A perceived human development index

The objective of the paper is to build a Perceived Human Development Index (PHDI) framework by assembling the HDI components, namely indicators on income, health and education on their subjective version. We propose here to introduce a fourth dimension linked to perceptions on work conditions, given its role in the “happiness” literature and in social policy making. We study how perceptions on satisfaction about the individual’s satisfaction with income, education, work and health are related to their objective counterparts. We use a sample of LAC countries where we take advantage of a larger set of questions on the four groups of social variables mentioned included in the Gallup World Poll by the IADB. We emphasize the impacts of objective income and age on perceptions. Complementarily, in the appendix we use the full sample of 132 countries where a smaller set of variables can be included, which provides a greater degree of freedom to study the impact of objective HDI components observed at country level on the formation of individual’s perception on income, education, work, health and life satisfaction. These exercises provide useful insights about the workings of beneficiaries’ point of view to understand the transmission mechanism of key social policy ingredients into perceptions. In particular, the so-called PHDI may provide a complementary subjective reference to the HDI. We also study how one’s satisfaction with life is established, measuring the relative importance given to income vis-à-vis health and education. Estimating these “instantaneous happiness functions” will help to assess the relative weights attributed to income, health and education in the HDI, which is a benchmark in the multidimensional social indicators toolbox used in practice.

The limits of human development and the use of energy and natural resources

The development of nations is an unquestionable requirement. A lot of challenges concerning health, education and economy are present. A discussion on these development models has occupied the minds of decision makers in recent years. When energy supply and demand is considered, the situation becomes critical and the crucial question is: how to improve the quality of life of developing countries based on available models of development that are related to the life style of developed countries, for which the necessary use and waste of energy are present? How much energy is essential to humanity for not so as to endangering the survival conditions of future generations? the human development index (HDI) establishes the relationship among energy use, economic growth and social growth. Here it can be seen that 75% of the world population has a significant energy consumption potential. This is a strong reason to consider that the sustainable development concepts on energy policies are strategic to the future of the planet. This paper deals with the importance of seeking alternative development models for human development balance, natural resources conservation and environment through rational energy use concepts. (c) 2004 Elsevier Ltd. All rights reserved.

Childbirth care: contributing to the debate on human development

Com a finalidade de subsidiar gestores da área de saúde da mulher, na formulação de políticas públicas, voltadas ao desenvolvimento humano, realizou-se esta investigação, cujo objetivo foi avaliar a estrutura e o processo da atenção ao parto e ao neonato desenvolvido em região do interior paulista. Estudo epidemiológico, voltado para avaliação dos serviços de saúde, baseou-se na observação da assistência prestada pelo Sistema Único de Saúde em 12 maternidades e 134 partos, adotando-se padrões estabelecidos pelo Ministério da Saúde ou Organização Mundial de Saúde para comparação. Os resultados apontam problemas relacionados à estrutura em algumas maternidades, mostrando que práticas úteis ao parto normal ainda são pouco utilizadas, enquanto que outras prejudiciais ou ineficazes ainda são utilizadas rotineiramente. Reverter esse quadro será essencial para oferecer atendimento de qualidade às mulheres, com conseqüente redução nas taxas de mortalidade materna e neonatal, para que a região atinja as metas estabelecidas para ampliação do desenvolvimento humano no milênio.

e-Health in Uruguay: development and challenges

Includes bibliography

A proposal for a modified Human Development Index

Includes bibliography.

EMERGENT CONDITIONAL RELATIONS IN A GO/NO-GO PROCEDURE: FIGURE-GROUND AND STIMULUS-POSITION COMPOUND RELATIONS

Past research has demonstrated emergent conditional relations using a go/no-go procedure with pairs of figures displayed side-by-side on a computer screen. The present Study sought to extend applications Of this procedure. In Experiment, 1, we evaluated whether emergent conditional relations Could be demonstrated when two-component stimuli were displayed in figure-ground relationships-abstract figures displayed on backgrounds of different colors. Five normal)), capable adults participated. During training, each two-component stimulus Was presented successively. Responses emitted in the presence of some Stimulus pairs (A1B1, A2B2, A3B3, B1C1, B2C2 and B3C3) were reinforced, whereas responses emitted in the presence of other pairs (A1B2, A1B3, A2B1, A2B3, A3B1, A3B2, B1C2, B1C3, B2C1, B2C3, B3C1 and B3C2) were not. During tests, new configurations (AC and CA) were presented, thus emulating structurally the matching-to-sample tests employed in typical equivalence Studies. All participants showed emergent relations consistent with stimulus equivalence during testing. In Experiment 2, we systematically replicated the procedures with Stimulus compounds consisting Of four figures (A1, A2, C1 and C2) and two locations (left - B1 and right - 132). A,11 6 normally capable adults exhibited emergent stimulus-stimulus relations. Together, these experiments show that the go/no-go procedure is a potentially useful alternative for Studying emergent. conditional relations when matching-to-sample is procedurally cumbersome or impossible to use.

