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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.

Interaction with the environment appears necessary for the maturation of sensorimotor and cognitive functions in early life. In rats, a model of sensorimotor restriction (SMR) from postnatal day 1 (P1) to P28 has shown that low and atypical sensorimotor activities induced the perturbation of motor behavior due to muscle weakness and the functional disorganization of the primary somatosensory and motor cortices. In the present study, our objective was to understand how SMR affects the muscle–brain dialogue. We focused on irisin, a myokine secreted by skeletal muscles in response to exercise. FNDC5/irisin expression was determined in hindlimb muscles and brain structures by Western blotting, and irisin expression in blood and cerebrospinal fluid was determined using an ELISA assay at P8, P15, P21 and P28. Since irisin is known to regulate its expression, Brain-Derived Neurotrophic Factor (BDNF) levels were also measured in the same brain structures. We demonstrated that SMR increases FNDC5/irisin levels specifically in the soleus muscle (from P21) and also affects this protein expression in several brain structures (as early as P15). The BDNF level was increased in the hippocampus at P8. To conclude, SMR affects FNDC5/irisin levels in a postural muscle and in several brain regions and has limited effects on BDNF expression in the brain.

Physical exercise (EX) is well established for its positive impact on brain health. However, conventional EX may not be feasible for certain individuals. In this regard, this study explores electromyostimulation (EMS) as a potential alternative for enhancing cognitive function. Conducted on both human participants and rats, the study involved two sessions of EMS applied to the quadriceps with a duration of 30 min at one-week intervals. The human subjects experienced assessments of cognition and mood, while the rats underwent histological and biochemical analyses on the prefrontal cortex, hippocampus, and quadriceps. Our findings indicated that EMS enhanced executive functions and reduced anxiety in humans. In parallel, our results from the animal studies revealed an elevation in brain-derived neurotrophic factor (BDNF), specifically in the hippocampus. Intriguingly, this increase was not associated with heightened neuronal activity or cerebral hemodynamics; instead, our data point towards a humoral interaction from muscle to brain. While no evidence of increased muscle and circulating BDNF or FNDC5/irisin pathways could be found, our data highlight lactate as a bridging signaling molecule of the muscle–brain crosstalk following EMS. In conclusion, our results suggest that EMS could be an effective alternative to conventional EX for enhancing both brain health and cognitive function.

Mars's magnetosphere is a sensitive system, varying due to external and internal factors, such as solar wind conditions and crustal magnetic fields. A signature of this influence can be seen in the position of two boundaries; the bow shock and the induced magnetospheric boundary (IMB). The bow shock moves closer to Mars during times of high solar activity, and both the bow shock and IMB bulge away from Mars over crustal magnetic fields in the southern hemisphere. This study investigates whether large-scale atmospheric events at Mars have any signature in these two magnetic boundaries, by investigating the 2007 storm. The 2007 global storm lasted for several months and increased atmospheric temperatures and densities of both water vapor and carbon dioxide in the atmosphere, leading to an increase in atmospheric escape. Using Mars Express, we identified boundary locations before, during, and after the event, and compared these to modeled boundary locations and areographical locations on Mars. We find that, while it is unclear whether the bow shock position is impacted by the storm, the IMB location does change significantly, despite the orbital bias introduced by Mars Express. The terminator distance for the IMB peaks at longitudes 0°–40° and 310°–360°, leaving a depression around 180° longitude, where the boundary usually extends to higher altitudes due to the crustal magnetic fields. We suggest this may be due to the confinement of ionospheric plasma over crustal fields preventing mixing with the dust, creating a dip in ionospheric pressure here.

The positive effects of physical exercise (EX) are well known to be mediated by cerebral BDNF (brain-derived neurotrophic factor), a neurotrophin involved in learning and memory, the expression of which could be induced by circulating irisin, a peptide derived from Fibronectin type III domain-containing protein 5 (FNDC5) produced by skeletal muscle contraction. While the influence of EX modalities on cerebral BDNF expression was characterized, their effect on muscle FNDC5/Irisin expression and circulating irisin levels remains to be explored. The present study involved Wistar rats divided into four experimental groups: sedentary (SED), low- (40% of maximal aerobic speed, MAS), intermediate- (50% of MAS) and high- (70% of MAS) intensities of treadmill EX (30 min/day, 7 days). Soleus (SOL) versus gastrocnemius (GAS) FNDC5 and hippocampal BDNF expressions were evaluated by Western blotting. Additionally, muscular FNDC5/Irisin localization and serum/hippocampal irisin levels were studied by immunofluorescence and ELISA, respectively. Our findings revealed that (1) serum irisin and hippocampal BDNF levels vary with EX intensity, showing a threshold intensity at 50% of MAS; (2) hippocampal BDNF levels positively correlate with serum irisin but not with hippocampal FNDC5/Irisin; and (3) GAS, in response to EX intensity, overexpresses FNDC5/Irisin in type II muscle fibers. Altogether, peripheral FNDC5/Irisin levels likely explain EX-dependent hippocampal BDNF expression.

