoding GPIbα containing the Trp498 → stop were transiently transfected into CHOβIX, the surface expression of GPIbα was barely detectable compared with the WT GPIbα. Thus, this newly described compound heterozygous defect produces Bernard-Soulier syndrome by a combination of synthesis of a nonfunctional protein and of a truncated protein that fails to insert into the platelet membrane and is found circulating in plasma.
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Bailey, Merridee L. "The Ties that Bind: Siblings, Family, and Society in Early Modern England, written by Capp, Bernard." Emotions: History, Culture, Society 3, no. 2 (November 15, 2019): 321–23. http://dx.doi.org/10.1163/2208522x-02010063.

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Hudiarto, Hudiarto. "Kajian Perolehan Sertifikasi Profesi Internasional Bagi Lulusan Jurusan Sistem Informasi." ComTech: Computer, Mathematics and Engineering Applications 2, no. 2 (December 1, 2011): 1254. http://dx.doi.org/10.21512/comtech.v2i2.2939.

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Having a professional certificate in information systems and information technology fields means having the recognition for related skills and knowledge requested by the industry. Some countries and institutions have tried to bridge these needs by organizing conferences and seminars. Information systems department of Bina Nusantara University always tries to meet those needs. One effort is to introduce the Enterprise Architecture method initiated by Bernard for use in the course of information systems and information technology strategic planning. The results of this activity suggest that obtaining international certification requires the implementation of learning in a referenced standard. This approach is expected to accelerate the acquisition of professional certification for graduates majoring in information systems and technology.
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Pereira, Cláudia Sousa. "Corpo, espaço com tempo: as dores de crescimento em Supergigante de Ana Pessoa e Bernardo P. Carvalho." FronteiraZ. Revista do Programa de Estudos Pós-Graduados em Literatura e Crítica Literária, no. 26 (July 8, 2021): 116–31. http://dx.doi.org/10.23925/1983-4373.2021i26p116-131.

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Partilhamos uma leitura de um caso central da literatura juvenil portuguesa contemporânea. Supergigante (2014) é também um objeto estético que se toca, vê e lê de acordo com várias gramáticas. Pretendemos usá-las para trabalhar, intratextualmente, a personagem do adolescente que, no mesmo dia, experiencia a perda do avô e o seu primeiro beijo num violento choque de emoções; e, paratextualmente, descodificar a materialização da leitura literária que, através do texto de Ana Pessoa e da ilustração de Bernardo P. Carvalho, se faz jogando também com as dificuldades em lutar com o peso gravitacional do lugar e do tempo na adolescência. Joga-se com a intensidade, a velocidade, do tempo de ser e de dizer, tudo em excesso. Edgar, protagonista e narrador, é um corpo que adolesce abruptamente como numa explosão cósmica. Exprimi-lo é confessar logo na primeira linha: “Eu corro e não avanço.” TRANSLATE with x EnglishArabicHebrewPolishBulgarianHindiPortugueseCatalanHmong DawRomanianChinese SimplifiedHungarianRussianChinese TraditionalIndonesianSlovakCzechItalianSlovenianDanishJapaneseSpanishDutchKlingonSwedishEnglishKoreanThaiEstonianLatvianTurkishFinnishLithuanianUkrainianFrenchMalayUrduGermanMalteseVietnameseGreekNorwegianWelshHaitian CreolePersian // TRANSLATE with COPY THE URL BELOW Back EMBED THE SNIPPET BELOW IN YOUR SITE Enable collaborative features and customize widget: Bing Webmaster PortalBack//
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Ziegler, Hannes. "Bernard Capp, The Ties that Bind. Siblings, Family, and Society in Early Modern England. Oxford, Oxford University Press 2018." Historische Zeitschrift 310, no. 3 (June 1, 2020): 746–47. http://dx.doi.org/10.1515/hzhz-2020-1205.

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Kerrigan, Steven W., Ian Douglas, Ann Wray, Jason Heath, Michael F. Byrne, Desmond Fitzgerald, and Dermot Cox. "A role for glycoprotein Ib in Streptococcus sanguis–induced platelet aggregation." Blood 100, no. 2 (July 15, 2002): 509–16. http://dx.doi.org/10.1182/blood.v100.2.509.

