Relevant bibliographies by topics / BamHI

Academic literature on the topic 'BamHI'

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Published: 10 March 2023

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Journal articles on the topic "BamHI"

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Kang, Y. K., H. B. Lee, M. J. Noh, N. Y. Cho, and O. J. Yoo. "Different Effects of Base Analog Substitutions in BamHI Restriction Site on Recognition by BamHI Endonuclease and Bamhi Methylase." Biochemical and Biophysical Research Communications 206, no. 3 (January 1995): 997–1002. http://dx.doi.org/10.1006/bbrc.1995.1141.

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Kim, W. K., R. L. Innes, and E. R. Kerber. "Ribosomal DNA repeat unit polymorphism in six Aegilops species." Genome 35, no. 3 (June 1, 1992): 510–15. http://dx.doi.org/10.1139/g92-075.

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Total genomic DNA of 27 accessions representing six Aegilops species was restricted with BamHI, EcoRI, and BamHI plus EcoRI, and the restriction fragments were probed with the ribosomal clones pMF2 containing the ribosomal RNA coding regions. The rDNA repeat lengths varied between 9.0 and 10.8 kb. Intraspecific variation among the 10 accessions of Ae. squarrosa var. strangulata ranged from 9.0 to 9.6 kb, suggesting a diversity of genotypes within as well as between species. These variations were not related to their geographical distributions. Each of 24 accessions had two BamHI sites in the coding region (type A), while three accessions of Ae. squarrosa var. strangulata had four BamHI sites (type B, two sites in the intergenic region). Results for these three accessions of Ae. squarrosa var. strangulata suggest genotypic diversity in this species. In BamHI restriction of each accession, a third DNA fragment, ranging between 9.0 and 10.8 kb in type A and 6.0 kb in type B, resulted from lack of digestion at the 26S BamHI site. In double digestion, all rDNA repeat units were restricted by EcoRI, yielding 3.9-, 0.9-, and 4.8-kb fragments, the last of which arose from the lack of digestion at the 26S BamHI site, estimated to occur in 5–20% of the repeat units, depending on the accession.Key words: Triticum tauschii, RFLP, diversity.
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Melani Maskoen, Ani, Saskia L Nasroen, Prima Nanda Fauziah, Eky Setiawan Soeria Soemantri, and Basri A Gani. "EXPRESSION OF TRANSFORMING GROWTH FACTOR ALPHA BAMHI AND RSAI GENE VARIANTS ASSOCIATED WITH NON-SYNDROMIC CLEFT PALATE OF INDONESIAN SUBJECTS USING POLYMERASE CHAIN REACTION METHOD." Asian Journal of Pharmaceutical and Clinical Research 11, no. 4 (April 1, 2018): 351. http://dx.doi.org/10.22159/ajpcr.2018.v11i4.24242.

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Objective: This study aimed to detect and analyze transforming growth factor alpha (TGFA) BamHI and RsaI gene variants which associated with the risk factor of non-syndromic cleft palate only (NS CPO) of Indonesian subject.Methods: This was case-control study using samples from 32 NS CPO subjects and 28 control subjects. DNA was extracted from venous blood, and the TGFA gene was amplified using polymerase chain reaction technique, then digestion product from TaqI and RsaI restriction enzyme was evaluated. Statistical analysis to determine significant differences of gene variant frequency among NS CPO subject and control was χ2. The odds ratio (OR) was used to determine a risk factor of NS CPO.Results: The study results showed that the TGFA BamHI gene variant was not identified in NS CPO among Indonesian but TGFA RsaI gene variant was identified. The frequency of TT/B1B1 homozygous mutant genotype was 80.0% in NS CPO subjects and 20.0% in control subjects (OR=3.857; 95% confidence interval=0.405–36.749).Conclusion: TGFA RsaI gene can be considered a risk factor of NS CPO compared TGFA BamH1 gene of Indonesian subjects.
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Molnar, Stephen J., and George Fedak. "Polymorphism in ribosomal DNA repeat units of 12 Hordeum species." Genome 32, no. 6 (December 1, 1989): 1124–27. http://dx.doi.org/10.1139/g89-565.

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Total genomic DNA was isolated from leaves of individual accessions of 12 Hordeum species. SacI, HindIII, and BamHI restriction fragments hybridizing to the wheat rDNA probe pTA71 were compared. Thirteen rDNA repeat unit length variants were recovered, which combined to produce 11 distinct phenotypes. All rDNA repeat units had two SacI sites and no HindIII sites. The rDNA repeat units of H. secalinum, H. hrasdanicum, and H. distichum all had 3 BamHI sites, but in different configurations. The rDNA repeat units of the other species had at least 4 BamHI sites. Ladders of small hybridizing fragments in 8 of 9 of the latter accessions indicated the presence of occasional BamHI sites in some subrepeats within the intergenic spacer regions of the rDNA repeat units. Different distributions of BamHI restriction site maps within the Hordeum sections strengthen the concept of using variation in rDNA restriction sites as a taxonomic character.Key words: Hordeum, ribosomal DNA, polymorphism.
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Litz, CE, JS McClure, CM Copenhaver, and RD Brunning. "Duplication of small segments within the major breakpoint cluster region in chronic myelogenous leukemia." Blood 81, no. 6 (March 15, 1993): 1567–72. http://dx.doi.org/10.1182/blood.v81.6.1567.1567.

