Land use dynamics under the Bolsa Floresta Program: a case study of the Uatumã Sustainable Development Reserve (Amazonas, Brazil)

Original ArticleThe effectiveness of a program of payment for environmental services (PES) in the Brazilian Amazon was analyzed through an accurate mapping of deforested areas. The Bolsa Floresta Program (BFP) in Amazonas state (Brazil) was chosen as an example of a PES program that aims to compensate farmers for their commitment to zero deforestation of primary forests while opening swiddens only in secondary vegetation areas. However, the official measurement of opened swiddens is not effective since only deforested areas larger than 6.25 ha are mapped, whereas most areas opened for cassava crops are approximately 1 ha in size. The effectiveness of the BFP was evaluated in the Uatumã Sustainable Development Reserve (SDR). We tested a methodology for mapping areas from 0.45 ha upwards that have been opened for cassava swiddens. The years 2006 (before the implementation of the BFP), 2011, 2015 and 2019 were analyzed. The results indicated that 88% of the areas opened for swiddens were between 0.45 and 6.25 ha in size. After the implantation of the BFP, the cumulative total deforested area decreased, and there was a reduction in deforested areas in primary forests. An intensification of swidden cultivation was also observed, which could cause a decline in productivity. The monitoring by land-use zoning showed that the majority of opened areas were located in intensive use zones, following the rules of the SDR management plan. The results show the efforts of local families to fulfill the BFP rulesinfo:eu-repo/semantics/publishedVersio

Deciphering the evolution of the Milky Way discs: Gaia APOGEE Kepler giant stars and the Besançon Galaxy Model

[Context] Thanks to ongoing efforts to compute accurate stellar ages, we are able to characterise stars in different regions of the Milky Way. The Gaia and Kepler space-missions, along with ground-based spectroscopic surveys such as APOGEE, provide a unique way to study the chemo-kinematics relations as a function of age through the Galactic stellar populations and provide new constraints to Galactic evolution models. [Aims] We investigate the properties of the double sequences of the Milky Way discs visible in the [α/Fe] versus [Fe/H] diagram, which are usually associated to the chemical thin and thick discs at the solar circle. In the framework of Galactic formation and evolution, we discuss the complex relationships between age, metallicity, [α/Fe], and the radial, azimuthal, and vertical components of the space velocities. [Methods] We study stars with measured chemical and seismic properties from the APOGEE spectroscopic survey and the Kepler satellite, respectively. In addition, astrometry from the Gaia satellite is available for the majority of the sample. We separate the [α/Fe]-[Fe/H] diagram into three stellar populations: the thin disc, the high-α metal-poor thick disc, and the high-α metal-rich thick disc and characterise each of these in the age-chemo-kinematics parameter space. Because of the model-dependent nature of the ages inferred from asteroseismology, and because they depend on the quality of the input spectroscopic information, we compare results obtained from different APOGEE data releases (DR14 and DR16). We also use age determinations from two recent works in the literature. In addition, we use the Besançon stellar populations synthesis model to highlight selection biases and mechanisms (such as mergers and secular evolution) not included in the model. [Results] The thin disc exhibits a flat age-metallicity relation while [α/Fe] increases with stellar age. We confirm no correlation between radial and vertical velocities with [Fe/H], [α/Fe], and age for each stellar population. Considering both samples, Vφ decreases with age for the thin disc, while Vφ increases with age for the high-α metal-poor thick disc. We show that this difference is not due to sample selection. Although the age distribution of the high-α metal-rich thick disc is very close to that of the high-α metal-poor thick disc between 7 and 14 Gyr, its kinematics seems to follow that of the thin disc. This feature, not predicted by the hypotheses included in the Besançon Galaxy Model, suggests a different origin and history for this population. Finally, we show that there is a maximum dispersion of the vertical velocity, σZ, with age for the high-α metal-poor thick disc around 8 Gyr. The comparisons with the Besançon Galaxy Model simulations suggest a more complex chemo-dynamical scheme to explain this feature, most likely including mergers and radial migration effects.F.F., A.F., R.M., M.R., T.A. acknowledge support by the Spanish Ministry of Science, Innovation and University (MICIU/FEDER, UE) through grant RTI2018-095076-B-C21, the Institute of Cosmos Sciences University of Barcelona (ICCUB, Unidad de Excelencia “María de Maeztu”) through grant CEX2019-000918-M, the Ramon y Cajal Fellowship RYC2018-025968-I. This project has received funding from the European Union’s Horizon 2020 research and innovation programme under the Marie Sklodowska-Curie grant agreement No. 800502. AM acknowledges funding from the European Research Council (ERC) under the European Union’s Horizon 2020 research and innovation programme (grant agreement No. 772293 – project ASTEROCHRONOMETRY, https://www.asterochronometry.eu

Reduced IgG anti-small nuclear ribonucleoprotein autoantibody production in systemic lupus erythematosus patients with positive IgM anti-cytomegalovirus antibodies

