Responses of soil microbial communities to prescribed burning in two paired vegetation sites in southern China

Prescribed burning is a common site preparation practice for forest plantation in southern China. However, the effects of prescribed burning on soil microbial communities are poorly understood. This study examined changes in microbial community structure, measured by phospholipid fatty acids (PLFAs), after a single prescribed burning in two paired vegetation sites in southern China. The results showed that the total amount of PLFA (totPLFA) was similar under two vegetation types in the wet season but differed among vegetation type in the dry season, and was affected significantly by burning treatment only in the wet season. Bacterial PLFA (bactPLFA) and fungal PLFA (fungPLFA) in burned plots all decreased compared to the unburned plots in both seasons (P = 0.059). Fungi appeared more sensitive to prescribed burning than bacteria. Both G⁺ bacterial PLFA and G⁻ bacterial PLFA were decreased by the burning treatment in both dry and wet seasons. Principal component analysis of PLFAs showed that the burning treatment induced a shift in soil microbial community structure. The variation in soil microbial community structure was correlated significantly to soil organic carbon, total nitrogen, available phosphorus and exchangeable potassium. Our results suggest that prescribed burning results in short-term changes in soil microbial communities but the long-term effects of prescribed burning on soil microbial community remain unknown and merit further investigation.     

Electrogenerated chemiluminescence of ruthenium complex immobilized in a highly cross‐linked polymer and its analytical applications

Electrogenerated chemiluminescence (ECL) of a ruthenium complex polymer modified carbon paste electrode and its analytical applications were investigated. The ruthenium complex polymer was prepared using bis(2,2‐bipyridine) (4,4‐dicarboxy‐2,2‐bipyridine) ruthenium(II). The ECL behaviours of ruthenium complex polymer modified carbon paste electrode were investigated in the absence and presence of tripropylamine (TPA). The modified carbon paste electrode exhibited long‐term stability and fine reproducibility. The ECL intensity of the modified carbon paste electrode was linear with the concentration of TPA in the range 2.0 × 10^–6–3.8 × 10^–3 mol/L, with a detection limit (S:N = 3) of 6 × 10^–7 mol/L. It was also found that raceanisodamine could enhance the ECL intensity of the modified electrode. The ECL intensity of the modified carbon paste electrode was linear with the concentration of raceanisodamine in the range 1.1 × 10^–5–6.0 × 10^–4 mol/L, with a detection limit (S:N = 3) of 6 × 10^–6 mol/L. This work demonstrates that the entrapment of ruthenium complex in a highly cross‐linked polymer is a promising approach to construct an ECL modified electrode with long‐term stability and fine reproducibility. The modified electrode designed has a potential application in the ECL detector. Copyright © 2008 John Wiley & Sons, Ltd.     

Extreme learning machine classification method for lower limb movement recognition

In order to identify the lower limb movements accurately and quickly, a recognition method based on extreme learning machine (ELM) is proposed. The recognizing target set is constructed by decomposing the daily actions into different segments. To get the recognition accuracy of seven movements based on the surface electromyography, the recognition feature vector space is established by integrating short-time statistical characteristics under time domain, and locally linear embedding algorithm is used to reduce the computational complexity and improve robustness of algorithm. Compared with BP, the overall recognition accuracy for each subject in the best dimension with ELM is above 95%.     

Assessment of Heavy Metal Contamination in the Sediments of the Shuangtaizi Estuary Using Multivariate Statistical Techniques

In order to assess heavy metal pollution of sediment samples collected from Shuangtaizi estuary, contamination factor (CF) and multivariate statistical analyses, including principal component analysis (PCA), cluster analysis (CA) and correlation analysis, are carried out in this paper. CF confirms that Pb, Cu and Hg concentrations are very low and all fall within the range of background, while Zn and Cd demonstrate moderate contamination (in A10, A13, A15, A16 and A17 sites) and very high contamination (in A10, A13, A15 and A17 sites), respectively. The PCA indicates that four significant principal components (PCs) are extracted, explaining 88.959% of total variance, which suggests that Pb, Cu and Zn are mainly associated with organic carbon (OC). The result from CA is consistent with that obtained from PCA, classifying that the heavy metals in two clusters derive from different sources. Correlation analysis supports the conclusions from PCA and CA, elucidating the relationships between heavy metals and particle sizes of the sediments.     