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Abstract The t(9;22) in chronic myelogenous leukemia (CML) may be reciprocal or, in a minority of cases, may result in an extensive deletion of a portion of the major breakpoint cluster region (M-bcr) of the BCR. This report provides evidence of the duplication of small segments within the M-bcr in a small group of patients with CML. Southern blots of Bgl II and Bgl II/BamHI double-digested DNA from the blood or bone marrow of 46 patients with CML were probed with a 5' 1.4-kb Taq I/HindIII M- bcr probe and a 3' 2-kb HindIII/BamHI M-bcr probe. In three patients, rearrangements were noted with both probes in Bgl II-digested DNA, but were not present in Bgl II/BamHI-digested DNA with either probe. Southern analysis of DNA samples double-digested with Bgl II and BspHI from two of these three cases showed no rearrangements with either probe; the M-bcr BspHI site is located 26 bp 3' of the BamHI site in the second intron of the M-bcr. The presence of a rearranged M-bcr with both probes in Bgl II-digested DNA and the lack of rearrangement in Bgl II/BamHI and Bgl II/BspHI double-digested DNA suggest the presence of M- bcr BamHI and BspHI sites on both 9q+ chromosome (9q+) and the Philadelphia chromosome (Ph). This implies a duplication of at least the 26-bp M-bcr BamHI/BspHI fragment in these two samples. Sequence data from one of these two cases confirmed the M-bcr breakpoints to be staggered; the Ph M-bcr breakpoint occurred 258 bp downstream from the 9q+ M-bcr breakpoint. It is concluded that a duplication of small segments within the M-bcr occurs in a small group of patients with CML, which may lead to pseudogermline patterns on Southern blot. Such a duplication may provide insight into the mechanism of some chromosomal translocations in neoplasia.
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Litz, CE, JS McClure, CM Copenhaver, and RD Brunning. "Duplication of small segments within the major breakpoint cluster region in chronic myelogenous leukemia." Blood 81, no. 6 (March 15, 1993): 1567–72. http://dx.doi.org/10.1182/blood.v81.6.1567.bloodjournal8161567.

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The t(9;22) in chronic myelogenous leukemia (CML) may be reciprocal or, in a minority of cases, may result in an extensive deletion of a portion of the major breakpoint cluster region (M-bcr) of the BCR. This report provides evidence of the duplication of small segments within the M-bcr in a small group of patients with CML. Southern blots of Bgl II and Bgl II/BamHI double-digested DNA from the blood or bone marrow of 46 patients with CML were probed with a 5' 1.4-kb Taq I/HindIII M- bcr probe and a 3' 2-kb HindIII/BamHI M-bcr probe. In three patients, rearrangements were noted with both probes in Bgl II-digested DNA, but were not present in Bgl II/BamHI-digested DNA with either probe. Southern analysis of DNA samples double-digested with Bgl II and BspHI from two of these three cases showed no rearrangements with either probe; the M-bcr BspHI site is located 26 bp 3' of the BamHI site in the second intron of the M-bcr. The presence of a rearranged M-bcr with both probes in Bgl II-digested DNA and the lack of rearrangement in Bgl II/BamHI and Bgl II/BspHI double-digested DNA suggest the presence of M- bcr BamHI and BspHI sites on both 9q+ chromosome (9q+) and the Philadelphia chromosome (Ph). This implies a duplication of at least the 26-bp M-bcr BamHI/BspHI fragment in these two samples. Sequence data from one of these two cases confirmed the M-bcr breakpoints to be staggered; the Ph M-bcr breakpoint occurred 258 bp downstream from the 9q+ M-bcr breakpoint. It is concluded that a duplication of small segments within the M-bcr occurs in a small group of patients with CML, which may lead to pseudogermline patterns on Southern blot. Such a duplication may provide insight into the mechanism of some chromosomal translocations in neoplasia.
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Lupton, S., and A. J. Levine. "Mapping genetic elements of Epstein-Barr virus that facilitate extrachromosomal persistence of Epstein-Barr virus-derived plasmids in human cells." Molecular and Cellular Biology 5, no. 10 (October 1985): 2533–42. http://dx.doi.org/10.1128/mcb.5.10.2533-2542.1985.

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The Epstein-Barr virus (EBV) genome becomes established as a multicopy plasmid in the nucleus of infected B lymphocytes. A cis-acting DNA sequence previously described within the BamHI-C fragment of the EBV genome (J. Yates, N. Warren, D. Reisman, and B. Sugden, Proc. Natl. Acad. Sci. USA 81:3806-3810, 1984) allows stable extrachromosomal plasmid maintenance in latently infected cells, but not in EBV-negative cells. In agreement with the findings of Yates et al., deletion analysis permitted the assignment of this function to a 2,208-base-pair region (nucleotides 7315 to 9517 of the B95-8 strain of EBV) of the BamHI-C fragment that contained a striking repetitive sequence and an extended region of dyad symmetry. A recombinant vector, p410+, was constructed which carried the BamHI-K fragment (nucleotides 107565 to 112625 of the B95-8 strain, encoding the EBV-associated nuclear antigen EBNA-1), the cis-acting sequence from the BamHI-C fragment, and a dominant selectable marker gene encoding G-418 resistance in animal cells. After being transfected into HeLa cells, this plasmid persisted extrachromosomally at a low copy number, with no detectable rearrangements or deletions. Two mutations in the BamHI-K-derived portion of p410+, a large in-frame deletion and a linker insertion frameshift mutation, both of which alter the carboxy-terminal portion of EBNA-1, destroyed the ability of the plasmid to persist extrachromosomally in HeLa cells. A small in-frame deletion and linker insertion mutation in the region encoding the carboxy-terminal portion of EBNA-1, which replaced 19 amino acid codons with 2, had no effect on the maintenance of p410+ in HeLa cells. These observations indicate that EBNA-1, in combination with a cis-acting sequence in the BamHI-C fragment, is in part responsible for extrachromosomal EBV-derived plasmid maintenance in HeLa cells. Two additional activities have been localized to the BamHI-C DNA fragment: (i) a DNA sequence that could functionally substitute for the simian virus 40 enhancer and promoter elements controlling the expression of G-418 resistance and (ii) a DNA sequence which, although not sufficient to allow extrachromosomal plasmid maintenance, enhanced the frequency of transformation to G-418 resistance in EBV-positive (but not EBV-negative) cells. These findings suggest that the BamHI-C fragment contains a lymphoid-specific or EBV-inducible promoter or enhancer element or both.
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Lupton, S., and A. J. Levine. "Mapping genetic elements of Epstein-Barr virus that facilitate extrachromosomal persistence of Epstein-Barr virus-derived plasmids in human cells." Molecular and Cellular Biology 5, no. 10 (October 1985): 2533–42. http://dx.doi.org/10.1128/mcb.5.10.2533.

