Fragm. lat. I 98 - Biblia (Is 43,9 - 21; 43,24 - 44,8; 45,24 - 46,10; 46,13 - 47,9)

Trägerband: Ms. Praed. 133; Vorbesitzer: Dominikanerkloster Frankfurt am Main

Fragm. lat. I 63 - Biblia (Sir 41,22 - 43,26)

Trägerband: 'M 11 14 BIB. des Recoll.'

Fragm. lat. IV 37 - Conclusiones Sententiarum (IV 37,3 - 43)

Trägerbände: Inc. qu. 1058a; war ursprünglich Bestandteil von Ms. Praed. 73 (ein dort zwischen Bl. 23/24 fehlendes Blatt); Vorbesitzer: Dominikanerkloster Frankfurt am Main

Fragm. lat. V 43 - Notariatsinstrument

Trägerband: Inc. qu. 1028a; Vorbesitzer: Dominikanerkloster Frankfurt am Main

Fragm. lat. IX 43 - Psalterium feriatum

Trägerband: Inc. qu. 927; Vorbesitzer: Dominikanerkloster Frankfurt am Main

Na 1 Nachlass Max Horkheimer, 803 - "Dialektik der Aufklärung" von Max Horkheimer und Theodor W. Adorno (p. XI 6.43 - XI 6.106)