VEGF165 induces differentiation of hair follicle stem cells into endothelial cells and plays a role in in vivo angiogenesis

Within the vascular endothelial growth factor (VEGF) family of five subtypes, VEGF165 secreted by endothelial cells has been identified to be the most active and widely distributed factor that plays a vital role in courses of angiogenesis, vascularization and mesenchymal cell differentiation. Hair follicle stem cells (HFSCs) can be harvested from the bulge region of the outer root sheath of the hair follicle and are adult stem cells that have multi‐directional differentiation potential. Although the research on differentiation of stem cells (such as fat stem cells and bone marrow mesenchymal stem cells) to the endothelial cells has been extensive, but the various mechanisms and functional forms are unclear. In particular, study on HFSCs’ directional differentiation into vascular endothelial cells using VEGF165 has not been reported. In this study, VEGF165 was used as induction factor to induce the differentiation from HFSCs into vascular endothelial cells, and the results showed that Notch signalling pathway might affect the differentiation efficiency of vascular endothelial cells. In addition, the in vivo transplantation experiment provided that HFSCs could promote angiogenesis, and the main function is to accelerate host‐derived neovascularization. Therefore, HFSCs could be considered as an ideal cell source for vascular tissue engineering and cell transplantation in the treatment of ischaemic diseases.     

Distinct roles of RIP1–RIP3 hetero- and RIP3–RIP3 homo-interaction in mediating necroptosis

Necroptosis is mediated by a signaling complex called necrosome, containing receptor-interacting protein (RIP)1, RIP3, and mixed-lineage kinase domain-like (MLKL). It is known that RIP1 and RIP3 form heterodimeric filamentous scaffold in necrosomes through their RIP homotypic interaction motif (RHIM) domain-mediated oligomerization, but the signaling events based on this scaffold has not been fully addressed. By using inducible dimer systems we found that RIP1–RIP1 interaction is dispensable for necroptosis; RIP1–RIP3 interaction is required for necroptosis signaling, but there is no necroptosis if no additional RIP3 protein is recruited to the RIP1–RIP3 heterodimer, and the interaction with RIP1 promotes the RIP3 to recruit other RIP3; RIP3–RIP3 interaction is required for necroptosis and RIP3–RIP3 dimerization is sufficient to induce necroptosis; and RIP3 dimer-induced necroptosis requires MLKL. We further show that RIP3 oligomer is not more potent than RIP3 dimer in triggering necroptosis, suggesting that RIP3 homo-interaction in the complex, rather than whether RIP3 has formed homo polymer, is important for necroptosis. RIP3 dimerization leads to RIP3 intramolecule autophosphorylation, which is required for the recruitment of MLKL. Interestingly, phosphorylation of one of RIP3 in the dimer is sufficient to induce necroptosis. As RIP1–RIP3 heterodimer itself cannot induce necroptosis, the RIP1–RIP3 heterodimeric amyloid fibril is unlikely to directly propagate necroptosis. We propose that the signaling events after the RIP1–RIP3 amyloid complex assembly are the recruitment of free RIP3 by the RIP3 in the amyloid scaffold followed by autophosphorylation of RIP3 and subsequent recruitment of MLKL by RIP3 to execute necroptosis.Necroptosis is a type of programmed necrosis characterized by necrotic morphological changes, including cellular organelle swelling, cell membrane rupture,^{1, 2, 3} and dependence of receptor-interacting protein (RIP)1⁴ and RIP3.^{5, 6, 7} Physiological function of necroptosis has been illustrated in host defense,^{8, 9, 10, 11} inflammation,^{12, 13, 14, 15, 16} tissue injury,^{10, 17, 18} and development.^{19, 20, 21}Necroptosis can be induced by a number of different extracellular stimuli such as tumor necrosis factor (TNF). TNF stimulation leads to formation of TNF receptor 1 (TNFR1) signaling complex (named complex I), and complex II containing RIP1, TRADD, FAS-associated protein with a death domain (FADD), and caspase-8, of which the activation initiates apoptosis. If cells have high level of RIP3, RIP1 recruits RIP3 to form necrosome containing FADD,^{22, 23, 24} caspase-8, RIP1, and RIP3, and the cells undergo necroptosis.^{25, 26} Caspase-8 and FADD negatively regulates necroptosis,^{27, 28, 29, 30} because RIP1, RIP3, and CYLD are potential substrates of caspase-8.^{31, 32, 33, 34} Necrosome also suppresses apoptosis but the underlying mechanism has not been described yet. Mixed-lineage kinase domain-like (MLKL) is downstream of RIP3,^{35, 36} and phosphorylation of MLKL is required for necroptosis.^{37, 38, 39, 40, 41, 42}Apoptosis inducing complex (complex II) and necrosome are both supramolecular complexes.^{43, 44, 45} A recent study showed that RIP1 and RIP3 form amyloidal fibrils through their RIP homotypic interaction motif⁴⁶ (RHIM)-mediated polymerization, and suggested that amyloidal structure is essential for necroptosis signaling.⁴⁷ The RIP1–RIP3 heterodimeric amyloid complex is believed to function as a scaffold that brings signaling proteins into proximity to permit their activation. However, RIP1 and RIP3 also can each form fibrils on their own RHIM domains in vitro. It is unclear how the homo- and hetero-interactions are coordinated and organized on the amyloid scaffold to execute their functions in necroptosis. Here, we used inducible dimerization systems to study the roles of RIP1–RIP1, RIP1–RIP3, and RIP3–RIP3 interactions in necroptosis signaling. Our data suggested that it is the RIP1–RIP3 interaction in the RIP1–RIP3 heterodimeric amyloid complex that empowers to recruit other free RIP3; homodimerization of RIP3 triggers its autophosphorylation and only the phosphorylated RIP3 can recruit MLKL to execute necroptosis.     

