934 resultados para Felt deprivation
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Individual well-being is multidimensional and various aspects of the quality of life need to be jointly considered in its measurement. The axiomatic literature on the subject has proposed many indices of multidimensional poverty and deprivation and explored the properties that are at the basis of these measures. The purpose of this chapter is to add intertemporal considerations to the analysis of material deprivation. We employ the EU-SILC panel data set, which includes information on different aspects of well-being over time. EU countries are compared based on measures that take this additional intertemporal information into consideration. Journal of Economic Literature Classi cation No.: D63.
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We propose and characterize a generalization of the classical linear index of individual deprivation based on income shortfalls. Unlike the original measure, our class allows for increases in the income of a higher-income individual to have a stronger impact on a person’s deprivation the closer they occur to the income of the individual whose deprivation is being assessed. The subclass of our measures with this property is axiomatized in our second result.
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In this paper we seriously entertain the question, “Is maternal deprivation the root of all evil?” Our consideration of this question is broken down into three parts. In the fi rst part, we discuss the nature of evil, focusing in particular on the legal concept of depravity. In the second part, we discuss the nurture of evil, focusing in particular on the common developmental trajectory seen in those who are depraved. In the third part, we discuss the roots of evil, focusing in particular on the animal and human research regarding maternal deprivation. Our conclusion is that maternal deprivation may actually be the root of all evil, but only because depraved individuals have been deprived of normative maternal care, which is the cradle of our humanity.
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It is well established that brain ischemia can cause neuronal death via different signaling cascades. The relative importance and interrelationships between these pathways, however, remain poorly understood. Here is presented an overview of studies using oxygen-glucose deprivation of organotypic hippocampal slice cultures to investigate the molecular mechanisms involved in ischemia. The culturing techniques, setup of the oxygen-glucose deprivation model, and analytical tools are reviewed. The authors focus on SUMOylation, a posttranslational protein modification that has recently been implicated in ischemia from whole animal studies as an example of how these powerful tools can be applied and could be of interest to investigate the molecular pathways underlying ischemic cell death.
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Human breast cancer cells (MCF-7, T-47-D and ZR-75-1) can adapt to circumvent any reduced growth rate during long-term oestrogen deprivation, and this provides three model systems to investigate mechanisms of endocrine resistance in breast cancer. In this paper we report consistent differences in the effects of three growth inhibitors following long-term oestrogen deprivation in all three cell models. Long-term oestrogen deprivation of MCF-7, T-47-D and ZR-75-1 cells resulted in reduced growth inhibition by PD98059 (2–10 µg/ml), implying a loss of dependence on mitogen-activated protein kinase pathways for growth. The growth inhibitor LY294002 (2–10 µM) inhibited growth of both oestrogen-maintained and oestrogen-deprived cells with similar dose–responses, implying continued similar dependence on phosphoinositide 3-kinase (PI3K) pathways with no alteration after adaptation to oestrogen independent growth. However, by contrast, long-term oestrogen deprivation resulted in an increased sensitivity to growth inhibition by rapamycin, which was not reduced by readdition of oestradiol. The enhanced inhibition of long-term oestrogen-deprived MCF-7-ED, T-47-D-ED and ZR-75-1-ED cell growth by combining rapamycin with LY294002 at concentrations where each alone had little effect, offers preclinical support to the development of therapeutic combinations of rapamycin analogues with other PI3K inhibitors in endocrine-resistant breast cancer.
