61 research outputs found

    Risque d'Ă©rosion hydrique entre fragilitĂ© des Ă©quilibres environnementaux et perspectives de durabilitĂ©: Cas du bassin d’Oued El Abed (Maroc nord-est)

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    The objective of this work is to study water erosion phenomenon in El Abed watershed in North Eastern Morocco. With this in mind, we have analyzed the quantitative and qualitative information available on the one hand, and on the other hand, we have carried out field measurements by rain simulation (60 mm/h during 10 mn). Soil loss was estimated using the universal soil loss equation (USLE). The qualitative analysis based on the inventory of the various forms of water erosion showed a strong morphodynamic activity, characterized by diffuse and concentrated streaming, gullying and side extensions of valleys. The quantitative analysis of soil losses using USLE model made it possible to estimate that 4,7% of the watershed surface area are strongly eroded and that average specific degradation is estimated to be 6,4 t/ha/an. Measurements of rain simulation tests showed clear differences between the various land uses. Indeed, runoff coefficient is low on the vegetation covered plots of and the plots cultivated parallel to contour lines. On the other hand, runoff coefficient is high on steeply bare soils. The amount of detached soil varied from 0.014 t/ha for the covered plots to 2.9 t/ha for the steeply bare soils. It should be underlined that the extent of water erosion in El Abed watershed is due to its natural settings, but also to anthropic activities (cultivation and overgrazing).  Keywords: Water erosion, USLE, El Abed watershed, MoroccoL'Ă©rosion hydrique est l’un des risques inquiĂ©tants qui menacent le milieu physique et la stabilitĂ© humaine. Le bassin d’oued El Abed, est sujet Ă  ce phĂ©nomĂšne depuis longtemps, ce qui a induit des mutations importantes et a touchĂ© divers domaines Ă©conomiques, sociaux et environnementaux. Ainsi, la problĂ©matique de cette Ă©tude est axĂ©e sur l’étude de l’érosion et son Ă©valuation dans ce bassin. Le bassin d’oued El Abed est situĂ© au sud-ouest de Taourirt, dans la partie ouest du couloir de Guercif-Oujda et comprend une partie de la plaine de Tafrata. Sa surface est de 317 kmÂČ Ă  sa confluence avec oued Moulouya. Pour Ă©tudier l'Ă©rosion dans ce bassin, nous avons, d’une part analysĂ© les donnĂ©es quantitatives et qualitatives disponibles et, d’autre part, rĂ©alisĂ© des mesures sur le terrain par simulation de pluie (intensitĂ© de 60 mm/h durant 10 mn). L'estimation de la perte en sol a Ă©tĂ© faite en se basant sur l'Ă©quation universelle de perte en sol (USLE). L'inventaire des diverses manifestations et formes d'Ă©rosion hydrique dans le bassin de l'oued El-Abed montre clairement qu'il s'agit d'une forte activitĂ© morphodynamique caractĂ©risĂ©e par un ruissellement diffus et concentrĂ©, des ravinements, des extensions latĂ©rales des vallĂ©es. AprĂšs avoir calculĂ© les diffĂ©rents facteurs de l’USLE, on a constatĂ© que 4,7% de la surface du bassin serait fortement Ă©rodĂ©e. La dĂ©gradation spĂ©cifique moyenne a Ă©tĂ© estimĂ©e Ă  6,4 tonnes/ha/an. Les mesures de simulation de pluie ont montrĂ© des diffĂ©rences nettes entre les utilisations des terres. En effet, les coefficients de ruissellement sont faibles dans les parcelles couvertes de vĂ©gĂ©tation et celles cultivĂ©es parallĂšlement aux courbes de niveau. Par contre, sur les sols nus et les pentes fortes, ce coefficient est Ă©levĂ©. Les quantitĂ©s de sols dĂ©tachĂ©es varient de 0,014 pour les parcelles couvertes Ă  2,9 t/ha pour celles nues et Ă  forte pente. L’érosion dans le bassin d’El Abed est due Ă  sa fragilitĂ© naturelle mais surtout aux actions anthropiques (mise en culture, surpĂąturage). Mots clĂ©s: Érosion hydrique, USLE, Bassin d’oued El-Abed, Maroc nord-es

