41 research outputs found

    Lessons learnt from case studies : TOOLBOX OF KNOWLEDGE, EXPERIENCES AND GOOD PRACTICES. Outcome of the TRACKs project

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    The project Transition Children and Kindergarten (TRACKs) is funded by the Erasmus+ European program and it is carried out in partnership with different institutions in three partner countries: Poland, Italy and Belgium. The University institutions are the Jagiellonian University of Krakow in Poland, the University of Bologna in Italy, and the University of Ghent in Belgium. Other local educational organizations collaborating are Artevelde University College in Belgium, the Komensky Institute in Poland, and the Cooperativa Assistenza Disabili Infermi Anziani Infanzia (CADIAI) in Italy. The purpose of our project is to focus on the voices of practitioners \u2013 such as Early Childhood Education and Care (ECEC) professionals currently working with children aged 1 to 6 years old \u2013 and future ECEC professionals, such as early years educators and pre-school teachers still in training. The project\u2019s foundation rests on the dynamic exchange of knowledge and practice between the two target groups in the three countries involved in the project. This transnational exchange between the ECEC professionals across the three European Member States is intended to improve quality of learning, assuming that the international contexts can feed into each other, exchange solutions and practices and respond to shared challenges. A further essential purpose of the project is providing high quality learning opportunities and nurturing environments for all children, especially those coming from multiply marginalized backgrounds, and those that are experiencing social inequalities, poverty and racism. Drawing on the method of video-coaching and video-analysis, the project encourages high-quality interaction of ECEC professionals with children (Fukkink & Lont, 2007; Fukkink & Tavecchio, 2010; Fukkink, Trienekens & Kramer, 2010). The research teams and professionals from the different countries observe the video recordings collectively, or in one-to-one sessions, and reflect on the interactions between professionals and children and among children. This report will shed light on the contextual conditions where such tools and methods were implemented and how. The purpose is to show how the video-coaching methodology can be implemented in different ways in relation to diverse contexts (\u2018no one model fits all\u2019). This will also facilitate reflection by trainers/pedagogical leaders/coordinators who might want to use this methodology in their services/with their teams on how to develop context-appropriate procedures and tools that make it relevant to the settings/professionals within which/with whom they are working

    Cadmium-Induced Oxidative Stress and Apoptotic Changes in the Testis of Freshwater Crab, Sinopotamon henanense

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    Cadmium (Cd), one of the most toxic environmental and industrial pollutants, is known to exert gonadotoxic and spermiotoxic effects. In the present study, we examined the toxic effect of Cd on the testis of freshwater crab, Sinopotamon henanense. Crabs were exposed to different Cd concentrations (from 0 to 116.00 mg·L−1) for 7 d. Oxidative stress and apoptotic changes in the testes were detected. The activities of SOD, GPx and CAT initially increased and subsequently decreased with increasing Cd concentrations, which was accompanied with the increase in malondialdehyde (MDA) and H2O2 content in a concentration-dependent manner. Typical morphological characteristic and physiological changes of apoptosis were observed using a variety of methods (HE staining, AO/EB double fluorescent staining, Transmission Electron Microscope observation and DNA fragmentation analysis), and the activities of caspase-3 and caspase-9 were increased in a concentration-dependent manner after Cd exposure. These results led to the conclusion that Cd could induced oxidative damage as well as apoptosis in the testis, and the apoptotic processes may be mediated via mitochondria-dependent apoptosis pathway by regulating the activities of caspase-3 and caspase-9

