Effect of bone char addition on the fractionation and bio-accessibility of Pb and Zn in combined contaminated soil

Effect of bone char addition on the fractionation and bio-accessibility of lead (Pb) and Zinc (Zn) in combined contaminated soil was studied by batch soil column incubation experiment. Four treatments were designed: control (without bone char), 1%, 2% and 5% bone char addition (by weight). The results showed that all treatments with bone char addition could significantly decrease the concentration of HOAc extractable Pb (P < 0.05). Compared with the control the concentration of HOAc extractable Pb was decreased by 66.85%, 83.69% and 97.40%, respectively, in 1%, 2% and 5% bone char amended soils after 3 months incubation. The treatment with 5% bone char addition significantly decreased (P < 0.05) the concentration of HOAc extractable Zn by 47.80%, 43.63% and 41.35%, respectively, after 1, 2 and 3 months incubation. All treatments, including 1%, 2% and 5% bone char addition, significantly decreased (P < 0.05) the concentration of bio-accessible Pb after 3 months incubation, however, only the treatment with 5% bone char addition significantly decreased (P < 0.05) the concentration of bio-accessible Zn after 3 months incubation. The results highlighted the potential of bone char amendments to reduce the bioavailability of Pb and Zn in contaminated soil.     

青藏高原高寒草原生态系统植被碳密度分布规律及其与气候因子的关系

根据青藏高原高寒草原生态系统中以降水量为主要驱动力的东西样带和以气温为主要驱动力的南北样带内植被土壤的实测数据,分析了这一区域植被碳密度的分布特征及其与气候因子之间的关系.结果表明,在南北样带内(北纬28°46′～31°40′),植被碳密度首先随纬度的增加而增加,当纬度达到约北纬30°16′处,植被碳密度达到最大值0.873 1 kg·m-2,之后,则随纬度的增加而减少,植被碳密度总体上呈现出南北低、中间高的分布特征;在东西样带内(东经80°02′～91°50′),植被碳密度随经度的增加而增加,呈现出东高西低的分布特征.在南北样带内植被碳密度与年均降水量和年均气温之间的偏相关系数均达到极显著水平,而在东西样带内植被碳密度与年均降水量和年均气温之间的偏相关系数也均达到显著水平;在南北样带内植被碳密度先随年均气温和年均降水量的增加而增加,当年均气温达到约-1.5 ℃、年均降水量达到约497.0 mm时,植被碳密度达到最大值1.329 6 kg·m-2,之后,随年均气温和年均降水量的增加而减少;在东西样带内植被碳密度也先随年均气温和年均降水量的增加而增加,当年均气温达到约0.7 ℃、年均降水量达到约409.0 mm时,植被碳密度达到最大值1.208 3 kg·m-2,之后,随年均气温和年均降水量的增加而减少.研究结果显示,青藏高原高寒草原生态系统南北样带和东西样带内的植被碳密度分布均是年均气温和年均降水量综合作用的结果,且年均降水量的作用大于年均气温.     

超声波骨密度测量技术的最新进展

骨质疏松等中老年的常见病和多发病也呈年轻化发展,如何进行有效的骨状况诊断,拥有一台可以信赖的、可以方便地应用的骨测量仪器显得更为重要。超声波骨测量技术是使用范围比较广泛的一种,本文对超声波测量法的最新发展进行了阐述。     

Identification of Epithelial to Mesenchymal Transition as a Novel Source of Fibroblasts in Intestinal Fibrosis

Intestinal fibrosis is a major complication of Crohn disease (CD), but the precise mechanism by which it occurs is incompletely understood. As a result, specific therapies to halt or even reverse fibrosis have not been explored. Here, we evaluated the contribution of epithelial to mesenchymal transition (EMT) to intestinal fibrosis associated with a mouse model of CD and also human inflammatory bowel disease. Mice administered intrarectal 2,4,6-trinitrobenzene sulfonic acid (TNBS) develop inflammation and fibrosis that resembles CD both histologically and by immunologic profile. We utilized this model to molecularly probe the contribution of EMT to intestinal fibrosis. Additionally, we utilized double-transgenic VillinCre;R26Rosa-lox-STOP-lox-LacZ mice, in which removal of the STOP cassette by Cre recombinase in villin⁺ intestinal epithelial cells activates permanent LacZ expression, to lineage trace epithelial cells that might undergo EMT upon TNBS administration. TNBS-induced fibrosis is associated with the presence of a significant number of cells that express both epithelial and mesenchymal markers. In the lineage tagged transgenic mice, the appearance of LacZ⁺ cells that also express the fibroblast marker FSP1 unequivocally demonstrates EMT. Transforming growth factor (TGF)-β1, a known inducer of EMT in epithelial cells, induces EMT in rat intestinal epithelial cells in vitro, and bone morphogenic protein-7, an antagonist of TGF-β1, inhibits EMT and fibrosis both in vitro and in the TNBS-treated mice. Our study demonstrates that EMT contributes to intestinal fibrosis associated with the TNBS-induced model of Crohn colitis and that inhibition of TGF-β1 with recombinant human bone morphogenic protein-7 prevents this process and prevents fibrosis.     