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Abstract Numerous studies have implicated bacteria in cardiovascular disease, but there is a paucity of information on the mechanism involved. In this study we show how the common oral bacteriumStreptococcus sanguis can directly interact with platelets, resulting in activation and aggregate formation. Platelet aggregation was dependent on glycoprotein IIb/IIIa (GPIIb/IIIa) and thromboxane. Platelets could also directly bind to S sanguis, but this interaction was not inhibited by GPIIb/IIIa antagonists. Antibodies to GPIb could inhibit both platelet aggregation and platelet adhesion to bacteria. This suggested a direct interaction between GPIb and S sanguis; however, this interaction did not require von Willebrand factor, the normal ligand for GPIb. By use of a range of monoclonal antibodies to GPIb and the enzyme mocharagin, which cleaves GPIb at amino acid 282, the interaction was localized to a region within the N-terminal 1-225 portion of GPIbα. Furthermore S sanguisfailed to induce aggregation of platelets from a patient with Bernard-Soulier disease, the organism bound to Chinese hamster ovary cells transfected with the GPIbα gene but did not bind to mock-transfected cells and biotin-labeled S sanguis cells bound to purified GPIb in ligand blots. It is suggested that the interaction between S sanguis and GPIb is important in the pathogenesis of infective endocarditis and may also play a contributory role in some cases of myocardial infarction.
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Metz, Holly. "McFeely Muscle: The Campaign to Ruin George Harper." New Jersey Studies: An Interdisciplinary Journal 2, no. 1 (January 13, 2016): 11. http://dx.doi.org/10.14713/njs.v2i1.24.

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<p>The twenty-two-year reign of Hoboken political boss Bernard N. McFeely (including seventeen as mayor) has long been under-reported in the national press and almost completely overlooked by historians. Bernard McFeely’s extensive FBI file, recently released under the Freedom of Information Act, provides an opportunity to remedy this lapse, and to consider his rule (1925-1947) alongside other post-World War I urban political machines. Unlike his over-boss, Jersey City mayor and statewide machine leader Frank Hague, or machine bosses in Boston, Memphis, and Kansas City—all of whom retained power by matching bullying with programs that gained the affection of poor and working class constituents—McFeely was stingy with public funds and mostly relied on force to secure his hold. The coercion and beatings attributed to McFeely and his cohorts in oral histories and court records are detailed in his FBI file. This article focuses on one series of documents, relating to a 1937-1938 campaign to ruin the milk business of George Harper, who was said to have displeased then-mayor McFeely by consorting with his political opponents. Harper provided the FBI with daily records of the enforced boycott of his business; they provide a blow-by-blow account of McFeely bossism in action.</p><p><span style="font-family: 'Times New Roman',serif; font-size: 10pt; mso-fareast-font-family: 'MS Mincho'; mso-fareast-theme-font: minor-fareast; mso-ansi-language: EN-US; mso-fareast-language: EN-US; mso-bidi-language: AR-SA;">A version of this talk was originally delivered at the NJ Forum Conference, Kean University, on November 22, 2014. </span></p>
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Stricker, RB, and MA Shuman. "Quinidine purpura: evidence that glycoprotein V is a target platelet antigen." Blood 67, no. 5 (May 1, 1986): 1377–81. http://dx.doi.org/10.1182/blood.v67.5.1377.1377.

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Abstract Quinidine-induced thrombocytopenia has been associated with both immune complex and autoantibody binding to platelets. In the present study, serum antibody from six of six patients with quindine purpura was shown by immunoblotting to bind to a single platelet membrane protein of mol wt 80,000. This target protein was absent from Bernard-Soulier (BSS) platelets. F(ab)2 prepared from one patient's serum also bound to this protein, indicating autoantibody rather than immune complex binding to the target antigen. Antibody binding to the 80-kd protein was preserved after treatment of platelets with concentrations of trypsin or chymotrypsin that completely removed glycoprotein Ib (GPIb). Preincubation of platelet proteins with one patient's serum blocked binding of a polyclonal rabbit antibody against glycoprotein V (GPV), indicating that these antibodies recognize the same antigen. By wheat germ affinity chromatography, GPV was shown to copurify with GPIb. Quinidine-induced antibody bound to the wheat germ-purified GPV but not to GPIb. We conclude that quinidine purpura is associated with autoantibody directed against platelet GPV.
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Stricker, RB, and MA Shuman. "Quinidine purpura: evidence that glycoprotein V is a target platelet antigen." Blood 67, no. 5 (May 1, 1986): 1377–81. http://dx.doi.org/10.1182/blood.v67.5.1377.bloodjournal6751377.

