Littérature et sociologie : analyse de l'expérience moderne chez Joseph Roth, Thomas Mann et Max Weber

Ce présent mémoire est animé par une forte conviction : les frontières disciplinaires entre les sociologues et les écrivains ne doivent pas se transmuer en barbelés obstruant un éclairage de sens renouvelé sur la réalité sociale. Alors qu’au tournant du siècle dernier, le roman réaliste et la sociologie allemande se sont mutuellement inspirés, au fil du temps les canaux de communication se sont progressivement brouillés. Notre démarche consiste donc à renouer avec la tradition du monde germanophone à l’orée du 20e siècle, période au cours de laquelle la sociologie émerge comme discipline propre. Plus précisément, nous chercherons à faire converser les deux régimes d’écriture afin d’une part, d’explorer les vertus cognitives de la littérature pour la sociologie et d’autre part de mieux comprendre comment les hommes contemporains aux premiers sociologues entrevoyaient l’époque des temps modernes. Pour ce faire, nous nous appuierons sur la sociologie de Max Weber (1864-1920), un des pères fondateurs de la discipline, ainsi que sur l’analyse de trois romans réalistes, signés par deux romanciers germanophones du début du 20e siècle, c’est-à-dire Joseph Roth (1894-1939) et Thomas Mann (1875-1955).

Joseph Roth

Lutz Weltmann

Joseph Roth: Radetzkymarsch [Rezension]

M-x.

Juden auf Wanderschaft

von Joseph Roth

Na 1 Nachlass Max Horkheimer, 44 - Korrespondenzen u.a. mit Marthe Roth (p. I 21, 313-463)

2 Briefe und 1 Lebenslauf von Max Horkheimer an Arthur Rosenberg, 1939, 1941; 2 Briefe zwischen Kurt Rosenfeld und Karl Brandt, 22.04.1937, 27.04.1937; 5 Briefe von Kurt Rosenfeld an Max Horkheimer, 1937-19378; 4 Brief und Beilage an Kurt Rosenfeld, 1937-1943; 11 Briefe zwischen Hans W. Rosenhaupt und Max Horkheimer, 1935, 1941, 1942, 1947; 4 Briefe zwischen Samuel I. Roseman und Max Horkheimer, 1939, 03.01.1940; 2 Briefe zwischen J. Rosenstock und Max Horkheimer, 15.07.1946; 2 Briefe zwischen Joseph Adolphe Rosenthal und Max Horkheimer, 09.04.1941, 08.05.1941, sowie Briefwechsel mit Sophie Ries; 2 Briefe zwischen Sophie Ries und Max Horkheimer, 08.05.1941, 11.05.1941; 1 Brief von Max Horkheimer an Lore Woedthke, 08.05.1941; 2 Briefe zwischen Morris Rosenthal und Max Horkheimer, 01.10.1935, 04.10.1935; 1 Brief von Max Horkheimer an das Rosenwald Capital Outlay Fund New York, 30.01.1940; 1 Brief B. Lifschitz an Marthe Roth, 21.04.1937; 1 Brief von Chamorel et Simond an Marthe Roth, 11.06.1937; 1 Brief von F.K. Sung an Marthe Roth, 24.06.1937; 12 Briefe zwischen Marthe Roth und Max Horkheimer, Juli 1937-1938, sowie Briefwechsel mit Louis Vogt; 4 Briefe zwischen Louis Vogt und Max Horkheimer, 10.08.1937, 1937; 1 Brief von Max Horkheimer an Dr. Rothen, 31.01.1935; 1 Umzugsmitteilung von Hans Rothmann; 2 Briefe zwischen Richard C. Rothschild und Max Horkheimer, 11.05.1940, 13.05.1940; 4 Briefe zwischen Ludwig Rothschild, Hilde Rothschild und Max Horkheimer, 1936-15.09.1939; 2 Briefe zwischen S. Rothschildt und Max Horkheimer, 23.11.1940, 29.11.1940; 4 Brief zwischen J. S. Roucek und Max Horkheimer, 1941; 1 Brief von Joseph Rovan an Max Horkheimer, 11.05.1948; 2 Brief zwischen Wilmina Rowland und Max Horkheimer, 13.03.1949, 11.04.1949; 2 Briefe zwischen dem Royal Automobile Club und Max Horkheimer, 26.08.1937, 22.09.1937; 2 Briefe zwischen Royal Motors Inc. und Max Horkheimer, 05.02.1940, 06.03.1940; 1 Beitrag von Nina Rubinstein zur Soziologie des Fremden; 1 Brief von Theodor W. Adorno an Rudd, 09.09.1940; 1 Brief von Jay Rumney an Goldstein, 18.06.1936; 20 Briefe und Beilage zwischen Jay Rumney und Max Horkheimer, 1934- 1937, 1949 sowie Briefwechsel mit D. Mitrany; 3 Briefe zwischen D. Mitrany und Max Horkheimer, 01.12.1937, 1937; 3 Briefe von Theodor W. Adorno an Dagobert D. Runes, 1941; 1 Brief und 1 Beilage von N. Waterman an Georg Rusche, 03.05.1939; 12 Briefe und Beilage zwischen Georg Rusche und Max Horkheimer, 1939-1942 sowie Briefwechsel mit N. Waterman; 1 Brief von N. Waterman an Georg Rusche, 03.04.1939; 2 Briefe zwischen N. Waterman und Max Horkheimer, 21.04.1939, 05.05.1939; 1 Brief von Ruth an Max Horkheimer;

