Academic literature on the topic 'Deprivation'

The paper presents the results of an empirical study of prison deprivations suffered by women, conducted at the Female Department of Correctional Facility in Pozarevac within the scope of a wider study of women's prison system. It was supposed that female prisoners in this penal institution face similar prison experience and suffer the same or similar deprivations as women in other penal institutions do. The research sample included female prisoners sentenced to more than one year, staying in prison for more than a year (54 female prisoners, i.e. more than 50% prisoners sentenced to long prison terms). Prisoners were interviewed employing a questionnaire measuring different types of deprivations using 26 indicators. Using the method of factor analysis - which was here used for the first time to study prison deprivations - six factors of women's prison deprivations were extracted: deprivation of maternity; deprivation of autonomy; deprivation of individuality; deprivation of human kindness and empathy; deprivation of a key role - a woman's role, and deprivation of friendship relations. The outcomes of this research, together with the findings of other researchers, affirm the assumption that these types of deprivations are realistic and dominant types of women's prison deprivations.

The study applies the counting approach to explain the deprivation concept among children under 5 years of age using the 2008 DHS data. Five dimensions of deprivation were used: safe drinking water, sanitation, housing, health, and nutrition largely recognized in the SDGs. In all, a total of 13561 children were sampled. About half of the children were males with a mean age of 28.27 months old. The assessment of dimensional deprivation showed that children are most deprived in sanitation, health, and access to safe drinking water while they were least deprived in nutrition. The situation is also marked with regional disparities with northern regions reporting higher deprivation rates than the southern regions but this rate was significantly higher in the sanitation dimension across regions. Considering deprivation counts, 33.9% of children suffer from more than three deprivations and approximately 85.2% from at least two deprivations. Child deprivation should be tackled using a holistic approach through social protection programmes to resolve children’s problems in an integrated manner which would in this case be more efficient and effective in safeguarding children’s rights to survival and development. Identifying the children suffering from single and multiple deprivations can help to target the interventions.

The article reveals political protest as one of the major factors of political system development in society. In particular, possibilities of methodological synthesis, deprivation theory in terms of political protest development are considered. Deprivation phenomenon's psychological nature is stressed. Distinc-tions between relative deprivation and absolute one are considered. The authors prove the deprivation's influence on mobilization of protest movements providing examples. The relative deprivation's classifica¬tion including progressive, aspirational and decremental deprivation is used. The relative deprivation theory refers to the ideas that frustration and feelings of discontent de¬pend on purposes of a person or a group of people. Relative deprivation feelings emerge when important tagets of people tunr out to be unreal or blocked by political elites or society. As the central concept in the explanation of protest movements relative deprivation is often considered as well as the central concept in when explaining protest movements also it is used to describe and give understanding to the factors that trigger social movements. Protest activity appears from relative deprivation collective feelings. Absolute deprivation is a key factor of protest movements in poor countries, unlike relative deprivation.

A dominant conception of poverty among many researchers is that it is a form of deprivation. There is, however, more focus on the idea of poverty as physical deprivation than there is on psychological deprivation. I argue that poverty is as much a psychological deprivation as it is a physical deprivation and propose a new index that explicitly takes the psychological into account in poverty measurement. I show that most extant literature tends to focus more on physical deprivations which poverty causes. I discuss some poverty indices which are employed to measure levels of poverty and highlight their inadequacy. Employing the conversational method, I tap into Odera Oruka’s ideas to offer the Human Minimum Measure (HMM) as a model that might also be desirable if the reality of psychological deprivation is taken seriously.

This essay presents a critical review of the recent book by Alkire et al. entitled Multidimensional Poverty Measurement and Analysis, and, in the course of doing so, it also discusses some general issues that come up in this context. We outline the basic structure of the problem of measuring multidimensional deprivation and critically evaluate the methodology adopted by Alkire et al. (2015). In particular, we discuss some problems associated with the methods used by them to identify the deprived and to aggregate individual deprivations so as to derive an index of social deprivation. We examine the interpretation in terms of unfreedoms of individuals, which Alkire et al. put on one of their measures of social deprivation. We also suggest a variant of their methodology for measuring multidimensional deprivation.( JEL C38, E02, I32, Z13)

Abstract Objective. The aim of the present investigation was to study the impact of glucose and gluta-mine deprivations on the expression of genes encoding EDN1 (endothelin-1), its cognate receptors (EDNRA and EDNRB), and ECE1 (endothelin converting enzyme 1) in U87 glioma cells in response to knockdown of ERN1 (endoplasmic reticulum to nucleus signaling 1), a major signaling pathway of endoplasmic reticulum stress, for evaluation of their possible implication in the control of glioma growth through ERN1 and nutrient limitations. Methods. The expression level of EDN1, its receptors and converting enzyme 1 in control U87 glioma cells and cells with knockdown of ERN1 treated by glucose or glutamine deprivation by quantitative polymerase chain reaction was studied. Results. We showed that the expression level of EDN1 and ECE1 genes was significantly up-regulated in control U87 glioma cells exposure under glucose deprivation condition in comparison with the glioma cells, growing in regular glucose containing medium. We also observed up-regulation of ECE1 gene expression in U87 glioma cells exposure under glutamine deprivation as well as down-regulation of the expression of EDN1 and EDNRA mRNA, being more significant for EDN1. Furthermore, the knockdown of ERN1 signaling enzyme function significantly modified the response of most studied gene expressions to glucose and glutamine deprivation conditions. Thus, the ERN1 knockdown led to a strong suppression of EDN1 gene expression under glucose deprivation, but did not change the effect of glutamine deprivation on its expression. At the same time, the knockdown of ERN1 signaling introduced the sensitivity of EDNRB gene to both glucose and glutamine deprivations as well as completely removed the impact of glucose deprivation on the expression of ECE1 gene. Conclusions. The results of this study demonstrated that the expression of endothelin-1, its receptors, and ECE1 genes is preferentially sensitive to glucose and glutamine deprivations in gene specific manner and that knockdown of ERN1 significantly modified the expression of EDN1, EDNRB, and ECE1 genes in U87 glioma cells. It is possible that the observed changes in the expression of studied genes under nutrient deprivation may contribute to the suppressive effect of ERN1 knockdown on glioma cell proliferation and invasiveness.

