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Добірка наукової літератури з теми "TnAg"

Автор: Grafiati

Опубліковано: 15 вересня 2021

Оновлено: 1 лютого 2022

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Статті в журналах з теми "TnAg"

hÓgáin, Fionnán Ó. "Bíodh TnaG Againn!" Comhar 51, no. 5 (1992): 220. http://dx.doi.org/10.2307/25571800.

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Feinneadha, Ciarán Ó. "TnaG - an ród a bhí romhainn." Comhar 54, no. 5 (1995): 10. http://dx.doi.org/10.2307/25572644.

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Konan, Kouacou Vincent, and Charles Yanofsky. "Role of Ribosome Release in Regulation oftna Operon Expression in Escherichia coli." Journal of Bacteriology 181, no. 5 (1999): 1530–36. http://dx.doi.org/10.1128/jb.181.5.1530-1536.1999.

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ABSTRACT Expression of the degradative tryptophanase (tna) operon of Escherichia coli is regulated by catabolite repression and tryptophan-induced transcription antitermination. In cultures growing in the absence of added tryptophan, transcription of the structural genes of the tna operon is limited by Rho-dependent transcription termination in the leader region of the operon. Tryptophan induction prevents this Rho-dependent termination, and requires in-frame translation of a 24-residue leader peptide coding region, tnaC, that contains a single, crucial, Trp codon. Studies with a lacZ reporter construct lacking the spacer region between tnaC and the first major structural gene,tnaA, suggested that tryptophan induction might involvecis action by the TnaC leader peptide on the ribosome translating the tnaC coding region. The leader peptide was hypothesized to inhibit ribosome release at thetnaC stop codon, thereby blocking Rho’s access to the transcript. Regulatory studies with deletion constructs of thetna operon of Proteus vulgaris supported this interpretation. In the present study the putative role of thetnaC stop codon in tna operon regulation inE. coli was examined further by replacing the naturaltnaC stop codon, UGA, with UAG or UAA in atnaC-stop codon-tnaA′-′lacZ reporter construct. Basal level expression was reduced to 20 and 50% when the UGA stop codon was replaced by UAG or UAA, respectively, consistent with the finding that in E. coli translation terminates more efficiently at UAG and UAA than at UGA. Tryptophan induction was observed in strains with any of the stop codons. However, when UAG or UAA replaced UGA, the induced level of expression was also reduced to 15 and 50% of that obtained with UGA as the tnaC stop codon, respectively. Introduction of a mutant allele encoding a temperature-sensitive release factor 1, prfA1, increased basal level expression 60-fold when the tnaC stop codon was UAG and 3-fold when this stop codon was UAA; basal level expression was reduced by 50% in the construct with the natural stop codon, UGA. In strains with any of the three stop codons and the prfA1mutation, the induced levels of tna operon expression were virtually identical. The effects of tnaC stop codon identity on expression were also examined in the absence of Rho action, using tnaC-stop codon-′lacZ constructs that lack the tnaC-tnaA spacer region. Expression was low in the absence of tnaC stop codon suppression. In most cases, tryptophan addition resulted in about 50% inhibition of expression when UGA was replaced by UAG or UAA and the appropriate suppressor was present. Introduction of the prfA1 mutant allele increased expression of the suppressed construct with the UAG stop codon; tryptophan addition also resulted in ca. 50% inhibition. These findings provide additional evidence implicating the behavior of the ribosome translating tnaC in the regulation of tna operon expression.

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Tovey, Hilary. "Book Review: Comparison of the Campaigns for Raidio na Gaeltachta and TnaG." Irish Journal of Sociology 11, no. 2 (2002): 147–49. http://dx.doi.org/10.1177/079160350201100209.

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Konan, Kouacou Vincent, and Charles Yanofsky. "Rho-Dependent Transcription Termination in the tnaOperon of Escherichia coli: Roles of the boxASequence and the rut Site." Journal of Bacteriology 182, no. 14 (2000): 3981–88. http://dx.doi.org/10.1128/jb.182.14.3981-3988.2000.

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ABSTRACT Expression of the tryptophanase (tna) operon ofEscherichia coli is regulated by catabolite repression and by tryptophan-induced transcription antitermination. Tryptophan induction prevents Rho-dependent transcription termination in the leader region of the operon. Induction requires translation of a 24-residue leader peptide-coding region, tnaC, containing a single, crucial Trp codon. Studies with a lacZ reporter construct lacking the tnaC-tnaA spacer region suggest that, in the presence of excess tryptophan, the TnaC leader peptide acts incis on the ribosome translating tnaC to inhibit its release. The stalled ribosome is thought to block Rho's access to the transcript. In this paper we examine the roles of theboxA sequence and the rut site in Rho-dependent termination. Deleting six nucleotides (CGC CCT) of boxA or introducing specific point mutations in boxA results in high-level constitutive expression. Some constitutive changes introduced in boxA do not change the TnaC peptide sequence. We confirm that deletion of the rut site results in constitutive expression. We also demonstrate that, in each constitutive construct, replacement of the tnaC start codon by a UAG stop codon reduces expression significantly, suggesting that constitutive expression requires translation of the tnaCcoding sequence. Addition of bicyclomycin, an inhibitor of Rho, to these UAG constructs increases expression, demonstrating that reduced expression is due to Rho action. Combining a boxA point mutation with rut site deletion results in constitutive expression comparable to that of a maximally induced operon. These results support the hypothesis that in the presence of tryptophan the ribosome translating tnaC blocks Rho's access to theboxA and rut sites, thereby preventing transcription termination.

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Almansour, Haidara, Johann Jacoby, Heiko Baumgartner, Marie K. Reumann, Konstantin Nikolaou, and Fabian Springer. "Injury of the Tibial Nutrient Artery Canal during External Fixation for Lower Extremity Fractures: A Computed Tomography Study." Journal of Clinical Medicine 9, no. 7 (2020): 2235. http://dx.doi.org/10.3390/jcm9072235.

