Publications by authors named "Pueyo S"

Increasing evidence-synthesized in this paper-shows that economic growth contributes to biodiversity loss via greater resource consumption and higher emissions. Nonetheless, a review of international biodiversity and sustainability policies shows that the majority advocate economic growth. Since improvements in resource use efficiency have so far not allowed for absolute global reductions in resource use and pollution, we question the support for economic growth in these policies, where inadequate attention is paid to the question of how growth can be decoupled from biodiversity loss.

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Fires and herbivores shape tropical vegetation structure, but their effects on the stability of tree cover in different climates remain elusive. Here, we integrate empirical and theoretical approaches to determine the effects of climate on fire- and herbivore-driven forest-savanna shifts. We analyzed time series of remotely sensed tree cover and fire observations with estimates of herbivore pressure across the tropics to quantify the fire-tree cover and herbivore-tree cover feedbacks along climatic gradients.

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Context: Precariousness is increasing among all populations and especially among women. The access to healthcare is increasingly unequal upon the population and particularly in access to contraception methods or abortion according to their vulnerability level.

Objective: Our main object is to describe the socio-demographic specifications, the different steps involved in the healthcare itinerary to contraception and abortion, according to the level of social vulnerability for a woman population sample requesting an abortion.

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Recent studies have interpreted patterns of remotely sensed tree cover as evidence that forest with intermediate tree cover might be unstable in the tropics, as it will tip into either a closed forest or a more open savanna state. Here we show that across all continents the frequency of wildfires rises sharply as tree cover falls below ~40%. Using a simple empirical model, we hypothesize that the steepness of this pattern causes intermediate tree cover (30‒60%) to be unstable for a broad range of assumptions on tree growth and fire-driven mortality.

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Wildfires burn large parts of the tropics every year, shaping ecosystem structure and functioning. Yet the complex interplay between climate, vegetation and human factors that drives fire dynamics is still poorly understood. Here we show that on all continents, except Australia, tropical fire regimes change drastically as mean annual precipitation falls below 550 mm.

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An increasing number of authors agree in that the maximum entropy principle (MaxEnt) is essential for the understanding of macroecological patterns. However, there are subtle but crucial differences among the approaches by several of these authors. This poses a major obstacle for anyone interested in applying the methodology of MaxEnt in this context.

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We test for two critical phenomena in Amazonian ecosystems: self-organized criticality (SOC) and critical transitions. SOC is often presented in the complex systems literature as a general explanation for scale invariance in nature. In particular, this mechanism is claimed to underlie the macroscopic structure and dynamics of terrestrial ecosystems.

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Why does the neutral theory, which is based on unrealistic assumptions, predict diversity patterns so accurately? Answering questions like this requires a radical change in the way we tackle them. The large number of degrees of freedom of ecosystems pose a fundamental obstacle to mechanistic modelling. However, there are tools of statistical physics, such as the maximum entropy formalism (MaxEnt), that allow transcending particular models to simultaneously work with immense families of models with different rules and parameters, sharing only well-established features.

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Vandermeer and Perfecto (Reports, 17 February 2006, p. 1000) maintain that a mutualist ant disrupts the power law distribution of scale insect abundances. However, reanalysis of the data reveals that ants cause an increase in the range of the power law and modify its exponent.

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In 61 antiretroviral-naive HIV-2-infected patients starting triple therapy at a median CD4 cell count of 136 cells/microl, the median increase was 41 cells/microl at month 12, which was no different among those on protease inhibitors or triple nucleoside analogues. Despite virological response, as the median plasma load was under the detectable threshold from month 3, CD4 cell recovery remained poor in treated HIV-2 infection. Our results raise the question of the optimal regimen to recommend in HIV-2-infected patients.

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We developed a new assay for human immunodeficiency virus type 2 plasma RNA quantification based on a previous format. The new version performed significantly better than the original regarding the detection of subtype B, allowing the detection of 14 out of 36 plasma RNAs in the subtype B-infected patients not detected with the original version.

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We described the baseline polymorphism of the human immunodeficiency virus type 2 (HIV-2) protease gene from 94 treatment-naive patients and the longitudinal follow-up of 17 protease inhibitor-treated patients. Compared to the HIV-2 consensus sequences, baseline polymorphism involved 47 positions. Substitutions selected under treatment were observed at positions corresponding to HIV-1 resistance mutations as well as at positions of currently unknown impact on HIV-1.