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Background: MCF-7, T-47-D, ZR-75-1 human breast cancer cell lines are dependent on oestrogen for growth but can adapt to grow during long-term oestrogen deprivation. This serves as a model for identification of therapeutic targets in endocrine-resistant breast cancer. Methods: An overlooked complication of this model is that it involves more than non-addition of oestrogen, and inadequate attention has been given to separating molecular events associated with each of the culture manipulations. Results: Insulin and oestradiol were shown to protect MCF-7 cells against upregulation of basal growth, demonstrating a crosstalk in the growth adaptation process. Increased phosphorylation of p44/42MAPK and c-Raf reflected removal of insulin from the medium and proliferation of all three cell lines was inhibited to a lesser extent by PD98059 and U0126 following long-term oestrogen/insulin withdrawal, demonstrating a reduced dependence on the MAPK pathway. By contrast, long-term oestrogen/insulin deprivation did not alter levels of phosphorylated Akt and did not alter the dose-response of growth inhibition with LY294002 in any of the three cell lines. The IGF1R inhibitor picropodophyllin inhibited growth of all MCF-7 cells but only in the long-term oestrogen/insulin-deprived cells was this paralleled by reduction in phosphorylated p70S6K, a downstream target of mTOR. Long-term oestrogen/insulin-deprived MCF-7 cells had higher levels of phosphorylated p70S6K and developed increased sensitivity to growth inhibition by rapamycin. Conclusions: The greater sensitivity to growth inhibition by rapamycin in all three cell lines following long-term oestrogen/insulin deprivation suggests rapamycin-based therapies might be more effective in breast cancers with acquired oestrogen resistance. Keywords Akt, breast cancer cells, endocrine resistance, insulin, MAPK, MCF-7 cells, mTOR, oestrogen, oestrogen-deprived, PI3K, picropodophyllin, rapamycin, T-47-D cells, ZR-75-1 cells
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Hippocampal CA1 pyramidal neurons are highly sensitive to ischemic damage, whereas neighboring CA3 pyramidal neurons are less susceptible. It is proposed that switching of AMPA receptor (AMPAR) subunits on CA1 neurons during an in vitro model of ischemia, oxygen/glucose deprivation (OGD), leads to an enhanced permeability of AMPARs to Ca2+, resulting in delayed cell death. However, it is unclear whether the same mechanisms exist in CA3 neurons and whether this underlies the differential sensitivity to ischemia. Here, we investigated the consequences of OGD for AMPAR function in CA3 neurons using electrophysiological recordings in rat hippocampal slices. Following a 15 min OGD protocol, a substantial depression of AMPAR-mediated synaptic transmission was observed at CA3 associational/commissural and mossy fiber synapses but not CA1 Schaffer collateral synapses. The depression of synaptic transmission following OGD was prevented by metabotropic glutamate receptor 1 (mGluR1) or A3 receptor antagonists, indicating a role for both glutamate and adenosine release. Inhibition of PLC, PKC, or chelation of intracellular Ca2+ also prevented the depression of synaptic transmission. Inclusion of peptides to interrupt the interaction between GluA2 and PICK1 or dynamin and amphiphysin prevented the depression of transmission, suggesting a dynamin and PICK1-dependent internalization of AMPARs after OGD. We also show that a reduction in surface and total AMPAR protein levels after OGD was prevented by mGluR1 or A3 receptor antagonists, indicating that AMPARs are degraded following internalization. Thus, we describe a novel mechanism for the removal of AMPARs in CA3 pyramidal neurons following OGD that has the potential to reduce excitotoxicity and promote neuroprotection
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Escherichia coli O157: H7 and Cryptosporidium parvum infections of man have been associated with direct contact with small ruminants. Colostrum protects neonates against gastrointestinal pathogens, and orphan lambs, which are common on petting farms, may be deprived of this protection. In a recent study, it was demonstrated that high shedding of E coli O157 : H7 by an 8-week-old goat kid was associated with coincidental C. parvum infection. Furthermore, both pathogens were co-located in the distal gastrointestinal tract. It was hypothesized that colostrum deprivation and pre-infection with C. parvum predisposed young ruminants to colonization and increased shedding of E coli O157: H7. To test this, 21 lambs 5 weeks of age were divided into four groups as follows: (A) colostrum-deprived and inoculated with E coli O157: H7, (B) colostrum-deprived and inoculated with C. parvum and then E coli O157: H7, (C) conventionally reared and inoculated with E coli O157: H7, (D) conventionally reared and inoculated with C. parvum and then E coli O15 7: H7. C. parvum was detected between 8 and 12 days post-inoculation in most of the infected lambs. At 24 h post-inoculation with E coli O157: H7, all lambs were shedding between 5 x 10(4) and 5 x 10(7) c.f.u. E coli O157: H7 per gram of faeces. E coli O157: H7 was shed in higher numbers in the groups pre-inoculated with C. parvum, whether conventionally reared or colostrum-deprived. Interestingly, for the colostrum-deprived lambs on day 3, a significant difference in shedding of E coli O157: H7 was observed (P= 0-038), with the lambs inoculated with E coli alone yielding higher counts than those pre-inoculated with C. parvum. From day 15 onwards, shedding of E coli O157: H7 was highest from the colostrum-deprived C. parvum-infected lambs, then (in descending order of shedding) the colostrum-deprived lambs, the conventionally reared lambs infected with C. parvum, and the conventionally reared animals. In total, four animals were euthanized, two at 24 h and two at 96 h post inoculation with E coli 0 157: H7 (two conventionally reared and two colostrum-deprived). All animals euthanized were from groups pre-inoculated with C. parvum prior to challenge with E coli O157 : H7. On examination of tissues, in three of the four animals examined, multifocal attaching and effacing lesions were observed in the caecum, colon, rectum and at the recto-anal junction, and were confirmed by immunolhistochemistry to be associated with E coli O157: H7.
