Historical carbon emissions and uptake from the agricultural frontier of the Brazilian Amazon

Tropical ecosystems play a large and complex role in the global carbon cycle. Clearing of natural ecosystems for agriculture leads to large pulses of CO(2) to the atmosphere from terrestrial biomass. Concurrently, the remaining intact ecosystems, especially tropical forests, may be sequestering a large amount of carbon from the atmosphere in response to global environmental changes including climate changes and an increase in atmospheric CO(2). Here we use an approach that integrates census-based historical land use reconstructions, remote-sensing-based contemporary land use change analyses, and simulation modeling of terrestrial biogeochemistry to estimate the net carbon balance over the period 1901-2006 for the state of Mato Grosso, Brazil, which is one of the most rapidly changing agricultural frontiers in the world. By the end of this period, we estimate that of the state`s 925 225 km(2), 221 092 km(2) have been converted to pastures and 89 533 km(2) have been converted to croplands, with forest-to-pasture conversions being the dominant land use trajectory but with recent transitions to croplands increasing rapidly in the last decade. These conversions have led to a cumulative release of 4.8 Pg C to the atmosphere, with similar to 80% from forest clearing and 20% from the clearing of cerrado. Over the same period, we estimate that the residual undisturbed ecosystems accumulated 0.3 Pg C in response to CO2 fertilization. Therefore, the net emissions of carbon from Mato Grosso over this period were 4.5 Pg C. Net carbon emissions from Mato Grosso since 2000 averaged 146 Tg C/yr, on the order of Brazil`s fossil fuel emissions during this period. These emissions were associated with the expansion of croplands to grow soybeans. While alternative management regimes in croplands, including tillage, fertilization, and cropping patterns promote carbon storage in ecosystems, they remain a small portion of the net carbon balance for the region. This detailed accounting of a region`s carbon balance is the type of foundation analysis needed by the new United Nations Collaborative Programmme for Reducing Emissions from Deforestation and Forest Degradation (REDD).

Greenhouse gas emissions from alternative futures of deforestation and agricultural management in the southern Amazon

The Brazilian Amazon is one of the most rapidly developing agricultural areas in the world and represents a potentially large future source of greenhouse gases from land clearing and subsequent agricultural management. In an integrated approach, we estimate the greenhouse gas dynamics of natural ecosystems and agricultural ecosystems after clearing in the context of a future climate. We examine scenarios of deforestation and postclearing land use to estimate the future (2006-2050) impacts on carbon dioxide (CO(2)), methane (CH(4)), and nitrous oxide (N(2)O) emissions from the agricultural frontier state of Mato Grosso, using a process-based biogeochemistry model, the Terrestrial Ecosystems Model (TEM). We estimate a net emission of greenhouse gases from Mato Grosso, ranging from 2.8 to 15.9 Pg CO(2)-equivalents (CO(2)-e) from 2006 to 2050. Deforestation is the largest source of greenhouse gas emissions over this period, but land uses following clearing account for a substantial portion (24-49%) of the net greenhouse gas budget. Due to land-cover and land-use change, there is a small foregone carbon sequestration of 0.2-0.4 Pg CO(2)-e by natural forests and cerrado between 2006 and 2050. Both deforestation and future land-use management play important roles in the net greenhouse gas emissions of this frontier, suggesting that both should be considered in emissions policies. We find that avoided deforestation remains the best strategy for minimizing future greenhouse gas emissions from Mato Grosso.

The Amazon Frontier of Land-Use Change: Croplands and Consequences for Greenhouse Gas Emissions

