Ecological Footprint Inequality: A methodological review and some results

Scarcities of environmental services are no longer merely a remote hypothesis. Consequently, analysis of their inequalities between nations becomes of paramount importance for the achievement of sustainability in terms either of international policy, or of Universalist ethical principles of equity. This paper aims, on the one hand, at revising methodological aspects of the inequality measurement of certain environmental data and, on the other, at extending the scarce empirical evidence relating to the international distribution of Ecological Footprint (EF), by using a longer EF time series. Most of the techniques currently important in the literature are revised and then tested on EF data with interesting results. We look in depth at Lorenz dominance analyses and consider the underlying properties of different inequality indices. Those indices which fit best with environmental inequality measurements are CV2 and GE(2) because of their neutrality property, however a trade-off may occur when subgroup decompositions are performed. A weighting factor decomposition method is proposed in order to isolate weighting factor changes in inequality growth rates. Finally, the only non-ambiguous way of decomposing inequality by source is the natural decomposition of CV2, which additionally allows the interpretation of marginal term contributions. Empirically, this paper contributes to the environmental inequality measurement of EF: this inequality has been quite stable and its change over time is due to per capita vector changes rather than population changes. Almost the entirety of the EF inequality is explainable by differences in the means between the countries of the World Bank group. This finding suggests that international environmental agreements should be attempted on a regional basis in an attempt to achieve greater consensus between the parties involved. Additionally, source decomposition warns of the dangers of confining CO2 emissions reduction to crop-based energies because of the implications for basic needs satisfaction.

Menores, educación y conflicto armado: un análisis desde la realidad africana 15 años después del Informe Machel

Si bien en los últimos años África Subsahariana ha registrado un notable descenso del número de conflictos armados, un buen número de países sigue padeciendo las consecuencias de la violencia armada, especialmente algunos contextos como el de la República Democrática del Congo, la región de Darfur (oeste de Sudán) o Somalia, por citar algunos ejemplos. Tal y como desde el ámbito institucional (Naciones Unidas u ONG) o el académico llevan señalando desde hace varios años, la principal víctima de la violencia suele ser la población civil, principalmente los menores y las mujeres. El presente artículo tiene como objetivo analizar el impacto que los conflictos armados africanos tienen en la infancia y en aspectos tan importantes como su educación. Este objeto de estudio cuenta en los últimos años con un importante referente como fue la publicación en el año 1996 del denominado «Informe Machel». Quince años después de la aparición de este documento, resulta de interés hacer un pequeño balance sobre algunos de los avances, déficits y principales retos de la protección de los menores en conflictos armados.

Comprehensive evaluation of the IEEE 802.15.4 MAC layer performance with retransmissions

Supported by IEEE 802.15.4 standardization activities, embedded networks have been gaining popularity in recent years. The focus of this paper is to quantify the behavior of key networking metrics of IEEE 802.15.4 beacon-enabled nodes under typical operating conditions, with the inclusion of packet retransmissions. We corrected and extended previous analyses by scrutinizing the assumptions on which the prevalent Markovian modeling is generally based. By means of a comparative study, we singled out which of the assumptions impact each of the performance metrics (throughput, delay, power consumption, collision probability, and packet-discard probability). In particular, we showed that - unlike what is usually assumed - the probability that a node senses the channel busy is not constant for all the stages of the backoff procedure and that these differences have a noticeable impact on backoff delay, packet-discard probability, and power consumption. Similarly, we showed that - again contrary to common assumption - the probability of obtaining transmission access to the channel depends on the number of nodes that is simultaneously sensing it. We evidenced that ignoring this dependence has a significant impact on the calculated values of throughput and collision probability. Circumventing these and other assumptions, we rigorously characterize, through a semianalytical approach, the key metrics in a beacon-enabled IEEE 802.15.4 system with retransmissions.

15 years of new growth economics: What have we learnt?

This paper evaluates the empirical and theoretical contributions of theEconomic Growth Literature since the publication of Paul Romer s seminalpaper in 1986.

