Sediments in urban river basins: identification of sediment sources within the Lago Paranoá catchment, Brasilia DF, Brazil - using the fingerprint approach.

The development of effective sediment management strategies is a key requirement in tropical areas with fast urban development, like Brasilia DF, Brazil, because of the limited resources available. Accurate identification and management of sediment sources areas, however, is hampered by the dearth of reliable information on the primary sources of sediment. Few studies have attempted to quantify the source of sediment within fast urbanizing, mixed used, tropical catchments. In this study, statistically verified composite fingerprints and a multivariate mixing model have been used to identify the main land use specific sources of sediment deposited in the artificial Lago Paranoá, Central Brazil. Because of the variability of urban land use types within the Lago Paranoá sub-catchments, the fingerprinting approach was additionally undertaking for the Riacho Fundo sub-catchment. The main contributions from individual source types (i.e. surface materials from residential areas, constructions sites, road deposited sediment, cultivated areas, pasture, farm tracks, woodland and natural gullies) varied between the whole catchment and the Riacho Fundo sub-catchment, reflecting the different proportions of land uses. The sediments deposited in the silting zones of the Lago Paranoá originate largely from urban sources (85 ± 4%). Areas with (semi-) natural vegetation and natural gullies contribute 10 ± 2% of the sediment yield. Agricultural sites have only a minor sediment contribution of about 5 ± 4% within the whole catchment. Within the Riacho Fundo sub-catchment there is a significant contribution from urban (53 ± 4%) source, such as residential areas with semi-detached housings (42 ± 3%) with unpaved roads (12 ± 3%) and construction sites (20 ± 3%) and agricultural areas (31 ± 2%). The relative contribution from land use specific sources to the sediment deposition in the silting zone of the Lago Paranoá demonstrated that most of the sediment is derived from sites with high anthropogenic impact.

Geochemical signature and properties of sediment sources and alluvial sediments within the Lago Paranoá catchment, Brasilia DF: a study on anthropogenic introduced chemical elements in an urban river basin.

One of the largest urban agglomerations in Brazil is the capital Brasilia and its surrounding area. Due to fast urban sprawl and accelerated land use changes, available water supplies are near their limits. The water supply depends largely on surface water collected in reservoirs. There are increasing concerns regarding water shortages due to sediment aggradations, and of water quality due to geochemical modification of sediments from human activities. The concentration of 18 chemical elements and five sediment properties was analyzed from different potential land-based sediment sources and deposited alluvial sediment within the Lago Paranoà catchment. The goal of this study was to assess the distribution of chemical elements and geochemical/physical properties of potential sediment sources in the Lago Paranoá catchment. Principal component analysis and hierarchical cluster analysis were used to investigate the influence of different land use types on the geochemistry of sediments. Geochemical fingerprints of anthropogenic activities were developed based on the results of the cluster analysis grouping. The anthropogenic input of land use specific geochemical elements was examined and quantified by the calculation of enrichment factors using the local geological background as reference. Through comparison of the geochemical signature of potential sediment sources and alluvial sediments of the Lago Paranoá and sub-catchments, the relative contribution of land use specific sediment sources to the sediment deposition of the main water reservoir were estimated. The existing findings suggest a strong relationship between land use and quantifiable features of sediment geochemistry and indicate that urban land use had the greatest responsibility for recent silting in the Lago Paranoá. This assessment helps to characterize the role of human activities in mixed-used watersheds on sediment properties, and provides essential information to guide management responses towards more effective source-reduction strategies.

E2F1 loss induces spontaneous tumour development in Rb-deficient epidermis.

The specific ablation of Rb1 gene in epidermis (Rb(F/F);K14cre) promotes proliferation and altered differentiation but does not produce spontaneous tumour development. These phenotypic changes are associated with increased expression of E2F members and E2F-dependent transcriptional activity. Here, we have focused on the possible dependence on E2F1 gene function. We have generated mice that lack Rb1 in epidermis in an inducible manner (Rb(F/F);K14creER(TM)). These mice are indistinguishable from those lacking pRb in this tissue in a constitutive manner (Rb(F/F);K14cre). In an E2F1-null background (Rb(F/F);K14creER(TM); and E2F1(-/-) mice), the phenotype due to acute Rb1 loss is not ameliorated by E2F1 loss, but rather exacerbated, indicating that pRb functions in epidermis do not rely solely on E2F1. On the other hand, Rb(F/F);K14creER(TM);E2F1(-/-) mice develop spontaneous epidermal tumours of hair follicle origin with high incidence. These tumours, which retain a functional p19(arf)/p53 axis, also show aberrant activation of ß-catenin/Wnt pathway. Gene expression studies revealed that these tumours display relevant similarities with specific human tumours. These data demonstrate that the Rb/E2F1 axis exerts essential functions not only in maintaining epidermal homoeostasis, but also in suppressing tumour development in epidermis, and that the disruption of this pathway may induce tumour progression through specific alteration of developmental programs.