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Quinidine-induced thrombocytopenia has been associated with both immune complex and autoantibody binding to platelets. In the present study, serum antibody from six of six patients with quindine purpura was shown by immunoblotting to bind to a single platelet membrane protein of mol wt 80,000. This target protein was absent from Bernard-Soulier (BSS) platelets. F(ab)2 prepared from one patient's serum also bound to this protein, indicating autoantibody rather than immune complex binding to the target antigen. Antibody binding to the 80-kd protein was preserved after treatment of platelets with concentrations of trypsin or chymotrypsin that completely removed glycoprotein Ib (GPIb). Preincubation of platelet proteins with one patient's serum blocked binding of a polyclonal rabbit antibody against glycoprotein V (GPV), indicating that these antibodies recognize the same antigen. By wheat germ affinity chromatography, GPV was shown to copurify with GPIb. Quinidine-induced antibody bound to the wheat germ-purified GPV but not to GPIb. We conclude that quinidine purpura is associated with autoantibody directed against platelet GPV.
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Dissertations / Theses on the topic "Bernardo Bini"

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Jürgensen, Inga. "Patrice Chéreaus Inszenierungen von Koltés' Dans la solitude des champs de coton und ihre Filmfassungen als intermedialer Transfer Begegnungen /." [S.l. : s.n.], 2001. http://deposit.ddb.de/cgi-bin/dokserv?idn=969687435.

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Niwano, Hiroshi Munehiro. ""Being in love" : religious conversion in Bernard Lonergan and the Lotus Sutra /." Rom, 2007. http://opac.nebis.ch/cgi-bin/showAbstract.pl?sys=000253520.

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Hilker, Annette. "Karnevalisierung als Medium der Aufklärung Fontenelle, Fénelon, Voltaire, Diderot." Hannover-Laatzen Wehrhahn, 2004. http://deposit.ddb.de/cgi-bin/dokserv?id=2686765&prov=M&dok_var=1&dok_ext=htm.

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CAPORALI, ALESSIO. "Bernardo Bini, un banchiere fiorentino alla corte di Leone X: architettura e commissioni artistiche fra Roma e Firenze nel primo Cinquecento." Doctoral thesis, 2017. http://hdl.handle.net/2158/1075933.

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Il presente contributo delinea la figura di Bernardo di Piero Bini (1461-1548), ricco mercante fiorentino e abile uomo politico, il quale, durante il pontificato di Leone X, è uno dei banchieri più potenti dello Stato della Chiesa. Attraverso lo studio del mecenatismo di questo personaggio è stato possibile ricostruire la storia di opere d’arte e di palazzi poco conosciuti ma che si inseriscono a pieno titolo nel panorama artistico rinascimentale. In questo contesto, l’individuazione nell’Archivio Bini Smaghi Bellarmini dei registri contabili relativi alle spese personali di papa Leone X ha permesso di identificare pagamenti inediti intestati ad alcuni protagonisti del Rinascimento, come Raffaello Sanzio, Michelangelo Buonarroti, Giovan Francesco da Sangallo e Giulio Romano.
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"Salvation and affectivity: the affective integration in the theology of charles andré bernard." Tese, MAXWELL, 2004. http://www.maxwell.lambda.ele.puc-rio.br/cgi-bin/db2www/PRG_0991.D2W/SHOW?Cont=4979:pt&Mat=&Sys=&Nr=&Fun=&CdLinPrg=pt.