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The Epstein-Barr virus (EBV) genome becomes established as a multicopy plasmid in the nucleus of infected B lymphocytes. A cis-acting DNA sequence previously described within the BamHI-C fragment of the EBV genome (J. Yates, N. Warren, D. Reisman, and B. Sugden, Proc. Natl. Acad. Sci. USA 81:3806-3810, 1984) allows stable extrachromosomal plasmid maintenance in latently infected cells, but not in EBV-negative cells. In agreement with the findings of Yates et al., deletion analysis permitted the assignment of this function to a 2,208-base-pair region (nucleotides 7315 to 9517 of the B95-8 strain of EBV) of the BamHI-C fragment that contained a striking repetitive sequence and an extended region of dyad symmetry. A recombinant vector, p410+, was constructed which carried the BamHI-K fragment (nucleotides 107565 to 112625 of the B95-8 strain, encoding the EBV-associated nuclear antigen EBNA-1), the cis-acting sequence from the BamHI-C fragment, and a dominant selectable marker gene encoding G-418 resistance in animal cells. After being transfected into HeLa cells, this plasmid persisted extrachromosomally at a low copy number, with no detectable rearrangements or deletions. Two mutations in the BamHI-K-derived portion of p410+, a large in-frame deletion and a linker insertion frameshift mutation, both of which alter the carboxy-terminal portion of EBNA-1, destroyed the ability of the plasmid to persist extrachromosomally in HeLa cells. A small in-frame deletion and linker insertion mutation in the region encoding the carboxy-terminal portion of EBNA-1, which replaced 19 amino acid codons with 2, had no effect on the maintenance of p410+ in HeLa cells. These observations indicate that EBNA-1, in combination with a cis-acting sequence in the BamHI-C fragment, is in part responsible for extrachromosomal EBV-derived plasmid maintenance in HeLa cells. Two additional activities have been localized to the BamHI-C DNA fragment: (i) a DNA sequence that could functionally substitute for the simian virus 40 enhancer and promoter elements controlling the expression of G-418 resistance and (ii) a DNA sequence which, although not sufficient to allow extrachromosomal plasmid maintenance, enhanced the frequency of transformation to G-418 resistance in EBV-positive (but not EBV-negative) cells. These findings suggest that the BamHI-C fragment contains a lymphoid-specific or EBV-inducible promoter or enhancer element or both.
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Patel, P., G. I. Bell, R. C. Turner, and J. S. Wainscoat. "BamHI RFLP at the GLUT3 locus." Nucleic Acids Research 18, no. 16 (1990): 4967. http://dx.doi.org/10.1093/nar/18.16.4967.

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Cao, Y., J. K. Wagner, A. Eblé, P. Hindmarsh, and P. E. Mullis. "BamHI RFLP for the GHRHR locus." Human Molecular Genetics 3, no. 4 (1994): 682. http://dx.doi.org/10.1093/hmg/3.4.682.

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Dissertations / Theses on the topic "BamHI"

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Kirby, Helen Elizabeth. "Characterisation of regulatory sequences at the Epstein-Barr virus BamHI W promoter." Thesis, University of Birmingham, 2000. http://ethos.bl.uk/OrderDetails.do?uin=uk.bl.ethos.393823.

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Kao, Kuan-Yu. "Control of the EBV growth transformation programme : the importance of the Bamhi W repeats." Thesis, University of Birmingham, 2011. http://etheses.bham.ac.uk//id/eprint/1493/.

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Epstein-Barr virus (EBV), a human gammaherpesvirus, possesses a unique set of latent genes whose constitutive expression in B cells leads to cell growth transformation. The initiation of this B-cell growth transformation programme depends on the activation of a viral promoter, Wp, present in each tandemly arrayed BamHI W repeat of the EBV genome. In order to examine the role of the BamHI W region in B cell infection and growth transformation, we constructed a series of recombinant EBVs carrying different numbers of BamHI W repeats and carried out B cell infection experiments. We concluded that EBV requires at least 2 copies of BamHI W repeats to be able to activate transcription and transformation in resting B cells in vitro. At least 5 copies of BamHI W were required for optimal transcription and transformation; while increasing the number beyond 5 copies had no further effect. Experiments to try to rescue the impaired virus indicated that the expression of sufficient levels of EBNA-LP and EBNA2 from Wp are the key determinants of virus-driven B cell transformation. We believe that EBV has evolved to contain multiple copies of BamHI W repeats to ensure high levels of Wp-initiated transcripts immediately post infection.
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Sanosyan, Armen. "Control of chronic Epstein-Barr virus infection : consequences of altered B lymphocyte activation." Thesis, Montpellier, 2016. http://www.theses.fr/2016MONTT089.