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The tibial nutrient artery (TNA) is the major diaphyseal artery of the tibia supplying two thirds of the inner osseous cortex. Hence, iatrogenic injury of the TNA endangers the integrity of the tibial blood supply and may compromise fracture healing. The incidence of its injury in the setting of external fixation for lower limb fractures has not been previously investigated. The aim of this study was to evaluate the incidence of TNA injury in the context of external fixation and to characterize the topography of the fixator pins in relation to the TNA canal (TNAC). Patients who underwent external fixation for distal femoral fractures and for tibial (proximal, shaft, and distal) fractures and had a postoperative computed tomography study were retrospectively included. The following parameters were retrieved: 1) Pin characteristics (orientation and cortical position of the pins), 2) The anatomic relationship between the TNAC and external fixation pin (topography above/below and at the level of the TNAC, and the distance between the pin and medial tibial plateau and/or the medial malleolus), and 3) The incidence of TNAC injury (complete/partial disruption of TNA lumen). A total of 105 patients with 214 tibial pins were analyzed. In 27 patients (26%), the TNAC was completely injured by the pins of the external fixator. In 13 patients (12%), the TNAC was partially injured. Of the 214 analyzed pins, 85 pins (40%) were located at the level of the TNAC (the TNAC and the pin are seen on the same axial slice). Most pins that were applied at the level of the TNAC belonged to a knee-bridging external fixator. Of those, ninety-three percent of the pins were anteromedially applied according to published surgical guidelines. Six percent of the pins were applied through the tibial crest and 1% anterolaterally. Of those 85 pins, 42 pins (49%) injured the TNAC at least partially. Based on the analyzed pins and the incidence of partial and complete injury of the TNAC, we observed that the tibial segment at which the tibial nutrient artery is endangered was located approximately (95% CI: 13–15 cm) from the medial tibia plateau and (95% CI: 22–25 cm) from the medial malleolus. Thus, TNAC injury by external fixation pins in the context of lower limb fractures can be considered common. Almost half of the pins applied at the middle third of the tibia injured the TNA, despite adherence to published surgical guidelines for external fixation. When possible, pin application at the middle third of tibia should be avoided to circumvent iatrogenic injury of the TNA and to safeguard tibial blood supply.

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Manicardi, G. C., D. Bizzaro, E. Galli, and U. Bianchi. "Heterochromatin heterogeneity in the holocentric X chromatin of Megoura viciae (Homoptera, Aphididae)." Genome 39, no. 2 (1996): 465–70. http://dx.doi.org/10.1139/g96-059.

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Holocentric chromosomes, prepared by spreading embryo cells obtained from Megoura viciae parthenogenetic females, have been C-banded, enzymatically digested in situ using the specific endonucleases DdeI (C↓TNAG), DraI (TTT↓AAA), Tru9I (TT↓AA), and CfoI (GCG↓C), and subsequently stained with Giemsa, DAPI, CMA3, and AgNO3. We observed that the X chromosome had the best defined banding patterns. In the M. viciae X chromosome there is a certain amount of heterogeneity in heterochromatic DNA composition. In fact, the GC-rich NOR-associated heterochromatin differs from other heterochromatic bands that are characterized by AT-rich DNAs. Our data also indicate that, in M. viciae holocentric chromosomes, all heterochromatic blocks are accessible to in situ enzyme attack, the only limit to the digestion being the presence or absence of recognition targets. This is an interesting point, since, in monocentric chromosomes, it is well known that in situ endonuclease digestion is heavily affected not only by DNA base composition but also by chromatin compactness that may limit enzyme accessibility to their specific targets. Key words : heterochromatin, holocentric chromosomes, aphids.

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Cruz-Vera, Luis R., and Charles Yanofsky. "Conserved Residues Asp16 and Pro24 of TnaC-tRNAPro Participate in Tryptophan Induction of tna Operon Expression." Journal of Bacteriology 190, no. 14 (2008): 4791–97. http://dx.doi.org/10.1128/jb.00290-08.

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ABSTRACT In Escherichia coli, interactions between the nascent TnaC-tRNAPro peptidyl-tRNA and the translating ribosome create a tryptophan binding site in the ribosome where bound tryptophan inhibits TnaC-tRNAPro cleavage. This inhibition delays ribosome release, thereby inhibiting Rho factor binding and action, resulting in increased tna operon transcription. Replacing Trp12 of TnaC with any other amino acid residue was previously shown to prevent tryptophan binding and induction of tna operon expression. Genome-wide comparisons of TnaC amino acid sequences identify Asp16 and Pro24, as well as Trp12, as highly conserved TnaC residues. Replacing these residues with other residues was previously shown to influence tryptophan induction of tna operon expression. In this study, in vitro analyses were performed to examine the potential roles of Asp16 and Pro24 in tna operon induction. Replacing Asp16 or Pro24 of TnaC of E. coli with other amino acids established that these residues are essential for free tryptophan binding and inhibition of TnaC-tRNAPro cleavage at the peptidyl transferase center. Asp16 and Pro24 are in fact located in spatial positions corresponding to critical residues of AAP, another ribosome regulatory peptide. Sparsomycin-methylation protection studies further suggested that segments of 23S RNA were arranged differently in ribosomes bearing TnaCs with either the Asp16Ala or the Pro24Ala change. Thus, features of the amino acid sequence of TnaC of the nascent TnaC-tRNAPro peptidyl-tRNA, in addition to the presence of Trp12, are necessary for the nascent peptide to create a tryptophan binding/inhibition site in the translating ribosome.

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Cruz-Vera, Luis R., Rui Yang, and Charles Yanofsky. "Tryptophan Inhibits Proteus vulgaris TnaC Leader Peptide Elongation, Activating tna Operon Expression." Journal of Bacteriology 191, no. 22 (2009): 7001–6. http://dx.doi.org/10.1128/jb.01002-09.

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ABSTRACT Expression of the tna operon of Escherichia coli and of Proteus vulgaris is induced by l-tryptophan. In E. coli, tryptophan action is dependent on the presence of several critical residues (underlined) in the newly synthesized TnaC leader peptide, WFNIDXXL/IXXXXP. These residues are conserved in TnaC of P. vulgaris and of other bacterial species. TnaC of P. vulgaris has one additional feature, distinguishing it from TnaC of E. coli; it contains two C-terminal lysine residues following the conserved proline residue. In the present study, we investigated l-tryptophan induction of the P. vulgaris tna operon, transferred on a plasmid into E. coli. Induction was shown to be l-tryptophan dependent; however, the range of induction was less than that observed for the E. coli tna operon. We compared the genetic organization of both operons and predicted similar folding patterns for their respective leader mRNA segments. However, additional analyses revealed that l-tryptophan action in the P. vulgaris tna operon involves inhibition of TnaC elongation, following addition of proline, rather than inhibition of leader peptide termination. Our findings also establish that the conserved residues in TnaC of P. vulgaris are essential for l-tryptophan induction, and for inhibition of peptide elongation. TnaC synthesis is thus an excellent model system for studies of regulation of both peptide termination and peptide elongation, and for studies of ribosome recognition of the features of a nascent peptide.