43. - 62. Sammlung B: "Konzepte als Zugabe zur Festschrift für Friedrich Pollock" [GS 12, S. 250 - 295]. 64 Blatt; 43. "Zum Problem der Bedürfnisse". Typoskript, 6 Blatt; 44. "Dichtung und Moral". Typoskript, 5 Blatt; 45. "Geschichte der amerikanischen Arbeiterschaft". Typoskript, 1 Blatt; 46. "Kein Weg zur Wahrheit". Typoskript, 1 Blatt; 47. "Zur Rechtsphilosophie". Typoskript mit eigenen Korrekturen, 2 Blatt; 48. "Strafgefangene". Typoskript, 1 Blatt; 49. "Jüdischer Charakter". Typoskript, 1 Blatt; 50. "Solidarität". Typoskript, 2 Blatt; 51. "Unmöglichkeit der Dichtung". Typoskript, 1 Blatt; 52. "Theorie des Verbrechers". Typoskript, 14 Blatt; 53. "Erbsünde und Kopula". Typoskript, 2 Blatt; 54. "Feind". Typoskript, 2 Blatt; 55. "Haupt- und Nebensatz". Typoskript, 3 Blatt; 56. "Bewußtsein". Typoskript, 1 Blatt; 57. "Kampf und Gewaltlosigkeit". Typoskript, 6 Blatt; 58. "Umschlag der idealistischen Dialektik". Typoskript, 1 Blatt; 59. "Die Rackets und der Geist". Typoskript, 7 Blatt; 60. "Altmodische Probleme". Typoskript mit eigenen Korrekturen, 2 Blatt; 61. "Physiognomik". Typoskript, 1 Blatt; 62. "Religionspsychologie". Typoskript, 2 Blatt; 63. - 106. Sammlung C: "New Yorker Notizen [I]"; 63. "Dialektik der Aufklärung Nr. 7". Typoskript mit eigenen Korrekturen, 12 Blatt; 64. Aus der "Dialektik der Aufklärung"; Kapitel: "Elemente des Antisemitismus", Abschitt VII:; 64a) Typoskript mit eigenen Korrekturen, 11 Blatt; 64b) Teilstück, Typoskript, 2 Blatt; 64c) Teilstück, Typoskript, 1 Blatt; 64d) Teilstück, Typoskript, 1 Blatt; 65. "Bemerkungen zu These VII" [zu: 64]; Über Antisemitismus und Stalinismus, [von Theodor W. Adorno]. Typoskript, 3 Blatt; 66. "Verwandlung der Idee in Gesinnung":; 66a) Typoskript, 5 Blatt; 66b) Typoskript mit eigenen Korrekturen, 4 Blatt; 66c) Typoskript, 5 Blatt; 67. "Zum Problem der Bedürfnisse". Typoskript mit eigenen Korrekturen, 6 Blatt; 68. "Dichtung und Moral":; 68a) Typoskript, 5 Blatt; 68b) Typoskript mit eigenen Korrekturen, 4 Blatt; 68c) Typoskript mit eigenen Korrekturen, 4 Blatt; 68d) Typoskript mit eigenen Korrekturen, 5 Blatt; 69. "Geschichte der amerikanischen Arbeiterschaft":; 69a) Typoskript, 1 Blatt; 69b) Typoskript; 1 Blatt; 70. "Straftheorie. Zur Rechtsphilosophie":; 70a) Typoskript mit eigenen Korrekturen, 3 Blatt; 70b) Typoskript mit eigenen Korrekturen, 3 Blatt; 70c) Typoskript mit eigenen Korrekturen, 3 Blatt; 70d) Typoskript, 3 Blatt; 71. "Jüdischer Charakter". Typoskript, 1 Blatt; 72. "Solidarität". Typoskript, 2 Blatt; 73. "Theorie des Verbrechens". Typoskript mit eigenen Korrekturen, 17 Blatt; 74. "Erbsünde und Copula":; 74a) Typoskript, 2 Blatt; 74b) Typoskript mit eigenen Korrekturen, 3 Blatt; 75. "Geschichtsphilosophischer Exkurs zur Odysee" [von Theodor W. Adorno ?]