Silicates,Silicate Weathering,and Microbial Ecology

Mineralogy, microbial ecology, and mineral weathering in the subsurface are an intimately linked biogeochemical system. Although bacteria have been implicated indirectly in the accelerated weathering of minerals, it is not clear if this interaction is simply the coincidental result of microbial metabolism, or if it represents a specific strategy offering the colonizing bacteria a competitive ecological advantage. Our studies provide evidence that silicate weathering by bacteria is sometimes driven by the nutrient requirements of the microbial consortium, and therefore depends on the trace nutrient content of each aquifer mineral. This occurrence was observed in reducing groundwaters where carbon is abundant but phosphate is scarce; here, even resistant feldspars are weathered rapidly. This suggests that the progression of mineral weathering may be influenced by a mineral's nutritional potential, with microorganisms destroying only beneficial minerals. The rock record, therefore, may contain a remnant mineralogy that reflects early microbial destruction of biologically valuable minerals, leaving a residuum of "useless" minerals, where "value" depends on the organism, its metabolic needs, and the diagenetic environment. Conversely, the subsurface distribution of microorganisms may, in part, be controlled by the mineralogy and by the ability of an organism to take advantage of mineral-bound nutrients.     

The Alteration of MiR-222 and Its Target Genes in Nickel-Induced Tumor

Nickel is an important kind of metal and a necessary trace element in people’s production and livelihood; it is also a well-confirmed human carcinogen. In the past few years, researchers did a large number of studies about the molecular mechanisms of nickel carcinogenesis, and they focused on activation of proto-oncogenes and inactivation of anti-oncogenes caused by gene point mutation, gene deletion, gene amplification, DNA methylation, chromosome condensation, and so on that were induced by nickel. However, the researches on tumorigenic molecular mechanisms regulated by microRNAs (miRNAs) are rare. In this study, we established nickel-induced tumor by injecting Ni₃S₂ compounds to Wistar Rattus. By establishing a cDNA library of miRNA from rat muscle tumor tissue induced by Ni₃S₂, we found that the expression of miR-222 was significantly upregulated in tumor tissue compared with the normal tissue. As we expected, the expression levels of target genes of miR-222, CDKN1B and CDKN1C, were downregulated in the nickel-induced tumor. The same alteration of miR-222 and its target genes was also found in malignant 16HBE cells induced with Ni₃S₂ compounds. We conclude that miR-222 may promote cell proliferation infinitely during nickel-induced tumorigenesis in part by regulating the expression of its target genes CDKN1B and CDKN1C. Our study elucidated a novel molecular mechanism of nickel-induced tumorigenesis.     

Zinc Transporter 7 Induced by High Glucose Attenuates Epithelial-to-Mesenchymal Transition of Peritoneal Mesothelial Cells

Zinc (Zn) is an essential micronutrient and cytoprotectant involved in preventing many types of epithelial-to-mesenchymal transition (EMT)-driven fibrosis in vivo. The zinc-transporter family SLC30A (ZnT) is a pivotal factor in the regulation of Zn homeostasis. However, its function in EMT in peritoneal mesothelial cells (PMCs) remains unknown. This study explored the regulation of zinc transporters and the role they play in cell EMT, particularly in rat peritoneal mesothelial cells (RPMCs), surrounding glucose concentrations and the molecular mechanism involved. The effects of high glucose (HG) on zinc transporter gene expression were measured in RPMCs by real-time PCR. We explored ZnT7 (Slc30A7): the effect of ZnT7 over-expression and siRNA-mediated knock-down on HG-induced EMT was investigated as well as the underlying molecular mechanisms. Over-expression of ZnT7 resulted in significantly inhibited HG-induced EMT in RPMCs, while inhibition of ZnT7 expression using a considerable siRNA-mediated knock-down of RPMCs increased the levels of EMT. Furthermore, over-expression of ZnT7 is accompanied by down-regulation of TGF-β/Smad pathway, phospho-Smad3,4 expression levels. The finding suggests that the zinc-transporting system in RPMCs is influenced by the exposure to HG. The ZnT7 may account for the inhibition of HG-induced EMT in RPMCs, likely through targeting TGF-β/Smad signaling.     