INTRODUCTION: Systemic lupus erythematosus is characterized by production of autoantibodies to RNA or DNA-protein complexes such as small nuclear ribonucleoproteins (snRNPs). A role of Epstein-Barr virus in the pathogenesis has been suggested. Similar to Epstein-Barr virus, cytomegalovirus (CMV) infects the majority of individuals at a young age and establishes latency with a potential for reactivation. Homology of CMV glycoprotein B (UL55) with the U1snRNP-70 kDa protein (U1-70 k) has been described; however, the role of CMV infection in production of anti-snRNPs is controversial. We investigated the association of CMV serology and autoantibodies in systemic lupus erythematosus. METHODS: Sixty-one Mexican patients with systemic lupus erythematosus were tested for CMV and Epstein-Barr virus serology (viral capsid antigen, IgG, IgM) and autoantibodies by immunoprecipitation and ELISA (IgG and IgM class, U1RNP/Sm, U1-70 k, P peptide, rheumatoid factor, dsDNA, beta2-glycoprotein I). RESULTS: IgG anti-CMV and IgM anti-CMV were positive in 95% (58/61) and 33% (20/61), respectively, and two cases were negative for both. Clinical manifestation and autoantibodies in the IgM anti-CMV+ group (n = 20) versus the IgM anti-CMV(-)IgG+ (n = 39) group were compared. Most (19/20) of the IgM anti-CMV+ cases were IgG anti-CMV+, consistent with reactivation or reinfection. IgM anti-CMV was unrelated to rheumatoid factor or IgM class autoantibodies and none was positive for IgM anti-Epstein-Barr virus-viral capsid antigen, indicating that this is not simply due to false positive results caused by rheumatoid factor or nonspecific binding by certain IgM. The IgM anti-CMV+ group has significantly lower levels of IgG anti-U1RNP/Sm and IgG anti-U1-70 k (P = 0.0004 and P = 0.0046, respectively). This finding was also confirmed by immunoprecipitation. Among the IgM anti-CMV(-) subset, anti-Su was associated with anti-U1RNP and anti-Ro (P < 0.05). High levels of IgG anti-CMV were associated with production of lupus-related autoantibodies to RNA or DNA-protein complex (P = 0.0077). CONCLUSIONS : Our findings suggest a potential role of CMV in regulation of autoantibodies to snRNPs and may provide a unique insight to understand the pathogenesis

Observations of the First Electromagnetic Counterpart to a Gravitational-wave Source by the TOROS Collaboration

We present the results of prompt optical follow-up of the electromagnetic counterpart of the gravitational-wave event GW170817 by the Transient Optical Robotic Observatory of the South Collaboration. We detected highly significant dimming in the light curves of the counterpart (Δg = 0.17 ± 0.03 mag, Δr = 0.14 ± 0.02 mag, Δi = 0.10 ± 0.03 mag) over the course of only 80 minutes of observations obtained ∼35 hr after the trigger with the T80-South telescope. A second epoch of observations, obtained ∼59 hr after the event with the EABA 1.5 m telescope, confirms the fast fading nature of the transient. The observed colors of the counterpart suggest that this event was a \ blue kilonova\ relatively free of lanthanides

Mesenchymal stem cell-like properties of CD133+ glioblastoma initiating cells

Glioblastoma is composed of dividing tumor cells, stromal cells and tumor initiating CD133+ cells. Recent reports have discussed the origin of the glioblastoma CD133+ cells and their function in the tumor microenvironment. The present work sought to investigate the multipotent and mesenchymal properties of primary highly purified human CD133+ glioblastoma-initiating cells. To accomplish this aim, we used the following approaches: i) generation of tumor subspheres of CD133+ selected cells from primary cell cultures of glioblastoma; ii) analysis of the expression of pluripotency stem cell markers and mesenchymal stem cell (MSC) markers in the CD133+ glioblastoma-initiating cells; iii) side-by-side ultrastructural characterization of the CD133+ glioblastoma cells, MSC and CD133+ hematopoietic stem cells isolated from human umbilical cord blood (UCB); iv) assessment of adipogenic differentiation of CD133+ glioblastoma cells to test their MSC-like in vitro differentiation ability; and v) use of an orthotopic glioblastoma xenograft model in the absence of immune suppression. We found that the CD133+ glioblastoma cells expressed both the pluripotency stem cell markers (Nanog, Mush-1 and SSEA-3) and MSC markers. In addition, the CD133+ cells were able to differentiate into adipocyte-like cells. Transmission electron microscopy (TEM) demonstrated that the CD133+ glioblastoma-initiating cells had ultrastructural features similar to those of undifferentiated MSCs. In addition, when administered in vivo to non-immunocompromised animals, the CD133+ cells were also able to mimic the phenotype of the original patient’s tumor. In summary, we showed that the CD133+ glioblastoma cells express molecular signatures of MSCs, neural stem cells and pluripotent stem cells, thus possibly enabling differentiation into both neural and mesodermal cell types

Genome-wide meta-analysis of cerebral white matter hyperintensities in patients with stroke.

