Dynamics, patterns and causes of fires in Northwestern Amazonia

According to recent studies, two widespread droughts occurred in the Amazon basin, one during 2005 and one during 2010. The drought increased the prevalence of climate-driven fires over most of the basin. Given the importance of human-atmosphere-vegetation interactions in tropical rainforests, these events have generated concerns over the vulnerability of this area to climate change. This paper focuses on one of the wettest areas of the basin, Northwestern Amazonia, where the interactions between the climate and fires are much weaker and where little is known about the anthropogenic drivers of fires. We have assessed the response of fires to climate over a ten-year period, and analysed the socio-economic and demographic determinants of fire occurrence. The patterns of fires and climate and their linkages in Northwestern Amazonia differ from the enhanced fire response to climate variation observed in the rest of Amazonia. The highest number of recorded fires in Northwestern Amazonia occurred in 2004 and 2007, and this did not coincide with the periods of extreme drought experienced in Amazonia in 2005 and 2010. Rather, during those years, Northwestern Amazonia experienced a relatively small numbers of fire hotspots. We have shown that fire occurrence correlated well with deforestation and was determined by anthropogenic drivers, mainly small-scale agriculture, cattle ranching (i.e., pastures) and active agricultural frontiers (including illegal crops). Thus, the particular climatic conditions for air convergence and rainfall created by proximity to the Andes, coupled with the presence of one of the most active colonisation fronts in the region, make this region differently affected by the general drought-induced fire patterns experienced by the rest of the Amazon. Moreover, the results suggest that, even in this wet region, humans are able to modify the frequency of fires and impact these historically well preserved forests.     

Cyclin-dependent kinases 4 and 6 control tumor progression and direct glucose oxidation in the pentose cycle

Cyclin-dependent kinases CDK4 and CDK6 are essential for the control of the cell cycle through the G(1) phase. Aberrant expression of CDK4 and CDK6 is a hallmark of cancer, which would suggest that CDK4 and CDK6 are attractive targets for cancer therapy. Herein, we report that calcein AM (the calcein acetoxymethyl-ester) is a potent specific inhibitor of CDK4 and CDK6 in HCT116 human colon adenocarcinoma cells, inhibiting retinoblastoma protein (pRb) phosphorylation and inducing cell cycle arrest in the G(1) phase. The metabolic effects of calcein AM on HCT116 cells were also evaluated and the flux between the oxidative and non-oxidative branches of the pentose phosphate pathway was significantly altered. To elucidate whether these metabolic changes were due to the inhibition of CDK4 and CDK6, we also characterized the metabolic profile of a CDK4, CDK6 and CDK2 triple knockout of mouse embryonic fibroblasts. The results show that the metabolic profile associated with the depletion of CDK4, CDK6 and CDK2 coincides with the metabolic changes induced by calcein AM on HCT116 cells, thus confirming that the inhibition of CDK4 and CDK6 disrupts the balance between the oxidative and non-oxidative branches of the pentose phosphate pathway. Taken together, these results indicate that low doses of calcein can halt cell division and kill tumor cells. Thus, selective inhibition of CDK4 and CDK6 may be of greater pharmacological interest, since inhibitors of these kinases affect both cell cycle progression and the robust metabolic profile of tumors.     

CPT1c is localized in endoplasmic reticulum of neurons and has carnitine palmitoyltransferase activity

CPT1c is a carnitine palmitoyltransferase 1 (CPT1) isoform that is expressed only in the brain. The enzyme has recently been localized in neuron mitochondria. Although it has high sequence identity with the other two CPT1 isoenzymes (a and b), no CPT activity has been detected to date. Our results indicate that CPT1c is expressed in neurons but not in astrocytes of mouse brain sections. Overexpression of CPT1c fused to the green fluorescent protein in cultured cells demonstrates that CPT1c is localized in the endoplasmic reticulum rather than mitochondria and that the N-terminal region of CPT1c is responsible for endoplasmic reticulum protein localization. Western blot experiments with cell fractions from adult mouse brain corroborate these results. In addition, overexpression studies demonstrate that CPT1c does not participate in mitochondrial fatty acid oxidation, as would be expected from its subcellular localization. To identify the substrate of CPT1c enzyme, rat cDNA was overexpressed in neuronal PC-12 cells, and the levels of acylcarnitines were measured by high-performance liquid chromatography-mass spectrometry. Palmitoylcarnitine was the only acylcarnitine to increase in transfected cells, which indicates that palmitoyl-CoA is the enzyme substrate and that CPT1c has CPT1 activity. Microsomal fractions of PC-12 and HEK293T cells overexpressing CPT1c protein showed a significant increase in CPT1 activity of 0.57 and 0.13 nmol.mg(-1).min(-1), respectively, which is approximately 50% higher than endogenous CPT1 activity. Kinetic studies demonstrate that CPT1c has similar affinity to CPT1a for both substrates but 20-300 times lower catalytic efficiency.     

