996 resultados para PRENATAL STRESS


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Stress in local isolation structures is studied by micro‐Raman spectroscopy. The results are correlated with predictions of an analytical model for the stress distribution and with cross‐sectional transmission electron microscopy observations. The measurements are performed on structures on which the Si3N4 oxidation mask is still present. The influence of the pitch of the periodic local isolation pattern, consisting of parallel lines, the thickness of the mask, and the length of the bird"s beak on the stress distribution are studied. It is found that compressive stress is present in the Si substrate under the center of the oxidation mask lines, with a magnitude dependent on the width of the lines. Large tensile stress is concentrated under the bird"s beak and is found to increase with decreasing length of the bird"s beak and with increasing thickness of the Si3N4 film.

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A new approach to the local measurement of residual stress in microstructures is described in this paper. The presented technique takes advantage of the combined milling-imaging features of a focused ion beam (FIB) equipment to scale down the widely known hole drilling method. This method consists of drilling a small hole in a solid with inherent residual stresses and measuring the strains/displacements caused by the local stress release, that takes place around the hole. In the presented case, the displacements caused by the milling are determined by applying digital image correlation (DIC) techniques to high resolution micrographs taken before and after the milling process. The residual stress value is then obtained by fitting the measured displacements to the analytical solution of the displacement fields. The feasibility of this approach has been demonstrated on a micromachined silicon nitride membrane showing that this method has high potential for applications in the field of mechanical characterization of micro/nanoelectromechanical systems.

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Stress induced by accumulation of unfolded proteins at the endoplasmic reticulum (ER) is a classic feature of secretory cells and is observed in many tissues in human diseases including cancer, diabetes, obesity, and neurodegeneration. Cellular adaptation to ER stress is achieved by the activation of the unfolded protein response (UPR), an integrated signal transduction pathway that transmits information about the protein folding status at the ER to the nucleus and cytosol to restore ER homeostasis. Inositol-requiring transmembrane kinase/endonuclease-1 (IRE1α), the most conserved UPR stress sensor, functions as an endoribonuclease that processes the mRNA of the transcription factor X-box binding protein-1 (XBP1). IRE1α signaling is a highly regulated process, controlled by the formation of a dynamic scaffold onto which many regulatory components assemble, here referred to as the UPRosome. Here we provide an overview of the signaling and regulatory mechanisms underlying IRE1α function and discuss the emerging role of the UPR in adaptation to protein folding stress in specialized secretory cells and in pathological conditions associated with alterations in ER homeostasis.

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The origin of the microscopic inhomogeneities in InxGa12xAs layers grown on GaAs by molecular beam epitaxy is analyzed through the optical absorption spectra near the band gap. It is seen that, for relaxed thick layers of about 2.8 mm, composition inhomogeneities are responsible for the band edge smoothing into the whole compositional range (0.05,x,0.8). On the other hand, in thin enough layers strain inhomogeneities are dominant. This evolution in line with layer thickness is due to the atomic diffusion at the surface during growth, induced by the strain inhomogeneities that arise from stress relaxation. In consequence, the strain variations present in the layer are converted into composition variations during growth. This process is energetically favorable as it diminishes elastic energy. An additional support to this hypothesis is given by a clear proportionality between the magnitude of the composition variations and the mean strain.

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OBJECTIVES: To evaluate prenatal diagnosis of congenital heart diseases by ultrasound investigation in well-defined European populations. DESIGN: Data from 20 registries of congenital malformations in 12 European countries were included. The prenatal ultrasound screening programs in the countries ranged from no routine screening to three ultrasound investigations per patient routinely performed. RESULTS: There were 2454 cases with congenital heart disease with an overall prenatal detection rate of 25%. Termination of pregnancy was performed in 293 cases (12%). There was considerable variation in prenatal detection rate between regions, with the lowest detection rates being in countries without ultrasound screening (11%) and in Eastern European countries (Croatia, Lithuania and Ukraine; 8%). In Western European countries with ultrasound screening, detection rate ranged from 19-48%. There was a significant difference in prenatal detection rate and proportion of induced abortions between isolated congenital heart disease and congenital heart disease associated with chromosome anomalies, multiple malformations and syndromes (P < 0.0001). There were 1694 cases with isolated congenital heart disease of which 16% were diagnosed prenatally. Malformations affecting the size of the ventricles were detected prenatally in half of the cases. CONCLUSIONS: Prenatal detection rate of congenital heart disease varies significantly between countries even with the same screening recommendations. The presence of associated malformations significantly increases the prenatal detection rate.