Enhanced Healing of Rat Calvarial Critical Size Defect with Selenium-Doped Lamellar Biocomposites

A 3D porous lamellar selenium-containing nano-hydroxyapatite (SeHAN)/chitosan (CS) biocomposite was synthesized. The selenium-containing hydroxyapatite (HA) grains of 150～200 nm in length and 20～30 nm in width were observed by dynamic light scattering and transmission electron microscopy. A combination of X-ray diffraction, Fourier-transform infrared spectroscopy, and SEM indicated that HA particles were uniformly dispersed in chitosan matrix and there was a chemical interaction between chitosan and HA. Then, a standard critical size calvarial bone defect was created in Wistar rats. In group 1, no implant was made in the defect. In groups 2 and 3, HA nanoparticles (HAN)/CS biocomposite and SeHAN/CS biocomposite were implanted into the defect, respectively. After 4 weeks, the histological assessment clearly exhibited no significant changes, only found some living cells anchored in the periphery of the implants. After 8 and 12 weeks, most newly formed osteoid tissue was found in the SeHAN/CS implant group. Additionally, the newly formed osteoid tissue, both at the edge and in the center of implants, was bioactive and neovascularized. Microfocus computerized tomography measurements also confirmed the much better quality of the newly formed bone tissue in SeHAN/CS implant group than that in HAN/CS implant group (p?<?0.01). Collectively, the SeHAN/CS biocomposite, as a bioactive bone grafting substitute, significantly enhanced the repair of bone defect.     

Characterization in biological traits of entomopathogenic nematodes isolated from North China

In a series of bioassays, thirty-one isolates that were collected from diverse locations in northern China and the laboratory kept isolate Steinernema carpocapsae All, were compared in order to select superior isolates for biological control of Bradysia odoriphaga. Virulence of the isolates against B. odoriphaga was significantly different among nematode isolates. Tolerance of infective juveniles (IJs) to heat, cold, and desiccation differed significantly among and within species. Strains from S. carpocapsae, S. ceratophorum, S. longicaudum, Heterorhabditis indica, and H. bacteriophora were more heat tolerant than strains from S. feltiae, S. hebeiense, S. monticolum, and H. megidis. Heterorhabditis megidis, H. bacteriophora, and S. carpocapsae showed better cold tolerance than the other species. High desiccation tolerance was recorded for S. carpocapsae, S. hebeiense, and S. ceratophorum. The infectivity of IJ of these species against Galleria mellonella larvae was not significantly different between the treated and non-treated IJ after the nematodes had been exposed to 40 °C for 2 h, −5 °C for 8 h or 25% glycerin for 72 h. Nematode survival was significantly affected by exposure time and IJ concentration when exposed to 40 °C or −5 °C. All nematode isolates lost their infectivity against G. mellonella after exposure to −5 °C for 16 h, except for H. megidis LFS10, which had a low infectivity of 3.3%. A hierarchical classification analysis classified the isolates in four main clusters. The fourth cluster, composed of 13 isolates, grouped the isolates that scored well for most traits.     

Zero effect of Bt rice on expression of genes coding for digestion,detoxification and immune responses and developmental performances of Brown Planthopper Nilaparvata lugens (Stål)

Transgenic Cry1Ac, Cry2Aa and Cry1Ca (Bt toxins) rice lines are well developed to manage lepidopteron pests in China. The impact of transgenic Bt rice on the non-target Brown Planthopper (BPH) has become an essential part of environmental risk assessment, however, scanty evidence is found addressing on developmental and molecular responses of BPH to the ingestion of Bt protein from transgenic rice. The focus of the current study is to examine the developmental characteristics and the expression profiles of gene in relation to digestion, detoxification and immune responses were examined. Our study strongly revealed that the tested Bt rice strains have no unfavorable effect on fecundity, survival and growth of BPH. Furthermore, each of the tested genes did not exhibit distinct expression pattern responding to non Bt parental cultivar, thus, it could be concluded that Bt rice have no detrimental effects on the physiological processes of digestion, detoxification and immune responses of BPH.     

Betaine attenuates Alzheimer‐like pathological changes and memory deficits induced by homocysteine

Hyperhomocysteinemia (Hhcy) may induce memory deficits with β‐amyloid (Aβ) accumulation and tau hyperphosphorylation. Simultaneous supplement of folate and vitamin B12 partially restored the plasma homocysteine level and attenuated tau hyperphosphorylation, Aβ accumulation and memory impairments induced by Hhcy. However, folate and vitamin B12 treatment have no effects on Hhcy which has the methylenetetrahydrofolate reductase genotype mutation. In this study, we investigated the effects of simultaneous supplement of betaine on Alzheimer‐like pathological changes and memory deficits in hyperhomocysteinemic rats after a 2‐week induction by vena caudalis injection of homocysteine (Hcy). We found that supplementation of betaine could ameliorate the Hcy‐induced memory deficits, enhance long‐term potentiation (LTP) and increase dendritic branches numbers and the density of the dendritic spines, with up‐regulation of NR1, NR2A, synaptotagmin, synaptophysin, and phosphorylated synapsin I protein levels. Supplementation of betaine also attenuated the Hcy‐induced tau hyperphosphorylation at multiple AD‐related sites through activation protein phosphatase‐2A (PP2A) with decreased inhibitory demethylated PP2A_C at Leu309 and phosphorylated PP2A_C at Tyr307. In addition, supplementation of betaine also decreased Aβ production with decreased presenilin‐1 protein levels. Our data suggest that betaine could be a promising candidate for arresting Hcy‐induced AD‐like pathological changes and memory deficits.     