Intervenciones de identidad territorial en el proceso global de construcción de imagen de marca de los destinos turísticos

La competitividad emergente entre destinos turísticos ha puesto de manifiesto la necesidad de enfatizar las estrategias de comunicación –con el fin de crear un valor añadido intangible para el potencial cliente- encaminadas a crear una imagen favorable de los espacios que se pretenden promocionar, mediante el diseño de acciones de comunicación con objetivos que van más allá del mero interés promocional o informativo. En este sentido, tanto los emplazamientos que conciben el turismo como una solución de diversificación económica (destinos emergentes), como las localizaciones geográficas que ya disponen de una cierta solera en relación a su tradición turística (destinos maduros), aúnan esfuerzos en aras de consolidar una identidad territorial acorde con sus posibilidades turísticas. Si además se tiene en cuenta que, en la actualidad, el consumo de imágenes percibidas a priori representa, de antemano, un primer viaje simbólico previo a un posterior viaje real, se puede llegar a vislumbrar el papel decisivo que desempeña la interpretación del consumidor (creación de imaginarios individuales y colectivos) en un escenario global de comercialización del territorio. Por tanto, el valor añadido en una situación de dura competencia entre destinos, radica en los valores que se asocian a la imagen de marca turística, que representa la primera carga de sensaciones y emociones que percibe el potencial turista y/o visitante antes de decidirse por uno u otro destino.

Muscle protein waste in tumor-bearing rats is effectively antagonized by a beta 2-adrenergic agonist (clenbuterol). Role of the ATP-ubiquitin-dependent proteolytic pathway.

Tissue protein hypercatabolism (TPH) is a most important feature in cancer cachexia, particularly with regard to the skeletal muscle. The rat ascites hepatoma Yoshida AH-130 is a very suitable model system for studying the mechanisms involved in the processes that lead to tissue depletion, since it induces in the host a rapid and progressive muscle waste mainly due to TPH (Tessitore, L., G. Bonelli, and F. M. Baccino. 1987. Biochem. J. 241:153-159). Detectable plasma levels of tumor necrosis factor-alpha associated with marked perturbations in the hormonal homeostasis have been shown to concur in forcing metabolism into a catabolic setting (Tessitore, L., P. Costelli, and F. M. Baccino. 1993. Br. J. Cancer. 67:15-23). The present study was directed to investigate if beta 2-adrenergic agonists, which are known to favor skeletal muscle hypertrophy, could effectively antagonize the enhanced muscle protein breakdown in this cancer cachexia model. One such agent, i.e., clenbuterol, indeed largely prevented skeletal muscle waste in AH-130-bearing rats by restoring protein degradative rates close to control values. This normalization of protein breakdown rates was achieved through a decrease of the hyperactivation of the ATP-ubiquitin-dependent proteolytic pathway, as previously demonstrated in our laboratory (Llovera, M., C. García-Martínez, N. Agell, M. Marzábal, F. J. López-Soriano, and J. M. Argilés. 1994. FEBS (Fed. Eur. Biochem. Soc.) Lett. 338:311-318). By contrast, the drug did not exert any measurable effect on various parenchymal organs, nor did it modify the plasma level of corticosterone and insulin, which were increased and decreased, respectively, in the tumor hosts. The present data give new insights into the mechanisms by which clenbuterol exerts its preventive effect on muscle protein waste and seem to warrant the implementation of experimental protocols involving the use of clenbuterol or alike drugs in the treatment of pathological states involving TPH, particularly in skeletal muscle and heart, such as in the present model of cancer cachexia.

The Impact of Monetary Union on EU-15 Sovereign Debt Yield Spreads

With European Monetary Union (EMU), there was an increase in the adjusted spreads (corrected from the foreign exchange risk) of euro participating countries' sovereign securities over Germany and a decrease in those of non-euro countries. The objective of this paper is to study the reasons for this result, and in particular, whether the change in the price assigned by markets was due to domestic factors such as credit risk and/or market liquidity, or to international risk factors. The empirical evidence suggests that market size scale economies have increased since EMU for all European markets, so the effect of the various risk factors, even though it differs between euro and non-euro countries, is always dependent on the size of the market.