OBSERVING BEHAVIOR AND ATYPICALLY RESTRICTED STIMULUS CONTROL

Restricted stimulus control refers to discrimination learning with atypical limitations in the range of controlling stimuli or stimulus features In the study reported here 4 normally capable individuals and 10 individuals with Intellectual disabilities (ID) performed two-sample delayed matching to sample Sample stimulus observing was recorded with an eye tracking apparatus High accuracy scores indicated stimulus control by both sample stimuli for the 4 nondisabled participants and 4 participants with ID and eye tracking data showed reliable observing of all stimuli Intermediate accuracy scores indicated restricted stimulus control for the remaining 6 participants Their eye tracking data showed that errors were related to failures to observe sample stimuli and relatively brief observing durations Five of these participants were then given interventions designed to improve observing behavior For 4 participants the interventions resulted initially in elimination of observing failures increased observing durations and Increased accuracy For 2 of these participants contingencies sufficient to maintain adequate observing were not always sufficient to maintain high accuracy subsequent procedure modifications restored It however For the 5th participant initial improvements in observing were not accompanied by improved accuracy in apparent Instance of observing without attending accuracy improved only after an additional intervention that imposed contingencies on observing behavior Thus interventions that control observing behavior seem necessary but may not always be sufficient for the remediation of restricted stimulus control

The impact of mortality from external causes on human development in the Brazilian borderland

This article estimates the impact of mortality from external causes on the human development index (HDI) along the Brazilian borderland from 2000 to 2005. Data obtained from Brazilian government agencies were combined using the methodology defined by the United Nations Development Program, revealing the HDI according to actual conditions. Subsequently, deaths from external causes were excluded in order to estimate their impact on the index, recalculating life expectancy using the technique of competing causes. HDI showed a gradual increase from North to South, with the most developed regions concentrated in the South, consistent with studies using other sets of economic indicators. By excluding mortality from external causes, the highest gains appeared in regions where the HDI (under actual conditions) were lower, and the magnitude of gains declined towards the South.

Evaluation of Viral Load Thresholds for Predicting New World Health Organization Stage 3 and 4 Events in HIV-Infected Children Receiving Highly Active Antiretroviral Therapy

Background: This study evaluated a wide range of viral load (VL) thresholds to identify a cut-point that best predicts new clinical events in children on stable highly active antiretroviral therapy (HAART). Methods: Cox proportional hazards modeling was used to assess the adjusted risk for World Health Organization stage 3 or 4 clinical events (WHO events) as a function of time-varying CD4, VL, and hemoglobin values in a cohort study of Latin American children on HAART >= 6 months. Models were fit using different VL cut-points between 400 and 50,000 copies per milliliter, with model fit evaluated on the basis of the minimum Akaike information criterion value, a standard model fit statistic. Results: Models were based on 67 subjects with WHO events out of 550 subjects on study. The VL cut-points of >2600 and >32,000 copies per milliliter corresponded to the lowest Akaike information criterion values and were associated with the highest hazard ratios (2.0, P = 0.015; and 2.1, P = 0.0058, respectively) for WHO events. Conclusions: In HIV-infected Latin American children on stable HAART, 2 distinct VL thresholds (>2600 and >32,000 copies/mL) were identified for predicting children at significantly increased risk for HIV-related clinical illness, after accounting for CD4 level, hemoglobin level, and other significant factors.

Neonatal outcomes of extremely preterm infants from the NICHD Neonatal Research Network.

OBJECTIVE: This report presents data from the Eunice Kennedy Shriver National Institute of Child Health and Human Development Neonatal Research Network on care of and morbidity and mortality rates for very low birth weight infants, according to gestational age (GA). METHODS: Perinatal/neonatal data were collected for 9575 infants of extremely low GA (22-28 weeks) and very low birth weight (401-1500 g) who were born at network centers between January 1, 2003, and December 31, 2007. RESULTS: Rates of survival to discharge increased with increasing GA (6% at 22 weeks and 92% at 28 weeks); 1060 infants died at CONCLUSION: Although the majority of infants with GAs of >or=24 weeks survive, high rates of morbidity among survivors continue to be observed.

Volumetric and anatomical MRI for hypoxic-ischemic encephalopathy: relationship to hypothermia therapy and neurosensory impairments.