In small, underdeveloped Chinese cities, the travel needs of economically disadvantaged residents have not been satisfactorily met for a long time, and thus, the problem of travel inequality has become increasingly serious. This study developed and applied a fuzzy multidimensional assessment approach of travel deprivation to assess the travel deprivations that arise because of this travel inequity. The resulting model includes both monetary and nonmonetary indicators, and involves multiple measurement items, dimensions, and related weights. Then, this fuzzy multidimensional assessment approach of travel deprivation is used to measure the travel deprivation in the underdeveloped, small city of Lhasa, China. The results identified both differences and similarities between different parts of the city. Among all measured dimensions, the following four dimensions cause strong travel deprivation: disposable income, travel service quality, travel time, and available transportation. Differences in the travel deprivation were identified between different parts of Lhasa, indicating multidimensional travel deprivation. Furthermore, an early warning analysis on travel deprivation and an assessment of different levels of residents’ travel deprivation in underdeveloped cities are presented. These findings provide an effective evaluation of the current situation of travel inequity in underdeveloped small cities.

ABSTRACT Plasma samples obtained at 4-h intervals from goats for at least 24 h before and then during 24 h of deprivation of water were analysed by radioimmunoassay for vasopressin and oxytocin concentrations. The samples were also analysed for osmolality and sodium concentration. The differential effect of night/day versus day/night deprivation was also studied. During the two periods before the two deprivations osmolality varied in a regular manner, with low values occurring at 08.00 h. Sodium concentration followed osmolality, whereas vasopressin did not vary during the period before deprivation. During deprivation vasopressin increased along with osmolality and sodium concentration, with the beginning of the increase occurring after the morning feed. Oxytocin levels did not increase during the period of deprivation. These results do not support the hypothesis of general release of neurohypophysial hormones in response to osmotic stimuli but instead indicate there are species variations with respect to hormonal response to water deprivation. J. Endocr. (1986) 110, 335–340

During specific rapid eye movement (REM) sleep deprivation its homeostatic regulation is expressed by progressively more frequent attempts to enter REM and by a compensatory rebound after the deprivation ends. The buildup of pressure to enter REM may be hypothesized to depend just on the time elapsed without REM or to be differentially related to non-REM (NREM) and wakefulness. This problem bears direct implications on the issue of the function of REM and its relation to NREM. We compared three protocols that combined REM-specific and total sleep deprivation so that animals underwent similar 3-h REM deprivations but different concomitant NREM deprivations for the first 2 (2T1R), 1 (1T2R), or 0 (3R) hours. Deprivation periods started at hour 6 after lights on. Twenty-two chronically implanted rats were recorded. The median amount of REM during all three protocols was ∼1 min. The deficits of median amount of NREM in minutes within the 3-h deprivation periods as compared with their baselines were, respectively for 2T1R, 1T2R, and 3R, 35 (43%), 25 (25%), and 7 (7%). Medians of REM rebound in the three succeeding hours, in minutes above baseline, were, respectively, 8 (44%), 9 (53%), and 9 (50%), showing no significant differences among protocols. Attempted transitions to REM showed a rising trend during REM deprivations reaching a final value that did not differ significantly among the three protocols. These results support the hypothesis that the build up of REM pressure and its subsequent rebound is primarily related to REM absence independent of the presence of NREM.

Background: The capability approach conceptualizes poverty as capability deprivation. Given that functionings and opportunities as key factors are diverse, the combination of a varied lack of functionings and opportunities will lead to different deprivation patterns. Therefore, we sought to investigate the association between the category of capacity deprivation and the subjective acquisition of rural households. Methods: Data were collected from the micro survey of 892 households in six provinces. The overall sense of acquisition was measured by self-assessment of life satisfaction and the relative sense of gain was measured by self-assessment of social status and communication confidence. Capability deprivation was assessed through evaluation functionings and opportunities for a better life, such as education, social security, medical and health services, living conditions and spiritual and cultural activities. The factor mixture models were used to investigate the group categories of capability deprivation and ordered probit regression was used to estimate the associations between the categories of capability deprivation and sense of gain. Results: There were mild, moderate and severe differences among the deprivation items reflecting functionings and opportunities. In addition, capability deprivation was grouped into four classes: double deprivation of functionings and opportunities, severe deprivation of opportunities, functionings deprivation and non-poverty. There was a significant negative relationship between deprivation classes and the subjective sense of gain. Conclusion: The deprivation from some social participation functions and services led to a reduced sense of acquisition. However, serious deprivations from educational opportunities and social participation opportunities were the main reason for the lower sense of gain. Eliminating the unequal educational opportunities and social participation opportunities for people is imperative to improving the subjective sense of gain.