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Gong, Ming, Luis R. Cruz-Vera, and Charles Yanofsky. "Ribosome Recycling Factor and Release Factor 3 Action Promotes TnaC-Peptidyl-tRNA Dropoff and Relieves Ribosome Stalling during Tryptophan Induction of tna Operon Expression in Escherichia coli." Journal of Bacteriology 189, no. 8 (2007): 3147–55. http://dx.doi.org/10.1128/jb.01868-06.

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ABSTRACT Upon tryptophan induction of tna operon expression in Escherichia coli, the leader peptidyl-tRNA, TnaC- \batchmode \documentclass[fleqn,10pt,legalpaper]{article} \usepackage{amssymb} \usepackage{amsfonts} \usepackage{amsmath} \pagestyle{empty} \begin{document} \(tRNA_{2}^{Pro}\) \end{document} , resists cleavage, resulting in ribosome stalling at the tnaC stop codon. This stalled ribosome blocks Rho factor binding and action, preventing transcription termination in the tna operon's leader region. Plasmid-mediated overexpression of tnaC was previously shown to inhibit cell growth by reducing uncharged \batchmode \documentclass[fleqn,10pt,legalpaper]{article} \usepackage{amssymb} \usepackage{amsfonts} \usepackage{amsmath} \pagestyle{empty} \begin{document} \(tRNA_{2}^{Pro}\) \end{document} availability. Which factors relieve ribosome stalling, facilitate TnaC- \batchmode \documentclass[fleqn,10pt,legalpaper]{article} \usepackage{amssymb} \usepackage{amsfonts} \usepackage{amsmath} \pagestyle{empty} \begin{document} \(tRNA_{2}^{Pro}\) \end{document} cleavage, and relieve growth inhibition were addressed in the current study. In strains containing the chromosomal tna operon and lacking a tnaC plasmid, the overproduction of ribosome recycling factor (RRF) and release factor 3 (RF3) reduced tna operon expression. Their overproduction in vivo also increased the rate of cleavage of TnaC- \batchmode \documentclass[fleqn,10pt,legalpaper]{article} \usepackage{amssymb} \usepackage{amsfonts} \usepackage{amsmath} \pagestyle{empty} \begin{document} \(tRNA_{2}^{Pro}\) \end{document} , relieving the growth inhibition associated with plasmid-mediated tnaC overexpression. The overproduction of elongation factor G or initiation factor 3 did not have comparable effects, and tmRNA was incapable of attacking TnaC- \batchmode \documentclass[fleqn,10pt,legalpaper]{article} \usepackage{amssymb} \usepackage{amsfonts} \usepackage{amsmath} \pagestyle{empty} \begin{document} \(tRNA_{2}^{Pro}\) \end{document} in stalled ribosome complexes. The stability of TnaC- \batchmode \documentclass[fleqn,10pt,legalpaper]{article} \usepackage{amssymb} \usepackage{amsfonts} \usepackage{amsmath} \pagestyle{empty} \begin{document} \(tRNA_{2}^{Pro}\) \end{document} was increased appreciably in strains deficient in RRF and RF3 or deficient in peptidyl-tRNA hydrolase. These findings reveal the existence of a natural mechanism whereby an amino acid, tryptophan, binds to ribosomes that have just completed the synthesis of TnaC- \batchmode \documentclass[fleqn,10pt,legalpaper]{article} \usepackage{amssymb} \usepackage{amsfonts} \usepackage{amsmath} \pagestyle{empty} \begin{document} \(tRNA_{2}^{Pro}\) \end{document} . Bound tryptophan inhibits RF2-mediated cleavage of TnaC- \batchmode \documentclass[fleqn,10pt,legalpaper]{article} \usepackage{amssymb} \usepackage{amsfonts} \usepackage{amsmath} \pagestyle{empty} \begin{document} \(tRNA_{2}^{Pro}\) \end{document} , resulting in the stalling of the ribosome translating tnaC mRNA. This stalling results in increased transcription of the structural genes of the tna operon. RRF and RF3 then bind to this stalled ribosome complex and slowly release TnaC- \batchmode \documentclass[fleqn,10pt,legalpaper]{article} \usepackage{amssymb} \usepackage{amsfonts} \usepackage{amsmath} \pagestyle{empty} \begin{document} \(tRNA_{2}^{Pro}\) \end{document} . This release allows ribosome recycling and permits the cleavage of TnaC- \batchmode \documentclass[fleqn,10pt,legalpaper]{article} \usepackage{amssymb} \usepackage{amsfonts} \usepackage{amsmath} \pagestyle{empty} \begin{document} \(tRNA_{2}^{Pro}\) \end{document} by peptidyl-tRNA hydrolase.

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Дисертації з теми "TnAg"

Forton, Fabienne. "Le rôle du Demodex dans la rosacée. La rosacée avec papulopustules :une démodécie." Doctoral thesis, Universite Libre de Bruxelles, 2021. http://hdl.handle.net/2013/ULB-DIPOT:oai:dipot.ulb.ac.be:2013/325373.