Muscle protein waste in tumor-bearing rats is effectively antagonized by a beta 2-adrenergic agonist (clenbuterol). Role of the ATP-ubiquitin-dependent proteolytic pathway.

Tissue protein hypercatabolism (TPH) is a most important feature in cancer cachexia, particularly with regard to the skeletal muscle. The rat ascites hepatoma Yoshida AH-130 is a very suitable model system for studying the mechanisms involved in the processes that lead to tissue depletion, since it induces in the host a rapid and progressive muscle waste mainly due to TPH (Tessitore, L., G. Bonelli, and F. M. Baccino. 1987. Biochem. J. 241:153-159). Detectable plasma levels of tumor necrosis factor-alpha associated with marked perturbations in the hormonal homeostasis have been shown to concur in forcing metabolism into a catabolic setting (Tessitore, L., P. Costelli, and F. M. Baccino. 1993. Br. J. Cancer. 67:15-23). The present study was directed to investigate if beta 2-adrenergic agonists, which are known to favor skeletal muscle hypertrophy, could effectively antagonize the enhanced muscle protein breakdown in this cancer cachexia model. One such agent, i.e., clenbuterol, indeed largely prevented skeletal muscle waste in AH-130-bearing rats by restoring protein degradative rates close to control values. This normalization of protein breakdown rates was achieved through a decrease of the hyperactivation of the ATP-ubiquitin-dependent proteolytic pathway, as previously demonstrated in our laboratory (Llovera, M., C. García-Martínez, N. Agell, M. Marzábal, F. J. López-Soriano, and J. M. Argilés. 1994. FEBS (Fed. Eur. Biochem. Soc.) Lett. 338:311-318). By contrast, the drug did not exert any measurable effect on various parenchymal organs, nor did it modify the plasma level of corticosterone and insulin, which were increased and decreased, respectively, in the tumor hosts. The present data give new insights into the mechanisms by which clenbuterol exerts its preventive effect on muscle protein waste and seem to warrant the implementation of experimental protocols involving the use of clenbuterol or alike drugs in the treatment of pathological states involving TPH, particularly in skeletal muscle and heart, such as in the present model of cancer cachexia.

Muscle protein waste in tumor-bearing rats is effectively antagonized by a beta 2-adrenergic agonist (clenbuterol). Role of the ATP-ubiquitin-dependent proteolytic pathway.

Tissue protein hypercatabolism (TPH) is a most important feature in cancer cachexia, particularly with regard to the skeletal muscle. The rat ascites hepatoma Yoshida AH-130 is a very suitable model system for studying the mechanisms involved in the processes that lead to tissue depletion, since it induces in the host a rapid and progressive muscle waste mainly due to TPH (Tessitore, L., G. Bonelli, and F. M. Baccino. 1987. Biochem. J. 241:153-159). Detectable plasma levels of tumor necrosis factor-alpha associated with marked perturbations in the hormonal homeostasis have been shown to concur in forcing metabolism into a catabolic setting (Tessitore, L., P. Costelli, and F. M. Baccino. 1993. Br. J. Cancer. 67:15-23). The present study was directed to investigate if beta 2-adrenergic agonists, which are known to favor skeletal muscle hypertrophy, could effectively antagonize the enhanced muscle protein breakdown in this cancer cachexia model. One such agent, i.e., clenbuterol, indeed largely prevented skeletal muscle waste in AH-130-bearing rats by restoring protein degradative rates close to control values. This normalization of protein breakdown rates was achieved through a decrease of the hyperactivation of the ATP-ubiquitin-dependent proteolytic pathway, as previously demonstrated in our laboratory (Llovera, M., C. García-Martínez, N. Agell, M. Marzábal, F. J. López-Soriano, and J. M. Argilés. 1994. FEBS (Fed. Eur. Biochem. Soc.) Lett. 338:311-318). By contrast, the drug did not exert any measurable effect on various parenchymal organs, nor did it modify the plasma level of corticosterone and insulin, which were increased and decreased, respectively, in the tumor hosts. The present data give new insights into the mechanisms by which clenbuterol exerts its preventive effect on muscle protein waste and seem to warrant the implementation of experimental protocols involving the use of clenbuterol or alike drugs in the treatment of pathological states involving TPH, particularly in skeletal muscle and heart, such as in the present model of cancer cachexia.