Ghrelin Causes a Decline in GABA Release by Reducing Fatty Acid Oxidation in Cortex

Lipid metabolism, specifically fatty acid oxidation (FAO) mediated by carnitine palmitoyltransferase (CPT) 1A, has been described to be an important actor of ghrelin action in hypothalamus. However, it is not known whether CPT1A and FAO mediate the effect of ghrelin on the cortex. Here, we show that ghrelin produces a differential effect on CPT1 activity and γ-aminobutyric acid (GABA) metabolism in the hypothalamus and cortex of mice. In the hypothalamus, ghrelin enhances CPT1A activity while GABA transaminase (GABAT) activity, a key enzyme in GABA shunt metabolism, is unaltered. However, in cortex CPT1A activity and GABAT activity are reduced after ghrelin treatment. Furthermore, in primary cortical neurons, ghrelin reduces GABA release through a CPT1A reduction. By using CPT1A floxed mice, we have observed that genetic ablation of CPT1A recapitulates the effect of ghrelin on GABA release in cortical neurons, inducing reductions in mitochondrial oxygen consumption, cell content of citrate and α-ketoglutarate, and GABA shunt enzyme activity. Taken together, these observations indicate that ghrelin-induced changes in CPT1A activity modulate mitochondrial function, yielding changes in GABA metabolism. This evidence suggests that the action of ghrelin on GABA release is region specific within the brain, providing a basis for differential effects of ghrelin in the central nervous system.     

The effect of dexamethasone treatment on the expression of the regulatory genes of ketogenesis in intestine and liver of suckling rats

The influence of the injection of dexamethasone on ketogenesis in 12 day old suckling rats was studied in intestine and liver by determining mRNA levels and enzyme activity of the two genes responsible for regulation of ketogenesis: carnitine palmitoyl transferase I (CPT 1) and mitochondrial HMG-CoA synthase. Dexamethasone produced a 2 fold increase in mRNA and activity of CPT I in intestine, but led to a decrease in mitt HMG-CoA synthase. In liver the mRNA levels and activity of both CPT I and mitt HMG-CoA synthase decreased. Comparison of these values with the ketogenic rate of both tissues following dexamethasone treatment suggests that mitt HMG-CoA synthase could be the main gene responsible for the regulation of ketogenesis in suckling rats. The changes produced in serum ketone bodies by dexamethasone, with a profile that is more similar to the ketogenic rate in the liver than that in the intestine, indicate that liver contributes more to ketone body synthesis in suckling rats. Two day treatment with dexamethasone produced no change in mRNA or activity levels for CPT I in liver or intestine. While mRNA levels for mitt HMG-CoA synthase changed little, the enzyme activity is decreased in both tissues.     