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Le Demodex, petit acarien vivant dans les follicules pilo-sébacés de tous les humains adultes, est reconnu responsable des démodécies chez l’homme mais n’est considéré dans la rosacée, au plus, que comme un facteur aggravant potentiel d’une inflammation préexistante. Toutes nos observations, depuis 1983, convergent vers la confirmation de son rôle pathogène dans la rosacée, et suggèrent des liens physiopathologiques clairs entre rosacées avec papulopustules (RPP) avec ou sans érythème permanent, rosacée érythématotélangiectasique (RET), pityriasis folliculorum et autres démodécies. (1) Dans les biopsies cutanées, le Demodex est associé à l’inflammation périfolliculaire. (2) Le concept de densité en Demodex a été introduit et une méthode de prélèvement standardisée permettant de mesurer cette densité a été développée, puis perfectionnée. (3) Elle a permis de montrer que cette densité était nettement supérieure chez les patients atteints de démodécie et de RPP, que chez ceux avec peau saine et ceux atteints d’autres dermatoses faciales, les patients avec RPP sans prolifération en Demodex étant exceptionnels. (4) Un test diagnostique hautement spécifique et sensible, utilisable facilement en consultation a été élaboré et validé. (5) Des signes cliniques discrets de ces dermatoses ont été mis en évidence, de même que la grande fréquence des démodécies en consultation de dermatologie (alors qu’elles sont très peu diagnostiquées). (6) L’effet acaricide sur le Demodex de six traitements topiques a été comparé in vivo et les meilleures molécules ont été utilisées pendant une vingtaine d’années :sur base des résultats collectés, l’efficacité du traitement a été démontrée, non seulement sur la densité en Demodex mais également sur les symptômes cliniques, tant parmi les démodécies que dans la RPP, ce qui prouve indirectement que la prolifération en parasites n’est pas un épiphénomène mais est bien la cause de la maladie. (7) Parmi les modalités comparées, les plus intenses ont une efficacité plus rapide et une meilleure compliance. (8) La RET peut correspondre à une démodécie subclinique et est probablement un facteur favorisant la prolifération des parasites, tout comme le sont probablement l’hyperplasie sébacée et l’hypothyroïdie, tandis que la cortisone semble limiter leur prolifération quand celle-ci est excessive. (9) Les similarités et les confusions nosologiques entre les démodécies et les différentes formes de rosacée ont été mises en évidence, afin de montrer que ces dermatoses ne sont vraisemblablement que des phénotypes d’une seule et même maladie :ce sont toutes des démodécies. (10) Trois systèmes d’attribution d’une cause à une maladie convergent pour confirmer le rôle pathogène du Demodex dans la RPP. Nos observations doivent être confirmées par des études longitudinales et des études contrôlées, mais d’ores et déjà, ajoutées aux données actuelles de la littérature, elles nous semblent suffisantes pour reconnaître le rôle pathogène du parasite en médecine humaine et dans la rosacée en particulier. Cette reconnaissance donnerait une définition principalement étiologique à la rosacée, la classerait parmi les démodécies, et en faciliterait la prise en charge et le traitement. Nous proposons une hypothèse physiopathologique originale où le Demodex se trouve au centre d’un réseau causal « en toile d’araignée », la RPP étant considérée comme une infection chronique s’accompagnant d’épuisement lymphocytaire. Demodex folliculorum and Demodex brevis are small mites living in the pilosebaceous follicles of all adult humans. They are known to be responsible for demodicosis in humans but in rosacea are generally considered only as a potential aggravating factor of pre-existing inflammation. However, our observations since 1983 converge towards a pathogenic role of the Demodex mite in rosacea, and suggest clear pathophysiological links between rosacea with papulopustules (PPR) with or without persistent erythema, erythematotelangiectatic rosacea (ETR), pityriasis folliculorum and other demodicoses. Summarising our findings: (1) In skin biopsies, Demodex is statistically associated with perifollicular inflammation. (2) The concept of Demodex density was introduced and a method to measure it using two consecutive standardized skin surface biopsies was developed and refined. (3) It was shown that Demodex density was significantly higher in patients with demodicosis and PPR than in those with healthy skin and with other facial dermatoses; patients with PPR without Demodex proliferation detected are rare, and the few cases that do occur likely correspond to false negative results linked to proliferation of the mites deep in the pilosebaceous follicles, thus not detected by the sampling method. (4) A highly specific and sensitive diagnostic test based on the results from two consecutive standardized skin surface biopsies was developed and validated and can be easily used during clinical consultation. (5) Less well-known clinical signs of these dermatoses were highlighted, as well as the high frequency of demodicoses in dermatologic consultations (although they are under-diagnosed). (6) The acaricidal effect of six topical treatments on Demodex was compared in vivo and the best molecules were used for about 20 years in our practice. From data collected from our patients during this time period, the efficacy of the treatment was demonstrated, not only on Demodex density but also on clinical symptoms, both in demodicosis and in PPR, indirectly showing that parasite proliferation is not an epiphenomenon, but is the cause of the disease. (7) Of the treatment modalities compared, those that were more intense worked more rapidly and had better compliance. (8) ETR may correspond to subclinical demodicosis and is probably a condition that favours parasite proliferation, as are sebaceous hyperplasia and hypothyroidism; cortisone seems initially to favour mite proliferation, but to limit it when Demodex density is very high. (9) The similarities and nosological confusion between demodicosis and the different forms of rosacea were highlighted, showing that these dermatoses are probably phenotypes of one and the same disease: they are all demodicoses. (10) Three systems used to attribute disease causality converge to confirm the pathogenic role of Demodex in PPR. Our observations need to be confirmed by longitudinal and controlled studies, but, combined with current data in the literature, they seem sufficient to recognise the pathogenic role of the parasite in human disease and in rosacea in particular. This recognition would enable a mainly aetiological definition to be given to rosacea, would classify it among the demodicoses, and would facilitate its management and treatment. We propose an original pathophysiological hypothesis in which Demodex is at the centre of a causal network, with PPR being considered a chronic infection accompanied by lymphocyte exhaustion. Doctorat en Sciences médicales (Médecine) info:eu-repo/semantics/nonPublished

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Ferrari, Cécilia. "Il y a plus de choses dans la salle et sur la scène que n’en montre votre scénographie : Étude spatiale et iconographique du « théâtre populaire » à partir des expériences de Firmin GÉMIER : Festivals suisses, TNAG, Œdipe Roi de Thèbes (1903-1919) ; Jacques COPEAU : Savonarola, Florence (1935) ; Jean VILAR : La Tragédie du Roi Richard II, Avignon (1947)." Caen, 2014. http://www.theses.fr/2014CAEN1016.