The Lunar Orbital Platform - Gateway (LOP - Gateway, or simply Gateway) is a crewed platform that will be assembled and operated in the vicinity of the Moon by NASA and international partner organizations, including ESA, starting from the mid-2020s. It will offer new opportunities for fundamental and applied scientific research. The Moon is a unique location to study the deep space plasma environment. Moreover, the lunar surface and the surface-bounded exosphere are interacting with this environment, constituting a complex multi-scale interacting system. This paper examines the opportunities provided by externally mounted payloads on the Gateway in the field of space plasma physics, heliophysics and space weather, and also examines the impact of the space environment on an inhabited platform in the vicinity of the Moon. It then presents the conceptual design of a model payload, required to perform these space plasma measurements and observations. It results that the Gateway is very well-suited for space plasma physics research. It allows a series of scientific objectives with a multi-disciplinary dimension to be addressed.

Abstract 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.

Elevation of cerebral blood flow (CBF) may contribute to the cerebral benefits of the regular practice of physical exercise. Surprisingly, while electrically induced contraction of a large muscular mass is a potential substitute for physical exercise to improve cognition, its effect on CBF remains to be investigated. Therefore, the present study investigated CBF in the cortical area representing the hindlimb, the hippocampus and the prefrontal cortex in the same anesthetized rats subjected to either acute (30 min) or chronic (30 min for 7 days) electrically induced bilateral hindlimb contraction. While CBF in the cortical area representing the hindlimb was assessed from both laser doppler flowmetry (LDFCBF) and changes in p-eNOSSer1177 levels (p-eNOSCBF), CBF was evaluated only from changes in p-eNOSSer1177 levels in the hippocampus and the prefrontal cortex. The contribution of increased cardiac output and increased neuronal activity to CBF changes were examined. Stimulation was associated with tachycardia and no change in arterial blood pressure. It increased LDFCBF with a time- and intensity-dependent manner as well as p-eNOSCBF in the area representing the hindlimb. By contrast, p-eNOSCBF was unchanged in the two other regions. The augmentation of LDFCBF was partially reduced by atenolol (a ß1 receptor antagonist) and not reproduced by the administration of dobutamine (a ß1 receptor agonist). Levels of c-fos as a marker of neuronal activation selectively increased in the area representing the hindlimb. In conclusion, electrically induced bilateral hindlimb contraction selectively increased CBF in the cortical area representing the stimulated muscles as a result of neuronal hyperactivity and increased cardiac output. The absence of CBF changes in cognition-related brain regions does not support flow-dependent neuroplasticity in the pro-cognitive effect of electrically induced contraction of a large muscular mass.

Masonry construction is one of the oldest building systems and practiced since the early stage of human civilization. Even though industrialized nations developed new building practices using steel and concrete materials, most developing countries still use unreinforced masonry buildings. Evidence from past events shows that masonry structures sometimes performed well and survived several earthquake events, particularly in the area where earthquake events struck regularly and enough to show how structures behave. However, an alteration from the traditional cultural building practice is seen due to the lack of proper scientific knowledge about such local construction cultures. Amongst traditional construction technics, one captured authorities' and scientists' attention as showing excellent properties: seismic bands that can be found in many parts of Nepal. After the 2015 Gorkha earthquake, reconstruction works started adopting the guidelines developed by DUDBC and National Building code that suggest using such seismic bands. The evidence of using such band dates to 2500 BCE, and qualitative studies of those applications have proven to enhance the performance in the masonry structure. However, the experiment's quantitative parameters using various materials are needed to carry out the parametrical analysis to optimize seismic band's use. To provide quantitative results, we have started with two specimens, one without a band and one with a timber seismic band, and incorporate the digital image correlation (DIC) technique to obtain the localized information. The quasi-static cyclic test is carried out for our specimens to compare the behavior concerning the energy dissipation, and the surface area of the crack formed during the loading cyclic. This work clearly shows the seismic band's advantage in limiting the crack propagation and improving masonry structure integrity.