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Study Objectives: Chronic sleep deprivation of rats causes hyperphagia without body weight gain. Sleep deprivation hyperphagia is prompted by changes in pathways governing food intake; hyperphagia may be adaptive to sleep deprivation hypermetabolism. A recent paper suggested that sleep deprivation might inhibit ability of rats to increase food intake and that hyperphagia may be an artifact of uncorrected chow spillage. To resolve this, a palatable liquid diet (Ensure) was used where spillage is insignificant. Design: Sleep deprivation of male Sprague Dawley rats was enforced for 10 days by the flowerpot/platform paradigm. Daily food intake and body weight were measured. On day 10, rats were transcardially perfused for analysis of hypothalamic mRNA expression of the orexigen, neuropeptide Y (NPY). Setting: Morgan State University, sleep deprivation and transcardial perfusion; University of Maryland, NPY in situ hybridization and analysis. Measurements and Results: Using a liquid diet for accurate daily measurements, there was no change in food intake in the first 5 days of sleep deprivation. Importantly, from days 6-10 it increased significantly, peaking at 29% above baseline. Control rats steadily gained weight but sleep-deprived rats did not. Hypothalamic NPY mRNA levels were positively correlated to stimulation of food intake and negatively correlated with changes in body weight. Conclusion: Sleep deprivation hyperphagia may not be apparent over the short term (i.e., <= 5 days), but when extended beyond 6 days, it is readily observed. The timing of changes in body weight and food intake suggests that the negative energy balance induced by sleep deprivation prompts the neural changes that evoke hyperphagia.
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This research has resulted of investigations appeared from our work experience as psychologist in a prison of the state Rio Grande do Norte. It deals with the meeting with prisoner in the search for the rescue of the human being dignity, discovering the being that finds annulled by backwards of the prison. The current debate on the prisoners in Brazil has as focus the creation of efficient strategies in the combat to the criminal acts, not being worried in understanding the historical and social conditions in the context in which such acts develop. Our objective was to reach an understanding of the experience of the prisoner in the situation of freedom deprivation in Natal (RN) city. Its significant social relevance meets in emphasized thematic which intends to be revealing of the not-said one of these citizens. The epistemological space and the vision of adopted human being support in the humanist ideas of the Centered Approach in the Person and construct self, central nucleus of the personality theory proposal by Carl Rogers. We opt to the phenomenological method as way of access to the singularity of the experience of each one of the participants, supporting us in the strategy of the narrative as expression of the lived world. The results had pointed that the investigated experience is through suffering, that is, the way to be in the world of prisoner in the situation of freedom deprivation is felt by him/her as difficult to support. This reality is had by him/her as difficult to control, having a negative emotional repercussion for the self, leading the citizen to the alienation of his/her existential flow in these circumstances. The reflections produced in this work take us to consider that the punishment practices on behalf of a normalization of the behavior, linked to the recovery idea, do not meet to the intention of the arrests, that come demonstrating to the inefficacy of the objectives shown in the law as well as the loss of the human being dignity