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Entre la fin du XIXe et le début du XXe siècle, plusieurs hommes de théâtre désignent le public qu’ils visent à rassembler par le terme peuple et leur théâtre par l’expression théâtre populaire. Leur attention se concentre sur la recherche d’un espace traduisant l’égalité propre à la société démocratique. Afin d’offrir à tous une bonne visibilité de la scène, ils choisissent le Festspielhaus de Bayreuth comme modèle de référence : le public est disposé face à la scène et la salle est plongée dans l’obscurité. Qui est le peuple que l’on place dans ce type d’espace où les échanges entre les spectateurs sont réduits et où chacun est fasciné par l’image scénique ? Pour répondre à cette question, la thèse propose d’étudier le dessin (projet de la scène et de la salle) de quelque spectacle populaire pour en mieux comprendre le dessein (acception du terme « populaire »). Grâce à l’élaboration d’une grille typologique analysant la scène, la salle et la scénographie, l’étude porte sur les expériences de Gémier (1903-1919) et le travail de Copeau pour Savonarola (1935). Ces exemples attestent la cristallisation du modèle frontal pour une réception de l’image-écran proposée par la figure naissante du metteur en scène. La grille est ensuite appliquée à une régie de Jean Vilar, La Tragédie du Roi Richard II (1947), spectacle n’utilisant ni le modèle frontal ni l’image illusionniste. En se faisant le régisseur d’une « scène illimitée » et d’une image polysémique confiée au spectateur, Vilar permet de passer de la réception passive à l’invention artistique. L’acception donnée au mot peuple se lit dans la scénographie : si l’on change de dessin, le dessein change aussi, ou vice versa Between the end of the XIX century and the beginning of the XX century, many theater’s men call the audience they want to reunite as peuple and their theater as théâtre populaire. Their major interest is the research of a space capable to transmit the equality of the democratic society. In order to offer to everyone a good view of the stage, they choose the Bayreuth’s Festspielhaus as a reference model: the entire public is in front of the stage in the middle of darkness. Who’s the peuple that you place in that kind of space where spectators can’t almost have no exchange and where everyone is fascinated by the stage? In order to answer this question, the thesis proposes to study the dessin (room and scenography’s project) of a popular spectacle to better understand the dessein (acceptation of the word « populaire »). Thanks’ to a typological grid that analyzes the stage, the room and the scenography, the study will bring us to the Firmin Gémier’s experiences (1903-1919) and Jacques Copeau’s work for Savonarola (1935). These examples show the frontal model’s crystallisation for a reception of the image-screen proposed by the new figure of the metteur en scène. The grid is the used with Jean Vilar’s work, La Tragédie du Roi Richard II (1947); a spectacle that doesn’t uses neither the frontal model nor the illusionist image. Becoming the régisseur of « ilimitated stage » and of a polysomic image given to the spectator, Vilar allows to pass from a passive reception to an artistic invention. The acceptation given to the word peuple read in the scenography: if we change the dessin, the dessein also changes, or vice versa

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Bieber, Nicole A. (Nicole Amanda). "SimLogo : improving simulations in StarLogo TNG." Thesis, Massachusetts Institute of Technology, 2011. http://hdl.handle.net/1721.1/66408.

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Thesis (M. Eng.)--Massachusetts Institute of Technology, Dept. of Electrical Engineering and Computer Science, 2011. Cataloged from PDF version of thesis. Includes bibliographical references (p. 59). StarLogo TNG (The Next Generation) is a graphical programming environment originally developed by the MIT Scheller Teacher Education Program as a means of improving computer literacy and programming skills in middle and high school students. The original goal of StarLogo TNG was to make computer programming more accessible to students by designing a programming framework, StarLogoBlocks, which could graphically represent the control flow and data structures of a program, and to introduce a "coolness" factor by permitting students to view their program's execution in a 3D game-like environment called SpaceLand. However, after the program was released, the team found that researchers and professionals were using StarLogo TNG for more complex agent-based simulations than it had been originally designed to support. This thesis outlines the design and implementation of a new suite of features, code-named SimLogo, which will improve the simulation capabilities of StarLogo TNG through the addition of true internal parallelism to the virtual machine. by Nicole A. Bieber. M.Eng.

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D'Ambrosio, Michael (Michael A. ). "Three dimensional terrain editing in StarLogo TNG." Thesis, Massachusetts Institute of Technology, 2009. http://hdl.handle.net/1721.1/53155.

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Thesis (M. Eng.)--Massachusetts Institute of Technology, Dept. of Electrical Engineering and Computer Science, 2009. Includes bibliographical references (p. 69-70). StarLogo TNG is a block based programming language designed to create models and simulations that are used to help middle and high school students understand mathematical and scientific concepts. However, there is a desire to use the program to help facilitate game creation but the tools do not exist. This thesis evaluates and discusses the design of some of the tools necessary in order to create richer 3-D environments and games within StarLogo TNG. by Michael D.Ambrosio. M.Eng.

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Wendel, Daniel J. "Design and editing 2.5-dimensional terrain in StarLogo TNG." Thesis, Massachusetts Institute of Technology, 2006. http://hdl.handle.net/1721.1/42120.

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Thesis (M. Eng.)--Massachusetts Institute of Technology, Dept. of Electrical Engineering and Computer Science, 2006. Includes bibliographical references (leaf 60). StarLogo TNG is "The Next Generation" in block-based decentralized programming for modeling and simulation software. Its aim is to make computer programming more appealing for students in middle school and high school. Part of the draw of StarLogo TNG is its 3-D rendered world called Spaceland where "agents" live on a terrain made of a grid of "patches". This thesis evaluates and outlines the redesign of Spaceland and its associated terrain editor based on user-task analysis, and discusses the design of new data structures to support the desired features. by Daniel J. Wendel. M.Eng.

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Jackman, John Daniel III. "A network development and runtime environment for StarLogo TNG." Thesis, Massachusetts Institute of Technology, 2007. http://hdl.handle.net/1721.1/41630.

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Thesis (M. Eng.)--Massachusetts Institute of Technology, Dept. of Electrical Engineering and Computer Science, 2007. Includes bibliographical references (leaf 44). StarLogo: The Next Generation aims to introduce students to programming. The StarLogo application is frequently used in a classroom setting, but the effectiveness of StarLogo is limited as long as students cannot interact with each other using the application. This thesis describes the design and implementation of a networked development and runtime environment for StarLogo. Hopefully, students will become more interested in programming when they can collaborate to create and run StarLogo programs. In addition, teachers will have more options available when choosing classroom activities using StarLogo. by John Daniel Jackman, III. M.Eng.

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McCaffrey, Corey (Corey Stanley Gordon). "StarLogo TNG : the convergence of graphical programming and text processing." Thesis, Massachusetts Institute of Technology, 2006. http://hdl.handle.net/1721.1/36904.

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Thesis (M. Eng. and S.B.)--Massachusetts Institute of Technology, Dept. of Electrical Engineering and Computer Science, 2006. This electronic version was submitted by the student author. The certified thesis is available in the Institute Archives and Special Collections. Includes bibliographical references (leaves 67-68). StarLogo TNG is a robust graphical programming environment for secondary students. Despite the educational advantages of graphical programming, TNG has sustained criticism from some who object to the exclusion of a textual language. Recognizing the benefits of text processing and the power of controlling software with a keyboard, I sought to incorporate text-processing techniques into TNG's graphical language. The key component of this work is an innovation dubbed "Typeblocking," by which users construct block code through the use of a keyboard. by Corey McCaffrey. M.Eng.and S.B.