Effects of Soil Compaction and Meloidogyne incognita on Cotton Root Architecture and Plant Growth

The effects of a soil hardpan and Meloidogyne incognita on cotton root architecture and plant growth were evaluated in microplots in 2010 and 2011. Soil was infested with M. incognita at four different levels with or without a hardpan. The presence of a hardpan resulted in increased plant height, number of main stem nodes, and root fresh weight for cotton seedlings both years. Meloidogyne incognita decreased height and number of nodes for seedlings in 2010. Nematode infestation increased seedling root length and enhanced root magnitude, altitude, and exterior path length in 2010. This was also the case for root length and magnitude in 2011 at lower infestation levels suggesting compensatory growth. A hardpan had no consistent effect on these root parameters but increased root volume in both years. A hardpan hastened crop maturity and increased the number of fruiting branches that were produced, while M. incognita infection delayed crop development and reduced plant height and number of bolls. Both M. incognita infection and a hardpan reduced taproot length and root dry weight below the hardpan in both years. Root topological indices under all the treatments ranged from 1.71 to 1.83 both years indicating that root branching followed a herringbone pattern. The techniques for characterizing root architecture that were used in this study provide a greater understanding of changes that result from disease and soil abiotic parameters affecting root function and crop productivity.     

A Single Divergent Exon Inhibits Ankyrin-B Association with the Plasma Membrane

Vertebrate ankyrin-B and ankyrin-G exhibit divergent subcellular localization and function despite their high sequence and structural similarity and common origin from a single ancestral gene at the onset of chordate evolution. Previous studies of ankyrin family diversity have focused on the C-terminal regulatory domain. Here, we identify an ankyrin-B-specific linker peptide connecting the ankyrin repeat domain to the ZU5₂-UPA module that inhibits binding of ankyrin-B to membrane protein partners E-cadherin and neurofascin 186 and prevents association of ankyrin-B with epithelial lateral membranes as well as neuronal plasma membranes. The residues of the ankyrin-B linker required for autoinhibition are encoded by a small exon that is highly divergent between ankyrin family members but conserved in the ankyrin-B lineage. We show that the ankyrin-B linker suppresses activity of the ANK repeat domain through an intramolecular interaction, likely with a groove on the surface of the ANK repeat solenoid, thereby regulating the affinities between ankyrin-B and its binding partners. These results provide a simple evolutionary explanation for how ankyrin-B and ankyrin-G have acquired striking differences in their plasma membrane association while maintaining overall high levels of sequence similarity.     

Extracellular Norepinephrine Clearance by the Norepinephrine Transporter Is Required for Skeletal Homeostasis

Changes in bone remodeling induced by pharmacological and genetic manipulation of β-adrenergic receptor (βAR) signaling in osteoblasts support a role of sympathetic nerves in the regulation of bone remodeling. However, the contribution of endogenous sympathetic outflow and nerve-derived norepinephrine (NE) to bone remodeling under pathophysiological conditions remains unclear. We show here that differentiated osteoblasts, like neurons, express the norepinephrine transporter (NET), exhibit specific NE uptake activity via NET and can catabolize, but not generate, NE. Pharmacological blockade of NE transport by reboxetine induced bone loss in WT mice. Similarly, lack of NE reuptake in norepinephrine transporter (Net)-deficient mice led to reduced bone formation and increased bone resorption, resulting in suboptimal peak bone mass and mechanical properties associated with low sympathetic outflow and high plasma NE levels. Last, daily sympathetic activation induced by mild chronic stress was unable to induce bone loss, unless NET activity was blocked. These findings indicate that the control of endogenous NE release and reuptake by presynaptic neurons and osteoblasts is an important component of the complex homeostatic machinery by which the sympathetic nervous system controls bone remodeling. These findings also suggest that drugs antagonizing NET activity, used for the treatment of hyperactivity disorders, may have deleterious effects on bone accrual.