53 research outputs found

    Un chantier de restauration à Angers à la fin du Moyen Âge : le compte de Jean Perier

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    In 1478, Jean Perier was appointed by the council of the city of Angers to begin the rehabilitation of a part of the ditches and walls within its boundaries. His accounts, a register of over a hundred folios, reported valuable information regarding the material organisation of the construction site, the delivery of the materials required in order to carry out the work, as well as the construction trades involved in the project. Throughout the register, the author of this account allows us to enter fully into the universe of this restoration project for which individuals from different socioeconomic backgrounds worked side by side. In this regard, the presence of several men sentenced by the court to undertake periods of work, sometimes stretching over an entire week, including Sundays, must also be mentioned. Jean Perier, who was in charge of monitoring the construction site and paying for work as it progressed, also became the spokesman for the everyday life of the construction site, sometimes including accidents and injuries. These pages also mention the women whose role was to distribute water or to care for the wounded

    Neurodegeneration: The Size Takes It All

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    SummaryThere is increasing computational evidence that the exceptionally high vulnerability of dopaminergic neurons in Parkinson’s disease may be due to their unique axonal architecture and resulting metabolic needs. A new experimental study has actually demonstrated this

    Investigating Street Art in Latin America. Interview with Olivier Dabène

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    contribution à un site webPolitical scientist Olivier Dabène is the author of Street Art and Democracy in Latin America, published by Palgrave Macmillan. The author presents the results of a several year long project in several cities of Latin America, during which he investigated and questioned the relation between street art and (local) democracy. Olivier Dabène has accepted to answer our questions and present his book. Interview by Miriam Perier, CERI

    Infectious disease does not impact the lying and grooming behaviour of post-parturient dairy cows

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    Behaviour is commonly used to detect sickness in animals, but the impact of sickness on lying and maternal behaviours around parturition is not well understood. The objective was to assess the effects of sickness on the lying and grooming behaviours of dairy cows in the first 24 h after giving birth. Cows were categorized as 'sick' (n = 8) if they had at least one rectal temperature ≥39.1 °C and one clinical sign of illness (mastitis, pneumonia or an unknown infection) within 24 h of calving. These cows were match-paired for parity with cows that had no rectal temperature ≥39.1 °C and no clinical signs of illness up to 3 d after calving (n = 8; 'not sick'). The duration and latency of cow behaviours (standing, lying, lying bouts, lying close to calf, and grooming of the calf) and calf behaviours (standing and lying) were recorded for 24 h post-partum. We found no differences in the behaviour of sick and not sick cows and their calves post-calving, except that sick cows took longer to lie down near their calf after calving compared to those without illness. Cows may be more motivated to groom and spend time with their calf than to express sickness behaviours immediately after giving birth

    Sunnis and Shi‘a. A Political History. Interview with Laurence Louër

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    contribution à un site webLaurence Louër is the author of recently published Sunnis and Shi‘a. A Political History, with Princeton University Press. A great specialist of Shia Islam and politics as well as identity politics in the Middle East, Laurence answers our questions and helps us better understand the – mimetic – rivalry between Shi‘a and Sunni and its relation to other identities and political objectives. Interview by Miriam Perier, CERI

    Mitochondrial Quality Control in Neurodegenerative Diseases : Focus on Parkinson's Disease and Huntington's Disease

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    In recent years, several important advances have been made in our understanding of the pathways that lead to cell dysfunction and death in Parkinson's disease (PD) and Huntington's disease (HD). Despite distinct clinical and pathological features, these two neurodegenerative diseases share critical processes, such as the presence of misfolded and/or aggregated proteins, oxidative stress, and mitochondrial anomalies. Even though the mitochondria are commonly regarded as the "powerhouses" of the cell, they are involved in a multitude of cellular events such as heme metabolism, calcium homeostasis, and apoptosis. Disruption of mitochondrial homeostasis and subsequent mitochondrial dysfunction play a key role in the pathophysiology of neurodegenerative diseases, further highlighting the importance of these organelles, especially in neurons. The maintenance of mitochondrial integrity through different surveillance mechanisms is thus critical for neuron survival. Mitochondria display a wide range of quality control mechanisms, from the molecular to the organellar level. Interestingly, many of these lines of defense have been found to be altered in neurodegenerative diseases such as PD and HD. Current knowledge and further elucidation of the novel pathways that protect the cell through mitochondrial quality control may offer unique opportunities for disease therapy in situations where ongoing mitochondrial damage occurs. In this review, we discuss the involvement of mitochondrial dysfunction in neurodegeneration with a special focus on the recent findings regarding mitochondrial quality control pathways, beyond the classical effects of increased production of reactive oxygen species (ROS) and bioenergetic alterations. We also discuss how disturbances in these processes underlie the pathophysiology of neurodegenerative disorders such as PD and HD

    Mitochondrial Quality Control in Neurodegenerative Diseases: Focus on Parkinson's Disease and Huntington's Disease

    No full text
    In recent years, several important advances have been made in our understanding of the pathways that lead to cell dysfunction and death in Parkinson's disease (PD) and Huntington's disease (HD). Despite distinct clinical and pathological features, these two neurodegenerative diseases share critical processes, such as the presence of misfolded and/or aggregated proteins, oxidative stress, and mitochondrial anomalies. Even though the mitochondria are commonly regarded as the “powerhouses” of the cell, they are involved in a multitude of cellular events such as heme metabolism, calcium homeostasis, and apoptosis. Disruption of mitochondrial homeostasis and subsequent mitochondrial dysfunction play a key role in the pathophysiology of neurodegenerative diseases, further highlighting the importance of these organelles, especially in neurons. The maintenance of mitochondrial integrity through different surveillance mechanisms is thus critical for neuron survival. Mitochondria display a wide range of quality control mechanisms, from the molecular to the organellar level. Interestingly, many of these lines of defense have been found to be altered in neurodegenerative diseases such as PD and HD. Current knowledge and further elucidation of the novel pathways that protect the cell through mitochondrial quality control may offer unique opportunities for disease therapy in situations where ongoing mitochondrial damage occurs. In this review, we discuss the involvement of mitochondrial dysfunction in neurodegeneration with a special focus on the recent findings regarding mitochondrial quality control pathways, beyond the classical effects of increased production of reactive oxygen species (ROS) and bioenergetic alterations. We also discuss how disturbances in these processes underlie the pathophysiology of neurodegenerative disorders such as PD and HD

    Role of microRNAs in the Regulation of alpha-Synuclein Expression: a Systematic Review

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    Growing evidence suggests that increased levels of α-synuclein might contribute to the pathogenesis of Parkinson’s disease (PD) and therefore, it is crucial to understand the mechanisms underlying α-synuclein expression. Recently, microRNAs (miRNAs) have emerged as key regulators of gene expression involved in several diseases such as PD and other neurodegenerative disorders. A systematic literature search was performed here to identify microRNAs that directly or indirectly impact in α-synuclein expression/accumulation and describe its mechanism of action. A total of 27 studies were incorporated in the review showing evidences that 6 microRNAs directly bind and regulate α-synuclein expression while several miRNAs impact on α-synuclein expression indirectly by targeting other genes. In turn, α-synuclein overexpression also impacts miRNAs expression, indicating the complex network between miRNAs and α-synuclein. From the current knowledge on the central role of α-synuclein in PD pathogenesis/progression, miRNAs are likely to play a crucial role at different stages of PD and might potentially be considered as new PD therapeutic approaches
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