A Web-based planning support tool for sediment management in a meso-scale river basin in Western Central Brazil.

In scope of an IWRM concept for the Federal District, Western Central Brazil we developed a planning support tool, which enables non-experts to test the effects of land-use and land-cover change (LULCC) on landscape processes and landscape functions (LPF) related to sediment generation and retention. For this purpose we developed the web-based tool Letsmap do Brasil. The tool has two principal layers. The upper layer contains information on land use and its effect on LPF, i.e. sediment retention, runoff control, nitrogen loss control and agronomic value. The parameterized relation between land use and LPF is the core of the whole system. For each LPF a value specific to land use has been assigned. A second layer contains information on landscape properties and potentials (LPP), e.g. potential for sediment input in river networks and runoff potential. By linking land use and LPPs the system provides a spatially explicit assessment of effects of LULCC on landscape processes and functions (LPF). Letsmap do Brasil might have two major purposes. (1) It will support decision-making in river basin management and sediment management. By creating their own land-use/cover pattern non-expert users are enabled to test effects of LULCC on LPFs. (2) It will support and train non-experts to participate in decision processes in land-use planning. Because of its high adaptability, transparency, and simple handling Letsmap do Brasil might be used as tool in river basin management and land-use planning.

Testing the indicative value of magnetic susceptibility measurements for concluding on site potentials and risks provoked by fly ash deposition.

The article presents results of testing the indicative value of magnetic susceptibility for fly ash deposition and its effects on forest site properties. Base saturation and concentrations of Ca and Mg were used as indicators for nutrient pools resulting from fly ash deposition. Concentrations of Fe, Al, Mn, Cd and Black Carbon were used as indicators for risks of leaching. The correlation of magnetic susceptibility with concentrations of nutrient, acidic cations, heavy metals, base saturation and Black Carbon was calculated. Additionally, we tested the suitability of magnetic susceptibility as a parameter in a linear regression based model to predict the concentrations of Ca, Mg, Fe, Al, Mn, Cd and Black Carbon. We were able to show a positive correlation between magnetic susceptibility and the selected indicators. In contrast to previous studies, we were also able to demonstrate the suitability of magnetic susceptibility to predict the size of fly ash deposition influenced nutrient pools mainly for humus layers, especially for Oa horizons. The spatial distribution of magnetic susceptibility showed also a positive correlation with regionalized base saturation. However, because of the data base and other factors impacting the measurement and modeling results, some shortcomings of using a linear regression model must be noted. From these results, we concluded that magnetic susceptibility might be a valuable parameter in a multiple regression based approach, but should not be used alone for predicting effects of fly ash deposition.

GIS-based probability assessment of natural hazards in forested landscapes of Central and South-Eastern Europe.

We assessed the probability of three major natural hazards--windthrow, drought, and forest fire--for Central and South-Eastern European forests which are major threats for the provision of forest goods and ecosystem services. In addition, we analyzed spatial distribution and implications for a future oriented management of forested landscapes. For estimating the probability of windthrow, we used rooting depth and average wind speed. Probabilities of drought and fire were calculated from climatic and total water balance during growing season. As an approximation to climate change scenarios, we used a simplified approach with a general increase of pET by 20%. Monitoring data from the pan-European forests crown condition program and observed burnt areas and hot spots from the European Forest Fire Information System were used to test the plausibility of probability maps. Regions with high probabilities of natural hazard are identified and management strategies to minimize probability of natural hazards are discussed. We suggest future research should focus on (i) estimating probabilities using process based models (including sensitivity analysis), (ii) defining probability in terms of economic loss, (iii) including biotic hazards, (iv) using more detailed data sets on natural hazards, forest inventories and climate change scenarios, and (v) developing a framework of adaptive risk management.

How to support forest management in a world of change: results of some regional studies.

