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"Garnier, Philippe"
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الإنسان والمدينة : 13 مقالة في هذه المواضيع لمحاضرين ومفكرين فرنسين
كتاب \"الإنسان والمدينة\" هو عبارة 13 مقالة لمحاضرين ومفكرين فرنسين ويتناول الكتاب بشكل مفصل مفهوم العلاقة بين الإنسان والمدينة ويطرح الكتاب عدة تساؤلات : كيف نتصور المدينة ؟ ايمكن أن نضع دستوراً لمعادلة السكن الانساني ؟ ماهي الاساليب المقترحة وما هي حسنات كلَّ منها ؟ صحراء او سجن ، هل المدينة تولد العنف؟ اهناك علاج لهذا المرض العالمي ؟ ومن خلال الكتاب سنرى كيف يجيب الكتاب عن هذه التساؤلات.
Book
Time dependence of entanglement entropy on the fuzzy sphere
A
bstract
We numerically study the behaviour of entanglement entropy for a free scalar field on the noncommutative (“fuzzy”) sphere after a mass quench. It is known that the entanglement entropy before a quench violates the usual area law due to the non-local nature of the theory. By comparing our results to the ordinary sphere, we find results that, despite this non-locality, are compatible with entanglement being spread by ballistic propagation of entangled quasi-particles at a speed no greater than the speed of light. However, we also find that, when the pre-quench mass is much larger than the inverse of the short-distance cutoff of the fuzzy sphere (a regime with no commutative analogue), the entanglement entropy spreads faster than allowed by a local model.
Journal Article
Molecular mechanisms underlying physical exercise-induced brain BDNF overproduction
Accumulating evidence supports that physical exercise (EX) is the most effective non-pharmacological strategy to improve brain health. EX prevents cognitive decline associated with age and decreases the risk of developing neurodegenerative diseases and psychiatric disorders. These positive effects of EX can be attributed to an increase in neurogenesis and neuroplastic processes, leading to learning and memory improvement. At the molecular level, there is a solid consensus to involve the neurotrophin brain-derived neurotrophic factor (BDNF) as the crucial molecule for positive EX effects on the brain. However, even though EX incontestably leads to beneficial processes through BDNF expression, cellular sources and molecular mechanisms underlying EX-induced cerebral BDNF overproduction are still being elucidated. In this context, the present review offers a summary of the different molecular mechanisms involved in brain’s response to EX, with a specific focus on BDNF. It aims to provide a cohesive overview of the three main mechanisms leading to EX-induced brain BDNF production: the neuronal-dependent overexpression, the elevation of cerebral blood flow (hemodynamic hypothesis), and the exerkine signaling emanating from peripheral tissues (humoral response). By shedding light on these intricate pathways, this review seeks to contribute to the ongoing elucidation of the relationship between EX and cerebral BDNF expression, offering valuable insights into the potential therapeutic implications for brain health enhancement.
Journal Article
The effect of exercise on memory and BDNF signaling is dependent on intensity
The aims of the present study were to investigate in brain of adult rats (1) whether exercise-induced activation of brain-derived neurotrophic factor (BDNF)/tropomyosin-related kinase B (TrkB) pathway is dependent on exercise intensity modality and (2) whether exercise-induced improvement of memory is proportional to this pathway activation. Wistar rats were subjected to low (12 m/min) or high (18 m/min) exercise intensity on horizontal treadmill (30 min/day, 7 consecutive days) that corresponds to ~ 40 and 70% of maximal aerobic speed, respectively. Animals treated with scopolamine to induce memory impairment were subjected to novel object recognition test to assess potential improvement in cognitive function. Expressions of BDNF, phosphorylated TrkB receptors, synaptophysin (a marker of synaptogenesis), c-fos (a neuronal activity marker) and phosphorylated endothelial nitric oxide synthase (a cerebral blood flow marker) were measured in prefrontal cortex and hippocampus of different groups of rats. In terms of cognition, our data reported that only the most intense exercise improves memory performance. Our data also revealed that BDNF pathway is dependent on intensity modality of exercise with a gradual effect in hippocampus whereas only the highest intensity leads to this pathway activation in prefrontal cortex. Our study revealed that memory improvement through BDNF pathway activation is dependent on exercise intensity. While reporting that our protocol is sufficient to improve cognition in animals with impaired memory, our data suggest that prefrontal cortex is possibly a more suitable structure than hippocampus when neuroplastic markers are used to mirror potential improvement in memory performance.