The Brazilian Amazon is one of the most rapidly developing agricultural frontiers in the world. The authors assess changes in cropland area and the intensification of cropping in the Brazilian agricultural frontier state of Mato Grosso using remote sensing and develop a greenhouse gas emissions budget. The most common type of intensification in this region is a shift from single-to double-cropping patterns and associated changes in management, including increased fertilization. Using the enhanced vegetation index (EVI) from the Moderate Resolution Imaging Spectroradiometer (MODIS) sensor, the authors created a green-leaf phenology for 2001-06 that was temporally smoothed with a wavelet filter. The wavelet-smoothed green-leaf phenology was analyzed to detect cropland areas and their cropping patterns. The authors document cropland extensification and double-cropping intensification validated with field data with 85% accuracy for detecting croplands and 64% and 89% accuracy for detecting single-and double-cropping patterns, respectively. The results show that croplands more than doubled from 2001 to 2006 to cover about 100 000 km(2) and that new double-cropping intensification occurred on over 20% of croplands. Variations are seen in the annual rates of extensification and double-cropping intensification. Greenhouse gas emissions are estimated for the period 2001-06 due to conversion of natural vegetation and pastures to row-crop agriculture in Mato Grosso averaged 179 Tg CO(2)-e yr(-1),over half the typical fossil fuel emissions for the country in recent years.

Wavelet analysis of MODIS time series to detect expansion and intensification of row-crop agriculture in Brazil

Since 2000, the southwestern Brazilian Amazon has undergone a rapid transformation from natural vegetation and pastures to row-crop agricultural with the potential to affect regional biogeochemistry. The goals of this research are to assess wavelet algorithms applied to MODIS time series to determine expansion of row-crops and intensification of the number of crops grown. MODIS provides data from February 2000 to present, a period of agricultural expansion and intensification in the southwestern Brazilian Amazon. We have selected a study area near Comodoro, Mato Grosso because of the rapid growth of row-crop agriculture and availability of ground truth data of agricultural land-use history. We used a 90% power wavelet transform to create a wavelet-smoothed time series for five years of MODIS EVI data. From this wavelet-smoothed time series we determine characteristic phenology of single and double crops. We estimate that over 3200 km(2) were converted from native vegetation and pasture to row-crop agriculture from 2000 to 2005 in our study area encompassing 40,000 km(2). We observe an increase of 2000 km(2) of agricultural intensification, where areas of single crops were converted to double crops during the study period. (C) 2007 Elsevier Inc. All rights reserved.

Robust Control of Flight Simulator Motion Base

The purpose of this study is to apply robust inverse dynamics control for a six-degree-of-freedom flight simulator motion system. From an implementation viewpoint, simplification of the inverse dynamics control law is introduced by assuming control law matrices as constants. The robust control strategy is applied in the outer loop of the inverse dynamic control to counteract the effects of imperfect compensation due this simplification. The control strategy is designed using the Lyapunov stability theory. Forward and inverse kinematics and a full dynamic model of a six-degree-of-freedom motion base driven by electromechanical actuators are briefly presented. A describing function, acceleration step response and some maneuvers computed from the washout filter were used to evaluate the performance of the controllers.

FOOD, FUEL, FORESTS, AND THE PRICING OF ECOSYSTEM SERVICES

U.S. Department of Energy (DOE), Office of Science[DE-FG02-94ER61937]

Indirect Emissions from Biofuels: How Important?

A global biofuels program will lead to intense pressures on land supply and can increase greenhouse gas emissions from land-use changes. Using linked economic and terrestrial biogeochemistry models, we examined direct and indirect effects of possible land-use changes from an expanded global cellulosic bioenergy program on greenhouse gas emissions over the 21st century. Our model predicts that indirect land use will be responsible for substantially more carbon loss ( up to twice as much) than direct land use; however, because of predicted increases in fertilizer use, nitrous oxide emissions will be more important than carbon losses themselves in terms of warming potential. A global greenhouse gas emissions policy that protects forests and encourages best practices for nitrogen fertilizer use can dramatically reduce emissions associated with biofuels production.

Cross-cultural adaptation and validation of a Quality of Life questionnaire: The Nasal Obstruction Symptom Evaluation questionnaire

