Refine
Document Type
- Article (3)
Has Fulltext
- yes (3)
Is part of the Bibliography
- no (3)
Keywords
- Cerrado (1)
- MaxEnt (1)
- Per1−/−-mice (1)
- aging (1)
- agricultural commodity (1)
- autophagy (1)
- deforestation (1)
- hippocampus (1)
- infrastructure improvements (1)
- land-use/cover change modeling (1)
- lipofuscin (1)
- microglia (1)
- oxidative stress (1)
- tropical conservation (1)
- ß-amyloid (1)
Institute
Historically, the expansion of soy plantations has been a major driver of land-use/cover change (LUCC) in Brazil. While a series of recent public actions and supply-chain commitments reportedly curbed the replacement of forests by soy, the expansion of the agricultural commodity still poses a considerable threat to the Amazonian and Cerrado biomes. Identification of areas under high risk of soy expansion is thus paramount to assist conservation efforts in the region. We mapped the areas suitable for undergoing transition to soy plantations in the Legal Amazon with a machine-learning approach adopted from the ecological modeling literature. Simulated soy expansion for the year 2014 exhibited favorable validation scores compared to other LUCC models. We then used our model to simulate how potential future infrastructure improvements would affect the 2014 probabilities of soy occurrence in the region. In addition to the 2.3 Mha of planted soy in the Legal Amazon in 2014, our model identified another 14.7 Mha with high probability of soy conversion in the region given the infrastructure conditions at that time. Out of those, pastures and forests represented 9.8 and 0.4 Mha, respectively. Under the new infrastructure scenarios simulated, the Legal Amazonian area under high risk of soy conversion increased by up to 2.1 Mha (14.6%). These changes led to up to 11.4 and 51.4% increases in the high-risk of conversion areas of pastures and forests, respectively. If conversion occurs in the identified high-risk areas, at least 4.8 Pg of CO2 could be released into the atmosphere, a value that represents 10 times the total CO2 emissions of Brazil in 2014. Our results highlight the importance of targeting conservation policies and enforcement actions, including the Soy Moratorium, to mitigate future forest cover loss associated with infrastructure improvements in the region.
Die 15 bisher in der Gattung Conostomum eingeschlossenen Arten werden auf 7 reduziert. Conostomum aequinoctiale Schimp. ex C.Müll., C. lorentzii C. Müll., C. pentastichum (Brid.) Lindb., C. pusillum Hook. f. et Wils. und C. speirostichum C. Müll. sind synonym mit C. tetragonum,(Hedw.) Lindb. Conostomum giganteum Bartr. ist nicht mit C. pentastichum identisch, sondern eine gute Art, die bislang nur von der Typuslokalität in Neuseeland bekannt war und jetzt neu für Australien und die Campbell Islands angegeben wird. Conostomum crassinervium P. Varde, eine nur vom Mt. Kenia bekannte Art, besitzt nicht die für die Gattung typische 5reihige Beblätterung. Da die Art nur steril bekannt ist, ist ihre systematische Position nicht klar.
In humans, alterations of circadian rhythms and autophagy are linked to metabolic, cardiovascular and neurological dysfunction. Autophagy constitutes a specific form of cell recycling in many eukaryotic cells. Aging is the principal risk factor for the development of neurodegenerative diseases. Thus, we assume that both the circadian clock and autophagy are indispensable to counteract aging. We have previously shown that the hippocampus of Per1−/−-mice exhibits a reduced autophagy and higher neuronal susceptibility to ischemic insults compared to wild type (WT). Therefore, we chose to study the link between aging and loss of clock gene Per1−/−-mice. Young and aged C3H- and Per1−/−-mice were used as models to analyze the hippocampal distribution of Aβ42, lipofuscin, presenilin, microglia, synaptophysin and doublecortin. We detected several changes in the hippocampus of aged Per1−/−-mice compared to their wild type littermates. Our results show significant alterations of microglia morphology, an increase in Aβ42 deposition, overexpression of presenilin, decrease in synaptophysin levels and massive accumulation of lipofuscin in the hippocampus of 24-month-old Per1−/−-mice, without alteration of adult neurogenesis. We suggest that the marked lipofuscin accumulation, Aβ42 deposition, and overexpression of presenilin-2 observed in our experiments may be some of the consequences of the slowed autophagy in the hippocampus of aged Per1−/−-mice. This may lead during aging to excessive accumulation of misfolded proteins which may, consequently, result in higher neuronal vulnerability.