Cerebral Cortex Involvement In Machado-joseph Disease.

Machado-Joseph disease (MJD/SCA3) is the most frequent spinocerebellar ataxia, characterized by brainstem, basal ganglia and cerebellar damage. Few magnetic resonance imaging based studies have investigated damage in the cerebral cortex. The objective was to determine whether patients with MJD/SCA3 have cerebral cortex atrophy, to identify regions more susceptible to damage and to look for the clinical and neuropsychological correlates of such lesions. Forty-nine patients with MJD/SCA3 (mean age 47.7 ± 13.0 years, 27 men) and 49 matched healthy controls were enrolled. All subjects underwent magnetic resonance imaging scans in a 3 T device, and three-dimensional T1 images were used for volumetric analyses. Measurement of cortical thickness and volume was performed using the FreeSurfer software. Groups were compared using ancova with age, gender and estimated intracranial volume as covariates, and a general linear model was used to assess correlations between atrophy and clinical variables. Mean CAG expansion, Scale for Assessment and Rating of Ataxia (SARA) score and age at onset were 72.1 ± 4.2, 14.7 ± 7.3 and 37.5 ± 12.5 years, respectively. The main findings were (i) bilateral paracentral cortex atrophy, as well as the caudal middle frontal gyrus, superior and transverse temporal gyri, and lateral occipital cortex in the left hemisphere and supramarginal gyrus in the right hemisphere; (ii) volumetric reduction of basal ganglia and hippocampi; (iii) a significant correlation between SARA and brainstem and precentral gyrus atrophy. Furthermore, some of the affected cortical regions showed significant correlations with neuropsychological data. Patients with MJD/SCA3 have widespread cortical and subcortical atrophy. These structural findings correlate with clinical manifestations of the disease, which support the concept that cognitive/motor impairment and cerebral damage are related in disease.

Spinal Cord Damage In Machado-joseph Disease.

Machado-Joseph disease (SCA3) is the most frequent spinocerebellar ataxia worldwide and characterized by remarkable phenotypic heterogeneity. MRI-based studies in SCA3 focused in the cerebellum and connections, but little is known about cord damage in the disease and its clinical relevance. To evaluate the spinal cord damage in SCA3 through quantitative analysis of MRI scans. A group of 48 patients with SCA3 and 48 age and gender-matched healthy controls underwent MRI on a 3T scanner. We used T1-weighted 3D images to estimate the cervical spinal cord area (CA) and eccentricity (CE) at three C2/C3 levels based on a semi-automatic image segmentation protocol. The scale for assessment and rating of ataxia (SARA) was employed to quantify disease severity. The two groups-SCA3 and controls-were significantly different regarding CA (49.5 ± 7.3 vs 67.2 ± 6.3 mm(2), p < 0.001) and CE values (0.79 ± 0.06 vs 0.75 ± 0.05, p = 0.005). In addition, CA presented a significant correlation with SARA scores in the patient group (p = 0.010). CE was not associated with SARA scores (p = 0.857). In the multiple variable regression, we found that disease duration was the only variable associated with CA (coefficient = -0.629, p = 0.025). SCA3 is characterized by cervical cord atrophy and antero-posterior flattening. In addition, the spinal cord areas did correlate with disease severity. This suggests that quantitative analyses of the spinal cord MRI might be a useful biomarker in SCA3.