The removal of nanometric particles constitutes one of the main challenges for the Integrated Circuits manufacturing. A solution based on the polymer coating and removal without substrate consumption is described and its performances are evaluated. In our experiments, 60 nm SiO2 particles and 40–200 nm Si3N4 particles are used to contaminate Si wafers. Two polymer removal methods are compared, one is purely based on a chemical action while in the other one a chemical and a physical actions are coupled. We demonstrate that a physical action is required to remove particles. The process shows high Particle Removal Efficiency (PRE) up to 87% independently of the particle size and nature. The PRE stays at a constant value, around 85%, for 3 decades of aging time, but the particle removal is not uniform on all the wafer. Keywords: Polymer, Particle removal efficiency, Contamination, Particle size, Aging

The shake table test is one of the preferred techniques used to understand the dynamic response of a structure. However, due to the limited number of facilities available to perform such tests and their expensiveness, researchers often must rely on numerical models validated with the results of the static tests only. Moreover, most research papers concerning shake table tests lack details on how the tests were planned and executed. This paper explains the steps used for the preparation and execution of shake table tests on three reduced-scale buildings. These buildings were constructed outside the shake table surface, on a metallic base frame, and later moved to the shake table used for the tests in order to optimize the time of the experimental campaign. This approach enabled us to complete the tests in only 6 days. The approach presented in this paper may be helpful to researchers who want to increase the effectiveness of the available shake table facility and overcome the limitations of time and budget. Moreover, the solution presented in this article helps in the displacement of specimens without the use of a crane or other sophisticated hydraulic machinery. Thus, it could also be useful for testing specimens that have been aged and that are sensitive to displacements.

Cognitive abilities are largely dependent on activation of cerebral tropomyosin-related kinase B receptors (TrkB) by brain-derived neurotrophic factor (BDNF) that is secreted under a bioactive form by both neurons and endothelial cells. In addition, there is mounting evidence for a link between endothelial function and cognition even though the underlying mechanisms are not well known. Therefore, we investigated the cerebral BDNF pathway, either neuronal or endothelial, in rheumatoid arthritis (RA) that combines both endothelial dysfunction (ED) and impaired cognition. Adjuvant-induced arthritis (AIA) in rats was used as a model of RA. Clinical inflammatory symptoms were evaluated from an arthritis score and brains were collected at day 31 ± 2 post-immunization. Neuronal expression of BDNF and TrkB phosphorylated at tyrosine 816 (p-TrkB) was examined in brain slices. Endothelial BDNF and p-TrkB expression was examined on both brain slices (hippocampal arterioles) and isolated cerebral microvessels-enriched fractions (vessels downstream to arterioles). The connection between endothelial nitric oxide (NO) and BDNF production was explored on the cerebrovascular fractions using endothelial NO synthase (eNOS) levels as a marker of NO production, Nω-Nitro-L-arginine methyl ester hydrochloride (L-NAME) as a NOS inhibitor and glyceryl-trinitrate as a slow releasing NO donor. Brain slices displayed lower BDNF and p-TrkB staining in both neurons and arteriolar endothelial cells in AIA than in control rats. For endothelial cells but not neurons, a strong correlation was observed between BDNF and p-TrkB staining. Of note, a strong correlation was also observed between neuronal p-TrkB and endothelial BDNF staining. In cerebral microvessels-enriched fractions, AIA led to decreased BDNF and eNOS levels with a positive association between the 2 parameters. These effects coincided with decreased BDNF and p-TrkB staining in endothelial cells. The exposure of AIA cerebrovascular fractions to GTN increased BDNF levels while the exposure of control fractions to L-NAME decreased BDNF levels. Changes in the cerebral BDNF pathway were not associated with arthritis score. The present study reveals that AIA impairs the endothelial and neuronal BDNF/TrkB pathway, irrespective of the severity of inflammatory symptoms but dependent on endothelial NO production. These results open new perspectives for the understanding of the link between ED and impaired cognition.

The learning difficulties facing students with autism not only require an adaptation of the learning environment, (strategies and tools) but also require a personalized adaptation taking into account the specific skills and needs of students with autism. This personalized adaptation will be inserted into the collective learning of the class. If many studies have shown the interest of using information and communication technologies (ICT) in education for students with autism, these refer to making digital tools compatible with the teacher’s adapted pedagogical approach, in order for them to be fully employed into school practice. As a matter of fact, far from being a homogenous category, students with autism each have their own particularities, hence the need for information technology tools that are adapted to each pupil’s profile, whilst being in tune with the teacher’s pedagogical style. This article presents a collaborative research between a special teacher and a few researchers, concerning the introduction of a very personalized information technology tool. The grounded theory approach makes the process of inserting the information technology tools into a special teaching for students with autism, more intelligible.