. Teilstück, Typoskript, 1 Blatt; 76. "Feind":; 76a) Typoskript, 2 Blatt; 76b) Typoskript, 2 Blatt; 76c) Typoskript, 2 Blatt; 76d) Entwurf, englisch, Typoskript mit eigenen Korrekturen, 2 Blatt; 77. "Haupt- und Nebensatz":; 77a) Typoskript, 2 Blatt; 77b) Typoskript mit eigenen Korrekturen, 2 Blatt; 77c) Typoskript mit eigenen Korrekturen, 2 Blatt; 77d) Typoskript mit eigenen Korrekturen, 3 Blatt; 78. "Bewußtsein":; 78a) Typoskript, 1 Blatt; 78b) Typoskript mit eigenen Korrekturen, 1 Blatt; 79. "Kampf und Gewaltlosigkeit":; 79a) Typoskript, 6 Blatt; 79b) Typoskript, 6 Blatt; 79c) Teilstücke, Typoskript mit eigenen Korrekturen, 6 Blatt; 79d) Typoskript mit eigenen Korrekturen, 5 Blatt; 79e) Typoskript, 5 Blatt; 79f) Teilstück, Typoskript mit eigenen Korrekturen, 2 Blatt; 80. "Die Rackets und der Geist":; 80a) Typoskript mit eigenen Korrekturen, 2 Blatt; 80b) Typoskript mit eigenen Korrekturen, 6 Blatt; 81. "Altmodisches Problem". Typoskript, 2 Blatt; 82. "Physiognomik". Typoskript, 1 Blatt; 83. "Religionspsychologie":; 83a) Typoskript mit eigenen Korrekturen, 2 Blatt; 83b) Typoskript mit eigenen Korrekturen, 2 Blatt; 84. "Leeres Erschrecken":; 84a) Typoskript mit eigenen Korrekturen, 2 Blatt; 84b) Typoskript, 2 Blatt; 84c) Typoskript mit eigenen Korrekturen, 2 Blatt; 85. "Philosophie und Arbeitsteilung":; 85a) Typoskript mit eigenen Korrekturen, 3 Blatt; 85b) Typoskript mit eigenen Korrekturen, 3 Blatt; 85c) Typoskript, 3 Blatt; 85d) Typoskript mit handschriftlichen Korrekturen, 3 Blatt; 86. "Vorrede" zur Dialektik der Aufklärung. Typoskript mit eigenen Korrekturen, 11 Blatt; 87. ["Umschlag der idealistischen Dialektik"] Typoskript, 1 Blatt; 88. Über Erkenntnis und Sprache. Typoskript mit eigenen Korrekturen, 1 Blatt; 89. "Zur Kritik der Geschichtsphilosophie". Typoskript mit eigenen Korrekturen, 3 Blatt; 90. "Mensch und Tier":; 90a) Typoskript mit eigenen und handschriftlichen Korrekturen, 12 Blatt; 90b) Typoskript mit eigenen Korrekturen, 3 Blatt; 90c) Typoskript mit eigenen Korrekturen, 4 Blatt; 90d) Typoskript mit eigenen Korrekturen, 3 Blatt; 90e) Typoskript mit eigenen Korrekturen, 10 Blatt; 91. "Massengesellschaft". Typoskript, 1 Blatt; 92. "Zwei Welten". Typoskript, 2 Blatt; 93. "Zur Theorie der Gespenster":; 93a) Typoskript, 1 Blatt; 93b) Typoskript mit eigenen Korrekturen, 1 Blatt; 94. "Interesse am Körper":; 94a) Typoskript mit eigenen Korrekturen, 6 Blatt; 94b) Typoskript mit eigenen Korrekturen, 7 Blatt; 94c) Typoskript, 2 Blatt; 94d) Typoskript, 6 Blatt; 95. "Unmöglichkeit der Dichtung". Typoskript, 1 Blatt; 96. "Die Einseitigkeit der Negativität":; 96a) Typoskript, 2 Blatt; 96b) Typoskript mit eigenen Korrekturen, 2 Blatt; 96c) Typoskript, 2 Blatt; 97. "Widersprüche":; 97a) Typoskript, 4 Blatt; 97b) Typoskript mit eigenen Korrekturen, 4 Blatt; 98. "Zur Theorie der Dummheit":; 98a) Typoskript, 3 Blatt; 98b) Typoskript mit eigenen Korrekturen, 3 Blatt.; 99. "Gezeichnet". Typoskript, 2 Blatt; 100. "Quand-même":; 100a) Typoskript, 2 Blatt; 100b) Typoskript mit eigenen Korrekturen, 2 Blatt; 101. "Isolierung durch Verkehr":; 101a) Typoskript mit eigenen Korrekturen, 1 Blatt; 101b) Typoskript, 1 Blatt; 102. "Gegen Gescheitheit". Typoskript mit eigenen Korrekturen, 1 Blatt; 103. "Propaganda":; 103a) Typoskript mit eigenen Korrekturen, 2 Blatt; 103b) Typoskript, 2 Blatt; 103c) Typoskript mit eigenen Korrekturen, 2 Blatt; 104. "Der Gedanke". Typoskript mit eigenen Korrekturen, 1 Blatt; 105. Fragment aus der "Dialektik der Aufklärung", Exkurs II. Typoskript mit eigenen Korrekturen, 3 Blatt; 106. Zum Begriff des Individuums bei Leibniz und Hegel [GS 12, S. 314 - 315]. Typoskript mit eigenen Korrekturen, 2 Blatt;