This thesis is concerned with rights-based justifications for redistribution. Orthodox views are critically examined in three of the chapters. The case against fundamental moral rights to welfare, not derived from other more fundamental moral rights or principles, is pressed in chapter three. Chapter five distinguishes between rights-based and equality-based justifications for redistribution and argues that Ronald Dworkin's idea of a right to equal respect and concern is best understood as an equality-based justification. The enabling model of rights and deprivation is introduced in chapter six. This model says that liberty rights require that others ensure that the right-holder enjoys the means to do what he or she has the right to do as well as not interfere with him or her doing what he or she has the right to do. It is found to break down because it is unable to accommodate the right to do wrong. The other four chapters are concerned with defending an alternative model of rights and deprivation. The groundwork for this alternative model - the development model of rights and deprivation - is laid in chapters two and four. Chapter two presents a person-affecting theory of rights. The two principal conclusions of the development model of rights and deprivation are defended in chapter seven. It is argued, first, that from both of the abstract moral rights to liberty introduced in chapter four flow certain derivative rights against others to have one's needs met and, second, that the state is required to promote and protect particular forms of culture as well as to meet certain sorts of personal needs including special needs, collective needs, and the unmet personal needs that arise when the prevailing methods of meeting those needs breaks down. The final chapter discusses two general issues relating to the development model of rights and deprivation.

