Effect of insecticides and Plutella xylostella (Lepidoptera: Plutellidae) genotype on a predator and parasitoid and implications for the evolution of insecticide resistance

In the laboratory and in cages in the greenhouse, we evaluated the toxicity of two insecticides (lambda-cyhalothrin and spinosad) on the parasitoid, Diadegma insulare (Cresson), and the predator, Coleomegilla maculate (DeGeer), both natural enemies of the diamondback moth, Plutella xylostella (L.). Lambda-cyhalothrin was very toxic to both natural enemies. Spinosad was less toxic to C. maculata adults and larvae, and slightly toxic to D. insulare. Both natural enemies suppressed P. xylostella populations in cages with 80% spinosad-treated and 20% nontreated plants; such suppression was not seen when lambda-cyhalothrin was used. Using broccoli, Brassica oleracea L. variety italica, a common host for P. xylostella, we also studied direct and indirect effects of both natural enemies in the presence and absence of the two insecticides and to different P. xylostella genotypes: resistant to the insecticide, susceptible, or heterozygous. Neither natural enemy could distinguish host genotype if P. xylostella were feeding on nontreated plants. They could also not distinguish between larvae feeding on spinosad-treated plants and nontreated plants, but D. insulare could distinguish between larvae feeding on lambda-cyhalothrin treated and nontreated plants. Our studies suggest that lambda-cyhalothrin has direct toxicity to these two natural enemies, can affect their host foraging and acceptance of P. xylostella and consequently would not be compatible in conserving these natural enemies in a program for suppression of P. xylostella. In contrast, our studies suggest that treatment with spinosad has much less effect on these natural enemies and would allow them to help suppress populations of P. xylostella. These findings are discussed in relation to the evolution of insecticide resistance and suppression of the pest populations.     

Purification and expression of a protein elicitor from Alternaria tenuissima and elicitor-mediated defence responses in tobacco

A new protein elicitor, PeaT1, was purified from the mycelium of Alternaria tenuissima by column chromatography. PeaT1 was identified as a heat-stable and acidic protein. It induced systemic acquired resistance to tobacco mosaic virus (TMV) in tobacco plants but did not cause hypersensitive response. The elicitor-encoding gene was cloned by rapid amplification of cDNA ends method. Sequence analysis revealed that the cDNA is 624 bp in length and the open reading frame encodes for a polypeptide of 207 amino acids with a nascent polypeptide-associated complex domain. The peaT1 gene was cloned into the expression vector pET-28a and transformed into Escherichia coli BL21 (DE3). The recombinant elicitor also triggered defence responses in intact tobacco plants. The availability of the pure protein offers the possibility to isolate the corresponding receptor and links it to the downstream signalling pathway.     

MiR-489 regulates chemoresistance in breast cancer via epithelial mesenchymal transition pathway

To investigate the role of microRNAs in the development of chemoresistance and related epithelial–mesenchymal transition (EMT), we examined the effect of miR-489 in adriamycin (ADM)-resistant human breast cancer cells (MCF-7/ADM). MiR-489 was significantly suppressed in MCF-7/ADM cells compared with chemosensitive parental control MCF-7/WT cells. Forced-expression of miR-489 reversed chemoresistance. Furthermore, Smad3 was identified as the target of miR-489 and is highly expressed in MCF-7/ADM cells. Forced expression of miR-489 both inhibited Smad3 expression and Smad3 related EMT properties. Finally, the interactions between Smad3, miR-489 and EMT were confirmed in chemoresistant tumor xenografts and clinical samples, indicating their potential implication for treatment of chemoresistance.     

A Novel Phase of Li15Si4 Synthesized under Pressure

Li₁₅Si₄, the only crystalline phase that forms during lithiation of the Si anode in lithium‐ion batteries, is found to undergo a structural transition to a new phase at 7 GPa. Despite the large unit cell of Li₁₅Si₄ (152 atoms in the unit cell), ab initio evolutionary metadynamics (using the USPEX code) successfully predicts the atomic structure of this new phase (β‐Li₁₅Si₄), which has an orthorhombic structure with an Fdd2 space group. In the new β‐Li₁₅Si₄ phase Si atoms are isolated by Li atoms analogous to the original cubic phase (α‐Li₁₅Si₄), whereas the atomic packing is more efficient owing to the higher Si? Li coordination number and shorter Si? Li, Li? Li bonds. β‐Li₁₅Si₄ has substantially larger elastic moduli compared with α‐Li₁₅Si₄, and has a good electrical conductivity. As a result, β‐Li₁₅Si₄ has superior resistance to deformation and fracture under stress. The theoretical volume expansion of Si would decrease 25% if it transforms to β‐Li₁₅Si₄, instead of α‐Li₁₅Si₄, during lithiation. Moreover, β‐Li₁₅Si₄ can be recovered back to ambient pressure, providing opportunities to further investigate its properties and potential applications.     