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The objective of this study was to compare the effects of 24-h road transport or 24-h feed and water deprivation on acute-phase and performance responses of feeder cattle. Angus x Hereford steers (n = 30) and heifers (n = 15) were ranked by gender and BW (217 +/- 3 kg initial BW; 185 +/- 2 d initial age) and randomly assigned to 15 pens on d -12 of the experiment (3 animals/pen; 2 steers and 1 heifer). Cattle were fed alfalfa-grass hay ad libitum and 2.3 kg/animal daily (DM basis) of a corn-based concentrate throughout the experiment (d -12 to 28). on d 0, pens were randomly assigned to 1 of 3 treatments: 1) transport for 24 h in a livestock trailer for 1,200 km (TRANS), 2) no transport but feed and water deprivation for 24 h (REST), or 3) no transport and full access to feed and water (CON). Treatments were concurrently applied from d 0 to d 1. Total DMI was evaluated daily from d -12 to d 28. Full BW was recorded before treatment application (d -1 and 0) and at the end of experiment (d 28 and 29). Blood samples were collected on d 0, 1, 4, 7, 10, 14, 21, and 28. Mean ADG was greater (P < 0.01) in CON vs. TRANS and REST cattle but similar (P = 0.46) between TRANS and REST cattle (1.27, 0.91, and 0.97 kg/d, respectively; SEM = 0.05). No treatment effects were detected for DMI (P >= 0.25), but CON had greater G: F vs. TRANS (P < 0.01) and REST cattle (P = 0.08) whereas G: F was similar (P = 0.21) between TRANS and REST cattle. Plasma cortisol concentrations were greater (P <= 0.05) in REST vs. CON and TRANS cattle on d 1, 7, 14, and 28 and also greater (P = 0.02) in TRANS vs. CON cattle on d 1. Serum NEFA concentrations were greater (P < 0.01) in REST and TRANS vs. CON cattle on d 1 and greater (P < 0.01) in REST vs. TRANS cattle on d 1. Plasma ceruloplasmin concentrations were greater (P = 0.04) in TRANS vs. CON cattle on d 1, greater (P = 0.05) in REST vs. CON on d 4, and greater (P <= 0.05) in REST vs. TRANS and CON on d 14. Plasma haptoglobin concentrations were greater (P < 0.01) in TRANS vs. CON and REST cattle on d 1 and greater (P <= 0.05) for REST vs. TRANS and CON cattle on d 7. In conclusion, 24-h transport and 24-h nutrient deprivation elicited acute-phase protein reactions and similarly reduced feedlot receiving performance of feeder cattle. These results suggest that feed and water deprivation are major contributors to the acute-phase response and reduced feedlot receiving performance detected in feeder cattle transported for long distances.
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Adult rats deprived of water for 24-30 h were allowed to rehydrate by ingesting only water for 1-2 h. Rats were then given access to both water and 1.8% NaCl. This procedure induced a sodium appetite defined by the operational criteria of a significant increase in 1.8% NaCl intake (3.8 +/- 0.8 ml/2 h; n = 6). Expression of Fos (as assessed by immunohistochemistry) was increased in the organum vasculosum of the lamina terminalis (OVLT), median preoptic nucleus (MnPO), subfornical organ (SFO), and supraoptic nucleus (SON) after water deprivation. After rehydration with water but before consumption of 1.8% NaCl, Fos expression in the SON disappeared and was partially reduced in the OVLT and MnPO. However, Fos expression did not change in the SFO. Water deprivation also 1) increased plasma renin activity (PRA), osmolality, and plasma Na+; 2) decreased blood volume; and 3) reduced total body Na+; but 4) did not alter arterial blood pressure. Rehydration with water alone caused only plasma osmolality and plasma Na+ concentration to revert to euhydrated levels. The changes in Fos expression and PRA are consistent with a proposed role for ANG II in the control of the sodium appetite produced by water deprivation followed by rehydration with only water.
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Fundação de Amparo à Pesquisa do Estado de São Paulo (FAPESP)
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Water deprivation-induced thirst is explained by the double-depletion hypothesis, which predicts that dehydration of the two major body fluid compartments, the extracellular and intracellular compartments, activates signals that combine centrally to induce water intake. However, sodium appetite is also elicited by water deprivation. In this brief review, we stress the importance of the water-depletion and partial extracellular fluid-repletion protocol which permits the distinction between sodium appetite and thirst. Consistent enhancement or a de novo production of sodium intake induced by deactivation of inhibitory nuclei (e.g., lateral parabrachial nucleus) or hormones (oxytocin, atrial natriuretic peptide), in water-deprived, extracellular-dehydrated or, contrary to tradition, intracellular-dehydrated rats, suggests that sodium appetite and thirst share more mechanisms than previously thought. Water deprivation has physiological and health effects in humans that might be related to the salt craving shown by our species.