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But. - Investiguer l'influence d'une hospitalisation prénatale précédant une naissance préma¬turée sur les facteurs de stress parentaux et la relation parent-enfant lors de l'hospitalisation en néonatologie ainsi que sur les symptômes de stress post-traumatique parentaux. Population et méthodes. - Population : 51 enfants prématurés et 25 enfants nés à terme (groupe témoin). Quatre groupes : groupe témoin, prématurés sans hospitalisation prénatale, prématu¬rés avec hospitalisation courte (< 8 jours) et prématurés avec hospitalisation longue (> 8 jours). Instruments: le Parental Stressor Scale: Neonatal Intensive Care Unit (PSS: NICU, Miles et al., 1993 [14]) et le Perinatal PTSD Questionnaire (PPQ, Quinnell et Hynan, 1999 [16]). Résultats. -En cas d'hospitalisation prénatale, les parents se disent plus stressés par l'environnement du bébé en néonatologie. Les mères avec une hospitalisation prénatale courte (< 8 jours) se différencient significativement du groupe témoin par plus de symptômes de stress post-traumatique. Les parents présentant plus de symptômes post-traumatiques décrivent la relation avec leur bébé en néonatologie comme significativement plus difficile. Conclusion. - Cette étude indique l'attention à apporter aux patientes hospitalisées brièvement en prénatal (< 8 jours). Il s'agit d'un groupe plus à risque de présenter des symptômes de stress post-traumatique qui peuvent engendrer des troubles dans la relation à l'enfant.

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The aim of this study was to identify genes involved in solute and matric stress mitigation in the polycyclic aromatic hydrocarbon (PAH)-degrading Novosphingobium sp. strain LH128. The genes were identified using plasposon mutagenesis and by selection of mutants that showed impaired growth in a medium containing 450 mM NaCl as a solute stress or 10% (wt/vol) polyethylene glycol (PEG) 6000 as a matric stress. Eleven and 14 mutants showed growth impairment when exposed to solute and matric stresses, respectively. The disrupted sequences were mapped on a draft genome sequence of strain LH128, and the corresponding gene functions were predicted. None of them were shared between solute and matric stress-impacted mutants. One NaCl-affected mutant (i.e., NA7E1) with a disruption in a gene encoding a putative outer membrane protein (OpsA) was susceptible to lower NaCl concentrations than the other mutants. The growth of NA7E1 was impacted by other ions and nonionic solutes and by sodium dodecyl sulfate (SDS), suggesting that opsA is involved in osmotic stress mitigation and/or outer membrane stability in strain LH128. NA7E1 was also the only mutant that showed reduced growth and less-efficient phenanthrene degradation in soil compared to the wild type. Moreover, the survival of NA7E1 in soil decreased significantly when the moisture content was decreased but was unaffected when soluble solutes from sandy soil were removed by washing. opsA appears to be important for the survival of strain LH128 in soil, especially in the case of reduced moisture content, probably by mitigating the effects of solute stress and retaining membrane stability.

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Purpose: In the last years, MRI appears as a complementary diagnostic method to US in the diagnosis of congenital lung lesions. Focal homogeneous pulmonary hyperintensity on T2-WI constitutes a frequent pattern observed. Our purpose is to determine if this finding is associated with a characteristic pulmonary lesion. Materials and methods: Between 01.01.00 and 31.12.07, a total of 50 prenatal MRI in fetuses with echographic diagnosis of thoracic pathology were performed in our institution, including 12 cases of suspected congenital pulmonary lesions. Prenatal images were correlated with post-natal diagnosis. Results: In 12 cases, fetal MRI detected congenital pulmonary lesions. In 8 patients, typical signs (cystic lesions, septations, anomalous vasculature) clearly suggested a specific pathology. In 4 cases, MRI showed a focal homogeneous increase of the signal intensity (SI) on T2-WI of the pathologic lung related to the normal one. The final diagnosis of these fetuses included 1 patient with congenital cystic adenomatoid malformation type III, 1 patient with segmental emphysema and 2 cases of bronchial atresia. In all 4 cases, a significant post-natal reduction of the lesion size related to prenatal MRI studies was observed. Conclusion: Our study suggests that a focal increment of the SI of the lung on T2-WI is a non specific sign of congenital lung disease, present in different pathologies. Therefore, a prospective diagnosis is not possible.