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Le virus d'Epstein-Barr (EBV), est un gamma herpes virus exclusivement humain qui infecte près de 95% de la population adulte. EBV établit un cycle de latence dans les cellules B mémoires et les cellules épithéliales. EBV entre périodiquement dans une réplication lytique avec sécrétion des virions dans la salive. L’infection EBV est associée à l’apparition de lymphomes, de cancers et de maladies auto-immunes. Les conditions favorisant le développement de ces pathologies restent mal connues mais l’immunodépression et potentiellement l’activation des lymphocytes B nécessaire à la réplication d’EBV jouent un rôle clé.Nous avons examiné l’association entre activation des cellules B dans le compartiment systémique et le contrôle sur le réservoir de l’EBV. Deux situations cliniques d’activation chronique des cellules B ont été explorées ; le syndrome de Gougerot-Sjögren et la mastite subclinique dans le contexte de l’infection par le VIH.Dans ce travail de thèse, nous avons tout d’abord développé une PCR en temps réel pour la quantification de l'ADN de EBV ciblant la région répétée BamHI-W du génome. Le travail de validation de la technique a permis d’évaluer précisément le gain de sensibilité comparativement à une qPCR LMP2 (cible unique). L’impact des variations de répétition de la séquence BamHI-W suivant les souches et isolats EBV a également été analyse.Dans un deuxième travail, nous avons montré que, la mastite subclinique était fréquente au cours de l’allaitement et qu’elle était un facteur indépendant associé à une augmentation de l'excrétion EBV par le lait maternel. Cette sécrétion est associée localement à l’inflammation et à l’excrétion du VIH ce qui témoigne de phénomène de synergie entre les deux virus. Nous avons également démontré que l'ADN EBV dans le lait maternel peut être résistant à la DNase et que le virus était est probablement encapsidé dans le lait, donc potentiellement infectieux.Enfin, bénéficiant d’un accès aux prélèvements de la cohorte ASSESS nous avons recherché de possible anomalie du contrôle de l’infection EBV dans le compartiment sanguin au cours du syndrome de Gougerot-Sjögren primaire dans lequel les lésions glandulaires salivaires et lacrymales sont associées à la présence d’EBV. Nous avons démontré que le réservoir EBV et la réplication EBV dans le compartiment systémique sont bien contrôlées au cours du syndrome de Gougerot-Sjögren primaire. La réponse anticorps contre l’antigène précoce d’EBV (EA) n'était pas associée à une augmentation de l'ADN de EBV.Ce travail de thèse, souligne le lien entre l'activation des lymphocytes B, l'inflammation chronique et le contrôle sur le réservoir d’EBV. Dans la glande mammaire le contrôle de l’infection EBV est perturbé en cas de mastite subclinique. Au contraire dans le syndrome de Gougerot-Sjögren l’infection reste bien contrôlée dans le compartiment sanguin malgré l’activation des lymphocytes B et la présence renforcée du virus dans les lésions glandulaires
TEpstein-Barr virus (EBV), an ubiquitous human gammaherpesvirus affects 95% of adult human population and establishes a lifelong latency in memory B cells periodically entering into lytic replication with further propagation in oropharyngeal epithelia and shedding through saliva. Latent EBV infection is associated with lymphomas, carcinomas and autoimmune diseases. Although the conditions favoring the development of these pathologies are not completely understood, the immunosuppression and B cell activations play an important role in EBV-associated diseases.We examined the control over the EBV reservoir in a diseases associated with B cell activation. Two clinical situations associated with altered B cell activation were explored: primary Sjogren’s syndrome and subclinical mastitis in HIV-infected mothers.Primarily, we developed an in-house real-time PCR for EBV DNA quantification targeting the repetitive BamHI-W region of EBV DNA. The validation analyses enabled to evaluate the gain in sensitivity of the BamHI-W test relative to single repeat LMP2 qPCR. The impact of the variations in BamHI-W reiteration on EBV DNA quantification was further assessed on different EBV strains and clinical samples.In a second study, we showed that subclinical mastitis was common during breastfeeding, and it was an independent factor associated with increased EBV breast milk shedding. This secretion was associated with local inflammation and HIV shedding, reflecting synergy between the two viruses. We have also demonstrated that breast milk EBV DNA may be resistant to DNase, and the virus was probably encapsidated in the breast milk and thus potentially infectious.Finally, with an access to ASSESS cohort we looked for possible abnormal control over EBV infection in the blood compartment in primary Sjögren's syndrome, where salivary and lacrimal gland lesions were shown to be associated with the local activation of EBV. We have demonstrated that in primary Sjogren's syndrome EBV reservoir and replication in the systemic compartment are well controlled. The antibody response against EBV early antigen (EA) was not associated with increased DNA EBV.This thesis points out the link between the activation of B cells, chronic inflammation and control over the reservoir of EBV. In the mammary gland disturbed control of EBV infection is linked with subclinical mastitis. In contrast, in primary Sjogren’s syndrome EBV infection remains well controlled in the blood compartment despite the activation of B cells and the increased presence of the virus in glandular lesions
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Lehmann, Henrik. "Vad kommer hända Bambi? En visuell analys om förväntningar i reklamfilmen Bambi." Thesis, Malmö universitet, Fakulteten för kultur och samhälle (KS), 2020. http://urn.kb.se/resolve?urn=urn:nbn:se:mau:diva-22819.

