784 research outputs found

    Pyrolysis of organic side stream materials for the production of biochar as an amendment in green roofs: Characterization and field experiments

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    Green roofs offer a solution to worldwide problems in cities like: the urban heat island effect, floods and the loss of rural regions. Nevertheless, the widespread application of green roofs still faces some serious challenges, e.g. an excessive amount of drainage water, an excess of nutrients in this water, and plant mortality in periods of severe drought. Also, the production process of the components of these substrates, such as expanded clay, is not environmentally and energy-friendly. Biochar amendment in green roof substrates can help to overcome these problems because of its valuable properties like a high nutrient content, high waterholding capacity (WHC), low density and its self-sustaining production process. In this research, biochar is produced from six different side streams in a pilot-scale rotating kiln carbonization reactor (kg/hour input). These side streams consists out of: MDF, date palm, coffee skins, tree bark, olive stones and a waste wood mix. The produced biochars are characterized with multiple physico-chemical analyses like biochar yield, elemental composition, surface functional groups, morphology, WHC, cation exchange capacity and polyaromatic hydrocarbons (PAH’s). Furthermore, a techno-economical analysis is performed on the large-scale production of these biochars. Small scale (0,25 m2) and field experiments (2.5 m2) with biochar incorporated in commercially available green roof substrates in the temperate climate of the Netherlands and Belgium examine whether biochar can offer a solution to the described problems. Based on the analyses of the biochar, in particular the PAH’s and elemental composition, and the small scale growth experiments, two different biochars made from the waste wood mix and tree bark in concentrations of 1 and 5 % are selected for the field experiments. Growth of Sedum plants is monitored with digital imaging processing over a period of several months, starting from November 2018. Several chemical and physical parameters are monitored and linked to the properties of the biochar incorporated substrate like pH, conductivity, nutrient leaching and waterholding capacity

    Transgenic Mouse Model for Reducing Oxidative Damage in Bone

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    Exposure to musculoskeletal disuse and radiation result in bone loss; we hypothesized that these catabolic treatments cause excess reactive oxygen species (ROS), and thereby alter the tight balance between bone resorption by osteoclasts and bone formation by osteoblasts, culminating in bone loss. To test this, we used transgenic mice which over-express the human gene for catalase, targeted to mitochondria (MCAT). Catalase is an anti-oxidant that converts the ROS hydrogen peroxide into water and oxygen. MCAT mice were shown previously to display reduced mitochondrial oxidative stress and radiosensitivity of the CNS compared to wild type controls (WT). As expected, MCAT mice expressed the transgene in skeletal tissue, and in marrow-derived osteoblasts and osteoclast precursors cultured ex vivo, and also showed greater catalase activity compared to wildtype (WT) mice (3-6 fold). Colony expansion in marrow cells cultured under osteoblastogenic conditions was 2-fold greater in the MCAT mice compared to WT mice, while the extent of mineralization was unaffected. MCAT mice had slightly longer tibiae than WT mice (2%, P less than 0.01), although cortical bone area was slightly lower in MCAT mice than WT mice (10%, p=0.09). To challenge the skeletal system, mice were treated by exposure to combined disuse (2 wk Hindlimb Unloading) and total body irradiation Cs(137) (2 Gy, 0.8 Gy/min), then bone parameters were analyzed by 2-factor ANOVA to detect possible interaction effects. Treatment caused a 2-fold increase (p=0.015) in malondialdehyde levels of bone tissue (ELISA) in WT mice, but had no effect in MCAT mice. These findings indicate that the transgene conferred protection from oxidative damage caused by treatment. Unexpected differences between WT and MCAT mice emerged in skeletal responses to treatment.. In WT mice, treatment did not alter osteoblastogenesis, cortical bone area, moment of inertia, or bone perimeter, whereas in MCAT mice, treatment increased these parameters. Taken together, this typically catabolic treatment (disuse and irradiation) appeared to stimulate cortical expansion in MCAT mice but not WT mice. In conclusion, these results reveal the importance of mitochondrial ROS generation in skeletal remodeling and show that MCAT mice provide a useful animal model for bone studies

    Two European Cornus L. feeding leafmining moths, Antispila petryi Martini, 1899, sp. rev. and A. treitschkiella (Fischer von Röslerstamm, 1843) (Lepidoptera, Heliozelidae): an unjustified synonymy and overlooked range expansion