    Design and Implementation of Wireless Zigbee Sensor Based On Embedded 32-Bits FPGA Processor

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    Wireless Sensor Networks (WSN) has become an emerging area of research in recent years. Today this wireless sensors are used in many industrial and consumer applications, such as industrial process monitoring and control, machine health monitoring, automotive, home appliance, smart grid applications and so on. In this work, an intelligent wireless sensor system for real time functionality has been suggested. The proposed solution is based on the embedded FPGA design using a new Xilinx MicroBlaze Soft Processor to Increases the performance of the system. The effectiveness of the proposed method is verified by the experimental results. The hardware components include Xilinx FPGA board, XBee Series 2 wireless communication module and end device sensors to capture the physical or environmental quantity, such as temperature, sound or pressure..

    Resuscitation of Newborn Piglets. Short-Term Influence of FiO2 on Matrix Metalloproteinases, Caspase-3 and BDNF

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    Perinatal hypoxia-ischemia is a major cause of mortality and cerebral morbidity, and using oxygen during newborn resuscitation may further harm the brain. The aim was to examine how supplementary oxygen used for newborn resuscitation would influence early brain tissue injury, cell death and repair processes and the regulation of genes related to apoptosis, neurodegeneration and neuroprotection.Anesthetized newborn piglets were subjected to global hypoxia and then randomly assigned to resuscitation with 21%, 40% or 100% O(2) for 30 min and followed for 9 h. An additional group received 100% O(2) for 30 min without preceding hypoxia. The left hemisphere was used for histopathology and immunohistochemistry and the right hemisphere was used for in situ zymography in the corpus striatum; gene expression and the activity of various relevant biofactors were measured in the frontal cortex. There was an increase in the net matrix metalloproteinase gelatinolytic activity in the corpus striatum from piglets resuscitated with 100% oxygen vs. 21%. Hematoxylin-eosin (HE) staining revealed no significant changes. Nine hours after oxygen-assisted resuscitation, caspase-3 expression and activity was increased by 30-40% in the 100% O(2) group (n = 9/10) vs. the 21% O(2) group (n = 10; p<0.04), whereas brain-derived neurotrophic factor (BDNF) activity was decreased by 65% p<0.03.The use of 100% oxygen for resuscitation resulted in increased potentially harmful proteolytic activities and attenuated BDNF activity when compared with 21%. Although there were no significant changes in short term cell loss, hyperoxia seems to cause an early imbalance between neuroprotective and neurotoxic mechanisms that might compromise the final pathological outcome

    The Potential Role of Metalloproteinases in Neurogenesis in the Gerbil Hippocampus Following Global Forebrain Ischemia

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    BACKGROUND: Matrix metalloproteinases (MMPs) have recently been considered to be involved in the neurogenic response of adult neural stem/progenitor cells. However, there is a lack of information showing direct association between the activation of MMPs and the development of neuronal progenitor cells involving proliferation and/or further differentiation in vulnerable (Cornus Ammoni-CA1) and resistant (dentate gyrus-DG) to ischemic injury areas of the brain hippocampus. PRINCIPAL FINDINGS: We showed that dynamics of MMPs activation in the dentate gyrus correlated closely with the rate of proliferation and differentiation of progenitor cells into mature neurons. In contrast, in the damaged CA1 pyramidal cells layer, despite the fact that some proliferating cells exhibited antigen specific characteristic of newborn neuronal cells, these did not attain maturity. This coincides with the low, near control-level, activity of MMPs. The above results are supported by our in vitro study showing that MMP inhibitors interfered with both the proliferation and differentiation of the human neural stem cell line derived from umbilical cord blood (HUCB-NSCs) toward the neuronal lineage. CONCLUSION: Taken together, the spatial and temporal profiles of MMPs activity suggest that these proteinases could be an important component in neurogenesis-associated processes in post-ischemic brain hippocampus

    Fine-structural distribution of MMP-2 and MMP-9 activities in the rat skeletal muscle upon training: a study by high-resolution in situ zymography