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Uppsatsen syftar till att undersöka hur företag använder sig av narrativ och form i reklamfilmer för att forma en publiks förväntningar och marknadsföra en produkt, med hjälp av frågeställningen “På vilka sätt kan förväntningar för en viss publik skapas genom narrativ och form samt förkunskap och genre i reklamfilmen Bambi (2001), och hur använder sig Sony detta för att sälja en produkt?”. Materialet, en film som gör reklam för spelkonsolen Playstation 2, analyseras genom en visuell analys, kombinerat med en film- samt narrativ analys. Undersökningen resulterade i konstaterandet att filmskaparna har, med hjälp av narrativ, filmtekniska metoder som bild och ljud, samt tidigare erfarenheter av reklamfilmer, försökt forma en viss publiks förväntningar i syftet att sälja en spelkonsol.
The purpose of this thesis is to analyze how companies are using narrative and form in commercials in order to shape an audience's expectations and market a product, with the thesis question “In which ways can expectations for a certain audience be created through narrative and form as well as prior knowledge and genre in commercial Bambi (2001), and how is Sony using this to sell a product?”. The material, a film to market gaming console Playstation 2, is being analyzed through a visual analysis, combined with a film- and narrative analysis. The thesis resulted in the finding that the creators have, with the help of narrative, film technical methods such as picture and sound, as well as prior knowledge of commercials, tried to form a specific audience’s expectations with the purpose of selling a gaming console.
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Mecheri, Lamia. "L'écriture de l'histoire chez Salim Bachi." Paris 8, 2014. http://octaviana.fr/document/181110571#?c=0&m=0&s=0&cv=0.

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Salim Bachi, auteur algérien contemporain, figure parmi les écrivains les plus prometteurs de sa génération. Il a publié cinq romans et deux récits : Le Chien d’Ulysse (2001, Prix Goncourt du premier roman), « La Kahéna » (2003, Prix Tropiques), « Autoportrait avec Grenade » (2004), « Tuez-les tous » (2006), « Le Silence de Mahomet » (2008), « Le grand frère » (2010), « Amours et aventures de Sindbad le Marin » (2010) et « Moi, Khaled Kelkal » (2012), ainsi qu’un recueil de nouvelles intitulé « Les douze contes de minuit »(2007). Dès « Le Chien d’Ulysse », Salim Bachi se fait le chroniqueur de son pays en racontant l’histoire de l’Algérie pendant la décennie noire des années 90. Dans d’autres livres, il s’intéresse à des événements historiques importants qui ont marqué le monde entier, comme les attentats du 11 septembre 2001. Ce sont les modalités (imaginaires, stylistiques, narratives, etc. ) de cette présence de l’Histoire dans l’œuvre de cet auteur que nous tentons d’analyser dans notre thèse
Salim Bachi, a contemporary Algerian author, is one of the most promising writers of his generation. He has published five novels and two stories: "Le Chien d’Ulysse" (2001, Prix Goncourt du premier roman), "La Kahéna" (2003, Prix Tropiques), "Autoportrait avec Grenade" (2004), "Tuez-les tous" (2006), "Le Silence de Mahomet" (2008), "Le grand frère" (2010), "Amours et aventures de Sindbad le Marin" (2010) and "Moi, Khaled Kelkal" (2012), and a collection of short stories entitled "Les douze contes de minuit" (2007). With "Le Chien d’Ulysse", Salim Bachi became the chronicler of his country, recounting the history of Algeria during the black decade of the 90s. In other books, he focuses on important historical events affecting the whole world, such as the terrorist attacks of September 11, 2001. The purpose of our thesis is to analyze the different modalities (imaginary, stylistic, narrative) of the presence of History in the work of this author
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Mweze, Baguma. "Le Mariage chez les Bashi et ses transformations récentes." Lille 3 : ANRT, 1988. http://catalogue.bnf.fr/ark:/12148/cb376082910.

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Mühleib, Corinna [Verfasser], Mehran [Akademischer Betreuer] Baghi, and Robert [Akademischer Betreuer] Sader. "Immunologische Prognosefaktoren bei Patienten mit fortgeschrittenen Kopf-/Hals-Tumoren behandelt mit TPF-Induktionschemotherapie / Corinna Mühleib. Gutachter: Mehran Baghi ; Robert Sader. Betreuer: Mehran Baghi." Frankfurt am Main : Univ.-Bibliothek Frankfurt am Main, 2015. http://d-nb.info/1070581259/34.

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Kottmair, Mathias Verfasser], and Thomas [Gutachter] [Müller. "Bambi – Charakterisierung eines inhibitorischen BMP-Pseudorezeptors / Mathias Kottmair ; Gutachter: Thomas Müller." Würzburg : Universität Würzburg, 2014. http://d-nb.info/1122020767/34.

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Kottmair, Mathias [Verfasser], and Thomas [Gutachter] Müller. "Bambi – Charakterisierung eines inhibitorischen BMP-Pseudorezeptors / Mathias Kottmair ; Gutachter: Thomas Müller." Würzburg : Universität Würzburg, 2014. http://nbn-resolving.de/urn:nbn:de:bvb:20-opus-103530.

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Axelsson, Berg Lina. "Bambi : – en komparativ analys av Felix Saltens bok och Walt Disneys film." Thesis, Örebro universitet, Institutionen för humaniora, utbildnings- och samhällsvetenskap, 2017. http://urn.kb.se/resolve?urn=urn:nbn:se:oru:diva-60741.