1- ROLE OF SIRT1 IN THE REGULATION OF FATTY ACID OXIDATION AND KETOGENESIS UNDER DIFFERENT NUTRIONAL CHANGES. The homolog of the yeast silencing information regulator2 (SIRT1) has been implicated in several aspects of food limitation and caloric restriction in mammals. We have observed that there were no important changes, between wild type (WT) and SIRT1 liver-specific knockout (LKO) mice subjected to either CR or high fat diet (HFD), in the mRNA expression of Cpt1a, Cpt2 and Hmgcs2. SIRT1 had been shown to control hepatic glyconeogenic/glycolytic pathways in response to nutrients (Rodgers et al., 2005). So, we have hypothesized that SIRT1 could have a role in the metabolic adaptation to the changes of nutrient of weaning, when milk is replaced by the adult diet which contains less fat and more carbohydrate. Neither fatty acid oxidation (Cpt1a), ketogenesis (Hmgcs2), nor gluconeogenic (Pck1) liver pathways were significantly affected by the liver-specific knockdown of SIRT1, in both suckling and post-weaning conditions. If SIRT1 is involved in the response to aging, old LKO mice might be more susceptible to age-associated diseases as obesity, type 2 diabetes, hypertension, etc. To test this hypothesis we first weight and performed a glucose tolerance test in 7 months-old mice. There were no differences in weight neither in glucose tolerance between WT and LKO mice. Using a cell system, PPARα induced the expression of its known target genes CPT1A, HMGCS2, and FGF21 in HepG2 cells. SIRT1 overexpression by itself had almost no effect, although it increased PPARα induction of its target genes. We have interfered SIRT1 in these cells, and PPARα-induced expression of PEPCK and FGF21 was SIRT1-dependent. We have fasted WT and LKO mice for 15h and we found that the expression of Pck1 in liver was moderately but significantly induced in SIRT1-LKO mice after fasting, consistent with an increase in glucose levels. However, neither G6pase nor Pgc1α mRNA levels were affected. As expected, liver mRNA levels of Cpt1a, Hmgcs2, and Fgf21 were also induced upon fasting. However, Cpt1a and Hmgcs2 mRNA transcripts were comparable in fasted WT versus LKO mice, while Fgf21 expression was reduced around 40% in LKO mice liver. This result was consistent with the fact that fasting induction of FGF21 serum levels was also impaired in LKO mice. 2- ROLE OF SIRT1 IN THE HMGCS2 REGULATION OF FGF21 EXPRESSION. (Article 1: Human HMGCS2 regulates fatty acid oxidation and FGF21 expression in HepG2 cells. Vilà-Brau et al., 2011) Recently, our group has seen that HMGCS2 expression stimulates FGF21 expression and that these events are dependent on HMGCS2 activity. A catalytic dead mutant (C166A) failed to induce either fatty acid β-oxidation or FGF21 expression, whereas acetoacetate (an oxidized form of ketone bodies) could stimulate FGF21 mRNA expression in a dose-dependent manner. Because ketone bodies production implies the reduction of acetoacetate to β- hydroxybutyrate with the concomitant generation of NAD+ (Hegardt et al, 1999), and SIRT1 is a NAD+-dependent deacetylase enzyme, this specificity could explain why FGF21 fasting induction was affected in LKO-SIRT1 mice liver, while other PPARα target genes were not. We have treated HepG2 cells with the oxidizing (acetoacetate) partner of ketone bodies, and endogenous SIRT1 was knockdown by a specific siRNA. FGF21 induction was dependent on SIRT1 expression, since knocking down impaired acetoacetate response. 3- ACTIVATING TRANSCRIPTION FACTOR 4-DEPENDENT INDUCTION OF FGF21 DURING AMINO ACID DEPRIVTION (Article 2: De Sousa-Coelho et al., 2012) Considering the central role of PPARα in the regulation of metabolic homeostasis we sought to investigate how the turnover of PPARα affected the expression of its target genes. HepG2 cells were infected with PPARα and exposed to DMSO or to the 26S proteasome inhibitor MG132. As expected, MG132-treatment blocked the PPARα-dependent expression of HMGCS2, indicating that the transcriptional activity of PPARα is increased by protein degradation (Blanquart et al, 2004). Contrary to what we had predicted, the expression of FGF21 was strongly increased by the MG132 treatment. We hypothesized that proteasome inhibition in HepG2 could decrease the pool of free amino acids. We treated HepG2 cells with histidinol (HisOH) a potent and reversible inhibitor of protein synthesis, (Hansen et al, 1972). Amino acid deprivation produced a time-dependent induction of FGF21 mRNA. To test whether this induction was due to an increase in the FGF21 gene transcription, we measured the FGF21 primary transcript (hnRNA) levels; HisOH treatment clearly induced FGF21 hnRNA levels in a time-dependent manner. As expected, HisOH induced an increase in the ATF4 protein levels after 2h treatment. By analyzing the sequence of the 5’-flanking region of the human FGF21 gene, we found two putative ATF4 response elements (AARE) starting at positions -152 and -610 upstream of the transcription start site. HepG2 cells were transfected with pGL3b-hFGF21 promoter-luciferase constructs and an expression vector for human ATF4. The expression of ATF4 induced the WT reporter in a concentration dependent manner. This induction was totally obliterated either when the AARE1 was mutated or when both elements were deleted. Induction was diminished when AARE2 was mutated. To further analyze the functionality of this sequence we tested the binding of ATF4 by an EMSA, where ATF4 bound as a C/EBPβ heterodimer to both AARE sequence elements. We also confirmed the in vivo binding by ChIP experiments. The chromatin binding of ATF4 was greatly increased in both ATF4 responsive sequences in HisOH treated cells. To confirm if the induction of FGF21 produced by amino acid starvation was mediated by ATF4, we treated siCtl and siATF4 HepG2 cells with HisOH. FGF21 mRNA levels after HisOH treatment were significantly lower when ATF4 was depleted. To analyze the effect of amino acid deprivation on FGF21 expression in vivo, we fed mice with a leucine-deficient [(-)leu] diet or a control (Ctl, nutrionally complete) diet for 7 days. Fgf21 mRNA levels were greatly increased in liver from mice fed a (-)leu diet compared to control. The circulating FGF21 levels were also increased in the serum of leucine deprived animals, paralleling hepatic gene expression. 4- LEUCINE DEPRIVATION SIGNALING UNDER FASTING CONDITIONS. We were interested to know whether FGF21 induction by a (-)leu diet would affect, or be affected by, the adaptive fasting response. We have fed mice for 7 days within a Ctl or (-)leu diet. Weights and food intake were recorded daily. Then, mice were randomly separated in a total of 4 groups, where 2 groups (one from each diet) were fasted overnight. Leucine deprivation affected the levels of free fatty acids and ketone bodies in serum in the fed state, while it does not upon fasting. Although no changes between groups were observed in the fed state, after fasting the β-oxidation, ketogenesis and gluconeogenesis keygenes were further up-regulated in the (-)leu diet group compared to control. The highest induction was seen in the Pgc1α gene, a known coactivator on these processes. The fasting activation of FGF21 was impaired in mice fed with (-)leu diet, underlying a crosstalk between the fasting and amino acid deprivation signalling. 5- ROLE OF FGF21 IN THE LEUCINE DEPRIVATION PHENOTYPE IN MICE (Article 3: De Sousa-Coelho et al., in preparation). According with our previously reported results (De Sousa-Coelho et al., 2012) mice maintained on a leucine-deficient [(-)leu] diet show a dramatic increase in FGF21 circulating levels. To check its origin we analyzed the Fgf21 gene expression in liver, where Fgf21 mRNA levels paralleled those in serum; brown adipose tissue (BAT), where it were unchanged; and in epididymal white adipose tissue (eWAT), where unexpectedly it were significantly decreased in wild type mice maintained in (-)leu diet. Because upon (-)leu diet, mice undergo rapid weight loss (Cheng et al., 2010), we wanted to investigate whether this phenotype is FGF21-dependent. For this purpose, WT and FGF21-KO mice were fed a Ctl or (-)leu diet for 7 days. Weight loss was diminished in FGF21-KO, while food intake decrease by (-)leu was unchanged between genotypes. Histological analysis of WAT showed that leucine deprivation resulted in a reduction in adipocyte volume compared with mice fed a control diet, while it was only slightly reduced in (-)leu FGF21-KO mice. It has been previously described that leucine deprivation increases lipolysis in WAT (Cheng et al., 2010). Consistent with changes in body weight, lack of FGF21 significantly decreased levels of phosphorylated (P)-HSL in WAT, indicating an impaired lipolysis. Gene expression analysis revealed reduction in the mRNA levels of the lipogenic genes Fas, Srebp1c and Acc1 in the WAT of mice maintained in (-)leu diet. These changes were impaired in FGF21-KO. Consistent with previous results (Cheng et al., 2010), leucine deprivation increased levels of Ucp1 mRNA in WT mice BAT. This increase was not observed in the FGF21-KO mice. mRNA levels of Pgc1α, which regulates the expression of Ucp1 (Handschin and Spiegelman, 2006), were also increased, although did not differ between WT and FGF21-KO mice under either control or (-)leu diet conditions. It has been recently proposed a link between FGF21 and SREBP1c during lipogenesis in HepG2 cells (Zhang et al., 2011). We examined levels of Fas, Srebp1c and Acc1 mRNA in liver of WT and FGF21-KO. As expected (Guo and Cavener, 2007), lipogenic program was decreased upon (-)leu diet, but this reduction was blocked in FGF21-KO mice. However, the amino acid response program was correctly initiated in these mice as shown by the increased levels of ATF4 protein and the increase in mRNA levels of Asns, a prototypical ATF4 target gene. The liver staining showed a decreased lipid accumulation under (-)leu in WT animals that is not produced in the FGF21-KO mice. These results demonstrate an important role of FGF21 in the regulation of lipid metabolism during amino acid starvation. References: Blanquart C, Mansouri R, Fruchart JC, Staels B, & Glineur C (2004) Different ways to regulate the PPARalpha stability. Biochem Biophys Res Commun 319, 663-70. Cheng, Y., Meng, Q., Wang, C., Li, H., Huang, Z., Chen, S., Xiao, F., and Guo, F. (2010). Leucine deprivation decreases fat mass by stimulation of lipolysis in white adipose tissue and upregulation of uncoupling protein 1 (UCP1) in brown adipose tissue. Diabetes 59, 17-25. Guo, F., and Cavener, D.R. (2007). The GCN2 eIF2alpha kinase regulates fatty-acid homeostasis in the liver during deprivation of an essential amino acid. Cell Metab 5, 103-14. Handschin, C., and Spiegelman, B.M. (2006). Peroxisome proliferator-activated receptor gamma coactivator 1 coactivators, energy homeostasis, and metabolism. Endocr Rev 27, 728-735. Hansen BS, Vaughan MH, & Wang L (1972) Reversible inhibition by histidinol of protein synthesis in human cells at the activation of histidine. J Biol Chem 247, 3854-3857. Hegardt FG (1999) Mitochondrial 3-hydroxy-3-methylglutaryl-CoA synthase: a control enzyme in ketogenesis. Biochem J. 338, 569-582. Hotta, Y., Nakamura, H., Konishi, M., Murata, Y., Takagi, H., Matsumura, S., Inoue, K., Fushiki, T., and Itoh, N. (2009). Fibroblast growth factor 21 regulates lipolysis in white adipose tissue but is not required for ketogenesis and triglyceride clearance in liver. Endocrinology 150, 4625-4633. Rodgers JT, Lerin C, Haas W, Gygi SP, Spiegelman BM, Puigserver P (2005) Nutrient control of glucose homeostasis through a complex of PGC-1alpha and SIRT1. Nature 434, 113-8 Zhang, Y., Lei, T., Huang, J.F., Wang, S.B., Zhou, L.L., Yang, Z.Q., and Chen, X.D. (2011). The link between fibroblast growth factor 21 and sterol regulatory element binding protein 1c during lipogenesis in hepatocytes. Mol Cell Endocrinol 342, 41-47.
Durante su vida un individuo se somete a diversos cambios nutricionales. La capacidad de detectar la disponibilidad de nutrientes y regular la homeostasis energética es un proceso fundamental. SIRT1 es un regulador clave en el metabolismo energético. SIRT1 puede modular la expresión génica en tejidos metabólicamente activos en respuesta a la restricción calórica o el ayuno. La dependencia de la actividad deacetilasa de SIRT1 en los niveles de NAD+ constituye un vínculo fundamental entre el estado metabólico celular y la regulación de genes. FGF21 es una hormona que se induce en el ayuno y que afecta al metabolismo de los carbohidratos y de los lípidos. Recientemente se han demostrado sus efectos benéficos en la protección de la obesidad inducida por la dieta y en la mejoría en la resistencia a la insulina. En este trabajo hemos demostrado que en células hepáticas en cultivo, SIRT1 desempeña un papel importante en la activación por PPARα de la expresión de FGF21, CPT1A, HMGCS2, y PEPCK. También, que la actividad de SIRT1 regula los niveles de glicemia y la expresión de PCK1 en hígado, en la respuesta al ayuno. Aún así, hemos visto que la actividad de SIRT1 no afecta la expresión de los genes de la oxidación de los ácidos grasos o la cetogénesis en el hígado, en respuesta a diferentes cambios nutricionales, como la restricción calórica, la transición de la lactancia/destete, y el ayuno. Adicionalmente, hemos demostrado que la activación de FGF21 por SIRT1 depende de la actividad HMGCS2. También hemos descrito que FGF21 se induce por la privación de aminoácidos, de manera dependiente de ATF4, y hemos identificado dos elementos de respuesta funcionales en la región promotora del gene humano, altamente conservados entre las especies. Además, hemos demostrado que FGF21 interviene en la regulación del metabolismo de los lípidos en el hígado y el tejido adiposo blanco, y de la termogénesis en el tejido adiposo marrón, durante la privación de aminoácidos. De todas formas, hemos visto que la privación de leucina afecta a los niveles de ácidos grasos libres y cuerpos cetónicos en suero en el estado de alimentación, mientras que no lo hace en el ayuno; y la activación de FGF21 en el ayuno está afectada en los ratones alimentados con esta dieta, desvelando un “crosstalk” entre la señalización del ayuno y la privación de aminoácidos.