Influence of clay licks on the diversity and structure of an Amazonian forest

The spatial heterogeneity of resource availability is a major driver of biodiversity patterns. Some environmental conditions and resources are characterized by large‐scale patterns of variation within the landscape. Clumped local discontinuities or discrete elements also increase spatial heterogeneity, promoting local ‘biodiversity hot spots’ by modifying habitat characteristics and promoting plant–animal interactions. Clay licks are faunal attractors owing to their role in the nutritional ecology of the user species; nevertheless, the effect of their presence on the surrounding vegetation has been poorly quantified. Here, we use data from 100 × 10 m transects and evaluate the effects of the presence of clay licks on forest diversity and structure at local and landscape scales. In clay lick areas, there was a higher abundance of certain species, which helps to homogenize species composition between localities counteracting the natural distance‐decay of compositional similarity between transects without clay lick influence (controls). Compared to control sites, clay lick′s forests had higher palm densities, shorter but more variable individuals in the canopy and understory, a thinner canopy layer, and denser herbaceous and ground level covers. These differences were found along the whole length of transects in both sampled areas types. These results reveal that the presence of discrete elements (i.e., clay licks) may help to explain the compositional and structural heterogeneity of Amazonian forests influencing ecological processes such as seed dispersal and trampling. These considerations may be relevant for other biomes where clay licks are present and give weight to their inclusion in conservation initiatives in tropical forests.     

Long-Term Macroevaluation of Environmental Enrichment in Three Brown Bears (Ursus arctos) at Barcelona Zoo

The evaluation of enrichment programs is important to determine their effect on nonhuman animal welfare. The daily activity pattern and use of space of 3 brown bears (Ursus arctos) were used for long-term macroevaluation of enrichment to compare the baseline and enrichment phases. Focal sampling methods were used for data collection, and instantaneous scans were made at 2-min intervals during 15 sessions of 1 hr for each animal during the 2 study periods. The enrichment devices were categorized as feeding, occupational, and sensorial. The long-term macroevaluation in 3 bears showed statistically significant differences in some types of activity but not in others. There were also statistically significant differences for the use of space in 4 of the 8 zones in which the enclosures were divided. A more homogenous pattern in the use of space was only observed during the enrichment phase in the old female. The 3 brown bears followed different patterns concerning the enrichment program.     

Monospecies and multispecies probiotic formulations produce different systemic and local immunostimulatory effects in the gilthead seabream (Sparus aurata L.)

The effects of the oral administration of heat-inactivated Lactobacillus delbrüeckii ssp. lactis and Bacillus subtilis, individually or combined, on gilthead seabream immune responses were investigated both systemically and locally in the gut. In a first experiment, seabream (65 g) were fed for 3 weeks different diets supplemented with 1 x 10(7)CFU g(-1)Lactobacillus, 1 x 10(7)CFU g(-1)Bacillus, or 0.5 x 10(7)CFU g(-1)Lactobacillus plus 0.5 x 10(7)CFU g(-1)Bacillus. Controls were fed non-supplemented diet. Six fish per group were sampled at the end of the trial and some humoral and cellular systemic innate immune parameters were evaluated. Feeding the mixture of the two killed bacteria species significantly increased natural complement, serum peroxidase and phagocytic activities compared with controls. In a second experiment, juvenile seabream (13 g) were fed for 3 weeks the same experimental diets and total serum IgM and numbers of gut IgM(+) cells and acidophilic granulocytes were evaluated. All these parameters were significantly higher in the multispecies probiotic group compared to monospecies and control fed groups. The advantages provided by administration of killed probiotic bacteria as well as multispecies versus monospecies formulations are discussed in light of the results obtained and for their possible application in aquacultural practices.     

Kinetic modelling of aldolase-catalyzed addition between dihydroxyacetone phosphate and (S)-alaninal

This paper is focused on the development of a kinetic model for an aldolase-catalyzed reaction. The aldol addition between dihydroxyacetone phosphate (DHAP) and (S)-benzyloxycarbonyl-alaninal ((S)-Cbz-alaninal) catalyzed by the four DHAP-dependent aldolases is a promising way for the synthesis of four complementary diastereoisomers with potential biological activity. The reaction catalyzed by fuculose-1-phosphate aldolase (FucA) conducts to a synthesis product with a 100% diastereomeric excess. A kinetic model has been proposed including both the synthesis and a parallel non-desired secondary reaction. The model involved an ordered two-substrate mechanism for the synthesis and non-competitive inhibition by (S)-Cbz-alaninal and competitive inhibition by methylglyoxal byproduct in both reactions. The values of the model kinetic parameters were determined and the model validated in batch and fed-batch synthesis reactions. The obtained model could be extended to explain the behavior of other class II DHAP-dependent aldolases and exploited in simulation for reactor design purposes.