This article presents results of several studies in Middle, Eastern and Southeastern Europe on needs and application areas, desirable attributes and marketing potentials of forest management support tools. By comparing present and future application areas, a trend from sectoral planning towards landscape planning and integration of multiple stakeholder needs is emerging. In terms of conflicts, where management support tools might provide benefit, no clear tendencies were found, neither on local nor on regional level. In contrast, on national and European levels, support of the implementation of laws, directives, and regulations was found to be of highest importance. Following the user-requirements analysis, electronic tools supporting communication are preferred against paper-based instruments. The users identified most important attributes of optimized management support tools: (i) a broad accessibility for all users at any time should be guaranteed, (ii) the possibility to integrate iteratively experiences from case studies and from regional experts into the knowledge base (learning system) should be given, and (iii) a self-explanatory user interface is demanded, which is also suitable for users rather inexperienced with electronic tools. However, a market potential analysis revealed that the willingness to pay for management tools is very limited, although the participants specified realistic ranges of maximal amounts of money, which would be invested if the products were suitable and payment inevitable. To bridge the discrepancy between unwillingness to pay and the need to use management support tools, optimized financing or cooperation models between practice and science must be found.

[Transcriptomics illustrate a deadly TRAIL to diabetic nephropathy]. / La transcriptómica ilustra nuevas vías letales en la nefropatía diabética.

Diabetic nephropathy is the most common cause of endstage renal disease. Approaches targeting angiotensin II significantly delay its progression. However, many patients still need renal replacement therapy. High throughput techniques such as unbiased gene expression profiling and proteomics may identify new therapeutic targets. Cell death is thought to contribute to progressive renal cell depletion in chronic nephropathies. A European collaborative effort recently applied renal biopsy transcriptomics to identify novel mediators of renal cell death in diabetic nephropathy. Twenty-five percent of cell death regulatory genes were upor downregulated in diabetic kidneys. TNF-related apoptosisinducing ligand (TRAIL) and osteoprotegerin had the highest level of expression. In diabetic nephropathy, tubular cells and podocytes express TRAIL. Inflammatory cytokines, including MIF via CD74, upregulate TRAIL. A high glucose environment sensitized renal cells to the lethal effect of TRAIL, while osteoprotegerin is protective. These results suggest that, in addition to glucose levels, inflammation and TRAIL are therapeutic targets in diabetic nephropathy.

Cytokine cooperation in renal tubular cell injury: the role of TWEAK.

Tumor necrosis factor (TNF)-like weak inducer of apoptosis (TWEAK, TNFSF12) is a member of the TNF superfamily. TWEAK activates the Fn14 receptor, and may regulate apoptosis, proliferation, and inflammation, processes that play a significant role in pathological conditions. However, there is little information on the function and regulation of this system in the kidney. Therefore, TWEAK and Fn14 expression were studied in cultured murine tubular epithelial MCT cells and in mice in vivo. The effect of TWEAK on cell death was determined. We found that TWEAK and Fn14 expression was increased in experimental acute renal failure induced by folic acid. Cultured tubular cells express both TWEAK and the Fn14 receptor. TWEAK did not induce cell death in non-stimulated tubular cells. However, in cells costimulated with TNFalpha/interferon-gamma, TWEAK induced apoptosis through the activation of the Fn14 receptor. Apoptosis was associated with activation of caspase-8, caspase-9, and caspase-3, Bid cleavage, and evidence of mitochondrial injury. There was no evidence of endoplasmic reticulum stress. A pan-caspase inhibitor benzyloxycarbonyl-Val-Ala-DL-Asp prevented TWEAK-induced apoptosis, but it sensitized cells to necrosis via generation of reactive oxygen species. In conclusion, cooperation between inflammatory cytokines results in tubular cell death. TWEAK and Fn14 may play a role in renal tubular cell injury.

Lethal activity of FADD death domain in renal tubular epithelial cells.

Fas-associated death domain (FADD) is an adaptor protein that is required for the transmission of the death signal from lethal receptors of the tumor necrosis factor superfamily. FADD contains a death domain (DD) and a death effector domain (DED). As death receptors contribute to renal tubular injury and tubular cell FADD increases in acute renal failure, we have studied the function of FADD in tubular epithelium. FADD expression was studied in kidney samples from mice. In order to study the contribution of FADD to renal tubular cell survival, FADD or FADD-DD were overexpressed in murine tubular epithelium. FADD is expressed in renal tubules of the healthy kidney. Both FADD and FADD-DD induce apoptosis in primary cultures of murine tubular epithelium and in the murine cortical tubular cell line. Death induced by FADD-DD has apoptotic morphology, but differs from death receptor-induced apoptosis in that it is not blocked by inhibitors of caspases. Neither an inhibitor of serine proteases nor overexpression of antiapoptotic BclxL prevented cell death. However, the combination of caspase and serine protease inhibition was protective. FADD and FADD-DD overexpression decreased nuclear factor kappa B activity. These data suggest that FADD has a death regulatory function in renal tubular cells that is independent of death receptors. FADD-DD is sufficient to induce apoptosis in these cells. This information is relevant to understanding the role of FADD in tubular injury.