Antigen-43-mediated autoaggregation impairs motility in Escherichia coli

Functional interaction between bacterial surface-displayed autoaggregation proteins such as antigen 43 (Ag43) of Escherichia coli and motility organelles such as flagella has not previously been described. Here, it has been demonstrated for the first time that Ag43-mediated aggregation can inhibit bacterial motility. Ag43 overexpression produces a dominant aggregation phenotype that overrides motility in the presence of low levels of flagella. In contrast, induction of an increased flagellation state prevents Ag43-mediated aggregation. This phenomenon was observed in naturally occurring subpopulations of E coli as phase variants expressing and not expressing Ag43 revealed contrasting motility phenotypes. The effects were shown to be part of a general mechanism because other short adhesins capable of mediating autoaggregation (AIDA-I and TibA) also impaired motility. These novel insights into the function of bacterial autoaggregation proteins suggest that a balance between these two systems, i.e. autoaggregation and flagellation, influences motility.

NÃO TEMAS! GRITEI POR TEU NOME: Estudo da concepção materna de Javé em Dêutero- Isaías a partir da análise exegética de Is 43,1-7

O presente estudo exegético tem por objetivo demonstrar a face materna de Javé revelada nos textos de Dêutero-Isaías, tendo como fonte principal o oráculo de salvação de Is 43,1-7. Para tal, partimos da análise do contexto literário, histórico e religioso de Dêutero-Isaías, paraentão fazer a análise exegética do texto proposto, através da qual enfocaremos, dentre os diversos conteúdos, a característica materna apresentada na perícope. Compreendendo que um texto surge dentro de um ambiente social, evidenciaremos, com base nos escritos de Dêutero-Isaías, a comunidade exilada à qual se dirigem profetas e profetisas. Por fim, combinando os atributos maternos das deusas Asherah e Ishtar com a incipiente concepção materna de Javé apresentado por Oséias, propomos a face materna de Deus com base nos textos dêuteroisaiânicos, em especial, Is 43,1-7.

A quantitative study of the neuropathology of 32 sporadic and familial cases of frontotemporal lobar degeneration with TDP-43 proteinopathy (FTLD-TDP)

To further characterize the neuropathology of the heterogeneous molecular disorder frontotemporal lobar degeneration (FTLD) with transactive response (TAR) DNA-binding protein of 43 kDa (TDP-43) proteinopathy (FTLD-TDP).

Neuropathological heterogeneity in frontotemporal lobar degeneration with TDP-43 proteinopathy: a quantitative study of 94 cases using principal components analysis

Studies suggest that frontotemporal lobar degeneration with transactive response (TAR) DNA-binding protein of 43kDa (TDP-43) proteinopathy (FTLD-TDP) is heterogeneous with division into four or five subtypes. To determine the degree of heterogeneity and the validity of the subtypes, we studied neuropathological variation within the frontal and temporal lobes of 94 cases of FTLD-TDP using quantitative estimates of density and principal components analysis (PCA). A PCA based on the density of TDP-43 immunoreactive neuronal cytoplasmic inclusions (NCI), oligodendroglial inclusions (GI), neuronal intranuclear inclusions (NII), and dystrophic neurites (DN), surviving neurons, enlarged neurons (EN), and vacuolation suggested that cases were not segregated into distinct subtypes. Variation in the density of the vacuoles was the greatest source of variation between cases. A PCA based on TDP-43 pathology alone suggested that cases of FTLD-TDP with progranulin (GRN) mutation segregated to some degree. The pathological phenotype of all four subtypes overlapped but subtypes 1 and 4 were the most distinctive. Cases with coexisting motor neuron disease (MND) or hippocampal sclerosis (HS) also appeared to segregate to some extent. We suggest: 1) pathological variation in FTLD-TDP is best described as a ‘continuum’ without clearly distinct subtypes, 2) vacuolation was the single greatest source of variation and reflects the ‘stage’ of the disease, and 3) within the FTLD-TDP ‘continuum’ cases with GRN mutation and with coexisting MND or HS may have a more distinctive pathology.

A morphometric study of the spatial patterns of TDP-43 immunoreactive neuronal inclusions in frontotemporal lobar degeneration (FTLD) with progranulin (GRN) mutation