Background:The Nasal Obstruction Symptom Evaluation (NOSE) instrument is a disease-specific questionnaire for assessing the outcome of an intervention in nasal obstruction in trials. This instrument is only available in the English language and cross-culturally valid questionnaires are very important for all research, including nasal obstruction. The aim of the current study was to reproduce the cross-cultural adaptation process for the NOSE questionnaire in the Portuguese language (NOSE-p). Methodology: Cross-cultural adaptation and validation of the instrument were divided into two stages. Stage I involved four bilingual professionals, an expert committee and the author of the original instrument. In Stage 2, the NOSE-p was tested on 33 patients undergoing septoplasty for internal consistency, test-retest reliability, construct validity. discriminant validity, criterion validity, and response sensitivity. Results: The cross-cultural adaptation process was completed and the NOSE-p was demonstrated to be a valid instrument with satisfactory construct validity. It showed an adequate internal consistency reliability and adequate test-retest reliability. It could discriminate between patients with and without nasal obstruction and it has a high response sensitivity to change. Conclusions: The cross-cultural adaptation and validation process demonstrated to be valid and the NOSE-p proved to be applicable in Brazil.

Mutations in NOTCH2 cause Hajdu-Cheney syndrome, a disorder of severe and progressive bone loss

We used an exome-sequencing strategy and identified an allelic series of NOTCH2 mutations in Hajdu-Cheney syndrome, an autosomal dominant multisystem disorder characterized by severe and progressive bone loss. The Hajdu-Cheney syndrome mutations are predicted to lead to the premature truncation of NOTCH2 with either disruption or loss of the C-terminal proline-glutamate-serine-threonine-rich proteolytic recognition sequence, the absence of which has previously been shown to increase Notch signaling.

Association Between Polymorphisms in GRIK2 Gene and Obsessive-Compulsive Disorder: A Family-Based Study

Several studies support a genetic influence on obsessive-compulsive disorder (OCD) etiology. The role of glutamate as an important neurotransmitter affecting OCD pathophysiology has been supported by neuroimaging, animal model, medication, and initial candidate gene studies. Genes involved in glutamatergic pathways, such as the glutamate receptor, ionotropic, kainate 2 (GRIK2), have been associated with OCD in previous studies. This study examines GRIK2 as a candidate gene for OCD susceptibility in a family-based approach. Probands had full DSM-IV diagnostic criteria for OCD. Forty-seven OCD probands and their parents were recruited from tertiary care OCD specialty clinics from France and USA. Genotypes of single nucleotide polymorphism (SNP) markers and related haplotypes were analyzed using Haploview and FBAT software. The polymorphism at rs1556995 (P = 0.0027; permuted P-value = 0.03) was significantly associated with the presence of OCD. Also, the two marker haplotype rs1556995/rs1417182, was significantly associated with OCD (P = 0.0019, permuted P-value = 0.01). This study supports previously reported findings of association between proximal GRIK2 SNPs and OCD in a comprehensive evaluation of the gene. Further study with independent samples and larger sample sizes is required.

Further delineation of the 15q13 microdeletion and duplication syndromes: a clinical spectrum varying from non-pathogenic to a severe outcome

Background: Recurrent 15q13.3 microdeletions were recently identified with identical proximal (BP4) and distal (BP5) breakpoints and associated with mild to moderate mental retardation and epilepsy. Methods: To assess further the clinical implications of this novel 15q13.3 microdeletion syndrome, 18 new probands with a deletion were molecularly and clinically characterised. In addition, we evaluated the characteristics of a family with a more proximal deletion between BP3 and BP4. Finally, four patients with a duplication in the BP3-BP4-BP5 region were included in this study to ascertain the clinical significance of duplications in this region. Results: The 15q13.3 microdeletion in our series was associated with a highly variable intra-and inter-familial phenotype. At least 11 of the 18 deletions identified were inherited. Moreover, 7 of 10 siblings from four different families also had this deletion: one had a mild developmental delay, four had only learning problems during childhood, but functioned well in daily life as adults, whereas the other two had no learning problems at all. In contrast to previous findings, seizures were not a common feature in our series (only 2 of 17 living probands). Three patients with deletions had cardiac defects and deletion of the KLF13 gene, located in the critical region, may contribute to these abnormalities. The limited data from the single family with the more proximal BP3-BP4 deletion suggest this deletion may have little clinical significance. Patients with duplications of the BP3-BP4-BP5 region did not share a recognisable phenotype, but psychiatric disease was noted in 2 of 4 patients. Conclusions: Overall, our findings broaden the phenotypic spectrum associated with 15q13.3 deletions and suggest that, in some individuals, deletion of 15q13.3 is not sufficient to cause disease. The existence of microdeletion syndromes, associated with an unpredictable and variable phenotypic outcome, will pose the clinician with diagnostic difficulties and challenge the commonly used paradigm in the diagnostic setting that aberrations inherited from a phenotypically normal parent are usually without clinical consequences.