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    Antispila treitschkiella (Fischer von Röslerstamm, 1843) and A. petryi Martini, 1899, sp. rev. were regarded as synonymous since 1978, but are shown to be two clearly separated species with different hostplants, life histories, DNA barcodes and morphology. Antispila treitschkiella feeds on Cornus mas L., is bivoltine, and has, by following its ornamentally planted host, greatly expanded its range in north-western Europe. In contrast A. petryi feeds on the widespread native C. sanguinea L., is univoltine, and is one of only two Antispila species previously resident in the British Isles, the Netherlands and northern Europe. Consequently, the increase in abundance of A. treitschkiella in the Netherlands since the early 1990s and in Great Britain in recent years must be regarded as part of a recent expansion into north-western Europe, whereas the native A. petryi is hardly expanding and less abundant. In Britain, detailed surveys of parks and living collections confirmed the monophagy of these two species. A search of British herbarium samples provided no evidence for an earlier date of establishment. Information on recognition of all stages, including DNA barcodes, and distribution is provided, and these two species are compared with the third European Cornus L. leafminer, A. metallella (Denis & Schiffermüller, 1775)

    Ionizing Radiation Stimulates Expression of Pro-Osteoclastogenic Genes in Marrow and Skeletal Tissue

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    Exposure to ionizing radiation can cause rapid mineral loss and increase bone-resorbing osteoclasts within metabolically-active, cancellous-bone tissue leading to structural deficits. To better understand mechanisms involved in rapid, radiation-induced bone loss, we determined the influence of total-body irradiation on expression of select cytokines known both to stimulate osteoclastogenesis and contribute to inflammatory bone disease. Adult (16wk), male C57BL/6J mice were exposed to either 2Gy gamma rays (137Cs, 0.8Gy/min) or heavy ions (56Fe, 600MeV, 0.50-1.1Gy/min); this dose corresponds to either a single fraction of radiotherapy (typical total dose is 10Gy) or accumulates over long-duration, interplanetary missions. Serum, marrow, and mineralized tissue were harvested 4hrs-7d later. Gamma irradiation caused a prompt (2.6-fold within 4hrs) and persistent (peaking at 4.1-fold within 1d) rise in the expression of the obligate osteoclastogenic cytokine, receptor activator of nuclear factor kappaB-ligand (Rankl) within marrow cells over controls. Similarly, Rankl expression peaked in marrow cells within 3d of iron exposure (9.2-fold). Changes in Rankl expression induced by gamma irradiation preceded and overlapped with a rise in expression of other pro-osteoclastic cytokines in marrow (e.g., monocyte chemotactic protein-1 increased 11.9-fold, tumor necrosis factor-alpha increased 1.7- fold over controls). Marrow expression of the RANKL decoy receptor, osteoprotegerin (Opg), also rose after irradiation (11.3-fold). The ratio Rankl/Opg in marrow was increased 1.8-fold, a net pro-resorption balance. As expected, radiation increased a serum marker of resorption (tartrate resistant acid phosphatase) and led to cancellous bone loss (16% decrease in bone volume/total volume) through reduced trabecular struts. We conclude that total-body irradiation (gamma or heavy-ion) caused temporal, concerted regulation of gene expression within marrow and mineralized tissue for select cytokines which are responsible for osteoclastogenesis and elevated resorption; this is likely to account for rapid and progressive 52 deterioration of cancellous microarchitecture following exposure to ionizing radiation

    Effects of Simulated Spaceflight on Mitochondrial Oxidative Stress in Bone Remodelling

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    Microgravity and ionizing radiation may contribute to cellular stress; resulting in increased generation of reactive oxygen species (ROS), DNA damage, cell cycle arrest, and cell death. We hypothesized that suppression of excess ROS in osteoblasts and osteoclasts will improve bone microarchitecture. To test our hypothesis, we used irradiated transgenic mCAT mice overexpressing human anti-oxidant catalase gene targeted to the mitochondria (main site for ROS production). mCAT mice expressed the transgene and displayed elevated catalase activity in bone and ex vivo osteoblast and osteoclast cultures. Treated bone from wildtype mice showed elevated levels of oxidative damage whereas mCAT mice did not. Also, increased catalase activity correlated with decreased MDA levels and that increased oxidative damage correlated with decreased % bone volume. Ex-vivo osteoblast colony growth positively correlated with osteoblast catalase activity. mCAT mice displayed reduced % bone volume. Treatment caused significant bone loss in wildtype mice. Treatment also caused slight deficits in microarchitecture of mCAT mice. In conclusion, ROS signaling in both osteoblast and osteoclast lineage cells contribute to skeletal development and remodeling and quenching oxidative damage could play a role in bone loss prevention