The recombinant form of tissue plasminogen activator (rt-PA) is the only curative treatment for ischemic stroke. Recently, t-PA has been linked to the metabolism of brain-derived neurotrophic factor (BDNF), a major neurotrophin involved in post-stroke neuroplasticity. Thus, the objective of our study was to investigate the impact of rt-PA treatment on post-stroke circulating BDNF levels in humans and in animals. Serum BDNF levels and t-PA/plasmin activity were measured at hospital admission and at up to 90 days in stroke patients receiving (n = 24) or not (n = 14) rt-PA perfusion. We investigated the relationships between serum BDNF with concurrent t-PA/plasmin activity, neurological outcomes and cardiovascular scores at admission. In parallel, serum BDNF levels and t-PA/plasmin activity were assessed before and after (1, 4 and 24h) the induction of ischemic stroke in rats. Our study revealed higher serum BDNF levels and better neurological outcome in rt-PA-treated than non-treated patients. However, serum BDNF levels did not predict stroke outcome when the whole cohort of stroke patients was analyzed. By contrast, serum BDNF levels when measured at admission and at day 90 correlated with cardiovascular scores, and those at day 1 correlated with serum t-PA/plasmin activity in the whole cohort of patients whereas no association could be found in the rt-PA-treated group. In rats devoid of cardiovascular risk, no difference in post-stroke serum BDNF levels was detected between rt-PA- and vehicle-treated animals and no correlation was found between serum BDNF levels and t-PA/plasmin activity. Overall, the data suggest that serum BDNF levels may not be useful as a prognostic biomarker of stroke outcome and that endothelial dysfunction could be a confounding factor when serum BDNF levels after stroke are used to reflect of brain BDNF levels.

Neurons exposed to zinc exhibit activation of poly(ADP-ribose) polymerase-1 (PARP-1), an enzyme that normally participates in DNA repair but promotes cell death when extensively activated. Endogenous, vesicular zinc in brain is released to the extracellular space under conditions causing neuronal depolarization. Here, we used a rat model of insulin-induced hypoglycemia to assess the role of zinc release in PARP-1 activation and neuronal death after severe hypoglycemia. Zinc staining with N-(6-methoxy-8-quinolyl)-para-toluenesulfonamide (TSQ) showed depletion of presynaptic vesicular zinc from hippocampal mossy fiber terminals and accumulation of weakly bound zinc in hippocampal CA1 cell bodies after severe hypoglycemia. Intracerebroventricular injection of the zinc chelator calcium ethylene-diamine tetraacetic acid (CaEDTA) blocked the zinc accumulation and significantly reduced hypoglycemia-induced neuronal death. CaEDTA also attenuated the accumulation of poly(ADP-ribose), the enzymatic product of PARP-1, in hippocampal neurons. These results suggest that zinc translocation is an intermediary step linking hypoglycemia to PARP-1 activation and neuronal death.

Brain-derived neurotrophic factor (BDNF) through TrkB activation is central for brain functioning. Since the demonstration that plasmin is able to process pro-BDNF to mature BDNF and that these two forms have opposite effects on neuronal survival and plasticity, a particular attention has been paid to the link between tissue plasminogen activator (tPA)/plasmin system and BDNF metabolism. However, t-PA via its action on different N-methyl-D-aspartate (NMDA) receptor subunits is also considered as a neuromodulator of glutamatergic transmission. In this context, the aim of our study was to investigate the effect of recombinant (r)t-PA administration on brain BDNF metabolism in rats. In the hippocampus, we found that rt-PA (10 mg/kg) administration induced a progressive increase in mature BDNF levels associated with TrkB activation. In order to delineate the mechanistic involved, plasmin activity was assessed and its inhibition was attempted using tranexamic acid (30 or 300 mg/kg, i.v.) while NMDA receptors were antagonized with MK801 (0.3 or 3 mg/kg, i.p.) in combination with rt-PA treatment. Our results showed that despite a rise in rt-PA activity, rt-PA administration failed to increase hippocampal plasmin activity suggesting that the plasminogen/plasmin system is not involved whereas MK801 abrogated the augmentation in mature BDNF levels observed after rt-PA administration. All together, our results show that rt-PA administration induces increase in hippocampal mature BDNF expression and suggests that rt-PA contributes to the control of brain BDNF synthesis through a plasmin-independent potentiation of NMDA receptors signaling.