OBJECTIVE: To relate volumetric magnetic resonance imaging (MRI) findings to hypothermia therapy and neurosensory impairments. STUDY DESIGN: Newborns > or =36 weeks' gestation with hypoxic-ischemic encephalopathy who participated in the National Institute of Child Health and Human Development hypothermia randomized trial at our center were eligible. We determined the relationship between hypothermia treatment and usual care (control) to absolute and relative cerebral tissue volumes. Furthermore, we correlated brain volumes with death or neurosensory impairments at 18 to 22 months. RESULT: Both treatment groups were comparable before randomization. Total brain tissue volumes did not differ in relation to treatment assignment. However, relative volumes of subcortical white matter were significantly larger in hypothermia-treated than control infants. Furthermore, relative total brain volumes correlated significantly with death or neurosensory impairments. Relative volumes of the cortical gray and subcortical white matter also correlated significantly with Bayley Scales psychomotor development index. CONCLUSION: Selected volumetric MRI findings correlated with hypothermia therapy and neurosensory impairments. Larger studies using MRI brain volumes as a secondary outcome measure are needed.

Intensive care for extreme prematurity--moving beyond gestational age.

BACKGROUND: Decisions regarding whether to administer intensive care to extremely premature infants are often based on gestational age alone. However, other factors also affect the prognosis for these patients. METHODS: We prospectively studied a cohort of 4446 infants born at 22 to 25 weeks' gestation (determined on the basis of the best obstetrical estimate) in the Neonatal Research Network of the National Institute of Child Health and Human Development to relate risk factors assessable at or before birth to the likelihood of survival, survival without profound neurodevelopmental impairment, and survival without neurodevelopmental impairment at a corrected age of 18 to 22 months. RESULTS: Among study infants, 3702 (83%) received intensive care in the form of mechanical ventilation. Among the 4192 study infants (94%) for whom outcomes were determined at 18 to 22 months, 49% died, 61% died or had profound impairment, and 73% died or had impairment. In multivariable analyses of infants who received intensive care, exposure to antenatal corticosteroids, female sex, singleton birth, and higher birth weight (per each 100-g increment) were each associated with reductions in the risk of death and the risk of death or profound or any neurodevelopmental impairment; these reductions were similar to those associated with a 1-week increase in gestational age. At the same estimated likelihood of a favorable outcome, girls were less likely than boys to receive intensive care. The outcomes for infants who underwent ventilation were better predicted with the use of the above factors than with use of gestational age alone. CONCLUSIONS: The likelihood of a favorable outcome with intensive care can be better estimated by consideration of four factors in addition to gestational age: sex, exposure or nonexposure to antenatal corticosteroids, whether single or multiple birth, and birth weight. (ClinicalTrials.gov numbers, NCT00063063 [ClinicalTrials.gov] and NCT00009633 [ClinicalTrials.gov].).

Transcriptional regulation and functional analysis of the Wilms' tumor gene WT1

The Wilms' tumor gene, WT1, encodes a zinc finger transcription factor which functions as a tumor suppressor. Defects in the WT1 gene can result in the development of nephroblastoma. WT1 is expressed during development, primarily in the metanephric kidney, the mesothelial lining of the abdomen and thorax, and the developing gonads. WT1 expression is tightly regulated and is essential for renal development. The WT1 gene encodes a protein with a proline-rich N-terminus which functions as a transcriptional repressor and C-terminus contains 4 zinc fingers that mediate DNA binding. WT1 represses transcription from a number of growth factors and growth factor receptors. WT1 mRNA undergoes alternative splicing at two sites, resulting in 4 mRNA species and polypeptide products. Exon 5, encoding 17 amino acids is alternatively spliced, and is located between the transcriptional repression domain and the DNA binding domain. The second alternative splice is the terminal 9 nucleotides of zinc finger 3, encoding the tripeptide Lys-Thr-Ser (KTS). The presence or absence of KTS within the zinc fingers of WT1 alters DNA binding.^ I have investigated transcriptional regulation of WT1, characterizing two means of repressing WT1 transcription. I have cloned a transcriptional silencer of the WT1 promoter which is located in the third intron of the WT1 gene. The silencer is 460 bp in length and contains an Alu repeat. The silencer functions in cells of non-renal origin.^ I have found that WT1 protein can autoregulate the WT1 promoter. Using the autoregulation of the WT1 promoter as a functional assay, I have defined differential consensus DNA binding motifs of WT1 isoforms lacking and containing the KTS tripeptide insertion. With these refined consensus DNA binding motifs, I have identified two additional targets of WT1 transcriptional repression, the proto-oncogenes bcl-2 and c-myc.^ I have investigated the ability of the alternatively spliced exon 5 to influence cell growth. In cell proliferation assays, isoforms of WT1 lacking exon 5 repress cell growth. WT1 isoforms containing exon 5 fail to repress cell growth to the same extent, but alter the morphology of the cells. These experiments demonstrate that the alternative splice isoforms of WT1 have differential effects on the function of WT1. These findings suggest a role for the alternative splicing of WT1 in metanephric development. ^