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Lina Axelsson Berg (2017). Bambi – en komparativ analys av Felix Saltens bok och Walt Disneys film. (Bambi – a comparative analysis of Felix Salten’s book and Walt Disney’s film). Independent project, Swedish, Specialization in Grades 4-6, Advanced Course, 15 credits. School of Humanities, Education and Social Sciences. The aim of this study is to examine the changes that have occurred when Saltens novel Bambi was adapted to Disney’s Bambi. The specific elements that are examined are the scenes, some of the characters and the environment. This has been done through a comparative analysis. The results shows that the changes that has been done when Disney adapted Bambi is fairly small but the (for some) underlying meaning of Saltens Bambi, that it can be read as an allegory, is gone. There has been a change of characters, for Disney has chosen to ignore a couple of the significant characters in Salten and choose to add a couple of new characters which is a reason to why the underlying meaning of the story has changed. The study also examines if and how the story of Bambi (mostly Saltens) can be used in school subjects, primary when working with human values and how human treat animals. The result shows that the story can be used for that purpose but that the pedagogy who chooses to use is have to see to their own students and how they would react to a story like Saltens.
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Books on the topic "BamHI"

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Felix, Salten, and Disney Walt 1901-1966, eds. Bambi. Loughborough: Ladybird Books, 1993.

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Bambi. Montreal, Quebec, Canada: Produced and published by Phidal Publishing, Inc., 2011.

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Bambi. Brazil?]: BrasiLeitura, 2000.

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Carr, Jan. Bambi. New York: Scholastic, 1988.

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Rahat, M. A. Baghi. Lahore: Ali Mian, 1996.

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Company, Walt Disney. Bambi. Greenwich, CT: Twin Books, 1987.

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Batt, Razia. Baghi. Lahore: Sang-e-Mil, 1991.

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1901-1966, Disney Walt, and Walt Disney Productions, eds. Bambi. (Loughborough): Ladybird, 1994.

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Disney Enterprises. Pixar Animation Studios. Bambi. Bath: Parragon, 2010.

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Salten, Felix. Bambi. Chichester: Invader, 1992.

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Book chapters on the topic "BamHI"

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Andreas-Zietz, A., E. Keller, E. D. Albert, and E. J. Yunis. "RFLP Standardization Report for C4/BamHI." In Immunobiology of HLA, 770–71. New York, NY: Springer New York, 1989. http://dx.doi.org/10.1007/978-1-4612-3552-1_208.

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Andreas-Zietz, A., E. Keller, E. D. Albert, A. Bushell, and E. J. Yunis. "RFLP Standardization Report for 210H/BamHI." In Immunobiology of HLA, 788–89. New York, NY: Springer New York, 1989. http://dx.doi.org/10.1007/978-1-4612-3552-1_219.

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Andreas-Zietz, A., E. Keller, E. D. Albert, A. Bushell, and E. J. Yunis. "RFLP Standardization Report for BF/BamHI." In Immunobiology of HLA, 734. New York, NY: Springer New York, 1989. http://dx.doi.org/10.1007/978-1-4612-3552-1_186.

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Andreas-Zietz, A., E. Keller, E. D. Albert, and E. J. Yunis. "RFLP Standardization Report for C2/BamHI." In Immunobiology of HLA, 754. New York, NY: Springer New York, 1989. http://dx.doi.org/10.1007/978-1-4612-3552-1_198.

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Keller, E., A. Andreas-Zietz, E. D. Albert, B. O. Boehm, J. J. Hyldig-Nielsen, A. Bushell, and D. P. Singal. "RFLP Standardization Report for DQ Alpha/BamHI." In Immunobiology of HLA, 828. New York, NY: Springer New York, 1989. http://dx.doi.org/10.1007/978-1-4612-3552-1_240.

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Andreas-Zietz, A., E. Keller, E. D. Albert, B. O. Boehm, J. J. Hyldig-Nielsen, and D. P. Singal. "RFLP Standardization Report for DP Alpha/BamHI." In Immunobiology of HLA, 848. New York, NY: Springer New York, 1989. http://dx.doi.org/10.1007/978-1-4612-3552-1_251.

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Vanamee, É. Scheuring, H. Viadiu, C. M. Lukacs, and A. K. Aggarwal. "Two of A Kind: BamHI and BglII." In Restriction Endonucleases, 215–36. Berlin, Heidelberg: Springer Berlin Heidelberg, 2004. http://dx.doi.org/10.1007/978-3-642-18851-0_8.

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Hyldig-Nielsen, J. J., B. O. Boehm, K. J. Wood, A. R. Bushell, D. P. Singal, and A. Svejgaard. "RFLP Standardization Report for DR Beta/BamHI." In Immunobiology of HLA, 605–7. New York, NY: Springer New York, 1989. http://dx.doi.org/10.1007/978-1-4612-3552-1_129.

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Hyldig-Nielsen, J. J., B. O. Boehm, K. J. Wood, A. R. Bushell, D. P. Singal, and A. Svejgaard. "RFLP Standardization Report for DQ Beta/BamHI." In Immunobiology of HLA, 634–36. New York, NY: Springer New York, 1989. http://dx.doi.org/10.1007/978-1-4612-3552-1_141.

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Hyldig-Nielsen, J. J., B. O. Boehm, K. J. Wood, A. R. Bushell, D. P. Singal, and A. Svejgaard. "RFLP Standardization Report for DP Beta/BamHI." In Immunobiology of HLA, 667–69. New York, NY: Springer New York, 1989. http://dx.doi.org/10.1007/978-1-4612-3552-1_153.

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Conference papers on the topic "BamHI"

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Marchetti, G., S. Guerra, G. Ballerini, P. Patracchini, S. Volinia, and F. Bernardi. "A FREQUENT TAQI RFLP AND A GENE LESION OR RARE TAQI RFLP IN THE VON WILLEBRAND FACTOR GENE." In XIth International Congress on Thrombosis and Haemostasis. Schattauer GmbH, 1987. http://dx.doi.org/10.1055/s-0038-1642834.