Modulation of renal tubular cell survival: where is the evidence?

Tubular cell loss is prominent both in acute and chronic renal failure. Apoptosis and its regulatory mechanisms contribute to cell number regulation in the kidney. The potential role of apoptosis ranges from induction and progression to repair of renal injury. However, therapeutic interest has focused in preventing the apoptotic loss of tubular cells that leads to acute and chronic renal failure. Death ligands and receptors, such as tumor necrosis factor and Fas ligand, proapoptotic and antiapoptotic Bcl2 family members and caspases have all been shown to participate in apoptosis regulation in the course of renal cell injury. Nevertheless, the precise role of these proteins is unclear, and the participation of most known apoptosis regulatory proteins has not been studied. We now review the role of apoptosis in renal injury, the potential molecular targets of therapeutic intervention, the therapeutic weapons to modulate the activity of these targets and the few examples of therapeutic intervention on apoptosis, with emphasis in acute renal failure.

Isatin, an endogenous monoamine oxidase inhibitor, triggers a dose- and time-dependent switch from apoptosis to necrosis in human neuroblastoma cells.

Isatin is an endogenous indole that is increased in stress, inhibits monoamine oxidase (MAO) B and improves bradykinesia and striatal dopamine levels in rat models of Parkinson's disease. Consequently, it has been suggested that isatin might be a possible treatment for Parkinson's disease although little is known about its effects on neural cell growth and survival. The aim of this study was to investigate the survival of dopaminergic human neuroblastoma (SH-SY5Y) cells following treatment with increasing concentrations of isatin. SH-SY5Y cells were exposed to isatin for defined time points, after which cell survival was determined by MTT assay. A combination of Annexin V binding and propidium iodide (PI) exclusion was used to distinguish apoptosis from necrosis in flow cytometry experiments and FACS profiles of permeabilised PI-labelled cells were employed for the assessment of cell cycle distribution. Isatin treatment (1-400 microM) for 24h induced a significant dose-dependent increase in MTT metabolism by SH-SY5Y cells in culture, but this was not due to an increase in cell division. At the higher concentrations (200-400 microm) isatin triggered cell death, although MTT metabolism was still increased in the culture, suggesting that surviving cells were hypermetabolic. Following a longer (48 h) exposure, isatin was found to cause cell death in a dose-dependent manner; at lower concentrations (50 microM), the predominant mode of cell death was apoptosis while at the highest concentration (400 microm) increasing numbers of necrotic cells were also evident. Thus, in dopaminergic SH-SY5Y cells isatin induces cell death in dose- and time-dependent manner. This death occurred as a continuum of survival, apoptosis and necrosis. Our results re-emphasise that caution should be exercised when considering high doses of isatin as a putative anti-Parkinson's disease therapeutic.

Modeling and monitoring of long-term acidification in an upland catchment of the Western Ore Mountains, SE Germany.

Modeling and monitoring of acidification patterns in a limed forest catchment in the Ore Mountains, SE Germany are presented. A lumped-parameter model, MAGIC, satisfactorily reproduced the main parameters of stream water chemistry. Despite repeated whole-catchment liming, between 1993 and 1999 stream water pH increased from 4.3 to only 4.6, while calcium concentrations declined slightly. Stream water sulfate concentration declined from 687 to 396 microeq l(-1), and the pronounced effect of deposition decline during the 1990s was probably more important than liming.

Apoptotic cell death in renal injury: the rationale for intervention.

Cell number abnormalities are frequent in renal diseases, and range from the hypercellularity of postinfectious glomerulonephritis to the cell depletion of chronic renal atrophy. Recent research has shown that apoptosis and its regulatory mechanisms contribute to cell number regulation in the kidney. The potential role of apoptosis ranges from induction and progression to repair of renal injury. Death ligands and receptors, such as tumor necrosis factor and Fas ligand, proapoptotic and antiapoptotic Bcl2 family members and caspases have all been shown to participate in apoptosis regulation in the course of renal cell injury. However, the precise role of these proteins is unclear, and the participation of most known apoptosis regulatory proteins has not been studied. We now review the role of apoptosis in renal injury, the potential molecular targets of therapeutic intervention, the therapeutic weapons to modulate the activity of these targets and the few examples of therapeutic intervention on apoptosis, with emphasis on the acute tubular necrosis.

Contribution of apoptotic cell death to renal injury.