Journal Article
Long-term use of standardised ginkgo biloba extract for the prevention of Alzheimer's disease (GuidAge): a randomised placebo-controlled trial
Prevention strategies are urgently needed to tackle the growing burden of Alzheimer's disease. We aimed to assess efficacy of long-term use of standardised ginkgo biloba extract for the reduction of incidence of Alzheimer's disease in elderly adults with memory complaints.
In the randomised, parallel-group, double-blind, placebo-controlled GuidAge clinical trial, we enrolled adults aged 70 years or older who spontaneously reported memory complaints to their primary-care physician in France. We randomly allocated participants in a 1:1 ratio according to a computer-generated sequence to a twice per day dose of 120 mg standardised ginkgo biloba extract (EGb761) or matched placebo. Participants and study investigators and personnel were masked to study group assignment. Participants were followed-up for 5 years by primary-care physicians and in expert memory centres. The primary outcome was conversion to probable Alzheimer's disease in participants who received at least one dose of study drug or placebo, compared by use of the log-rank test. This study is registered with ClinicalTrials.gov, number NCT00276510.
Between March, 2002, and November, 2004, we enrolled and randomly allocated 2854 participants, of whom 1406 received at least one dose of ginkgo biloba extract and 1414 received at least one dose of placebo. By 5 years, 61 participants in the ginkgo group had been diagnosed with probable Alzheimer's disease (1·2 cases per 100 person-years) compared with 73 participants in the placebo group (1·4 cases per 100 person-years; hazard ratio [HR] 0·84, 95% CI 0·60–1·18; p=0·306), but the risk was not proportional over time. Incidence of adverse events was much the same between groups. 76 participants in the ginkgo group died compared with 82 participants in the placebo group (0·94, 0·69–1·28; p=0·68). 65 participants in the ginkgo group had a stroke compared with 60 participants in the placebo group (risk ratio 1·12, 95% CI 0·77–1·63; p=0·57). Incidence of other haemorrhagic or cardiovascular events also did not differ between groups.
Long-term use of standardised ginkgo biloba extract in this trial did not reduce the risk of progression to Alzheimer's disease compared with placebo.
Ipsen.
Journal Article
A Cardy formula for off-diagonal three-point coefficients; or, how the geometry behind the horizon gets disentangled
A
bstract
In the AdS/CFT correspondence eternal black holes can be viewed as a specific entanglement between two copies of the CFT: the thermofield double. The statistical CFT Wightman function can be computed from a geodesic between the two boundaries of the Kruskal extended black hole and therefore probes the geometry behind the horizon. We construct a kernel for the AdS
3
/CFT
2
Wightman function that is independent of the entanglement. This kernel equals the average off-diagonal matrix element squared of a primary operator. This allows us to compute the Wightman function for an arbitrary entanglement between the double copies and probe the emergent geometry between a leftand right-CFT that are not thermally entangled.
Journal Article
Gravitational Wilson lines in 3D de Sitter
A
bstract
We construct local probes in the static patch of Euclidean dS
3
gravity. These probes are Wilson line operators, designed by exploiting the Chern-Simons formulation of 3D gravity. Our prescription uses non-unitary representations of
so
(4) ≃
su
(2)
L
× su
(2)
R
, and we evaluate the Wilson line for states satisfying a singlet condition. We discuss how to reproduce the Green’s functions of massive scalar fields in dS
3
, the construction of bulk fields, and the quasinormal mode spectrum. We also discuss the interpretation of our construction in Lorentzian signature in the inflationary patch, via SL(2
,
ℂ) Chern-Simons theory.