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Gleizes, Marie. "Ectonucléotidases, adénosine et transmission synaptique." Thesis, Toulouse 3, 2017. http://www.theses.fr/2017TOU30306/document.

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Dans le cerveau, les fonctions de la phosphatase alcaline non spécifique des tissus (TNAP) ne sont pas clairement identifiées. La localisation et l'expression de cette enzyme au niveau neuronal suggère cependant, qu'elle joue un rôle important dans le développement et le fonctionnement du cerveau. Cela est supporté par la présence de graves crises d'épilepsie chez les humains porteurs d'une mutation de la TNAP. Ces crises d'épilepsie sont létales chez les souris KO pour la TNAP. Des études chez la souris montrent que la TNAP pourrait réguler l'inhibition postsynaptique médiée par le GABA et elle pourrait être impliquée dans l'inhibition présynaptique médiée par l'adénosine. L'adénosine est, en partie, synthétisée via la déphosphorylation successive de l'ATP en ADP puis en AMP par des ectonucléotidases. Parmi elles, la TNAP et l'ecto- 5'-nucléotidase (NT5E) catalysent l'hydrolyse de l'AMP en adénosine dans le cortex cérébral. L'adénosine agit principalement au niveau présynaptique par l'intermédiaire des récepteurs A1. Ainsi l'adénosine a une influence sur la transmission synaptique et sur la plasticité synaptique. Ceci pourrait expliquer, en partie, les crises d'épilepsie observées chez les souris KO pour la TNAP. Les deux objectifs principaux de ma thèse ont été : (1) évaluer la contribution de la TNAP dans la production d'adénosine dans le cerveau ; (2) étudier l'influence de l'adénosine sur la plasticité synaptique. Premièrement, l'étude de la contribution de la TNAP dans la production d'adénosine dans le cerveau a été réalisée au moyen de deux approches complémentaires. Une approche métabolomique (spectroscopie RMN du proton) sur des cerveaux entiers de souris KO pour la TNAP a permis de montrer que la TNAP participe, entre autre, à la synthèse d'adénosine dans le cerveau. Une deuxième approche, électrophysiologique sur tranches de cerveaux de souris in vitro, nous permet d'examiner les conséquences de l'inhibition des ectonucléotidases intervenant dans la synthèse de l'adénosine. Elle a révélé que l'inhibition des ectonucléotidases (TNAP et NT5E) ne supprime pas l'effet inhibiteur de l'AMP médiée par les récepteurs A1. Deuxièmement, nous avons étudié l'influence de l'adénosine sur la plasticité synaptique à courte terme. Nous avons enregistré des potentiels de champs dans la couche Ia du cortex piriforme en réponse à des stimulations électriques (3,125 à 100 Hz) présentée avec des fréquences recouvrant la gamme d'oscillations physiologiques. Nos résultats montrent qu'avec de fortes concentrations d'adénosine, la facilitation est accentuée par rapport à celle observée en situation contrôle. Cet effet est observé pour des fréquences supérieures ou égales à 25 Hz. De plus, cette accentuation est d'autant plus grande que la fréquence est élevée (maximum atteint à 100 Hz pour 100 µM). En bloquant l'action de l'adénosine endogène, l'effet contraire est observé : une facilitation déficitaire par rapport au contrôle et dont le défaut est croissant avec la fréquence de stimulation. Tous ces résultats convergent vers l'hypothèse qu'une déficience en TNAP, traduite par une absence d'adénosine, pourrait contribuer au maintien des processus épileptiques générés par un déséquilibre de l'inhibition et de l'excitation dû à une diminution de GABA. L'effet inhibiteur de l'AMP médié par les récepteurs A1 ne serait pas suffisant pour contrecarrer les crises d'épilepsie observées chez les sujets hypophosphatasiques et les souris KO pour la TNAP The functions of Tissue Nonspecific Alkaline Phosphatase (TNAP) in the brain are not clearly identified. The localization and expression of TNAP at the neuronal level, however, suggests that it plays a prominent role in the development and the function in the brain. This is supported by the presence of severe epileptic seizures in humans carrying TNAP mutation. These epileptic seizures are lethal in TNAP KO mice. Studies in mice show that TNAP could regulate GABA-mediated postsynaptic inhibition and may be involved in presynaptic inhibition mediated by adenosine. Adenosine is, partly, synthesized via the successive dephosphorylation of ATP to ADP and then to AMP by ectonucleotidases. Among them TNAP and ecto-5'-nucleotidase (NT5E) are able to hydrolyze AMP into adenosine. Adenosine acts mainly at the presynaptic level via A1 receptors activation. Adenosine has an influence on synaptic transmission and thus on synaptic plasticity. This could partly explain the epileptic seizures observed in TNAP knock-out mice. The two main purposes of my thesis were: (1) to evaluate the contribution of TNAP in adenosine production in the brain; (2) to study the influence of adenosine on synaptic plasticity. Firstly, the study of the contribution of TNAP in adenosine production in the brain was carried out using two complementary approaches. A metabolomic approach (proton NMR spectroscopy) on whole brains of TNAP KO mice showed that TNAP in involved in adenosine synthesis in the brain. In a second approach, in vitro electrophysiological recordings on mouse brain slices allowed us to examine the consequences of the inhibition of the ectonucleotidases involved in adenosine synthesis. This revealed that inhibition of ectonucleotidases (TNAP and NT5E) did not suppress the inhibitory effect of AMP mediated by A1 receptors. Secondly, we studied the influence of adenosine on short-term synaptic plasticity. Field potentials were recorded in response to electrical stimulations (3.125 to 100 Hz) applied with frequencies encompassing the range of physiological oscillation. Our results show that, with high adenosine concentrations, the facilitation is emphasized compared to that observed in the control situation. This effect is observed for frequencies greater than or equal to 25 Hz. In addition, the higher the frequency, the greater the facilitation. Finally, by blocking the action of endogenous adenosine, the opposite effect was observed: a deficient facilitation with respect to the control, whose defect was increasing with stimulation frequency. All these results converge towards the hypothesis that TNAP deficiency, expressed by absence of adenosine, could contribute to the maintenance of the epileptic processes generated by an imbalance of the neuronal inhibition and the excitation due to a decrease of GABA. AMP inhibitory effect mediated by A1 receptors, would not be sufficient to counteract epileptic seizures observed in hypophosphatasic patients and TNAP KO mice

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Garratt, Andrea. "The construction of the builder and searcher components of WWWLIB-TNG." Thesis, University of Wolverhampton, 2006. http://ethos.bl.uk/OrderDetails.do?uin=uk.bl.ethos.425248.