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    Matrix metalloproteinases (MMPs) are key regulators of extracellular matrix remodeling, but have also important intracellular targets. The purpose of this study was to examine the activity and subcellular localization of the gelatinases MMP-2 and MMP-9 in skeletal muscle of control and physically trained rats. In control hind limb muscle, the activity of the gelatinases was barely detectable. In contrast, after 5 days of intense exercise, in Soleus (Sol), but not Extensor digitorum longus (EDL) muscle, significant upregulation of gelatinolytic activity in myofibers was observed mainly in the nuclei, as assessed by high resolution in situ zymography. The nuclei of quiescent satellite cells did not contain the activity. Within the myonuclei, the gelatinolytic activity colocalized with an activated RNA Polymerase II. Also in Sol, but not in EDL, there were few foci of mononuclear cells with strongly positive cytoplasm, associated with apparent necrotic myofibers. These cells were identified as activated satellite cells/myoblasts. No extracellular gelatinase activity was observed. Gel zymography combined with subcellular fractionation revealed training-related upregulation of active MMP-2 in the nuclear fraction, and increase of active MMP-9 in the cytoplasmic fraction of Sol. Using RT-PCR, selective increase in MMP-9 mRNA was observed. We conclude that training activates nuclear MMP-2, and increases expression and activity of cytoplasmic MMP-9 in Sol, but not in EDL. Our results suggest that the gelatinases are involved in muscle adaptation to training, and that MMP-2 may play a novel role in myonuclear functions

    Meta-analysis of heterogeneous Down Syndrome data reveals consistent genome-wide dosage effects related to neurological processes

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    <p>Abstract</p> <p>Background</p> <p>Down syndrome (DS; trisomy 21) is the most common genetic cause of mental retardation in the human population and key molecular networks dysregulated in DS are still unknown. Many different experimental techniques have been applied to analyse the effects of dosage imbalance at the molecular and phenotypical level, however, currently no integrative approach exists that attempts to extract the common information.</p> <p>Results</p> <p>We have performed a statistical meta-analysis from 45 heterogeneous publicly available DS data sets in order to identify consistent dosage effects from these studies. We identified 324 genes with significant genome-wide dosage effects, including well investigated genes like <it>SOD1</it>, <it>APP</it>, <it>RUNX1 </it>and <it>DYRK1A </it>as well as a large proportion of novel genes (N = 62). Furthermore, we characterized these genes using gene ontology, molecular interactions and promoter sequence analysis. In order to judge relevance of the 324 genes for more general cerebral pathologies we used independent publicly available microarry data from brain studies not related with DS and identified a subset of 79 genes with potential impact for neurocognitive processes. All results have been made available through a web server under <url>http://ds-geneminer.molgen.mpg.de/</url>.</p> <p>Conclusions</p> <p>Our study represents a comprehensive integrative analysis of heterogeneous data including genome-wide transcript levels in the domain of trisomy 21. The detected dosage effects build a resource for further studies of DS pathology and the development of new therapies.</p

    Joining S100 proteins and migration:for better or for worse, in sickness and in health

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    The vast diversity of S100 proteins has demonstrated a multitude of biological correlations with cell growth, cell differentiation and cell survival in numerous physiological and pathological conditions in all cells of the body. This review summarises some of the reported regulatory functions of S100 proteins (namely S100A1, S100A2, S100A4, S100A6, S100A7, S100A8/S100A9, S100A10, S100A11, S100A12, S100B and S100P) on cellular migration and invasion, established in both culture and animal model systems and the possible mechanisms that have been proposed to be responsible. These mechanisms involve intracellular events and components of the cytoskeletal organisation (actin/myosin filaments, intermediate filaments and microtubules) as well as extracellular signalling at different cell surface receptors (RAGE and integrins). Finally, we shall attempt to demonstrate how aberrant expression of the S100 proteins may lead to pathological events and human disorders and furthermore provide a rationale to possibly explain why the expression of some of the S100 proteins (mainly S100A4 and S100P) has led to conflicting results on motility, depending on the cells used. © 2013 Springer Basel
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