Substituted aminobenzimidazole pyrimidines as cyclin-dependent kinase inhibitors

A series of aminobenzimidazole-substituted pyrimidines were synthesized and evaluated for biochemical activity against CDK1. A high-speed parallel synthesis approach enabled the identification of a potent lead series having improved potency in the CDK1 assay (IC(50)<10nM). Cell cycle analysis showed that the compounds induced a G2/M block. Docking studies were carried out with a CDK1 homology model, and provide a rationale for the observed activities.     

Predator-induced changes in morphology of a prey fish: the effects of food level and temporal frequency of predation risk

In a series of experiments, we investigated the effects of food availability and risk frequency on the dynamics of predator-induced changes in growth and morphology of prey fish using goldfish (Carassius auratus) as our test species. In experiment 1, we fed goldfish high or low food rations and exposed them to either alarm cues from conspecifics, cues from swordtails or a water control. After 60 days, goldfish in the alarm cue treatment significantly increased their body depth and body weight but had smaller body length than goldfish exposed to swordtails cues or water, likely reducing their vulnerability to gape-limited predators. Importantly, food level had an impact on the amplitude of the morphological changes. In experiment 2, goldfish were exposed to two different frequencies of predation cues or a water control for 50 days. The cues were either continued or discontinued from day 51 to 100, and all cues were resumed from day 101 to 150. We found that goldfish exposed to predation cues increased their depth and weight at a faster rate than did the goldfish exposed to water, and of particular significance was the fact that frequency of risk had an effect on the amplitude of the change. When the cues were interrupted, the increase in growth rate parameters was reduced to the level of the goldfish exposed to water. However, when the cues were resumed, the rate increased to match the growth rate of the goldfish that were continuously exposed to the cues. Finally, we staged encounters between goldfish of differing morphologies and yellow perch (Perca flavescens) and found that deep-bodied goldfish had better survival than the shallow-bodied ones. These experiments illustrate the dynamic nature of inducible morphological defences.