Socioeconomic deprivation (SED) is inversely associated with mortality. The most deprived are at a higher risk of all cause mortality and cardiovascular mortality. However, only limited study of the relationship between SED and non-fatal cardiovascular disease has been previously undertaken. In those studies that have examined the relationship between SED and non-fatal cardiovascular disease, analyses have been limited to one form of cardiovascular disease (CVD), such as myocardial infarction or stroke and often prevalent disease. Furthermore, these studies have often failed to examine the association between SED and CVD whilst adjusting analyses for cardiovascular risk factors which are more prevalent in the most deprived. The aim of this work was to examine the association between SED and a number of cardiovascular outcomes after adjusting for the traditional cardiovascular risk factors of age, sex, smoking, blood pressure, diabetes mellitus and cholesterol. To determine is SED is in fact a risk factor for CVD after adjustment for these other risk factors, the relationship between SED and a number of fatal and non-fatal cardiovascular outcomes was examined. A number of forms of CVD were examined, including all coronary heart disease, myocardial infarction, stroke and heart failure A cohort of over 15,000 men and women who participated in the Renfrew Paisley cohort study was examined. These individuals were enrolled between 1974 and 1976 and underwent comprehensive screening for cardiorespiratory risk factors. They have since been followed for hospitalisations and deaths for 28 years. SED was measured using the Registrar General’s social class system and the Carstairs Morris index of deprivation. Rates of fatal and non-fatal outcomes were calculated, as were a number of composite outcomes. Adjusted analyses using multivariable regression were conducted to account for the risk factors of age, sex, smoking, blood pressure, diabetes and cholesterol. Further adjustment for the risk factors of lung function as measured by forced expiratory volume in 1 second, cardiomegaly on chest x-ray, body mass index, and a history of bronchitis was also made. The association between SED and the risk of recurrent cardiovascular hospitalisations, the burden of cardiovascular disease, as well as mortality and premature mortality was assessed for SED. I found that SED was associated with higher rates of hospitalisation for CVD disease in men and women irrespective of the measure of SED, either social class or the area based score of the Carstairs Morris index. This association persisted after adjustment for the traditional cardiovascular risk factors of age, sex, smoking, systolic blood pressure and diabetes and cholesterol. Further adjustment for lung function, the presence of bronchitis, body mass index and cardiomegaly on a chest x-ray did not explain the relationship between SED and each outcome. This risk was long lasting and persisted to the end of follow up. The strength of association of SED with coronary heart disease, myocardial infarction and stroke and all cause mortality was similar. The risk of a recurrent CVD hospitalisation was not higher in the most deprived after adjustment for CVD risk factors. However, I observed that SED was associated with higher mortality following an admission to hospital with CVD, before and after adjustment for cardiovascular risk factors of age, sex, smoking, systolic blood pressure, cholesterol and diabetes and after adjusting for the year of first developing cardiovascular disease. All cause mortality and cardiovascular mortality was highest in the most deprived. Again this association persisted after adjustment for cardiovascular risk factors. The most deprived also experienced longer hospital stays than the least deprived for a number of cardiovascular diseases including myocardial infarction and stroke. As a result the costs associated with cardiovascular disease admissions to hospital were highest in the most deprived despite their higher risk of dying during follow up. The cost differential was also explained by the finding that the most deprived experienced a higher number of admissions per person. Finally, the population attributable risk associated with SED is comparable to that of other traditional cardiovascular risk factors. In conclusion, I have found that the risk of CVD in the most deprived is higher even after adjustment for a number of cardiovascular risk factors. The numbers of hospitalisations, costs and mortality are also highest in the most deprived. Efforts are required to redress this imbalance. This can be achieved at the level of the individual through health care interventions to reduce the absolute burden of cardiovascular risk factors and to treat disease. However, societal level interventions are also required to tackle this problem as SED exerts complex effects on health that seem to also be independent of risk factors.