OBJECTIVE: For 3,670 stroke patients from the United Kingdom, United States, Australia, Belgium, and Italy, we performed a genome-wide meta-analysis of white matter hyperintensity volumes (WMHV) on data imputed to the 1000 Genomes reference dataset to provide insights into disease mechanisms. METHODS: We first sought to identify genetic associations with white matter hyperintensities in a stroke population, and then examined whether genetic loci previously linked to WMHV in community populations are also associated in stroke patients. Having established that genetic associations are shared between the 2 populations, we performed a meta-analysis testing which associations with WMHV in stroke-free populations are associated overall when combined with stroke populations. RESULTS: There were no associations at genome-wide significance with WMHV in stroke patients. All previously reported genome-wide significant associations with WMHV in community populations shared direction of effect in stroke patients. In a meta-analysis of the genome-wide significant and suggestive loci (p < 5 × 10(-6)) from community populations (15 single nucleotide polymorphisms in total) and from stroke patients, 6 independent loci were associated with WMHV in both populations. Four of these are novel associations at the genome-wide level (rs72934505 [NBEAL1], p = 2.2 × 10(-8); rs941898 [EVL], p = 4.0 × 10(-8); rs962888 [C1QL1], p = 1.1 × 10(-8); rs9515201 [COL4A2], p = 6.9 × 10(-9)). CONCLUSIONS: Genetic associations with WMHV are shared in otherwise healthy individuals and patients with stroke, indicating common genetic susceptibility in cerebral small vessel disease.Funding for collection, genotyping, and analysis of stroke samples was provided by Wellcome Trust Case Control Consortium-2, a functional genomics grant from the Wellcome Trust (DNA-Lacunar), the Stroke Association (DNA-lacunar), the Intramural Research Program of National Institute of Ageing (Massachusetts General Hospital [MGH] and Ischemic Stroke Genetics Study [ISGS]), National Institute of Neurological Disorders and Stroke (Siblings With Ischemic Stroke Study, ISGS, and MGH), the American Heart Association/Bugher Foundation Centers for Stroke Prevention Research (MGH), Deane Institute for Integrative Study of Atrial Fibrillation and Stroke (MGH), National Health and Medical Research Council (Australian Stroke Genetics Collaborative), and Italian Ministry of Health (Milan). Additional support for sample collection came from the Medical Research Council, National Institute of Health Research Biomedical Research Centre and Acute Vascular Imaging Centre (Oxford), Wellcome Trust and Binks Trust (Edinburgh), and Vascular Dementia Research Foundation (Munich). MT is supported by a project grant from the Stroke Association (TSA 2013/01). HSM is supported by an NIHR Senior Investigator award. HSM and SB are supported by the NIHR Cambridge University Hospitals Comprehensive Biomedical Research Centre. VT and RL are supported by grants from FWO Flanders. PR holds NIHR and Wellcome Trust Senior Investigator Awards. PAS is supported by an MRC Fellowship. CML’s research is supported by the National Institute for Health Research Biomedical Research Centre (BRC) based at Guy's and St Thomas' NHS Foundation Trust and King's College London, and the BRC for Mental Health at South London and Maudsley NHS Foundation Trust and King’s College London. This is the final version of the article. It first appeared from Wolters Kluwer via http://dx.doi.org/10.1212/WNL.000000000000226

Life on Arginine for Mycoplasma hominis: Clues from Its Minimal Genome and Comparison with Other Human Urogenital Mycoplasmas

Mycoplasma hominis is an opportunistic human mycoplasma. Two other pathogenic human species, M. genitalium and Ureaplasma parvum, reside within the same natural niche as M. hominis: the urogenital tract. These three species have overlapping, but distinct, pathogenic roles. They have minimal genomes and, thus, reduced metabolic capabilities characterized by distinct energy-generating pathways. Analysis of the M. hominis PG21 genome sequence revealed that it is the second smallest genome among self-replicating free living organisms (665,445 bp, 537 coding sequences (CDSs)). Five clusters of genes were predicted to have undergone horizontal gene transfer (HGT) between M. hominis and the phylogenetically distant U. parvum species. We reconstructed M. hominis metabolic pathways from the predicted genes, with particular emphasis on energy-generating pathways. The Embden–Meyerhoff–Parnas pathway was incomplete, with a single enzyme absent. We identified the three proteins constituting the arginine dihydrolase pathway. This pathway was found essential to promote growth in vivo. The predicted presence of dimethylarginine dimethylaminohydrolase suggested that arginine catabolism is more complex than initially described. This enzyme may have been acquired by HGT from non-mollicute bacteria. Comparison of the three minimal mollicute genomes showed that 247 CDSs were common to all three genomes, whereas 220 CDSs were specific to M. hominis, 172 CDSs were specific to M. genitalium, and 280 CDSs were specific to U. parvum. Within these species-specific genes, two major sets of genes could be identified: one including genes involved in various energy-generating pathways, depending on the energy source used (glucose, urea, or arginine) and another involved in cytadherence and virulence. Therefore, a minimal mycoplasma cell, not including cytadherence and virulence-related genes, could be envisaged containing a core genome (247 genes), plus a set of genes required for providing energy. For M. hominis, this set would include 247+9 genes, resulting in a theoretical minimal genome of 256 genes