The Impact of Monetary Union on EU-15 Sovereign Debt Yield Spreads

With European Monetary Union (EMU), there was an increase in the adjusted spreads (corrected from the foreign exchange risk) of euro participating countries' sovereign securities over Germany and a decrease in those of non-euro countries. The objective of this paper is to study the reasons for this result, and in particular, whether the change in the price assigned by markets was due to domestic factors such as credit risk and/or market liquidity, or to international risk factors. The empirical evidence suggests that market size scale economies have increased since EMU for all European markets, so the effect of the various risk factors, even though it differs between euro and non-euro countries, is always dependent on the size of the market.

Cela Espín, X. i Revilla Calvo, V., Annexos de Jaume Buxeda i Garrigós i Miquel Ângel Cau Ontiveros; Mariana Pérez-Sala i Rodés; Eva Orri Terrado i Alicia Estrada Martín.: La transició del municipium d'Iluro a Alarona (Mataró). Cultura material i transformacions d"un espai urbà entre els segles V i VII dC. Laietania, 15, 2004

Aquest llibre reuneix un estudi arqueològic extraordinàriament acurat referit a tot un seguit d'actuacions detectades a partir del registre arqueològic, que caracteritzen l'espai urbà de l'antiga Iluro durant el període de l'Antiguitat tardana. S'hi estudia amb molt deteniment cadascuna de les accions detectades -així com tot el mobiliari ceràmic relacionat- amb la finalitat de situar-les correctament en el temps, però també per entendre, a través de la cultura material, la dinàmica que pren la ciutat a les darreries de l'Antiguitat; per a poder intuir, més que saber, quina societat es desenvolupa darrere d¿aquests contenidors plens de productes alimentaris arribats d¿un ultramar llunyà i alhora molt proper; una societat capaç de respondre a l¿estímul exterior amb una producció pròpia que competirà o substituirà una gran part de la que ve de fora.

The Effect of a Physical Activity Program on the Total Number of Primary Care Visits in Inactive Patients: A 15-Month Randomized Controlled Trial

Abstract Background: Effective promotion of exercise could result in substantial savings in healthcare cost expenses in terms of direct medical costs, such as the number of medical appointments. However, this is hampered by our limited knowledge of how to achieve sustained increases in physical activity. Objectives: To assess the effectiveness of a Primary Health Care (PHC) based physical activity program in reducing the total number of visits to the healthcare center among inactive patients, over a 15-month period. Research Design: Randomized controlled trial. Subjects: Three hundred and sixty-two (n = 362) inactive patients suffering from at least one chronic condition were included. One hundred and eighty-three patients (n = 183; mean (SD); 68.3 (8.8) years; 118 women) were randomly allocated to the physical activity program (IG). One hundred and seventy-nine patients (n = 179; 67.2 (9.1) years; 106 women) were allocated to the control group (CG). The IG went through a three-month standardized physical activity program led by physical activity specialists and linked to community resources. Measures: The total number of medical appointments to the PHC, during twelve months before and after the program, was registered. Self-reported health status (SF-12 version 2) was assessed at baseline (month 0), at the end of the intervention (month 3), and at 12 months follow-up after the end of the intervention (month 15). Results: The IG had a significantly reduced number of visits during the 12 months after the intervention: 14.8 (8.5). The CG remained about the same: 18.2 (11.1) (P = .002). Conclusions: Our findings indicate that a 3-month physical activity program linked to community resources is a shortduration, effective and sustainable intervention in inactive patients to decrease rates of PHC visits. Trial Registration: ClinicalTrials.gov NCT00714831

Muscle protein waste in tumor-bearing rats is effectively antagonized by a beta 2-adrenergic agonist (clenbuterol). Role of the ATP-ubiquitin-dependent proteolytic pathway.