Mestrado em Econometria Aplicada e Previsão
O objetivo deste trabalho é identificar os determinantes socio-económicos e demográficos da Intensidade da Privação Matéria, e investigar as suas alterações quando se considera diferentes contextos macroeconómicos - crescimento moderado versus recessão (Economia Portuguesa, anos 2004 e 2012) e os grupos complementares - Economicamente Pobres e Não-Pobres. Este trabalho usa os 9 indicadores de Privação Material presentemente usados pelo Eurostat nos 27 Estados Membros da União Europeia para modelar o Score de Privação Material. Dado que a nossa variável de interesse é uma variável de contagem, vamos aplicar métodos para modelação de dados de contagem, nomeadamente, o modelo de Poisson e o modelo Zero-Inflated Poisson. Os resultados mostram quais são os principais determinantes da Intensidade da Privação Material, e que estes não variam, de forma significativa, face aos diferentes cenários macroeconómicos e grupos considerados.
The aim of this dissertation is to determine the socio-economic and demographic determinants of Material Deprivation Intensity, and investigate their changes when considering different macroeconomic backgrounds - moderate growth versus recession (Portuguese economy, years 2004 and 2012), and the additional groups - Income and Non-Income Poor. This work uses the 9 Material Deprivation indicators currently in use by Eurostat in the 27 European Union Member States to model the Material Deprivation Score. Given that the interest variable is a count variable, we will apply methodological framework for count data modeling, more particularly, Poisson and Zero-Inflated Poisson models. The results have shown what are the key determinants of the Material Deprivation Intensity, and also that they don?t change, in a significant way, in face of the considered macroeconomic backgrounds and groups.