    Maternal high-fat diet prevents developmental programming by early-life stress

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    Anxiety disorders and depression are well-documented in subjects exposed to adverse childhood events. Recently, maternal obesity and/or maternal consumption of high-fat diets (HFD) have been also proposed as risk factors for offspring mental health. Here using an animal model in rats, we explored the combinatorial effects of a maternal HFD (40% of energy from fat without impact on maternal weight; during gestation and lactation) and maternal separation (MS) in offspring. In the prefrontal cortex (PFC) of pups, MS led to changes in the expression of several genes such as Bdnf (brain derived neurotrophic factor), 5HT-r1a (serotonin receptor 1a) and Rest4 (neuron-restrictive silencer element, repressor element 1, silencing transcription factor (Rest), splicing variant 4). Surprisingly, perinatal HFD strongly attenuated the developmental alterations induced by MS. Furthermore, maternal HFD totally prevented the endophenotypes (anxiety, spatial memory, social behavior, hypothalamic–pituitary–adrenal (HPA) axis response to stress, hippocampal neurogenesis and visceral pain) associated with MS at adulthood. Finally, we also demonstrated that HFD intake reduced anxiety and enhanced maternal care in stressed dams. Overall, our data suggest that a HFD restricted to gestation and lactation, which did not lead to overweight in dams, had limited effects in unstressed offspring, highlighting the role of maternal obesity, rather than fat exposure per se, on brain vulnerability during development.Environnement psychosocial précoce, empreintes biologiques et épigénétiques et état de santé à l'âge adult

    Lack of brain serotonin affects postnatal development and serotonergic neuronal circuitry formation

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    Despite increasing evidence suggests that serotonin (5-HT) can influence neurogenesis, neuronal migration and circuitry formation, the precise role of 5-HT on central nervous system (CNS) development is only beginning to be elucidated. Moreover, how changes in serotonin homeostasis during critical developmental periods may have etiological relevance to human mental disorders, remains an unsolved question. In this study we address the consequences of 5-HT synthesis abrogation on CNS development using a knock-in mouse line in which the tryptophan hydroxylase 2 (Tph2) gene is replaced by the eGFP reporter. We report that lack of brain 5-HT results in a dramatic reduction of body growth rate and in 60% lethality within the first 3 weeks after birth, with no gross anatomical changes in the brain. Thanks to the specific expression of the eGFP, we could highlight the serotonergic system independently of 5-HT immunoreactivity. We found that lack of central serotonin produces severe abnormalities in the serotonergic circuitry formation with a brain region- and time- specific effect. Indeed, we observed a striking reduction of serotonergic innervation to the suprachiasmatic and thalamic paraventricular nuclei, while a marked serotonergic hyperinnervation was found in the nucleus accumbens and hippocampus of Tph2∷eGFP mutants. Finally, we demonstrated that BDNF expression is significantly up-regulated in the hippocampus of mice lacking brain 5-HT, mirroring the timing of the appearance of hyperinnervation and thus unmasking a possible regulatory feedback mechanism tuning the serotonergic neuronal circuitry formation. On the whole, these findings reveal that alterations of serotonin levels during CNS development affect the proper wiring of the brain that may produce long-lasting changes leading to neurodevelopmental disorders

    Microglia morphological changes in the motor cortex of hsod1g93a transgenic als mice

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    Amyotrophic lateral sclerosis (ALS) is characterized by the progressive degeneration of spinal motor neurons as well as corticospinal (CSN) large pyramidal neurons within cortex layer V. An intense microglia immune response has been associated with both upper and lower motor neuron degeneration in ALS patients, whereas microgliosis occurrence in the motor cortex of hSOD1G93A mice—the best characterized model of this disease—is not clear and remains under debate. Since the impact of microglia cells in the neuronal environment seems to be crucial for both the initiation and the progression of the disease, here we analyzed the motor cortex of hSOD1G93A mice at the onset of symptoms by the immunolabeling of Iba1/TMEM119 double positive cells and confocal microscopy. By means of Sholl analysis, we were able to identify and quantify the presence of presumably activated Iba1/TMEM119-positive microglia cells with shorter and thicker processes as compared to the normal surveilling and more ramified microglia present in WT cortices. We strongly believe that being able to analyze microglia activation in the motor cortex of hSOD1G93A mice is of great importance for defining the timing and the extent of microglia involvement in CSN degeneration and for the identification of the initiation stages of this disease
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