Correlation among soil enzyme activities under different forest system management practices

Soil enzyme activities were performed in three permanent no-till and unfertilised plots located in the South of Salamanca province (Spain), the first in a Castanea sativa Mill. paraclimax coppice (CC), the second in a chestnut orchard (CO) and the third in a Quercus pyrenaica Wild. climax forest (Oak), adjacent to the CO plot.We hypothesized that the activities of dehydrogenases, ureases, acid phosphatases, arylsulphatases and β-glucosidases in different forest ecosystems are involved in the carbon, nitrogen and phosphorus cycling and we report their relationship with each other and with physical, chemical and general biochemical parameters of the soils. The main aim of the study was to detect biological criteria for sustainable development in natural degenerate forests of Mediterranean Europe. For this, we used sweet Chestnut (C. sativa Mill) and Oak Q. pyrenaica Wild as models to better define the ecological conditions of these natural resources in terms of nutrient balance, physiology and biological diversity of their communities, to relate them to the conditions of exploitation and land-use changes, for the characterization of sustainable ecological systems.Furthermore, soil respiration was high and significantly different in the chestnut coppice stand than the other two stands, chestnut orchard and oak.Correlations between soil biochemical and soil microbiological variables showed that the three different forest management practices had also a strong effect on soil function conditions. In a discriminate analysis, CC and Oak were discriminated clearly, while CO was in the middle of the biplot sharing some properties with each of the two different groups. Thus, we proposed a soil property transition from the best soil structure and function properties at one chestnut management properties with low tree densities (CC and CO) to other with the worst ones at highest tree density conditions (Oak). According to natural soil conditions in Oak, we assumed that most of the enzyme activities reached their highest levels at highest C and N soil contents but at lowest soil base saturation percentage while they were not at all associated with P soil availability.     

A Re-Appraisal of the Early Andean Human Remains from Lauricocha in Peru

The discovery of human remains from the Lauricocha cave in the Central Andean highlands in the 1960’s provided the first direct evidence for human presence in the high altitude Andes. The skeletons found at this site were ascribed to the Early to Middle Holocene and represented the oldest known population of Western South America, and thus were used in several studies addressing the early population history of the continent. However, later excavations at Lauricocha led to doubts regarding the antiquity of the site. Here, we provide new dating, craniometric, and genetic evidence for this iconic site. We obtained new radiocarbon dates, generated complete mitochondrial genomes and nuclear SNP data from five individuals, and re-analyzed the human remains of Lauricocha to revise the initial morphological and craniometric analysis conducted in the 1960’s. We show that Lauricocha was indeed occupied in the Early to Middle Holocene but the temporal spread of dates we obtained from the human remains show that they do not qualify as a single contemporaneous population. However, the genetic results from five of the individuals fall within the spectrum of genetic diversity observed in pre-Columbian and modern Native Central American populations.     

Phosphoenolpyruvate carboxykinase and glucose-6-phosphate dehydrogenase expression in fetal hepatocyte primary cultures under proliferative conditions

Fetal hepatocytes cultured for 64 h in the presence of glucagon and dexamethasone maintain a quiescent state, showing a low expression of glucose-6-phosphate dehydrogenase (G6PD) and a high induction of phosphoenolpyruvate carboxykinase (PEPCK). Under these culture conditions, the presence of EGF produced hepatocyte proliferation, with a concomitant increase of DNA synthesis, DNA content, and G6PD expression, meanwhile the expression of PEPCK was drastically reduced. The presence of forskolin plus IBMX nearly suppressed the increase in DNA synthesis and G6PD expression induced by EGF, showing a very high expression of PEPCK. Accordingly, it is possible to establish an inverse relation between G6PD, highly expressed in proliferating fetal hepatocytes, and PEPCK expression, highly expressed in quiescent fetal hepatocytes under specific hormonal stimulation.     