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Tu, Yaa-Lirng. "A framework for teaching biology using StarLogo TNG : from DNA to evolution." Thesis, Massachusetts Institute of Technology, 2009. http://hdl.handle.net/1721.1/53182.

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Thesis (M. Eng.)--Massachusetts Institute of Technology, Dept. of Electrical Engineering and Computer Science, 2009. Includes bibliographical references (p. 65-66). This thesis outlines a 10-unit biology curriculum implemented in StarLogo TNG. The curriculum moves through units on ecology, the DNA-protein relationship, and evolution. By combining the three topics, it aims to highlight the similarities among different scales and the relationships between them. In particular, through the curriculum, students can see how small-scale changes in molecular processes can create large-scale changes in entire populations. In addition, the curriculum encourages students to engage in problembased learning, by which they are trained to approach questions creatively and independently. by Yaa-Lirng Tu. M.Eng.

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Книги з теми "TnAg"

Fonta, Caroline, and László Négyessy, eds. Neuronal Tissue-Nonspecific Alkaline Phosphatase (TNAP). Springer Netherlands, 2015. http://dx.doi.org/10.1007/978-94-017-7197-9.

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Audrey, Rasmussen, and Taylor Robert H, eds. Working with Unicenter TNG. 2nd ed. Que, 1999.

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Jayaraj, S. Plant protection research in TNAU, 1960-1988: An annotated bibliography. Tamil Nadu Agricultural University, 1988.

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Zhou, De Shang Ed. Jia tng an quan yong yao 200 wen. B Ke Tu, 2000.

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Izumi, K. H. Descent strategy comparisons for TNAV-equipped aircraft under airplane-preferred operating conditions. National Aeronautics and Space Administration, Scientific and Technical Information Division, 1989.

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Friedman, Karen L. Stability studies of a total nutrient admixture (TNA) for total parental nutrition (TPN). National Library of Canada, 1990.

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Sternbach, Rick. Star trek, the next generation: Technical manual. Pocket Books, 1991.

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Star trek, the next generation: U.S.S. Enterprise NCC-1701-D blueprints. Pocket Books, 1996.

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Sternbach, Rick. Star trek, the next generation: Technical manual. Pocket Books, 1991.

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TNA: Quilting. Ramboro Books PLC, 1997.

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Частини книг з теми "TnAg"

Viswanath, Dabir S., Tushar K. Ghosh, and Veera M. Boddu. "1,3,3-Trinitroazetidine (TNAZ)." In Emerging Energetic Materials: Synthesis, Physicochemical, and Detonation Properties. Springer Netherlands, 2018. http://dx.doi.org/10.1007/978-94-024-1201-7_11.

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Kántor, Orsolya, Dorottya Cserpán, Béla Völgyi, Ákos Lukáts, and Zoltán Somogyvári. "The Retinal TNAP." In Subcellular Biochemistry. Springer Netherlands, 2015. http://dx.doi.org/10.1007/978-94-017-7197-9_6.

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Klopfer, Eric, Hal Scheintaub, Wendy Huang, and Daniel Wendel. "StarLogo TNG." In Artificial Life Models in Software. Springer London, 2009. http://dx.doi.org/10.1007/978-1-84882-285-6_6.

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Street, Sarah E., and Nathaniel A. Sowa. "TNAP and Pain Control." In Subcellular Biochemistry. Springer Netherlands, 2015. http://dx.doi.org/10.1007/978-94-017-7197-9_13.

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Bale, Gemma, Ajay Rajaram, Matthew Kewin, et al. "Multimodal Measurements of Brain Tissue Metabolism and Perfusion in a Neonatal Model of Hypoxic-Ischaemic Injury." In Advances in Experimental Medicine and Biology. Springer International Publishing, 2021. http://dx.doi.org/10.1007/978-3-030-48238-1_32.

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AbstractThis is the first multimodal study of cerebral tissue metabolism and perfusion post-hypoxic-ischaemic (HI) brain injury using broadband near-infrared spectroscopy (bNIRS), diffuse correlation spectroscopy (DCS), positron emission tomography (PET) and magnetic resonance spectroscopy (MRS). In seven piglet preclinical models of neonatal HI, we measured cerebral tissue saturation (StO2), cerebral blood flow (CBF), cerebral oxygen metabolism (CMRO2), changes in the mitochondrial oxidation state of cytochrome c oxidase (oxCCO), cerebral glucose metabolism (CMRglc) and tissue biochemistry (Lac+Thr/tNAA). At baseline, the parameters measured in the piglets that experience HI (not controls) were 64 ± 6% StO2, 35 ± 11 ml/100 g/min CBF and 2.0 ± 0.4 μmol/100 g/min CMRO2. After HI, the parameters measured were 68 ± 6% StO2, 35 ± 6 ml/100 g/min CBF, 1.3 ± 0.1 μmol/100 g/min CMRO2, 0.4 ± 0.2 Lac+Thr/tNAA and 9.5 ± 2.0 CMRglc. This study demonstrates the capacity of a multimodal set-up to interrogate the pathophysiology of HIE using a combination of optical methods, MRS, and PET.

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Bonanno, G., P. Bruno, R. Cosentino, et al. "TNG New Generation CCD Controller." In Optical Detectors For Astronomy II. Springer Netherlands, 2000. http://dx.doi.org/10.1007/978-94-011-4361-5_38.

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Narisawa, Sonoko. "Genetically Modified Mice for Studying TNAP Function." In Subcellular Biochemistry. Springer Netherlands, 2015. http://dx.doi.org/10.1007/978-94-017-7197-9_3.

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Négyessy, László, Balázs Györffy, János Hanics, Mihály Bányai, Caroline Fonta, and Fülöp Bazsó. "Signal Transduction Pathways of TNAP: Molecular Network Analyses." In Subcellular Biochemistry. Springer Netherlands, 2015. http://dx.doi.org/10.1007/978-94-017-7197-9_10.

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Coburn, Stephen P. "Vitamin B-6 Metabolism and Interactions with TNAP." In Subcellular Biochemistry. Springer Netherlands, 2015. http://dx.doi.org/10.1007/978-94-017-7197-9_11.

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Gratton, R. G., A. Cavazza, R. U. Claudi, et al. "SARG: The High Resolution Spectrograph of TNG." In The Three Galileos: The Man, the Spacecraft, the Telescope. Springer Netherlands, 1997. http://dx.doi.org/10.1007/978-94-015-8790-7_35.