Following the earthquake that struck Haiti in 2010, observations have demonstrated the relevance of certain traditional building techniques that succeeded in limiting the occupants’ exposure to the risk of severe injury. Identifying and understanding the specificities of existing building structures and know-how provides a starting-point for improving building methods and reinforcing skills in order to reduce the long-term vulnerability of local communities. This paper presents two research works that address, from complementary angles, the issues of building in a risk-prone environment. The first, from the field of architecture, outlines a participatory methodology for analyzing local building practices with a view to developing them and making technical improvements. The second, from an engineering perspective, focuses on an experimental computer-aided scientific study of a building system used for post-earthquake reconstruction.

Physical exercise constitutes an innovative strategy to treat deficits associated with stroke through the promotion of BDNF-dependent neuroplasticity. However, there is no consensus on the optimal intensity/duration of exercise. In addition, whether previous stroke changes the effect of exercise on the brain is not known. Therefore, the present study compared the effects of a clinically-relevant form of exercise on cerebral BDNF levels and localization in control versus stroke rats. For this purpose, treadmill exercise (0.3 m/s, 30 min/day, for 7 consecutive days) was started in rats with a cortical ischemic stroke after complete maturation of the lesion or in control rats. Sedentary rats were run in parallel. Mature and proBDNF levels were measured on the day following the last boot of exercise using Western blotting analysis. Total BDNF levels were simultaneously measured using ELISA tests. As compared to the striatum and the hippocampus, the cortex was the most responsive region to exercise. In this region, exercise resulted in a comparable increase in the production of mature BDNF in intact and stroke rats but increased proBDNF levels only in intact rats. Importantly, levels of mature BDNF and synaptophysin were strongly correlated. These changes in BDNF metabolism coincided with the appearance of intense BDNF labeling in the endothelium of cortical vessels. Notably, ELISA tests failed to detect changes in BDNF forms. Our results suggest that control beings can be used to find conditions of exercise that will result in increased mBDNF levels in stroke beings. They also suggest cerebral endothelium as a potential source of BDNF after exercise and highlight the importance to specifically measure the mature form of BDNF to assess BDNF-dependent plasticity in relation with exercise.

Background. Although diosmectite has demonstrated efficacy in the treatment of acute watery diarrhoea in children, its efficacy in adults still needs to be assessed. The objective of this study was therefore to assess the efficacy of diosmectite on the time to recovery in adults with acute diarrhoea. Methods. A total of 346 adults with at least three watery stools per day over a period of less than 48 hours were prospectively randomized to diosmectite (6 g tid) or placebo during four days. The primary endpoint was time to diarrhoea recovery. Results. In the intention-to-treat population, median time to recovery was 53.8 hours (range [3.7–167.3]) with diosmectite (n=166) versus 69.0 hours [2.2–165.2] with placebo, (n=163; P=.029), which corresponds to a difference of 15.2 hours. Diosmectite was well tolerated. Conclusion. Diosmectite at 6 g tid was well tolerated and reduced the time to recovery of acute watery diarrhoea episode in a clinically relevant manner.

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.

Since 2010, Haiti has been subject to many hazards. Earthquakes and cyclones have all caused significant damage to the building. However, in 2010, the observation of the impact of the earthquake had made it possible to make a clear distinction between the construction typologies. Not all had killed, not all had been completely destroyed, and some, although rather modest in appearance, had behaved well despite the intensity of the shock. Research carried out on these housing typologies, based on the use of timber-frame construction systems and “fillings” with locally available materials, led to original reconstruction proposals, promoting these ancient local practices. Those, met with reluctance in the Haitian development community, considered backward-looking. However, as soon as the first prototype was built, the potential advantages of the approach were understood. In addition, structural calculations later on followed by laboratory and shaking-table tests allowed recognition and certification by the MTPTC. The model could be disseminated with various variants, in particular by the NGO platform PADED. During the passage of hurricanes Irma and Matthew, these newly built habitats behaved rather well. Thus, other integrated organisations started participating in the dissemination of the concept of TCLA (Improved Local Construction Techniques). Most of the achievements having been made in the West and South of the country, many of them suffered the earthquake of August 14, 2021. This was a real-life test whose results appeared rather eloquent. As a result, at the end of August 2021, the Shelter Working Group produced an orientation document which mentioned the interest of the TCLA approach, because beyond the para-disaster performance it allows self-help and self-recovery at the local level, and on the long term. Does all this means that, like has already been observed in other regions of the world, the recent repetition of disasters will lead to a radical change in the culture of risk in Haiti? Could this new situation ultimately lead to better adaptation of housing solutions to the capacities and means of the Haitian populations, and better consideration of natural hazards with, ultimately, more resilience?