Putative association of a mutant ROM1 allele with retinitis pigmentosa

Retinitis pigmentosa (RP) is a clinically and genetically heterogeneous form of retinal degeneration. Several genes and loci have been shown to be involved in the disease, although each of them only accounts for a few cases. Mutations in the gene encoding ROM1, a rod-specific protein, have been putatively associated with several forms of RP. Here we describe a double-mutant allele of this gene, P60T and T108M, present in two affected sibs and also in two healthy members of a Spanish RP family. The same double-mutant allele was previously considered to be responsible for autosomal dominant RP in one family. We now report data that question the potential pathogenicity of these two ROM1 mutations. Received: 30 July 1996 / Revised: 13 December 1996     

Organellar proteomics of human platelet dense granules reveals that 14-3-3zeta is a granule protein related to atherosclerosis

Dense granules, a type of platelet secretory organelle, are known to accumulate high concentrations of small molecules such as calcium, adenine nucleotides, serotonin, pyrophosphate, and polyphosphate. Protein composition of these granules has been obscure, however. In this paper, we use proteomics techniques to describe, for the first time, the soluble protein composition of platelet dense granules. We have isolated highly enriched human platelet dense granule fractions that have been analyzed using two proteomics methods. Using this approach, we have identified 40 proteins, and most of them, such as actin-associated proteins, glycolytic enzymes, and regulatory proteins, have not previously been related to the organelle. We have focused our efforts on studying 14-3-3zeta, a member of a conserved family of proteins that interact with hundreds of different proteins. We have demonstrated that 14-3-3zeta is localized mostly on dense granules and that it is secreted after platelet activation. As some proteins secreted from activated platelets could promote the development of atherosclerosis and thrombosis, we have studied the expression of 14-3-3zeta in sections of human abdominal aorta of patients with aneurysm, identifying it at the atherosclerotic plaques. Together, our results reveal new details of the composition of the platelet dense granule and suggest an extracellular function for 14-3-3zeta associated with atherosclerosis.     

Accuracy vs. computational time: translating aortic simulations to the clinic

State of the art simulations of aortic haemodynamics feature full fluid-structure interaction (FSI) and coupled 0D boundary conditions. Such analyses require not only significant computational resource but also weeks to months of run time, which compromises the effectiveness of their translation to a clinical workflow. This article employs three computational fluid methodologies, of varying levels of complexity with coupled 0D boundary conditions, to simulate the haemodynamics within a patient-specific aorta. The most comprehensive model is a full FSI simulation. The simplest is a rigid walled incompressible fluid simulation while an alternative middle-ground approach employs a compressible fluid, tuned to elicit a response analogous to the compliance of the aortic wall. The results demonstrate that, in the context of certain clinical questions, the simpler analysis methods may capture the important characteristics of the flow field.     

Protein-tyrosine phosphatase 1B (PTP1B) deficiency confers resistance to transforming growth factor-β (TGF-β)-induced suppressor effects in hepatocytes

Transforming growth factor-β (TGF-β) plays a dual role in hepatocytes, mediating both tumor suppressor and promoter effects. The suppressor effects of the cytokine can be negatively regulated by activation of survival signals, mostly dependent on tyrosine kinase activity. The aim of our work was to study the role of the protein-tyrosine phosphatase 1B (PTP1B) on the cellular responses to TGF-β, using for this purpose immortalized neonatal hepatocytes isolated from both PTP1B(+/+) and PTP1B(-/-) mice. We have found that PTP1B deficiency conferred resistance to TGF-β suppressor effects, such as apoptosis and growth inhibition, correlating with lower Smad2/Smad3 activation. Both responses were recovered in the presence of the general tyrosine kinase inhibitor genistein. PTP1B(-/-) cells showed elevated NF-κB activation in response to TGF-β. Knockdown of the NF-κB p65 subunit increased cell response in terms of Smads phosphorylation and apoptosis. Interestingly, these effects were accompanied by inhibition of Smad7 up-regulation. In addition, lack of PTP1B promoted an altered NADPH oxidase (NOX) expression pattern in response to TGF-β, strongly increasing the NOX1/NOX4 ratio, which was reverted by genistein and p65 knockdown. Importantly, NOX1 knockdown inhibited nuclear translocation of p65, promoted Smad phosphorylation, and decreased Smad7 levels. In summary, our results suggest that PTP1B deficiency confers resistance to TGF-β through Smad inhibition, an effect that is mediated by NOX1-dependent NF-κB activation, which in turn, increases the level of the Smad inhibitor Smad7 and participates in a positive feedback loop on NOX1 up-regulation.