Mutations of the progranulin (GRN) gene are a major cause of familial frontotemporal lobar degeneration with transactive response (TAR) DNA-binding protein of 43 kDa (TDP-43) proteinopathy (FTLD-TDP). We studied the spatial patterns of TDP-43 immunoreactive neuronal cytoplasmic inclusions (NCI) and neuronal intranuclear inclusions (NII) in histological sections of the frontal and temporal lobe in eight cases of FTLD-TDP with GRN mutation using morphometric methods and spatial pattern analysis. In neocortical regions, the NCI were clustered and the clusters were regularly distributed parallel to the pia mater; 58% of regions analysed exhibiting this pattern. The NII were present in regularly distributed clusters in 35% of regions but also randomly distributed in many areas. In neocortical regions, the sizes of the regular clusters of NCI and NII were 400-800 µm, approximating to the size of the modular columns of the cortico-cortical projections, in 31% and 36% of regions respectively. The NCI and NII also exhibited regularly spaced clustering in sectors CA1/2 of the hippocampus and in the dentate gyrus. The clusters of NCI and NII were not spatially correlated. The data suggest degeneration of the cortico-cortical and cortico-hippocampal pathways in FTLD-TDP with GRN mutation, the NCI and NII affecting different clusters of neurons.

Spatial patterns of TDP-43 neuronal cytoplasmic inclusions (NCI) in fifteen cases of frontotemporal lobar degeneration with TDP-43 proteinopathy (FTLD-TDP)

Neuronal cytoplasmic inclusions (NCI) immunoreactive for transactive response DNA-binding protein (TDP-43) are the pathological hallmark of frontotemporal lobar degeneration with TDP-43 proteinopathy (FTLD-TDP). We studied the spatial patterns of the TDP-43 immunoreactive NCI in the frontal and temporal cortex of 15 cases of FTLD-TDP. The NCI were distributed parallel to the tissue boundary predominantly in regular clusters 50-400 µm in diameter. In five cortical areas, the size of the clusters approximated to the cells of the cortico-cortical pathways. In most regions, cluster size was smaller than 400 µm. There were no significant differences in spatial patterns between familial and sporadic cases. Cluster size of the NCI was not correlated with disease duration, brain weight, Braak stage, or disease subtype. The spatial pattern of the NCI was similar to that of neuronal inclusions in other neurodegenerative diseases and may reflect a common pattern of degeneration involving the cortico-cortical projections.

TDP-43-Immunoreactive pathology in frontotemporal lobar degeneration with TDP proteinopathy (FTLD-TDP) with and without associated motor neuron disease

A proportion of patients with motor neuron disease (MND) exhibit frontotemporal dementia (FTD) and some patients with FTD develop the clinical features of MND. Frontotemporal lobar degeneration (FTLD) is the pathological substrate of FTD and some forms of this disease (referred to as FTLD-U) share with MND the common feature of ubiquitin-immunoreactive, tau-negative cellular inclusions in the cerebral cortex and hippocampus. Recently, the transactive response (TAR) DNA-binding protein of 43 kDa (TDP-43) has been found to be a major protein of the inclusions of FTLD-U with or without MND and these cases are referred to as FTLD with TDP-43 proteinopathy (FTLD-TDP). To clarify the relationship between MND and FTLD-TDP, TDP-43 pathology was studied in nine cases of FTLD-MND and compared with cases of familial and sporadic FTLD–TDP without associated MND. A principal components analysis (PCA) of the nine FTLD-MND cases suggested that variations in the density of surviving neurons in the frontal cortex and neuronal cytoplasmic inclusions (NCI) in the dentate gyrus (DG) were the major histological differences between cases. The density of surviving neurons in FTLD-MND was significantly less than in FTLD-TDP cases without MND, and there were greater densities of NCI but fewer neuronal intranuclear inclusions (NII) in some brain regions in FTLD-MND. A PCA of all FTLD-TDP cases, based on TDP-43 pathology alone, suggested that neuropathological heterogeneity was essentially continuously distributed. The FTLD-MND cases exhibited consistently high loadings on PC2 and overlapped with subtypes 2 and 3 of FTLD-TDP. The data suggest: (1) FTLD-MND cases have a consistent pathology, variations in the density of NCI in the DG being the major TDP-43-immunoreactive difference between cases, (2) there are considerable similarities in the neuropathology of FTLD-TDP with and without MND, but with greater neuronal loss in FTLD-MND, and (3) FTLD-MND cases are part of the FTLD-TDP ‘continuum’ overlapping with FTLD-TDP disease subtypes 2 and 3.