Characterization of acid-base status in maintenance hemodialysis: physicochemical approach

Acidosis is a common and deleterious aspect of maintenance dialysis. Traditionally, it is considered to be an elevated anion gap acidosis caused by the inability to excrete nonvolatile anions. Stewart`s approach made it possible to identify real determinants of the acid-base status and allowed quantification of the components of these disturbances, especially the unmeasured anions. We performed a cross-sectional study to identify and quantify each component of acidosis in hemodialysis maintenance patients. Sixty-four maintenance hemodialysis patients and 14 controls were enrolled in this study. Gasometrical and biochemical analysis were performed before the midweek dialysis session. Quantitative physicochemical analysis was carried out using the Stewart methodology. Hemodialysis patients were found to have mild acidemia (mean pH: 7.33 +/- 0.06 versus 7.41 +/- 0.05) secondary to metabolic acidosis (serum bicarbonate: 18.8 +/- 0.26 versus 25.2 +/- 0.48 mEq/l). The metabolic acidosis was due to retention of unmeasured anions (6.5 +/- 0.29 versus 3.1 +/- 0.62 mEq/l), hyperchloremia (105.1 +/- 0.5 versus 101.8 +/- 0.7 mEq/l), and hyperphosphatemia (5.90 +/- 0.19 versus 3.66 +/- 0.14 mg/dl). Compared with control values, the unmeasured anions and hyperchloremia had a similar acidifying effect (3.4 and 3.3 mEq/l), corresponding to almost 90% of the metabolic acidosis. Unmeasured anions and hyperchloremia are important components of acidosis in maintenance hemodialysis, in addition to phosphorus. Future studies to determine the etiology and consequences of hyperchloremic acidosis are warranted.

Atrogin-1 and MuRF1 regulate cardiac MyBP-C levels via different mechanisms

Familial hypertrophic cardiomyopathy (FHC) is frequently caused by cardiac myosin-binding protein C (cMyBP-C) gene mutations, which should result in C-terminal truncated mutants. However, truncated mutants were not detected in myocardial tissue of FHC patients and were rapidly degraded by the ubiquitin-proteasome system (UPS) after gene transfer in cardiac myocytes. Since the diversity and specificity of UPS regulation lie in E3 ubiquitin ligases, we investigated whether the muscle-specific E3 ligases atrogin-1 or muscle ring finger protein-1 (MuRF1) mediate degradation of truncated cMyBP-C. Human wild-type (WT) and truncated (M7t, resulting from a human mutation) cMyBP-C species were co-immunoprecipitated with atrogin-1 after adenoviral overexpression in cardiac myocytes, and WT-cMyBP-C was identified as an interaction partner of MuRF1 by yeast two-hybrid screens. Overexpression of atrogin-1 in cardiac myocytes decreased the protein level of M7t-cMyBP-C by 80% and left WT-cMyBP-C level unaffected. This was rescued by proteasome inhibition. In contrast, overexpression of MuRF1 in cardiac myocytes not only reduced the protein level of WT- and M7t-cMyBP-C by > 60%, but also the level of myosin heavy chains (MHCs) by > 40%, which were not rescued by proteasome inhibition. Both exogenous cMyBP-C and endogenous MHC mRNA levels were markedly reduced by MuRF1 overexpression. Similar to cardiac myocytes, MuRF1-overexpressing (TG) mice exhibited 40% lower levels of MHC mRNAs and proteins. Protein levels of cMyBP-C were 29% higher in MuRF1 knockout and 34% lower in TG than in WT, without a corresponding change in mRNA levels. These data suggest that atrogin-1 specifically targets truncated M7t-cMyBP-C, but not WT-cMyBP-C, for proteasomal degradation and that MuRF1 indirectly reduces cMyBP-C levels by regulating the transcription of MHC.