Fluid Flow-induced Soluble Vascular Endothelial Growth Factor Isoforms Regulate Actin Adaptation in Osteoblasts

Although load-induced mechanical signals play a key role in bone formation and maintenance of bone mass and structure, the cellular mechanisms involved in the translation of these signals are still not well understood. Recent identification of a novel flow-induced mechanosignaling pathway involving VEGF in osteoblasts and the known VEGF regulation of actin reorganization in various cell types has led us to hypothesize that fluid shear stress-induced Vegf up-regulation underlies the actin cytoskeleton adaptation observed in osteoblasts during mechanotransduction. Our results show that MC3T3-E1 cells secrete significant VEGF in response to 5 h of pulsatile fluid shear stress (PFSS; 5 dynes/cm² at 1 Hz), whereas expression of VEGF receptors (VEGFR-1, VEGFR-2, or NRP1) is unaffected. These receptors, in particular VEGFR-2, participate in PFSS-induced VEGF release. Exposure to flow-conditioned medium or exogenous VEGF significantly induces stress fiber formation in osteoblasts that is comparable with PFSS-induced stress fiber formation, whereas VEGF knockdown abrogates this response to PFSS, thereby providing evidence that flow-induced VEGF release plays a role in actin polymerization. Using neutralizing antibodies against the receptors and VEGF isoforms, we found that soluble VEGFs, in particular VEGF₁₆₄, play a crucial role in transient stress fiber formation during osteoblast mechanotransduction, most likely through VEGFR-2 and NRP1. Based on these data we conclude that flow-induced VEGF release from osteoblasts regulates osteoblast actin adaptation during mechanotransduction and that VEGF paracrine signaling may provide potent cross-talk among bone cells and endothelial cells that is essential for fracture healing, bone remodeling, and osteogenesis.     

Vinculin Is Indispensable for Repopulation by Hematopoietic Stem Cells,Independent of Integrin Function

Vinculin is a highly conserved actin-binding protein that is localized in integrin-mediated focal adhesion complexes. Although critical roles have been proposed for integrins in hematopoietic stem cell (HSC) function, little is known about the involvement of intracellular focal adhesion proteins in HSC functions. This study showed that the ability of c-Kit⁺Sca1⁺Lin⁻ HSCs to support reconstitution of hematopoiesis after competitive transplantation was severely impaired by lentiviral transduction with short hairpin RNA sequences for vinculin. The potential of these HSCs to differentiate into granulocytic and monocytic lineages, to migrate toward stromal cell-derived factor 1α, and to home to the bone marrow in vivo were not inhibited by the loss of vinculin. However, the capacities to form long term culture-initiating cells and cobblestone-like areas were abolished in vinculin-silenced c-Kit⁺Sca1⁺Lin⁻ HSCs. In contrast, adhesion to the extracellular matrix was inhibited by silencing of talin-1, but not of vinculin. Whole body in vivo luminescence analyses to detect transduced HSCs confirmed the role of vinculin in long term HSC reconstitution. Our results suggest that vinculin is an indispensable factor determining HSC repopulation capacity, independent of integrin functions.     

Coping strategies in farmed African catfish Clarias gariepinus. Does it affect their welfare?

The objective of this study was to assess whether and how coping strategies affect the welfare of African catfish Clarias gariepinus housed at low and high densities. Group composition influenced feed intake; re‐active groups (comprised of 100% re‐active fish) had a lower specific growth rate (G) and feed intake and a higher feed conversion ratio (R_FC) than pro‐active groups. Furthermore, re‐active groups had a lower energy retention than pro‐active groups. The latter was fully due to differences in feed intake, since energy partitioning (on % total gross energy intake basis) was similar among the group composition treatments. Fish held at high stocking density showed a higher R_FC and feeding speed and a lower energy retention and agonistic behaviour. None of the measured variables was influenced by the interaction effect. In mixed groups, G and number of skin lesions seemed to be affected by different behavioural phenotypes at low stocking density, but not at high density. These results indicate that both stocking density and group composition affect physical and behavioural responses of C. gariepinus. Furthermore, physical and behavioural data of individual fish housed in mixed groups suggest that coping strategy affects the fitness of different behavioural phenotypes at low, but not at high, stocking density.     

Plasma levels of lipoprotein-associated phospholipase A2 are increased in patients with ��-thalassemia

Lipoprotein-associated phospholipase A₂ (Lp-PLA₂) is an independent cardiovascular risk factor. We investigated the plasma levels of Lp-PLA₂ activity and mass as a function of plasma lipid levels, LDL subclass profile, and oxidative stress in patients with β-thalassemia. Thirty-five patients with β-thalassemia major (β-TM) and 25 patients with β-thalassemia intermedia (β-TI) participated in the study. Lp-PLA₂ activity and mass were measured in total plasma, in apolipoprotein (apo)B-depleted plasma (HDL-Lp-PLA₂), and in LDL subclasses. Lp-PLA₂ activity produced and secreted from peripheral blood monocytes in culture was also determined. Patients with β-thalassemia are characterized by a predominance of small-dense LDL particles, increased oxidative stress, and very high plasma levels of Lp-PLA₂ mass and activity, despite low LDL-cholesterol levels. A significant positive correlation between plasma Lp-PLA₂ activity or mass and 8-isoprostane (8-epiPGF2a) and ferritin levels as well as intima-media thickness (IMT) values was observed. An increase in secreted and cell-associated Lp-PLA₂ activity from monocytes in culture was observed in both patient groups. The HDL-Lp-PLA₂ activity and mass as well as the ratio of HDL-Lp-PLA₂/plasma Lp-PLA₂ were significantly higher in both patient groups compared with the control group. In conclusion, patients with β-thalassemia exhibit high plasma Lp-PLA₂ levels, attributed to increased enzyme secretion from monocytes/macrophages and to the predominance of sdLDL particles in plasma. Plasma Lp-PLA₂ is correlated with carotid IMT, suggesting that this enzyme may be implicated in premature carotid atherosclerosis observed in β-thalassemia.