Modelling Hot Spots of Soil Loss by Wind Erosion (SoLoWind) in Western Saxony, Germany

Land Degradation and Development published by John Wiley & Sons, Ltd. While it needs yet to be assessed whether or not wind erosion in Western Saxony is a major point of concern regarding land degradation and fertility, it has already been recognized that considerable off-site effects of wind erosion in the adjacent regions of Saxony-Anhalt and Brandenburg are connected to the spread of herbicides, pesticides and dust. So far, no wind erosion assessment for Western Saxony, Germany, exists. The wind erosion model previously applied for Germany (DIN standard 19706) is considering neither changes in wind direction over time nor influences of field size. This study aims to provide a first assessment of wind erosion for Western Saxony by extending the existing DIN model to a multidirectional model on soil loss by wind (SoLoWind) with new controlling factors (changing wind directions, soil cover, mean field length and mean protection zone) combined by fuzzy logic. SoLoWind is used for a local off-site effect evaluation in combination with high-resolution wind speed and wind direction data at a section of the highway A72. The model attributes 3·6% of the arable fields in Western Saxony to the very-high-wind erosion risk class. A relationship between larger fields (greater than 116 ha) and higher proportions (51·7%) of very-high-wind erosion risk can be observed. Sections of the highway A72 might be under high risk according to the modelled off-site effects of wind erosion. The presented applications showed the potential of SoLoWind to support and consult management for protection measures on a regional scale. © 2016 The Authors. Land Degradation and Development published by John Wiley & Sons, Ltd.The authors would like to thank Jürgen Heinrich and Gudrun Mayer for the technical revision of the model conception and the German Weather Service, the Saxon State Office for the Environment, Agriculture and Geology, the Saxon State Office for Road Construction and Traffic, the Saxon State Ministry of the Environment and Agriculture, the Saxon State Spatial Data and Land Survey Corporation, the Saxon Road Maintenance Depots, OpenStreetMap and the National Aeronautics and Space Administration for providing the datasets. We would also like to thank three anonymous reviewers for helpful comments.info:eu-repo/semantics/publishedVersio

Variation in flexural, morphological, and biochemical leaf properties of eelgrass (Zostera marina) along the European Atlantic climate regions

Seagrasses need to withstand hydrodynamic forces; therefore, mechanical properties such as flexibility or breaking resistance are beneficial for survival. The co-variation of leaf breaking properties with biochemical traits in seagrasses has been documented, but it is unknown if the same patterns apply to leaf flexural properties. To interpret changes in the ecological function of seagrass ecosystems based on acclimation responses to environmental changes, it is necessary to understand the factors that affect flexural leaf properties. Here, morphological and flexural leaf properties of the perennial type of Zostera marina across different environmental conditions along European Atlantic climate regions are presented together with C:N ratio and neutral detergent fibre content as descriptors of biochemical leaf composition. Eelgrass leaves from cold regions were similar to threefold more elastic and similar to tenfold more flexible, were also narrower (1.7-fold), and contained similar to 1.9-fold higher fibre content than from plants growing in warmer regions. Eelgrass also showed acclimation to local conditions such as seasonality, water depth, and hydrodynamic exposure. Leaves collected from exposed or shallower locations or during winter were more flexible, suggesting an avoidance strategy to hydrodynamic forcing, which is generally higher under those conditions. Flexural rigidity was almost equally controlled by bending modulus (35%) and leaf thickness (37%), indicating functional differences compared to leaf breaking described in the literature. Overall, the findings indicate that Zostera marina has a high flexural plasticity and high acclimation capacity to some climate change effects such as sea level rise and increase in storm frequency and intensity.German Science FoundationGerman Research Foundation (DFG) [PA 2547/1-1]Royal Swedish Academy of Sciences (KVA travel grant)FCT-Foundation for Science and TechnologyPortuguese Foundation for Science and Technology [UID/Multi/04326/2019, SFRH/BPD/119344/2016

Stromal gene signatures in large-B-cell lymphomas.

BACKGROUND: The addition of rituximab to combination chemotherapy with cyclophosphamide, doxorubicin, vincristine, and prednisone (CHOP), or R-CHOP, has significantly improved the survival of patients with diffuse large-B-cell lymphoma. Whether gene-expression signatures correlate with survival after treatment of diffuse large-B-cell lymphoma is unclear. METHODS: We profiled gene expression in pretreatment biopsy specimens from 181 patients with diffuse large-B-cell lymphoma who received CHOP and 233 patients with this disease who received R-CHOP. A multivariate gene-expression-based survival-predictor model derived from a training group was tested in a validation group. RESULTS: A multivariate model created from three gene-expression signatures--termed germinal-center B-cell, stromal-1, and stromal-2 --predicted survival both in patients who received CHOP and patients who received R-CHOP. The prognostically favorable stromal-1 signature reflected extracellular-matrix deposition and histiocytic infiltration. By contrast, the prognostically unfavorable stromal-2 signature reflected tumor blood-vessel density. CONCLUSIONS: Survival after treatment of diffuse large-B-cell lymphoma is influenced by differences in immune cells, fibrosis, and angiogenesis in the tumor microenvironment