Mechanisms Involved in 3 `,5 `-Cyclic Adenosine Monophosphate-Mediated Inhibition of the Ubiquitin-Proteasome System in Skeletal Muscle

Although it is well known that catecholamines inhibit skeletal muscle protein degradation, the molecular underlying mechanism remains unclear. This study was undertaken to investigate the role of beta(2)-adrenoceptors (AR) and cAMP in regulating the ubiquitin-proteasome system (UPS) in skeletal muscle. We report that increased levels of cAMP in isolated muscles, promoted by the cAMP phosphodiesterase inhibitor isobutyl methylxanthine was accompanied by decreased activity of the UPS, levels of ubiquitin-protein conjugates, and expression of atrogin-1, a key ubiquitin-protein ligase involved in muscle atrophy. In cultured myotubes, atrogin-1 induction after dexamethasone treatment was completely prevented by isobutyl methylxanthine. Furthermore, administration of clenbuterol, a selective beta(2)-agonist, to mice increased muscle cAMP levels and suppressed the fasting-induced expression of atrogin-1 and MuRF-1, atrogin-1 mRNA being much more responsive to clenbuterol. Moreover, clenbuterol increased the phosphorylation of muscle Akt and Foxo3a in fasted rats. Similar responses were observed in muscles exposed to dibutyryl-cAMP. The stimulatory effect of clenbuterol on cAMP and Akt was abolished in muscles from beta(2)-AR knockout mice. The suppressive effect of beta(2)-agonist on atrogin-1 was not mediated by PGC-1 alpha (peroxisome proliferator-activated receptor-gamma coactivator 1 alpha known to be induced by beta(2)-agonists and previously shown to inhibit atrogin-1 expression), because food-deprived PGC-1 alpha knockout mice were still sensitive to clenbuterol. These findings suggest that the cAMP increase induced by stimulation of beta(2)-AR in skeletal muscles from fasted mice is possibly the mechanism by which catecholamines suppress atrogin-1 and the UPS, this effect being mediated via phosphorylation of Akt and thus inactivation of Foxo3. (Endocrinology 150: 5395-5404, 2009)

TAC3/TACR3 Mutations Reveal Preferential Activation of Gonadotropin-Releasing Hormone Release by Neurokinin B in Neonatal Life Followed by Reversal in Adulthood

Context: Mutations in TAC3 and TACR3 (encoding neurokinin B and its receptor) have been identified in Turkish patients with idiopathic hypogonadotropic hypogonadism (IHH), but broader populations have not yet been tested and genotype-phenotype correlations have not been established. Objective: A broad cohort of normosmic IHH probands was screened for mutations in TAC3/TACR3 to evaluate the prevalence of such mutations and define the genotype/phenotype relationships. Design and Setting: The study consisted of sequencing of TAC3/TACR3, in vitro functional assays, and neuroendocrine phenotyping conducted in tertiary care centers worldwide. Patients or Other Participants: 345 probands, 18 family members, and 292 controls were studied. Intervention: Reproductive phenotypes throughout reproductive life and before and after therapy were examined. Main Outcome Measure: Rare sequence variants in TAC3/TACR3 were detected. Results: In TACR3, 19 probands harbored 13 distinct coding sequence rare nucleotide variants [three nonsense mutations, six nonsynonymous, four synonymous (one predicted to affect splicing)]. In TAC3, one homozygous single base pair deletion was identified, resulting in complete loss of the neurokinin B decapeptide. Phenotypic information was available on 16 males and seven females with coding sequence variants in TACR3/TAC3. Of the 16 males, 15 had microphallus; none of the females had spontaneous thelarche. Seven of the 16 males and five of the seven females were assessed after discontinuation of therapy; six of the seven males and four of the five females demonstrated evidence for reversibility of their hypogonadotropism. Conclusions: Mutations in the neurokinin B pathway are relatively common as causes of hypogonadism. Although the neurokinin B pathway appears essential during early sexual development, its importance in sustaining the integrity of the hypothalamic-pituitary-gonadal axis appears attenuated over time. (J Clin Endocrinol Metab 95: 2857-2867, 2010)