Cell number abnormalities are frequent in renal diseases, and range from the hypercellularity of postinfectious glomerulonephritis to the cell depletion of chronic renal atrophy. Recent research has shown that apoptosis and its regulatory mechanisms contribute to cell number regulation in the kidney. The role of apoptosis ranges from induction to repair and progression of renal injury. Death ligands and receptors, such as TNF and FasL, proapoptotic and antiapoptotic Bcl-2 family members and caspases have all been shown to participate in apoptosis regulation in the course of renal injury. These proteins represent potential therapeutic targets, which should be further explored.

Role and regulation of apoptotic cell death in the kidney. Y2K update.

Apoptosis is an active form of cell death that, in balance with mitosis, regulates cell number. Cell number abnormalities are a frequent feature of renal disease. We now review current concepts on the molecular regulation of apoptotic cell death, including the influence of survival and lethal factors from the extracellular microenvironment as well as the role of intracellular regulators of apoptosis, such as death receptors, proapoptotic and antiapoptotic bcl2-related proteins, the mitochondria and caspases. In addition the role of apoptosis in the genesis, persistence and progression and remodeling and resolution of renal injury is discussed. Information on the expression and function of apoptosis regulatory proteins in specific renal syndromes is summarized. Finally, future perspectives in research and clinical intervention are discussed.

Expression of apoptosis regulatory proteins in tubular epithelium stressed in culture or following acute renal failure.

BACKGROUND: While tubular cell death is a characteristic of acute renal failure (ARF), the molecular mechanisms that modulate this cell death are unclear. Cell fate in acute renal failure hinges on a balance of survival and mortality factors in a changing environment. We further explored this issue by studying selected cell death-related proteins in experimental renal failure. METHOD: The expression of genes that promote (c-myc, Bax, BclxS) or protect (Bcl2, BclxL) from cell death was studied by Northern blot, Western blot, and immunohistochemistry in murine kidneys following ARF induced by folic acid or in renal tubular epithelial cells (MCT) stressed in culture. RESULTS: Renal mRNA levels encoding for c-myc and BclxL were elevated in ARF while the Bcl2/Bax ratio was decreased (Bcl2 decreased and Bax increased; P < 0.05). Protein levels of BclxL increased and Bcl2 protein decreased. Expression of tumor necrosis factor (TNF-alpha), a mediator of ARF, was also increased. Immunohistochemistry further demonstrated that BclxL was increased in some tubuli and absent in others, while Bcl2 expression decreased diffusely. Bax staining was also patchy among tubuli and individual cells in the tubular wall and lumen. As a relative deficit of survival factors is present in ARF, MCT epithelium were deprived of serum survival factors. This resulted in apoptosis, decreased Bcl2/Bax and BclxL/Bax ratios (P < 0.05) and sensitization to TNF-alpha-induced apoptosis (P < 0.05). The latter was prevented by enforced overexpression of BclxL (P < 0.01). TNF-alpha increased the mRNA levels encoding for c-myc and decreased BclxL expression. Neither MCT cells nor the kidney expressed BclxS. CONCLUSIONS: A relative deficit of survival factors likely contributes to changes in levels of BclxL and Bax in ARF. These deficits predispose to cell death induced by persistent lethal factors such as TNF-alpha that is increased in ARF and a potential source of increased c-myc, a downstream facilitator of cell death. These findings implicate members of the Bcl2 family of proteins as regulators of tubular cell death in ARF and single them out as potential therapeutic targets.

The Fas ligand/Fas system in renal injury.

The FasL-Fas system regulates renal cell apoptosis, as well as the immune and inflammatory responses. Evidence that FasL and Fas participate in renal injury may be summarized along modified Koch's postulates (Table 1): (i) FasL is expressed by renal cells and during renal injury, (ii) activation of the Fas receptor promotes apoptosis of cultured renal cells, (iii) Fas agonists induce glomerular injury but they may also decrease renal injury by limiting injurious immunological responses, (iv) mice with disrupted FasL/Fas systems are protected from tubular cell injury during ischaemia reperfusion, although they develop autoimmune glomerulonephritis if other genetic predisposing factors are present. FasL/Fas must be considered a new target for therapeutic intervention in renal injury. Therapeutic modulation of Fas should aim not only at protecting intrinsic glomerular or tubular epithelial cells from death, but also at modulating the immune, inflammatory, and fibrogenic responses. Possible therapeutic interventions include Fas agonists, soluble Fas receptors, or other antagonists, and targetting of Fas to undesired cells, such as fibroblasts, in order to decrease their numbers in a physiological manner through apoptosis. Any therapeutic attempt should carefully take into account the possible effects of interference with Fas in other 1833 cell systems. Given the complexities of the FasL/Fas system, further studies are warranted.