Inflammation, genetic background and longevity

Ageing is an inexorable intrinsic process that affects all cells, tissues, organs and individuals. Due to a diminished homeostasis and increased organism frailty, ageing causes a reduction of the response to environmental stimuli and, in general, is associated to an increased predisposition to illness and death. Actually, it is characterized by a state of reduced ability to maintain health and general homeodynamics of the organism.Alarge part of the ageing phenotype is explained by an imbalance between inflammatory and anti-inflammatory networks, which results in the low grade chronic pro-inflammatory status of ageing, ‘‘inflamm-ageing’’. It is strictly linked to immunosenescence, and on the whole they are the major contributory factors to the increased frequency of morbidity and mortality among elderly. Inflammageing is compatible with longevity; even if centenarians have an increased level of inflammatory mediators in comparison to old subjects and they are very frail, they also have high level of anti-inflammatory cytokines together with protective genotypes. Actually, data on case control studies performed in Italian centenarians suggest that a pro-inflammatory genotype is unfavourable to reach extreme longevity in good health and likely favours the onset of age-related diseases such as cardiovascular diseases and Alzheimer’s disease, the leading causes of mortality and disability in the elderly. However, many associations between gene variants and longevity have been found only in Italian population. This should not be unexpected, since ageing and longevity are complex traits resulting not only and not exclusively from genetics, but rather from the interactions between genetics, environment and chance

The integration of lipid-sensing and anti-inflammatory effects: how the PPARs play a role in metabolic balance

The peroxisomal proliferating-activated receptors (PPARs) are lipid-sensing transcription factors that have a role in embryonic development, but are primarily known for modulating energy metabolism, lipid storage, and transport, as well as inflammation and wound healing. Currently, there is no consensus as to the overall combined function of PPARs and why they evolved. We hypothesize that the PPARs had to evolve to integrate lipid storage and burning with the ability to reduce oxidative stress, as energy storage is essential for survival and resistance to injury/infection, but the latter increases oxidative stress and may reduce median survival (functional longevity). In a sense, PPARs may be an evolutionary solution to something we call the 'hypoxia-lipid' conundrum, where the ability to store and burn fat is essential for survival, but is a 'double-edged sword', as fats are potentially highly toxic. Ways in which PPARs may reduce oxidative stress involve modulation of mitochondrial uncoupling protein (UCP) expression (thus reducing reactive oxygen species, ROS), optimising forkhead box class O factor (FOXO) activity (by improving whole body insulin sensitivity) and suppressing NFkB (at the transcriptional level). In light of this, we therefore postulate that inflammation-induced PPAR downregulation engenders many of the signs and symptoms of the metabolic syndrome, which shares many features with the acute phase response (APR) and is the opposite of the phenotype associated with calorie restriction and high FOXO activity. In genetically susceptible individuals (displaying the naturally mildly insulin resistant 'thrifty genotype'), suboptimal PPAR activity may follow an exaggerated but natural adipose tissue-related inflammatory signal induced by excessive calories and reduced physical activity, which normally couples energy storage with the ability to mount an immune response. This is further worsened when pancreatic decompensation occurs, resulting in gluco-oxidative stress and lipotoxicity, increased inflammatory insulin resistance and oxidative stress. Reactivating PPARs may restore a metabolic balance and help to adapt the phenotype to a modern lifestyle

An overlooked connection: serotonergic mediation of estrogen-related physiology and pathology

BACKGROUND: In humans, serotonin has typically been investigated as a neurotransmitter. However, serotonin also functions as a hormone across animal phyla, including those lacking an organized central nervous system. This hormonal action allows serotonin to have physiological consequences in systems outside the central nervous system. Fluctuations in estrogen levels over the lifespan and during ovarian cycles cause predictable changes in serotonin systems in female mammals. DISCUSSION: We hypothesize that some of the physiological effects attributed to estrogen may be a consequence of estrogen-related changes in serotonin efficacy and receptor distribution. Here, we integrate data from endocrinology, molecular biology, neuroscience, and epidemiology to propose that serotonin may mediate the effects of estrogen. In the central nervous system, estrogen influences pain transmission, headache, dizziness, nausea, and depression, all of which are known to be a consequence of serotonergic signaling. Outside of the central nervous system, estrogen produces changes in bone density, vascular function, and immune cell self-recognition and activation that are consistent with serotonin's effects. For breast cancer risk, our hypothesis predicts heretofore unexplained observations of the opposing effects of obesity pre- and post-menopause and the increase following treatment with hormone replacement therapy using medroxyprogesterone. SUMMARY: Serotonergic mediation of estrogen has important clinical implications and warrants further evaluation