Tissue protein hypercatabolism (TPH) is a most important feature in cancer cachexia, particularly with regard to the skeletal muscle. The rat ascites hepatoma Yoshida AH-130 is a very suitable model system for studying the mechanisms involved in the processes that lead to tissue depletion, since it induces in the host a rapid and progressive muscle waste mainly due to TPH (Tessitore, L., G. Bonelli, and F. M. Baccino. 1987. Biochem. J. 241:153-159). Detectable plasma levels of tumor necrosis factor-alpha associated with marked perturbations in the hormonal homeostasis have been shown to concur in forcing metabolism into a catabolic setting (Tessitore, L., P. Costelli, and F. M. Baccino. 1993. Br. J. Cancer. 67:15-23). The present study was directed to investigate if beta 2-adrenergic agonists, which are known to favor skeletal muscle hypertrophy, could effectively antagonize the enhanced muscle protein breakdown in this cancer cachexia model. One such agent, i.e., clenbuterol, indeed largely prevented skeletal muscle waste in AH-130-bearing rats by restoring protein degradative rates close to control values. This normalization of protein breakdown rates was achieved through a decrease of the hyperactivation of the ATP-ubiquitin-dependent proteolytic pathway, as previously demonstrated in our laboratory (Llovera, M., C. García-Martínez, N. Agell, M. Marzábal, F. J. López-Soriano, and J. M. Argilés. 1994. FEBS (Fed. Eur. Biochem. Soc.) Lett. 338:311-318). By contrast, the drug did not exert any measurable effect on various parenchymal organs, nor did it modify the plasma level of corticosterone and insulin, which were increased and decreased, respectively, in the tumor hosts. The present data give new insights into the mechanisms by which clenbuterol exerts its preventive effect on muscle protein waste and seem to warrant the implementation of experimental protocols involving the use of clenbuterol or alike drugs in the treatment of pathological states involving TPH, particularly in skeletal muscle and heart, such as in the present model of cancer cachexia.

Muscle protein waste in tumor-bearing rats is effectively antagonized by a beta 2-adrenergic agonist (clenbuterol). Role of the ATP-ubiquitin-dependent proteolytic pathway.

Tissue protein hypercatabolism (TPH) is a most important feature in cancer cachexia, particularly with regard to the skeletal muscle. The rat ascites hepatoma Yoshida AH-130 is a very suitable model system for studying the mechanisms involved in the processes that lead to tissue depletion, since it induces in the host a rapid and progressive muscle waste mainly due to TPH (Tessitore, L., G. Bonelli, and F. M. Baccino. 1987. Biochem. J. 241:153-159). Detectable plasma levels of tumor necrosis factor-alpha associated with marked perturbations in the hormonal homeostasis have been shown to concur in forcing metabolism into a catabolic setting (Tessitore, L., P. Costelli, and F. M. Baccino. 1993. Br. J. Cancer. 67:15-23). The present study was directed to investigate if beta 2-adrenergic agonists, which are known to favor skeletal muscle hypertrophy, could effectively antagonize the enhanced muscle protein breakdown in this cancer cachexia model. One such agent, i.e., clenbuterol, indeed largely prevented skeletal muscle waste in AH-130-bearing rats by restoring protein degradative rates close to control values. This normalization of protein breakdown rates was achieved through a decrease of the hyperactivation of the ATP-ubiquitin-dependent proteolytic pathway, as previously demonstrated in our laboratory (Llovera, M., C. García-Martínez, N. Agell, M. Marzábal, F. J. López-Soriano, and J. M. Argilés. 1994. FEBS (Fed. Eur. Biochem. Soc.) Lett. 338:311-318). By contrast, the drug did not exert any measurable effect on various parenchymal organs, nor did it modify the plasma level of corticosterone and insulin, which were increased and decreased, respectively, in the tumor hosts. The present data give new insights into the mechanisms by which clenbuterol exerts its preventive effect on muscle protein waste and seem to warrant the implementation of experimental protocols involving the use of clenbuterol or alike drugs in the treatment of pathological states involving TPH, particularly in skeletal muscle and heart, such as in the present model of cancer cachexia.