Machado-Joseph disease versus hereditary spastic paraplegia: case report

Machado-Joseph disease (MJD) is the most common autosomal dominant spinocerebellar ataxia and presents great phenotypic variability. MJD presenting with spastic paraparesis was recently described in Japanese patients. We report the case of 41-year-old woman with the phenotype of complicated hereditary spastic paraplegia. Her father died at the age of 56 years due to an undiagnosed progressive neurological disease that presented parkinsonism. She had an expanded allele with 66 CAG repeats and a normal allele with 22 repeats in the gene of MJD. MJD should be considered in the differential diagnosis of autosomal dominant complicated HSP. A patient with the phenotype of complicated HSP and relatives with other clinical features of a neurodegenerative disease should raise the suspicion of MJD.

Identificação de compostos que modulam a patogénese da doença de Machado-Joseph em C.elegans: autofagia como alvo terapêutico: identification of small compounds that modulate pathogenesis of Machado-Joseph disease in a C.elegans model: targeting autophagy

A doença de Machado-Joseph (DMJ) ou ataxia espinocerebelosa do tipo 3 (SCA3), conhecida por ser a mais comum das ataxias hereditárias dominantes em todo o mundo, é uma doença neurodegenerativa autossómica dominante que leva a uma grande incapacidade motora, embora sem alterar o intelecto, culminando com a morte do doente. Atualmente não existe nenhum tratamento eficaz para esta doença. A DMJ é resultado de uma alteração genética causada pela expansão de uma sequência poliglutamínica (poliQ), na região C-terminal do gene que codifica a proteína ataxina-3 (ATXN3). Os mecanismos celulares das doenças de poliglutaminas que provocam toxicidade, bem como a função da ATXN3, não são ainda totalmente conhecidos. Neste trabalho, usamos, pela sua simplicidade e potencial genético, um pequeno animal invertebrado, o nemátode C. elegans, com o objetivo de identificar fármacos eficazes para o combate contra a patogénese da DMJ, analisando simultaneamente o seu efeito na agregação da ATXN3 mutante nas células neuronais in vivo e o seu impacto no comportamento motor dos animais. Este pequeno invertebrado proporciona grandes vantagens no estudo dos efeitos tóxicos de proteínas poliQ nos neurónios, uma vez que a transparência das suas 959 células (das quais 302 são neurónios) facilita a deteção de proteínas fluorescentes in vivo. Para além disso, esta espécie tem um ciclo de vida curto, é económica e de fácil manutenção. Neste trabalho testámos no nosso modelo transgénico da DMJ com 130Qs em C.elegans dois compostos potencialmente moduladores da agregação da ATXN3 mutante e da resultante disfunção neurológica, atuando pela via da autofagia. De modo a validar a possível importância terapêutica da ativação da autofagia os compostos candidatos escolhidos foram o Litío e o análogo da Rapamicina CCI-779, testados independentemente e em combinação. A neuroproteção conferida pelo Litío e pelo CCI-779 independentemente sugere que o uso destes fármacos possa ser considerado uma boa estratégia como terapia para a DMJ, a testar em organismos evolutivamente mais próximos do humano. A manipulação da autofagia, segundo vários autores, parece ser benéfica e pode ser a chave para o desenvolvimento de novos tratamentos para várias doenças relacionadas com a agregação proteica e o envelhecimento.

Depleção do DNA mitocondrial (mtDNA) em leucócitos de doentes com doença Machado-Joseph : um estudo piloto

Dissertação de Mestrado, Ciências Biomédicas, 5 de Outubro de 2015, Universidade dos Açores.

Development of triplet repeat primed PCR (TP-PCR) technique as a support of molecular test in Machado-Joseph disease

Dissertação de Mestrado, Ciências Biomédicas, 3 de Fevereiro de 2016, Universidade dos Açores.

Searching for therapeutic strategies in a mouse modelo of Machado-Joseph disease: targeting proteostases

Tese de Doutoramento em Ciências da Saúde

Pre-clinical trials for Machado-Joseph Disease: Hypothesis-based and hypothesis-free therapeutic approaches

Tese de Doutoramento em Ciências da Saúde