Journal Article
Estimate of the carbon footprint of astronomical research infrastructures
The carbon footprint of astronomical research is an increasingly topical issue with first estimates of research institute and national community footprints having recently been published. As these assessments have typically excluded the contribution of astronomical research infrastructures, we complement these studies by providing an estimate of the contribution of astronomical space missions and ground-based observatories using greenhouse gas emission factors that relates cost and payload mass to carbon footprint. We find that worldwide active astronomical research infrastructures currently have a carbon footprint of 20.3 ± 3.3 MtCO
2
equivalent (CO
2
e) and an annual emission of 1,169 ± 249 ktCO
2
e yr
−1
corresponding to a footprint of 36.6 ± 14.0 tCO
2
e per year per astronomer. Compared with contributions from other aspects of astronomy research activity, our results suggest that research infrastructures make the single largest contribution to the carbon footprint of an astronomer. We discuss the limitations and uncertainties of our method and explore measures that can bring greenhouse gas emissions from astronomical research infrastructures towards a sustainable level.
Astronomical research facilities, such as space telescopes, space probes or ground-based observatories, are the largest contributor to an astronomer’s carbon footprint, well beyond other activities such as flying to conferences or running computer simulations.
Journal Article
Endothelial cells are an important source of BDNF in rat skeletal muscle
BDNF (brain-derived neurotrophic factor) is present in skeletal muscle, controlling muscular metabolism, strength and regeneration processes. However, there is no consensus on BDNF cellular source. Furthermore, while endothelial tissue expresses BDNF in large amount, whether endothelial cells inside muscle expressed BDNF has never been explored. The aim of the present study was to provide a comprehensive analysis of BDNF localization in rat skeletal muscle. Cellular localization of BDNF and activated Tropomyosin-related kinase B (TrkB) receptors was studied by immunohistochemical analysis on soleus (SOL) and gastrocnemius (GAS). BDNF and activated TrkB levels were also measured in muscle homogenates using Western blot analysis and/or Elisa tests. The results revealed BDNF immunostaining in all cell types examined with a prominent staining in endothelial cells and a stronger staining in type II than type I muscular fibers. Endothelial cells but not other cells displayed easily detectable activated TrkB receptor expression. Levels of BDNF and activated TrkB receptors were higher in SOL than GAS. In conclusion, endothelial cells are an important and still unexplored source of BDNF present in skeletal muscle. Endothelial BDNF expression likely explains why oxidative muscle exhibits higher BDNF levels than glycolytic muscle despite higher the BDNF expression by type II fibers.
Journal Article
Microglial Involvement in Neuroplastic Changes Following Focal Brain Ischemia in Rats
The pathogenesis of ischemic stroke is a complex sequence of events including inflammatory reaction, for which the microglia appears to be a major cellular contributor. However, whether post-ischemic activation of microglial cells has beneficial or detrimental effects remains to be elucidated, in particular on long term brain plasticity events. The objective of our study was to determine, through modulation of post-stroke inflammatory response, to what extent microglial cells are involved in some specific events of neuronal plasticity, neurite outgrowth and synaptogenesis. Since microglia is a source of neurotrophic factors, the identification of the brain-derived neurophic factor (BDNF) as possible molecular actor involved in these events was also attempted. As a means of down-regulating the microglial response induced by ischemia, 3-aminobenzamide (3-AB, 90 mg/kg, i.p.) was used to inhibit the poly(ADP-ribose) polymerase-1 (PARP-1). Indeed, PARP-1 contributes to the activation of the transcription factor NF-kB, which is essential to the upregulation of proinflammatory genes, in particular responsible for microglial activation/proliferation. Experiments were conducted in rats subjected to photothrombotic ischemia which leads to a strong and early microglial cells activation/proliferation followed by an infiltration of macrophages within the cortical lesion, events evaluated at serial time points up to 1 month post-ictus by immunostaining for OX-42 and ED-1. Our most striking finding was that the decrease in acute microglial activation induced by 3-AB was associated with a long term down-regulation of two neuronal plasticity proteins expression, synaptophysin (marker of synaptogenesis) and GAP-43 (marker of neuritogenesis) as well as to a significant decrease in tissue BDNF production. Thus, our data argue in favour of a supportive role for microglia in brain neuroplasticity stimulation possibly through BDNF production, suggesting that a targeted protection of microglial cells could represent an innovative approach to potentiate post-stroke neuroregeneration.
Journal Article