My aim in this thesis is to examine whether there are some mitigating factors, i.e. reasons to punish an offender less for his crime than an otherwise similar offender (other than that the offender suffered from mental disorder or disturbance or other forms of irrationality at the time of offence), that are more applicable to socially deprived offenders than to non-socially deprived offenders. I will answer the thesis question through a critical examination of twelve arguments for claiming that there is a mitigating factor that is more applicable to socially deprived offenders, each proposing a different mitigating factor. My conclusions are as follows: (1) Most of the arguments that I examine fail, i.e. they either fail to highlight a genuine mitigating factor, or we do not have much evidence that the mitigating factor highlighted by the argument has a greater applicability to socially deprived offenders than to non-socially deprived offenders. (2) However, one argument, which can be called the no violation of natural duties argument, is successful. (3) Moreover, the improvement of the worst off argument, an argument that is not often discussed in the literature, is particularly noteworthy. If my discussion about that argument is correct, then even if, as I will argue, the mitigating factor highlighted by that argument may not be more applicable to socially deprived offenders than to non-socially deprived offenders, the remaining parts of that argument would still have profound influence on punishment in our unjust societies.

Synaptic connectivity is highly plastic in early development and undergoes extensive remodeling in response to changes in neuronal activity and sensory experience. Microglia, the resident central nervous system macrophages, participate in shaping mature neuronal circuits by dynamically surveying the brain parenchyma and pruning away less active synaptic connections. However, it is unknown how changes in neuronal activity regulates microglial pruning within circuits and whether this activity-dependent pruning is necessary to achieve plasticity. Using the rodent somatosensory circuit, I identified that microglia engulf and eliminate synapses in the cortex following early postnatal (P4) unilateral removal of mouse whiskers. I found this early life microglial synaptic remodeling requires specific chemokine signaling between neurons and microglia. Mice that lack expression of either the neuronal chemokine CX3CL1 (fractalkine), or its microglial receptor CX3CR1, have significantly reduced microglial synapse engulfment and fail to eliminate synapses following whisker removal. To gain more insight into how this signaling is regulated, I performed both single-cell RNA sequencing of the primary somatosensory cortex as well as microglia-specific Translating Ribosome Affinity Purification (TRAP) sequencing. I identified that the majority of central nervous system (CNS) cell populations in the somatosensory cortex, including microglia, undergo transcriptional changes following whisker removal. Further, the transcriptional changes in microglia after whisker cauterization require expression of the receptor CX3CR1. Importantly, I also found that Adam10, a gene encoding the metalloprotease known to post-translationally cleave CX3CL1 into a soluble chemokine, is upregulated in the deprived cortex after whisker ablation. Pharmacological inhibition of ADAM10 inhibits microglia-mediated removal of synapses in the deprived cortex. These data support a mechanism by which cleavage of membrane-bound CX3CL1 by ADAM10 is necessary for neuronal signaling to microglia via CX3CR1 to induce transcriptional changes within microglia upstream of synaptic engulfment and elimination following sensory deprivation.

Degradation of the retinal image for extended periods of time causes axial elongation and myopia ("deprivation myopia") in both animals and humans. In chickens, even little image degradation for short periods of time is sufficient to produce longer eyes and "deprivation myopia", given that no intermittant "normal" visual experience occurs. If chicks are kept in the dark for the remaining time, 3 hours of vision per day through frosted occluders is sufficient to produce deprivation myopia (Schwahn and Schaeffel, 1994). On the other hand, 30 minutes of intermittent normal vision reduce deprivation myopia down to 50% (e.g. Napper et al., 1995). There is plenty of evidence showing that the central pathways of accommodation have no major effect on induced refractive errors in animal models (e.g. Diether and Schaeffel, 1997), possibly with one exception (Wildsoet and Wallman, 1995). Therefore, in first approximation, one can restrict the analysis to a retinal mechanism.

This research examined whether socioeconomic status (SES) predicts reactions to situations in which a group member decides for the entire group, thereby depriving other group members of personal choice. We found, as predicted, that Americans with higher subjective SES accepted choice deprivation less and demanded personal choice more than subjectively lower SES Americans. Subjective SES was a better predictor for reactions to choice deprivation than objective indicators of SES. The degree to which participants interpreted the deprivation of choice as a violation of their personal freedom partially mediated the relationship between subjective SES and reactions to choice deprivation. The results highlight the role subjective SES measurements can play and the need to consider social status and associated models of agency when interpreting behavior and motivation related to choice in American contexts.