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Тези доповідей конференцій з теми "TnAg"

Elmakki, Tasneem, Fathima Sifani Zavahir, Mona Gulied, Norhan Ismail, Areeba Hameed, and Dong Suk Han. "Advanced Degradation of Organic Substance in Water Using No-Ferric Fenton Reaction on Titania Nanotube." In Qatar University Annual Research Forum & Exhibition. Qatar University Press, 2020. http://dx.doi.org/10.29117/quarfe.2020.0028.

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Highly reactive OH radicals facilitate advanced oxidation processes (AOPs). AOPs are irreplaceable in environmental remediation including but not limited to pollutant degradation. H2O2 leading to OH radicals in iron based fenton systems are well known and few other oxides of alumina and ceria in non-ferrous fenton systems. Majority of studied catalysts materials are in powder form, which limits the catalysts long term applicability in real systems due to separation and regeneration of the catalyst with required catalytic activity, which is costly. In this present work, we have studied anatase phased titania nanotube arrays (TNA) grown on Ti films prepared by an anodization approach for methyl orange (MO) dye degradation under photocatalytic conditions. Key findings reveal long stability of TNAs over fifty reaction cycles in batch process with higher degree of reproducible performance. Complete removal of MO was achieved after six hours of exposure in AM 1.5 G light (equivalent to 1 sun intensity), where hydrogen peroxide accounted for only 1/200th of the amount of initial dye concentration. This superior performance is ascribed to surface oxygen vacancies and Ti3+ sites promoting regeneration of peroxide in the ongoing reaction medium that is consequently transformed to OH radicals. This is further confirmed by the experiments conducted with formic acid, a known hydroxyl radical scavenger, where the dye degradation was observed to be minimal at a near zero rate even after six hours of reaction time, upon measurements with UV-visible spectroscopy. About 38% of the initial dye was oxidized after 1 h into the reaction under light irradiation in a typical system whereas activity was hugely promoted to over 55% when it was coupled with a Pt wire in an electroless process, without supply of additional power. In conclusion, this TNA based new material is highly regarded as environmentally sustainable, easily reusable, non-toxic and commercially viable candidate for real wastewater treatment plants where the treatment plants are usually large tanks constructed in the open space with access to freely available, energetically rich solar power.

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Goose, Stuart, Jonathan Dale, Wendy Hall, and David De Roure. "Microcosm TNG." In the eighth ACM conference. ACM Press, 1997. http://dx.doi.org/10.1145/267437.267472.

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Ragazzoni, Roberto, Andrea Baruffolo, Fabio Bortoletto, et al. "Adaptive optics module for TNG (AdOpt@TNG): a status report." In Optical Telescopes of Today and Tomorrow, edited by Arne L. Ardeberg. SPIE, 1997. http://dx.doi.org/10.1117/12.268971.

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Simpson, R. L., P. A. Urtiew, and C. M. Tarver. "Shock initiation of 1,3,3-trinitroazetidine (TNAZ)." In Proceedings of the conference of the American Physical Society topical group on shock compression of condensed matter. AIP, 1996. http://dx.doi.org/10.1063/1.50587.

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Ragazzoni, Roberto, Andrea Baruffolo, Fabio Bortoletto, et al. "AdOpt@TNG: an update." In Optical Science, Engineering and Instrumentation '97, edited by Robert K. Tyson and Robert Q. Fugate. SPIE, 1997. http://dx.doi.org/10.1117/12.279044.

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Mancini, Dario, and Pietro Schipani. "TNG motion control system." In Astronomical Telescopes and Instrumentation, edited by Thomas A. Sebring and Torben Andersen. SPIE, 2000. http://dx.doi.org/10.1117/12.393923.

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Oliva, E., L. Origlia, C. Baffa, et al. "The GIANO-TNG spectrometer." In SPIE Astronomical Telescopes + Instrumentation, edited by Ian S. McLean and Masanori Iye. SPIE, 2006. http://dx.doi.org/10.1117/12.670006.

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Lanzerotti, M. Y. D., J. Autera, and J. Sharma. "Crystal growth of TNAZ during high acceleration." In Proceedings of the conference of the American Physical Society topical group on shock compression of condensed matter. AIP, 1996. http://dx.doi.org/10.1063/1.50752.

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Sheffield, S. A., R. L. Gustavsen, and R. R. Alcon. "Hugoniot and initiation measurements on TNAZ explosive." In Proceedings of the conference of the American Physical Society topical group on shock compression of condensed matter. AIP, 1996. http://dx.doi.org/10.1063/1.50842.

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Bonoli, Carlotta, Enrico Giro, Paolo Conconi, and Valentina Zitelli. "Tunable filter for the TNG." In Astronomical Telescopes and Instrumentation, edited by Masanori Iye and Alan F. M. Moorwood. SPIE, 2003. http://dx.doi.org/10.1117/12.460307.

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Simpson, R. L., R. G. Garza, M. F. Foltz, D. L. Ornellas, and P. A. Utriew. Characterization of TNAZ. Office of Scientific and Technical Information (OSTI), 1994. http://dx.doi.org/10.2172/71573.

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Guimaraes, F. B. TNG-GENOA User's Manual. Office of Scientific and Technical Information (OSTI), 2001. http://dx.doi.org/10.2172/777610.

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Guimaraes, F. B., and C. Y. Fu. TNG-GENOA User's Manual. Office of Scientific and Technical Information (OSTI), 2000. http://dx.doi.org/10.2172/769249.

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Maron, Nancy, and Rebecca Griffiths. The National Archives (TNA) 2009. Ithaka S+R, 2015. http://dx.doi.org/10.18665/sr.22352.

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Maron, Nancy. The National Archives (TNA) 2011. Ithaka S+R, 2015. http://dx.doi.org/10.18665/sr.22382.

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Shibata, K., and C. Y. Fu. Recent improvements of the TNG statistical model code. Office of Scientific and Technical Information (OSTI), 1986. http://dx.doi.org/10.2172/5411068.

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Hill, L. G., W. L. Seitz, J. F. Kramer, D. M. Murk, and R. S. Medina. Wedge test data for three new explosives: LAX112, 2,4-DNI, and TNAZ. Office of Scientific and Technical Information (OSTI), 1995. http://dx.doi.org/10.2172/102142.

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McCollam, K. Analysis of Fe(n,x[gamma]) cross sections using the TNG nuclear reaction model code. Office of Scientific and Technical Information (OSTI), 1993. http://dx.doi.org/10.2172/6549441.

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