    Tectonic interactions during rift linkage: insights from analog and numerical experiments

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    Continental rifts evolve by linkage and interaction of adjacent individual segments. As rift segments propagate, they can cause notable re-orientation of the local stress field so that stress orientations deviate from the regional trend. In return, this stress re-orientation can feed back on progressive deformation and may ultimately deflect propagating rift segments in an unexpected way. Here, we employ numerical and analog experiments of continental rifting to investigate the interaction between stress re-orientation and segment linkage. Both model types employ crustal-scale two-layer setups wherein pre-existing linear heterogeneities are introduced by mechanical weak seeds. We test various seed configurations to investigate the effect of (i) two competing rift segments that propagate unilaterally, (ii) linkage of two opposingly propagating rift segments, and (iii) the combination of these configurations on stress re-orientation and rift linkage. Both the analog and numerical models show counterintuitive rift deflection of two sub-parallel propagating rift segments competing for linkage with an opposingly propagating segment. The deflection pattern can be explained by means of stress analysis in numerical experiments wherein stress re-orientation occurs locally and propagates across the model domain as rift segments propagate. Major stress re-orientations may occur locally, which means that faults and rift segment trends do not necessarily align perpendicularly to far-field extension directions. Our results show that strain localization and stress re-orientation are closely linked, mutually influence each other, and may be an important factor for rift deflection among competing rift segments as observed in nature.</p

    Learning intrinsic excitability in medium spiny neurons

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    We present an unsupervised, local activation-dependent learning rule for intrinsic plasticity (IP) which affects the composition of ion channel conductances for single neurons in a use-dependent way. We use a single-compartment conductance-based model for medium spiny striatal neurons in order to show the effects of parametrization of individual ion channels on the neuronal activation function. We show that parameter changes within the physiological ranges are sufficient to create an ensemble of neurons with significantly different activation functions. We emphasize that the effects of intrinsic neuronal variability on spiking behavior require a distributed mode of synaptic input and can be eliminated by strongly correlated input. We show how variability and adaptivity in ion channel conductances can be utilized to store patterns without an additional contribution by synaptic plasticity (SP). The adaptation of the spike response may result in either "positive" or "negative" pattern learning. However, read-out of stored information depends on a distributed pattern of synaptic activity to let intrinsic variability determine spike response. We briefly discuss the implications of this conditional memory on learning and addiction.Comment: 20 pages, 8 figure

    Dried Plum Diet Prevents Bone Loss Caused by Ionizating Radiation: Reduces Pro-Resorption Cytokine Expression, and Protects Marrow-Derived Osteoprogenitors

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    Future long duration missions outside the protection of the Earth's magnetosphere, or unshielded exposures to solar particle events, achieves total doses capable of causing cancellous bone loss. Cancellous bone loss caused by ionizing radiation occurs quite rapidly in rodents: Initially, radiation increases the number and activity of bone-resorbing osteoclasts, followed by decrease in bone forming osteoblast cells. Here we report that Dried Plum (DP) diet completely prevented cancellous bone loss caused by ionizing radiation (Figure 1). DP attenuated marrow expression of genes related to bone resorption (Figure 2), and protected the bone marrow-derived pre-osteoblasts ex vivo from total body irradiation (Figure 3). DP is known to inhibit resorption in models of aging and ovariectomy-induced osteopenia; this is the first report that dietary DP is radioprotective

    Novel Radiomitigator for Radiation-Induced Bone Loss

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    Radiation-induced bone loss can occur with radiotherapy patients, accidental radiation exposure and during long-term spaceflight. Bone loss due to radiation is due to an early increase in oxidative stress, inflammation and bone resorption, resulting in an imbalance in bone remodeling. Furthermore, exposure to high-Linear Energy Transfer (LET) radiation will impair the bone forming progenitors and reduce bone formation. Radiation can be classified as high-LET or low-LET based on the amount of energy released. Dried Plum (DP) diet prevents bone loss in mice exposed to total body irradiation with both low-LET and high-LET radiation. DP prevents the early radiation-induced bone resorption, but furthermore, we show that DP protects the bone forming osteoblast progenitors from high-LET radiation. These results provide insight that DP re-balances the bone remodeling by preventing resorption and protecting the bone formation capacity. This data is important considering that most of the current osteoporosis treatments only block the bone resorption but do not protect bone formation. In addition, DP seems to act on both the oxidative stress and inflammation pathways. Finally, we have preliminary data showing the potential of DP to be radio-protective at a systemic effect and could possible protect other tissues at risk of total body-irradiation such as skin, brain and heart
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