Estrogen receptor-beta mediates male-female differences in the development of pressure overload hypertrophy

The goal of this study was to determine the role of estrogen receptor subtypes in the development of pressure overload hypertrophy in mice. Epidemiological studies have suggested gender differences in the development of hypertrophy and heart disease, but the mechanism and the role of estrogen receptor subtypes are not established. We performed transverse aortic constriction (TAC) and sham operations in male and female wild-type (WT) mice and mice lacking functional estrogen receptor-alpha [alpha-estrogen receptor knockout (alpha-ERKO)] and mice lacking estrogen receptor-beta (beta-ERKO). Body, heart, and lung weights were measured 2 wk postsurgery. WT male mice subjected to TAC showed a 64% increase in the heart weight-to-body weight ratio (HW/BW) compared with sham, and WT males have increased lung weight at 2 wk. WT female mice subjected to TAC showed a 31% increase in HW/BW compared with sham, which was significantly less than their male counterparts and with no evidence of heart failure. alpha-ERKO females developed HW/BW nearly identical to that seen in WT littermate females in response to TAC, indicating that estrogen receptor-alpha is not essential for the attenuation of hypertrophy observed in WT females. In contrast, beta-ERKO females responded to TAC with a significantly greater increase in HW/BW than WT littermate females. beta-ERKO females have lower expression of lipoprotein lipase at baseline than WT or alpha-ERKO females. These data suggest an important role for estrogen receptor-beta in attenuating the hypertrophic response to pressure overload in females.     

Soluble NSF attachment protein receptors (SNAREs) in RBL-2H3 mast cells: functional role of syntaxin 4 in exocytosis and identification of a vesicle-associated membrane protein 8-containing secretory compartment

Mast cells upon stimulation through high affinity IgE receptors massively release inflammatory mediators by the fusion of specialized secretory granules (related to lysosomes) with the plasma membrane. Using the RBL-2H3 rat mast cell line, we investigated whether granule secretion involves components of the soluble N-ethylmaleimide-sensitive factor attachment protein receptor (SNARE) machinery. Several isoforms of each family of SNARE proteins were expressed. Among those, synaptosome-associated protein of 23 kDa (SNAP23) was central in SNARE complex formation. Within the syntaxin family, syntaxin 4 interacted with SNAP23 and all vesicle-associated membrane proteins (VAMPs) examined, except tetanus neurotoxin insensitive VAMP (TI-VAMP). Overexpression of syntaxin 4, but not of syntaxin 2 nor syntaxin 3, caused inhibition of FcepsilonRI-dependent exocytosis. Four VAMP proteins, i.e., VAMP2, cellubrevin, TI-VAMP, and VAMP8, were present on intracellular membrane structures, with VAMP8 residing mainly on mediator-containing secretory granules. We suggest that syntaxin 4, SNAP23, and VAMP8 may be involved in regulation of mast cell exocytosis. Furthermore, these results are the first demonstration that the nonneuronal VAMP8 isoform, originally localized on early endosomes, is present in a regulated secretory compartment.     

白背飞虱种群动态关联分析及预测模型的研究

根据灰色系统关联分析的基本原理,提出了白背飞虱种群动态的加权关联度预测法。衢县早稻后期白背飞虱发生量与历年6月25～30日平均百丛虫量X_1（t）、同期若虫比例X_2（t）、迟熟品种比例X_3（t）、6月下旬水分积分指数X_4（t）和平均气温X_5（t）等因素的关联序为：X_2（t）＞X_1（t）＞X_3（t）＞X_5（t）＞X_4（t）。据此建立的加权关联度预测模型,经12年资料回测和试报验证,结果令人满意。     

Inhibition by N′-nitrosonornicotine of the catalytic activity of glutamate dehydrogenase in α-ketoglutarate amination

The effect of N′-nitrosonornicotine (NNN), one of the tobacco-specific nitrosamines, on the catalytic activity of glutamate dehydrogenase (GLDH) in the α-ketoglutarate amination, using reduced nicotinamide adenine dinucleotide as coenzyme, was studied by a chronoamperometric method. The maximum reaction rate of the enzyme-catalyzed reaction and the Michaelis-Menten constant, or the apparent Michaelis-Menten constant, were determined in the absence and presence of NNN. NNN remarkably inhibited the bio-catalysis activity of GLDH, and was a reversible competitive inhibitior with K_i, estimated as 199?μmol?l^?1 at 25°C and pH 8.0.     