Genetic analysis of factors regulating mesenchymal cell fates

Formation of cartilage and bone involves sequential processes in which undifferentiated mesenchyme aggregates into primordial condensations which subsequently grow and differentiate, resulting in morphogenesis of the adult skeleton. While much has been learned about the structural molecules which comprise cartilage and bone, little is known about the nuclear factors which regulate chondrogenesis and osteogenesis. MHox is a homeobox-containing gene which is expressed in the mesenchyme of facial, limb, and vertebral skeletal precursors during mouse embryogenesis. MHox expression has been shown to require epithelial-derived signals, suggesting that MHox may regulate the epithelial-mesenchymal interactions required for skeletal organogenesis. To determine the functions of MHox, we generated a loss-of-function mutation in the MHox gene. Mice homozygous for a mutant MHox allele exhibit defects of skeletogenesis, involving the loss or malformation of craniofacial, limb and vertebral skeletal structures. The affected skeletal elements are derived from the cranial neural crest, as well as somitic and lateral mesoderm. Analysis of the mutant phenotype during ontogeny demonstrated a defect in the formation or growth of chondrogenic and osteogenic precursors. These findings provide evidence that MHox regulates the formation of preskeletal condensations from undifferentiated mesenchyme. In addition, generation of mice doubly mutant for the MHox and S8 homeobox genes reveal that these two genes interact to control formation of the limb and craniofacial skeleton. Mice carrying mutant alleles for S8 and MHox exhibit an exaggeration of the craniofacial and limb phenotypes observed in the MHox mutant mouse. Thus, MHox and S8 are components of a combinatorial genetic code controlling generation of the skeleton of the skull and limbs. ^

Structure-function analyses of {\it PAX6\/} and the molecular bases of aniridia

PAX6 is a transcription activator that regulates eye development in animals ranging from Drosophila to human. The C-terminal region of PAX6 is proline/serine/threonine-rich (PST) and functions as a potent transactivation domain when attached to a heterologous DNA-binding domain of the yeast transcription factor, GAL4. The PST region comprises 152 amino acids encoded by four exons. The transactivation function of the PST region has not been defined and characterized in detail by in vitro mutagenesis. I dissected the PST domain in two independent systems, a heterologous system using a GAL4 DNA-binding site and the native system of PAX6. In both systems, the results show consistently that all four constituent exons of the PST domain are responsible for the transactivation function. The four exon fragments act cooperatively to stimulate transcription, although none of them can function individually as an independent transactivation domain. Combinations of two or more exon fragments can reconstitute substantial transactivation activity when fused to the DNA-binding domain of GAL4, but they surprisingly do not produce much activity in the context of native PAX6 even though the mutant PAX6 proteins are stable and their DNA-binding function remains unaffected. I conclude that the PAX6 protein contains an unusually large transactivation domain that is evolutionarily conserved to a high degree, and that its full transactivation activity relies on the cooperative action of the four exon fragments.^ Most PAX6 mutations detected in patients with aniridia result in truncations of the protein. Some of the truncation mutations occur in the PST region of PAX6, resulting in mutant proteins that retain their DNA-binding ability but have no significant transactivation activity. It is not clear whether such mutants are true loss-of-function or dominant-negative mutants. I show that these mutants are dominant-negative if they are coexpressed with wild-type PAX6 in cultured cells and that the dominant-negative effects result from enhanced DNA-binding ability of these mutants due to removal of the PST domain. These mutants are able to repress the wild-type PAX6 activity not only at target genes with paired domain binding sites but also at target genes with homeodomain binding sites.^ Mutations in the human PAX6 gene produce various phenotypes, including aniridia, Peters' anomaly, autosomal dominant keratitis, and familial foveal dysplasia. The various phenotypes may arise from different mutations in the same gene. To test this theory, I performed a functional analysis of two missense mutations in the paired domain: the R26G mutation reported in a case of Peters' anomaly, and the I87R mutation identified in a patient with aniridia. While both the R26 and the I87 positions are conserved in the paired boxes of all known PAX genes, X-ray crystallography has shown that only R26 makes contact with DNA. I found that the R26G mutant failed to bind a subset of paired domain binding sites but, surprisingly, bound other sites and successfully transactivated promoters containing those sites. In contrast, the I87R mutant had lost the ability to bind DNA at all tested sites and failed to transactivate promoters. My data support the haploinsufficiency hypothesis of aniridia, and the hypothesis that R26G is a hypomorphic allele. ^