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A cDNA for vonWi11ebrand factor (vWf) has been used to investigate lesions and RFLPs in the vWf gene.In hybridizations with the 3'cDNA portion (a 2 Kb SacI fragment) a frequent polymorphism has been found with TaqI restriction enzyme. The alleles are 3.3 Kb and 2.6 Kb ; the frequencies of 0.51 and 0.49 respectively enable to investigate an appreciable portion of vW disease (vWd) families.In a patient with type III vWd an abnormal TaqI pattern has been observed. A 4.5 Kb band is absent and an additional band of 2.3 Kb is present.This pattern has been inherited from the consanguineous heterozygous parents and has been traced in several members of this large family. The presence of the abnormal gene pattern is related to total or partial vWf deficiency in the family and has not been found in several normal subjects. The BamHI and BglII restriction patterns are normal and suggest a small mutation originating a new TaqI site.These findings are compatible with a gene lesion or a rare RFLP.Work supported by Ricerca Sanitaria Finalizzata Regione Emilia Romagna.
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Mukohyama, Junko, Dai Iwakiri, Yoh Zen, Toru Mukohara, Hironobu Minami, Yoshihiro Kakeji, and Yohei Shimono. "Abstract 4822: Detection of EBV BamHI W region in surgical cancer specimen is a useful method to evaluate the risk of lymphomagenesis in patient-derived tumor xenografts." In Proceedings: AACR Annual Meeting 2017; April 1-5, 2017; Washington, DC. American Association for Cancer Research, 2017. http://dx.doi.org/10.1158/1538-7445.am2017-4822.

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Kojima, T., M. Tanimoto, T. Kamiya, Y. Obata, K. Kurachi, and H. Saito. "ANALYSIS OF FACTOR IX GENE IN NORMAL SUBJECTS AND HEMOPHILIA B PATIENTS IN JAPAN." In XIth International Congress on Thrombosis and Haemostasis. Schattauer GmbH, 1987. http://dx.doi.org/10.1055/s-0038-1644077.

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We have examined DNA samples from 25 hemophilia B patients (21 B- patients, 2 BR patients and 2 B+ patients) and 51 normal subjects with molecular probes (pHFIX and 2 genomic fragments). By structural gene analysis, 4 out of 7 patients who developed anti-factor IX antibodies were detected to have gross factor IX gene deletion. Although these four patients showed normal pattern of HPRT gene detected by pCDHPRT, the gene deletions were found to expand more than 34kb including with entire factor IX exons. Quantitative Southern blot analysis of factor IX gene of the patient's family members indicated that the gene deletion was inherited in one family, establishing the carrier status of 2 aunts, 2 cousins and one sister. The 'de novo' mutation of factor IX gene was also established in 2 families. Three patients with anti-factor IX antibodies and 17 patients without antibody to factor IX had normal pattern of factor IX gene by several restriction enzyme digestions. Analysis of factor IX gene of three patients with anti-factor IX antibodies and two B+ patients are now underway to detect the unique gene defects which may be responsible for the disease Phenotypes. Common RFLPs in factor IX gene were studied in normal Japanese subjects. More than 80 X chromosomes were analysed with BamHI, Ddel, MspI, TaqI or XmnI digestion, followed by hybridization with pHFIX. RFLPs produced by these enzymes were found to be uncommon or possibly absent in normal Japanese subjects. These results imply that racial differences in the frequency of gene polymorphisms should be seriously considered before initiating the gene counseling by the genetic probes.
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Wha Lin, Shu, J. Ware, H. Roberts, N. McGraw, W. McAllister, and D. Stafford. "EXPRESSION OF HUMAN FACTOR IX IN MAMMALIAN CELLS." In XIth International Congress on Thrombosis and Haemostasis. Schattauer GmbH, 1987. http://dx.doi.org/10.1055/s-0038-1643567.

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Human factor IX has been expressed in mammalian cells. A cloned factor IX cDNA missing the first 15 nucleotides of the 5’ end was modified by in vitro mutagenesis to restore the missing codons and add the translation consensus sequence, CCACC, proposed by Kozak to be optimal for translational initiation. Additionally, Bgl II and BamHI sites were added immediately upstream of the CCACC sequence for ease of portability of the fragment. This modified cDNA was inserted into a bovine papillomavirus (BPV) vector under the control of a mouse met alio thionein promoter. The constructed plasmid pBPV-IX was used to transfect a mouse fibroblast cell line C127. After 3 weeks, the transformed foci were isolated and the established cell lines were grown in the presence or absence of vitamin K. Media was collected at 3 day intervals and assayed for factor IX activity in a one stage clotting assay. A standard curve was constructed using purified human factor IX. Cells grown in the presence of vitamin K (3 mg/L) exhibited an activity equivalent to 350 ng/ml of factor IX in the cell media; no (less than 3 ng/ml) activity was detectable in the absence of vitamin K. A monoclonal antibody column specific for the Ca++ dependent form of human factor IX allowed the isolation of approximately 7 ug of purified factor IX from approximately 100 ml of culture medium. Western blot analysis of the purified factor IX revealed 2 protein bands which reacted with a goat anti-human factor IX antibody as well as a human specific monoclonal antibody. One of the immunoreactive bands migrates with authentic human factor IX and the other migrates slower. This expression system provides a convenient way to produce suitable amounts of factor IX and mutated factor IX protein for functional analyses.
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Liddell, M. B., D. S. Anson, D. P. Lillicrap, and I. R. Peake. "SEARCH FOR AND USE OF RESTRICTION FRAGMENT LENGTH POLYMORPHISMS (RFLPs) IN AND AROUND THE HUMAN FACTOR IX GENE." In XIth International Congress on Thrombosis and Haemostasis. Schattauer GmbH, 1987. http://dx.doi.org/10.1055/s-0038-1644078.