Abstract: Proper amount of sleep has a critical role in biological processes and overall health and is linked to negative health outcomes, such as diabetes, heart disease, brain stroke, weight changes, pain, mood swings, Alzheimer's disease, cognitive health, chromo-some changes etc. Despite dedicating one-third of our lives to sleep, a substantial por-tion of the world's population faces sleep deprivation. Insufficient sleep goes beyond simple tiredness, and it is affecting humans metabolic, cardiovascular, cognitive, and emotional dimensions. When it comes to physical activity and athletic performance, sleep deprivation manifests in compromised reaction time, accuracy, vigour, sub-maximal strength, and endurance. These challenges also affect athlete’s cognitive functions such as judgment and decision-making. In the context of athletic perfor-mance, even partial sleep deprivation can lead to significant impairments. Relation-ship between sleep and physical activity was found as emphasizing the importance of adequate sleep for optimal performance and shows that good sleep hygiene and rec-ommended amount of physical activity really go hand in hand contributing to overall well-being including physiological and mental health. Keywords: Sleep deprivation; Physical activity; Athletic performance, Metabolic health; Cognitive functions, Global prevalence.

Adverse effects of dense congenital unilateral cataracts on the developing visual system of infants may result from the direct effects of visual deprivation and, in addition, as a result of competition with the normal eye in establishing cortical structure and function during a critical period in visual development. One approach to evaluating these two amblyogenic factors has been to compare the effects of unilateral and bilateral cataracts on visual development. The rationale is that a developing visual system with dense bilateral cataracts suffers only the effects of early visual deprivation while the developing visual system with a dense unilateral cataract suffers the effects of visual deprivation and of competition with a normal eye.

A significant amount of IoT devices are essentially powered by batteries and implements mechanisms to save energy, such as the sleep mode. The decision-making process deployed in IoT devices to enter to and exit from sleep mode can be exploited by remote users through sleep deprivation attacks, reducing the battery's lifetime and causing a denial of service. This paper presents a new defensive technique to mitigate and prevent sleep deprivation attacks. It is based on the local battery consumption data, that is an input to control the sleep mode. Performance evaluation carried out in a system based on an ESP32 showed that the technique could increase the battery's lifetime by 51.2% in a scenario under a sleep deprivation attack.

This paper compares the dynamic consistency of targeting methodologies that use multidimensional welfare indicators with those based on means and proxy means tests using panel data from Mexico. To make these comparisons, an extension of the Alkire and Foster (2008) dual cutoff multidimensional poverty methodology is proposed. This extension provides a relative approach to multidimensional deprivation that ranks individuals according to an aggregate of their relative position in the distribution of a set of welfare attributes or outcomes. The extension gives particular importance to deprivations that affect smaller portions of the population, as these deprivations are especially critical in defining relative multidimensional welfare. The findings, disaggregated by geographical area (urban and rural), suggest that taking into account deprivation in multiple dimensions may lead to more dynamically consistent measures of well-being and thus more dynamically consistent targeting algorithms.

This report describes the development of the BrazDep small-area deprivation measure for the whole of Brazil. The measure uses the 2010 Brazilian Population Census data and is calculated for the smallest possible geographical area level, the census sectors. It combines three variables – (1) percent of households with per capita income ≤ 1/2 minimum wage; (2) percent of people not literate, aged 7+; and (3) average of percent of people with inadequate access to sewage, water, garbage collection and no toilet and bath/shower – into a single measure. Similar measures have previously been developed at the census sector level for some states or municipalities, but the deprivation measure described in this report is the first one to be provided for census sectors for the whole of Brazil. BrazDep is a measure of relative deprivation, placing the census sectors on a scale of material well-being from the least to the most deprived. It is useful in comparing areas within Brazil in 2010, but cannot be used to make comparisons across countries or time. Categorical versions of the measure are also provided, placing census sectors into groups of similar levels of deprivation. Deprivation measures, such as the one developed here, have been developed for many countries and are popular tools in public health research for describing the social patterning of health outcomes and supporting the targeting and delivery of services to areas of higher need. The deprivation measure is exponentially distributed, with a large proportion of areas having a low deprivation score and a smaller number of areas experiencing very high deprivation. There is significant regional variation in deprivation; areas in the North and Northeast of Brazil have on average much higher deprivation compared to the South and Southeast. Deprivation levels in the Central-West region fall between those for the North and South. Differences are also great between urban and rural areas, with the former having lower levels of deprivation compared to the latter. The measure was validated by comparing it to other similar indices measuring health and social vulnerability at the census sector level in states and municipalities where it was possible, and at the municipal level for across the whole of Brazil. At the municipal level the deprivation measure was also compared to health outcomes. The different validation exercises showed that the developed measure produced expected results and could be considered validated. As the measure is an estimate of the “true” deprivation in Brazil, uncertainty exists about the exact level of deprivation for all of the areas. For the majority of census sectors the uncertainty is small enough that we can reliably place the area into a deprivation category. However, for some areas uncertainty is very high and the provided estimate is unreliable. These considerations should always be kept in mind when using the BrazDep measure in research or policy. The measure should be used as part of a toolkit, rather than a single basis for decision-making. The data together with documentation is available from the University of Glasgow http: //dx.doi.org/10.5525/gla.researchdata.980. The data and this report are distributed under Creative Commons Share-Alike license (CC BY-SA 4.0) and can be freely used by researchers, policy makers or members of public.