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OBJECTIVE: It is known that exogenous lactate given as an i.v. energy infusion is able to counteract a neuroglycopenic state that developed during psychosocial stress. It is unknown, however, whether the brain under stressful conditions can induce a rise in plasma lactate to satisfy its increased needs during stress. Since lactate is i) an alternative cerebral energy substrate to glucose and ii) its plasmatic concentration is influenced by the sympathetic nervous system, the present study aimed at investigating whether plasma lactate concentrations increase with psychosocial stress in humans. METHODS: 30 healthy young men participated in two sessions (stress induced by the Trier Social Stress Test and a non-stress control session). Blood samples were frequently taken to assess plasma lactate concentrations and stress hormone profiles. RESULTS: Plasma lactate increased 47% during psychosocial stress (from 0.9 ± 0.05 to 1.4 ± 0.1 mmol/l; interaction time × stress intervention: F = 19.7, p < 0.001). This increase in lactate concentrations during stress was associated with an increase in epinephrine (R(2) = 0.221, p = 0.02) and ACTH concentrations (R(2) = 0.460, p < 0.001). CONCLUSION: Plasma lactate concentrations increase during acute psychosocial stress in humans. This finding suggests the existence of a demand mechanism that functions to allocate an additional source of energy from the body towards the brain, which we refer to as 'cerebral lactate demand'.

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The influence of social factors on birthweight and fetal and infant mortality was investigated in the Swiss birth cohort from 1979-85 (N = 519,933). The proportion of newborns with low-birthweight (less than 2500 g) was higher in lower social classes. Stillbirth-rate, neonatal and postneonatal mortality were higher in lower social classes, too. When controlling for birthweight, the increase in mortality in the lower social classes became somewhat less striking. Marked social differences in perinatal mortality were found in the newborns with normal weight, whereas almost no difference could be detected in the low-birthweight-group.

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Endoplasmic reticulum (ER) homeostasis alteration contributes to pancreatic β-cell dysfunction and death and favors the development of diabetes. In this study, we demonstrate that HDLs protect β-cells against ER stress induced by thapsigargin, cyclopiazonic acid, palmitate, insulin overexpression, and high glucose concentrations. ER stress marker induction and ER morphology disruption mediated by these stimuli were inhibited by HDLs. Using a temperature-sensitive viral glycoprotein folding mutant, we show that HDLs correct impaired protein trafficking and folding induced by thapsigargin and palmitate. The ability of HDLs to protect β-cells against ER stress was inhibited by brefeldin A, an ER to Golgi trafficking blocker. These results indicate that HDLs restore ER homeostasis in response to ER stress, which is required for their ability to promote β-cell survival. This study identifies a cellular mechanism mediating the beneficial effect of HDLs on β-cells against ER stress-inducing factors.

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Chemical pollution is known to affect microbial community composition but it is poorly understood how toxic compounds influence physiology of single cells that may lay at the basis of loss of reproductive fitness. Here we analyze physiological disturbances of a variety of chemical pollutants at single cell level using the bacterium Pseudomonas fluorescens in an oligotrophic growth assay. As a proxy for physiological disturbance we measured changes in geometric mean ethidium bromide (EB) fluorescence intensities in subpopulations of live and dividing cells exposed or not exposed to different dosages of tetradecane, 4-chlorophenol, 2-chlorobiphenyl, naphthalene, benzene, mercury chloride, or water-dissolved oil fractions. Because ethidium bromide efflux is an energy-dependent process any disturbance in cellular energy generation is visible as an increased cytoplasmic fluorescence. Interestingly, all pollutants even at the lowest dosage of 1 nmol/mL culture produced significantly increased ethidium bromide fluorescence compared to nonexposed controls. Ethidium bromide fluorescence intensities increased upon pollutant exposure dosage up to a saturation level, and were weakly (r(2) = 0.3905) inversely correlated to the proportion of live cells at that time point in culture. Temporal increase in EB fluorescence of growing cells is indicative for toxic but reversible effects. Cells displaying high continued EB fluorescence levels experience constant and permanent damage, and no longer contribute to population growth. The procedure developed here using bacterial ethidium bromide efflux pump activity may be a useful complement to screen sublethal toxicity effects of chemicals.