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The objective of the study was to determine retrospectively which substitutions in the reverse transcriptase (RT) gene are selected in vivo during nucleoside RT inhibitors (NRTI) containing regimen in HIV-2 infected subjects. Thirty-four HIV-2 patients having received NRTI-containing regimen with available specimens and amplifiable RT gene were studied. Analyses of RT gene were undertaken after a median NRTI exposure of 51 months (range: 5-128).

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Objectives: To identify factors associated with clinical progression in HIV-2 infected patients.

Design: French prospective cohort initiated in 1994.

Methods: Follow-up data are collected twice a year; viral load is assessed once a year by cellular viraemia, quantitative proviral DNA and plasma RNA.

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The searching trajectories of different animals can be described with a broad class of flight length (lj) distributions with P(lj) = lj-mu. Theoretical studies have shown that changes in these distributions (i.e.

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Human immunodeficiency virus type 2 (HIV-2) is much less pathogenic than HIV-1, and HIV-2 infection is associated with plasma viral loads significantly lower than those found in HIV-1 infection. We have developed a real-time quantitative PCR method for measuring the HIV-2 RNA load that covers the range of genetic diversity of HIV-2 isolates and that detects extremely low viral loads. Samples from 49 patients were studied.

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In order to define more accurately human immunodeficiency virus-infected patients at risk of developing toxoplasmic encephalitis (TE), we assessed the prognostic significance of the anti-Toxoplasma gondii immunoglobulin G (IgG) immunoblot profile, in addition to AIDS stage, a CD4(+) cell count <50/mm(3), and an antibody titer > or =150 IU/ml, in patients with CD4 cell counts <200/mm(3) and seropositive for T. gondii. Baseline serum samples from 152 patients included in the placebo arm of the ANRS 005-ACTG 154 trial (pyrimethamine versus placebo) were used.

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Among sexually transmitted diseases, infection by human papillomavirus (HPV) has become one of the most important. On the other hand, though epidemiological data show that some HPV types are closely associated with cervical cancer, few reports have been found with reference to penile carcinoma because of its rare occurrence. The aim of this study was to investigate the relationship between HPV infection and penile cancer in Argentina.

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In a single institution, we have used recombinant interferon- (IFN-) to treat 116 newly diagnosed Philadelphia-positive (Ph+) chronic myeloid leukemia (CML) patients and analyzed the predictive factors for response and survival. The patients whose median age was 50.3 years (range, 9 to 70) were administered IFN- (5 million units/m2/d) subcutaneously.

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The objective of this study was to assess whether patients with CD4+ cell counts <200 x 10(6)/L have a decreased survival after the occurrence of any AIDS-defining event; 187 patients from the placebo arm of a clinical trial of toxoplasmosis prophylaxis (ANRS005-ACTG154) were included. For this analysis, patients were HIV infected without any AIDS-defining event, had a CD4+ lymphocyte count < 200 x 10(6)/L, had a positive serology for Toxoplasma gondii, and had no severe liver, renal, or hematologic abnormalities. We used proportional hazards regression to study the relationships between baseline variables.

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Although drug-induced rash is frequent in human immunodeficiency virus (HIV)-infected patients, rash due to pyrimethamine has not been described previously. In a randomized, double-blind, placebo-controlled study of pyrimethamine as primary prophylaxis for toxoplasmic encephalitis, the incidence of rash (per hundred patient-years) was 8.1 in the pyrimethamine group versus 1.

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Objective: To study the predictive value of anti-Toxoplasma gondii antibody titres for the occurrence of toxoplasmic encephalitis (TE) in HIV-infected patients.

Methods: Data from the placebo arm of a trial of primary prophylaxis for TE (ANRS 005/ACTG 154) were analysed. Patients included had CD4+ cell counts < 200 x 10(6)/l and a positive Toxoplasma serology.

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Pyrimethamine (50 mg) with folinic acid (15 mg) given three times weekly was assessed as primary prophylaxis for toxoplasmic encephalitis (TE) in 554 human immunodeficiency virus-infected patients seropositive for Toxoplasma gondii and with < 200 CD4 cells/mm3. At 1 year, the incidence of TE was similar in pyrimethamine, 12%, and placebo, 13%, groups (relative risk [RR], 0.9; 95% confidence interval [CI], 0.

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To identify risk factors for cerebral toxoplasmosis (CT) in HIV patients (pts) with positive serology for Toxoplasma gondii and CD4 < 200/mm3, data from the placebo group (N = 280) of a primary prophylaxis trial, were analyzed. The probability of onset of CT (n = 46) was, at one year, 13.1%.

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