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Books on the topic "Bernardo Bini"

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interviewer, Momo Alberto, ed. Atlante sentimentale del cinema per il XXI secolo: Conversazioni con Abel Ferrara, Adolfo B. Alix jr., Aki Kaurismaki, Alberto Grifi, Aleksandr Sokurov, Amir Naderi, Amos Gitai, Andrej Ujica, Angela Ricci Lucchi, Atom Egoyan, Béla Tarr, David Lynch, Enrico Ghezzi, Franco Maresco, Frederick Wiseman, George Romero, Goutam Ghose, Hou Hsiao-hsien, Jean-Marie Straub, Jia Zhang-ke, John Torres, Johnnie To, Julio Bressane, Khavn de la Cruz, Kira Muratova, Kiyoshi Kurosawa, Lav Diaz, Lee Kang-sheng, Lisandro Alonso, Manoel de Oliveira, Mohsen Makhmalbaf, Monte Hellman, Naomi Kawase, Onde filippine, Otar Iosseliani, Paulo Rocha, Pedro Costa, Philippe Garrel, Quentin Tarantino, Raoul Ruiz, Raya Martin, Roger Corman, Shinya Tsukamoto, Stan Brakhage, Takeshi Kitano, Tonino De Bernardi, Tsai Ming-liang, Wai Ka-fai, Wang Bing, Werner Herzog, Yervant Gianikian, Želimir Žilnik. Roma: DeriveApprodi, 2013.

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Conference papers on the topic "Bernardo Bini"

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Estry, D. W., J. C. Mattson, and J. Chediak. "CONTACT ACTIVATED PLATELETS BIND VON WILLEBRAND FACTOR TO GPIIb-IIIa." In XIth International Congress on Thrombosis and Haemostasis. Schattauer GmbH, 1987. http://dx.doi.org/10.1055/s-0038-1643517.

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Using a rabbit polyclonal anti-von Willebrand factor (vWF) antibody, normal human adherent platelets extensively bind vWF in a diffuse pattern as detected by immunogold electron microscopy. This pattern differed significantly from the zonal pattern observed for direct fibrinogen-gold labelling in contact activated platelets. In order to determine if contact activated platelets bind vWF to GPIIb-IIIa or GPlb, the extent and pattern of bound vWF in platelets from patients with Glanzmann’s thrombasthenia (GT) and Bernard Soulier Syndrome (BSS) was determined. Virtually no bound VWF was detected by immunogold labeling in GT platelets previously characterized as being deficient in GPIIb-IIIa. On the other hand, BSS platelets, lacking GPlb, demonstrated extensive labeling of vWF in a pattern identical to that seen in normal platelets. This data is consistant with vWF binding to GPIIb-IIIa in contact induced adhesion and spreading.
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Jandrot-Perrus, M., D. Didry, M. C. Guillin, and A. T. Nurden. "CHEMICAL CROSS-LINKING OF HUMAN THROMBIN TO PLATELET MEMBRANE GLYCOPROTEIN Ib." In XIth International Congress on Thrombosis and Haemostasis. Schattauer GmbH, 1987. http://dx.doi.org/10.1055/s-0038-1643629.

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The interaction of thrombin with proteins at the platelet surface was assessed by chemical cross-linking with the membrane impermeable reagents DTSSP and BS3. Washed platelets were incubated with 125I-α-thrombin, 125I-TLCK-inactivated α-thrombin or 125I-γ-thrombin, and then with 0.1 mM DTSSP or BS3. The pattern of 3H-labeled glycoproteins (GP) was only slightly modified, with no measurable loss of GPIb, lib, Ilia, V and IX. Thrombin was detected in high molecular weight complexes migrating at the top of a 3 % acrylamide stacking gel and at the tap of the separating gel (7 %). In addition, a complex of Mr : 240 000 has been characterized. This complex was formed with 0.5 to 50 nM thrombin, after a short incubation time (30 sec) with active thrombin as well as with TLCK-thrombin. Hirudin added in excess before the crosslinker inhibited its formation. After analysis of soluble extracts by crossed Immunoelectrophoresis against a rabbit anti-whole platelet serum, 3 precipitates were labelled, among them the GPIIb-Illa complex and the most intense, a precipitate in the position of GPIb. Immunoprecipitation of GPIb using a murine monoclonal antibody allowed the isolation of the 240 000 complex. This complex was not observed with platelets from a patient with the Bernard-Soulier syndrome or with chymatrypsin-treated platelets lacking the outer portion of the GPIb αchain. 1125I-γ-thrombin was unable to bind to GPIb and form sucha complex. In each of these three examples of a defective binding, of thrombin toGPIb, the pattern of platelet aggregation and release reaction are characterized b a prolonged lag phase. Our results confirm the ability of GPIb to bindα-thrombin and support a role for this interaction in governing, the velocity of the platelet response.
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