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5 previously described RFLPs within the factor IX gene have been used for family studies (carrier detection) in 10 haemophilia B kindred. In all DNA from 91 individuals, including 25 obligate or possible carriers, was analysed by digestion with TaqI and XmnI and probing with the intragenomic probe VIII (all probes were provided by Professor G. G. Brownlee, Oxford). When noninformative, additional RFLPs (DdeI;probe XIII and MspI;probe II) were used. Of 12 possible carriers, 11 were diagnosed (6 as carriers, 5 normal). Of the confirmed carriers (6 diagnosed, 13 obligate) 15 were informative (heterozygous and phase known), and the overall incidence of heterozygosity was 72%. The recently reported BamHI RFLP was not found to be useful ( <1.0% frequency).Further RFLPs in and flanking the factor IX gene were sought by two procedures. Firstly cosmid pCHIXα, containing a 40kb insert including the 3' end of the factor IX gene and stretching some 35kb 3' to the gene was used as a large probe, with repetitive sequences being blocked by preannealing the probe with an excess of sonicated, denatured human DNA (Litt and White, PNAS 82, 6206). Results with 25 restriction enzymes (covering an estimated 1038 nucleotides) and DNA from 7 unrelated females were obtained, but only one low frequency PvuII RFLP (frequency about 1%) was identified. Similar experiments with further cosmid probes 3' to the gene are underway. The second technique was developed to analyse small DNA fragments (<1.0kb) generated by frequently cutting restriction enzymes. These fragments were separated on 3.5% polyacrylamide/0.5% agarose composite gels and then electroblotted onto hybond-N. Fragments of 150bp were readily visualised by this procedure. 3 frequently cutting enzymes have been used (Hinfl, Rsal and Mbol), and the blots probed with a factor IX c-DNA probe, or a unique sequence subclone of cosmid pCHIXα. To date no RFLPs have been identified. This search for further useful RFLP has illustrated the paucity of detectable sequence variation within this region of the X-chromosome.
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Geddes, V. A., G. V. Louie, G. D. Brayer, and R. T. A. MacGillivray. "MOLECULAR BASIS OF HEMOPHILIA B: IDENTIFICATION OF THE DEFECT IN FACTOR IX VANCOUVER." In XIth International Congress on Thrombosis and Haemostasis. Schattauer GmbH, 1987. http://dx.doi.org/10.1055/s-0038-1643872.

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Factor IX Vancouver (fIX-V) is the cause of a moderate form of hemophilia B. An individual presenting with this disorder had 2.6% of normal procoagulant activity in his plasma but had 62% of the normal factor IX antigen level. Specific antibodies showed that fIX-V contains epitopes for both the heavy and light chains of factor IXa. To identify the defect involved, DNA was isolated from the lymphocytes of the male hemophiliac. Southern blot analysis using a full-length factor IX cDNA as a hybridization probe showed no gross differences between the fIX-V gene and the normal factor IX gene. The DNA from the hemophiliac was then partially digested with Sau3A and the resulting fragments (10-20kbp in size) were ligated into the BamHI site of λEMBL3. The DNA was then packaged into phage particles in vitro, and the recombinant phage were screened with the factor IX cDNA as a probe. Eight phage were isolated that contained overlapping DNA covering the complete gene for fIX-V. DNA sequence analysis of the protein-encoding regions, the intron/exon junctions and 5'-and 3'-flanking sequences revealed a single nucleotide change from the normal factor IX gene. The codon for amino acid 397 was changed from ATA (lie) to ACA (Thr). This mutation is in the catalytic domain of factor IXa and is novel amongst those hemophilia B mutations reported to date. Based on the known three dimensional structures of the pancreatic serine proteases, trypsin, elastase and chymotrypsin, models have been constructed for the structures of the catalytic domains of both the normal and Thr-397 mutant of factor IXa. These results suggest that the Thr-397 mutation may alter the conformation of the substrate binding region in the active site of factor IXa Vancouver through the formation of a hydrogen bond between the hydroxyl group of the Thr-397 side chain and the main chain carbonyl group of Trp-385. The postulated conformational change would lead to reduced binding affinity for the factor IXa substrate resulting in a reduction in the catalytic activity of fIXa-Vancouver.Supported in part by grants from the Medical Research Council of Canada (to GDB and RTAM).
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Adam, Shuaibu Musa, Ashok Samraj Thangarajan, Mengyao Liu, Danny Hughes, and Ka Lok Man. "BaMbI, a battery free and energy harvesting smartphone." In MobiSys '22: The 20th Annual International Conference on Mobile Systems, Applications and Services. New York, NY, USA: ACM, 2022. http://dx.doi.org/10.1145/3498361.3538673.

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Vock, Christina, Lars Lunding, Gabriele Schramm, Michael Wegmann, and Heinz Fehrenbach. "The deletion of Bambi attenuates experimental asthma in mice." In ERS International Congress 2017 abstracts. European Respiratory Society, 2017. http://dx.doi.org/10.1183/1393003.congress-2017.pa1144.

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Wijaksono, Prayogi, Martono, and Awal Putra Suprianto. "Cultural Study: Ghumah Baghi Philosophy of Besemah Ethnic Society." In International Joint Conference on Arts and Humanities (IJCAH 2020). Paris, France: Atlantis Press, 2020. http://dx.doi.org/10.2991/assehr.k.201201.112.

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Santos, Ronnie E. S., J. Rafael Cordeiro, Yvan Labiche, Cleyton V. C. Magalhães, and Fabio Q. B. da Silva. "Bug! Falha! Bachi! Fallo! Défaut! 程序错误!" In ESEM '20: ACM / IEEE International Symposium on Empirical Software Engineering and Measurement. New York, NY, USA: ACM, 2020. http://dx.doi.org/10.1145/3382494.3422167.

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