3 resultados para early life exposure
em Universidade Federal do Rio Grande do Norte(UFRN)
Resumo:
In most primates, the mother is primarily responsible for care in early life of the infants, since, as in other mammals, infants depend on their mother to nutritional conditions. However, unlike most of them, in some species, infants are also dependent on other individuals with respect to transportation, supervision, and food sharing. To understand the distribution of care to offspring is essential to understand the social dynamics of the group. Several studies conducted in the natural environment, during the infant have been studied mainly through the careful transport of the infants. Our study approached the different forms of care to infants (transport, supervision and food sharing) and the development of behavioral repertoire throughout all phases of infant and juvenile seeking to better understand how to establish the development and survival of offspring of Callithrix jacchus, in natural environment. The seasonality in the caatinga was striking in this study and the collection had two distinct seasons for each of the sets observed, one dry and one rainy. These environmental changes seem to have influenced the distribution of activities in animal development. Yet the greater availability of resources in the rainy season seems to have been the main factor influencing the pattern of activities. Results will be presented in two manuscripts
Resumo:
Introduction: Infiltration of organic fluids and microorganisms at the abutment/implant interface may result in bacterial infection of peri-implant tissues. Internal colonization of periodontal pathogens may be caused by bacteria trapped during installation or penetration of abutment/implant leakage. The aim of this study was to detect periodontal pathogens in the internal area of dental implants before loading. Materials and Methods: Seventy-eight implants in 32 partially edentulous subjects were selected for this evaluation. A bacterial biofilm sample of the internal surface of each implant was taken and analyzed for the presence of 40 microorganisms by checkerboard DNA-DNA hybridization, prior to installation of healing or any other prosthetic abutment. Discussion: Bacteria were detected in 20 patients (62.5%), distributed in 41 implants (52.6%). Forty-seven percent of implants showed no bacterial detection. Spontaneous early implant exposure to oral cavity during the healing period was not significant (P >0.05) to increase bacterial prevalence, but implants placed at mandible had higher bacterial prevalence than maxillary ones. Conclusion: The internal surface of dental implants can serve as a reservoir of periodontal pathogens for future implant/abutment interface.
Resumo:
Autism comprises a heterogeneous group of neurodevelopmental disorders that affects the brain maturation and produces sensorial, motor, language and social interaction deficits in early childhood. Several studies have shown a major involvement of genetic factors leading to a predisposition to autism, which are possibly affected by environmental modulators during embryonic and post-natal life. Recent studies in animal models indicate that alterations in epigenetic control during development can generate neuronal maturation disturbances and produce a hyper-excitable circuit, resulting in typical symptoms of autism. In the animal model of autism induced by valproic acid (VPA) during rat pregnancy, behavioral, electrophysiological and cellular alterations have been reported which can also be observed in patients with autism. However, only a few studies have correlated behavioral alterations with the supposed neuronal hyper-excitability in this model. The aim of this project was to generate an animal model of autism by pre-natal exposure to VPA and evaluate the early post-natal development and pre-puberal (PND30) behavior in the offspring. Furthermore, we quantified the parvalbumin-positive neuronal distribution in the medial prefrontal cortex and Purkinje cells in the cerebellum of VPA animals. Our results show that VPA treatment induced developmental alterations, which were observed in behavioral changes as compared to vehicle-treated controls. VPA animals showed clear behavioral abnormalities such as hyperlocomotion, prolonged stereotipies and reduced social interaction with an unfamiliar mate. Cellular quantification revealed a decrease in the number of parvalbumin-positive interneurons in the anterior cingulate cortex and in the prelimbic cortex of the mPFC, suggesting an excitatory/inhibitory unbalance in this animal model of autism. Moreover, we also observed that the neuronal reduction occurred mainly in the cortical layers II/III and V/VI. We did not detect any change in the density of Purkinje neurons in the Crus I region of the cerebellar cortex. Together, our results strengthens the face validity of the VPA model in rats and shed light on specific changes in the inhibitory circuitry of the prefrontal cortex in this autism model. Further studies should address the challenges to clarify particular electrophysiological correlates of the cellular alterations in order to better understand the behavioral dysfunctions