The IL-6–STAT3 axis mediates a reciprocal crosstalk between cancer-derived mesenchymal stem cells and neutrophils to synergistically prompt gastric cancer progression

Emerging evidence indicate that mesenchymal stem cells (MSCs) affect tumor progression by reshaping the tumor microenvironment. Neutrophils are essential component of the tumor microenvironment and are critically involved in cancer progression. Whether the phenotype and function of neutrophils is influenced by MSCs is not well understood. Herein, we investigated the interaction between neutrophils and gastric cancer-derived MSCs (GC-MSCs) and explored the biological role of this interaction. We found that GC-MSCs induced the chemotaxis of neutrophils and protected them from spontaneous apoptosis. Neutrophils were activated by the conditioned medium from GC-MSCs with increased expression of IL-8, TNFα, CCL2, and oncostatin M (OSM). GC-MSCs-primed neutrophils augmented the migration of gastric cancer cells in a cell contact-dependent manner but had minimal effect on gastric cancer cell proliferation. In addition, GC-MSCs-primed neutrophils prompted endothelial cells to form tube-like structure in vitro. We demonstrated that GC-MSCs stimulated the activation of STAT3 and ERK1/2 pathways in neutrophils, which was essential for the functions of activated neutrophils. We further revealed that GC-MSCs-derived IL-6 was responsible for the protection and activation of neutrophils. In turn, GC-MSCs-primed neutrophils induced the differentiation of normal MSCs into cancer-associated fibroblasts (CAFs). Collectively, our results suggest that GC-MSCs regulate the chemotaxis, survival, activation, and function of neutrophils in gastric cancer via an IL-6–STAT3–ERK1/2 signaling cascade. The reciprocal interaction between GC-MSCs and neutrophils presents a novel mechanism for the role of MSCs in remodeling cancer niche and provides a potential target for gastric cancer therapy.Accumulating evidence suggest that neutrophils are critical for cancer initiation and progression.^{1, 2} The increased presence of intratumoral neutrophils has been linked to a poorer prognosis for patients with renal cancer, hepatocellular carcinoma (HCC), melanoma, head and neck squamous cell carcinoma (HNSCC), pancreatic cancer, colorectal carcinoma, and gastric adenocarcinoma.³ Recent studies using murine tumor models or involving cancer patients have suggested an important functional role of neutrophils during tumor progression.^{4, 5, 6, 7} Neutrophils-derived factors promote genetic mutations leading to tumorigenesis or promote tumor cell proliferation,⁸ migration, and invasion.^{9, 10} Neutrophils have also been demonstrated to induce tumor vascularization by the production of pro-angiogenic factors^{11, 12}The infiltration of neutrophils into tumors has been shown to be mediated by factors produced by both tumor and stromal cells. Recent reports suggest that tumor cells actively modulate the functions of neutrophils. Tumor-derived CXCL5 modulates the chemotaxis of neutrophils, which in turn enhances the migration and invasion of human HCC cells.¹³ HNSCC cells-derived MIF induces the recruitment and activation of neutrophils through a p38-dependent manner.^{14, 15} Neutrophils respond to hyaluronan fragments in tumor supernatants via PI3K/Akt signaling, leading to prolonged survival and stimulating effect on HCC cell motility.¹⁶ Kuang et al.¹⁷ suggest that IL-17 promotes the migration of neutrophils into HCC through epithelial cell-derived CXC chemokines, resulting in increased MMP-9 production and angiogenesis at invading tumor edge However, much less is known about the role of stromal cells in modulating the phenotype and function of neutrophils in cancer thus far.Cancer-associated fibroblasts (CAFs) have a key role in cancer mainly through secretion of soluble factors, as growth factors or inflammatory mediators, as well as production of extracellular matrix proteins and their proteases. These activated fibroblasts are involved in creating a niche for cancer cells, promoting their proliferation, motility and chemoresistance. Activated fibroblasts express several mesenchymal markers such as α-smooth muscle actin (α-SMA), fibroblast activation protein (FAP), and vimentin. CAFs actively participate in reciprocal interaction with tumor cells and with other cell types in the microenvironment, contributing to a tumor-permissive niche and promoting tumor progression.Mesenchymal stem cells (MSCs) are adult stromal cells with self-renewal and pluripotent differentiation abilities. MSCs can be mobilized from bone marrow to the site of damage, respond to the local microenvironment, and exert wound repair and tissue regeneration functions upon injury and inflammation conditions.¹⁸ MSCs have been considered as one of the major components of the tumor stroma and are believed to be the precursors of CAFs.^{19, 20} We have previously demonstrated that human bone marrow MSCs prompt tumor growth in vivo.²¹ In addition, we have recently isolated MSCs-like cells from the gastric cancer tissues (GC) and the adjacent normal tissues (GCN) and shown that the gastric cancer-derived MSCs (GC-MSCs) possess the properties of CAFs.^{22, 23} As tumor-derived MSCs are often exposed to distinct inflammatory cells and factors in the tumor microenvironment, they may acquire novel functions that are not present in normal MSCs, and these unique functions may have a role in reshaping the tumor microenvironment and ultimately affect tumor progression. As neutrophils are key mediators of tumor progression and tumor angiogenesis, it is likely that an intense interaction may exist between the tumor-derived MSCs and tumor-infiltrating neutrophils.The emerging roles of CAFs in cancer immunoeditting led us to investigate whether GC-MSCs are able to regulate the phenotype and function of neutrophils in gastric cancer. We have shown that there is a reciprocal interaction between GC-MSCs and neutrophils. GC-MSCs enhanced the chemotaxis of peripheral blood-derived neutrophils and protected them from spontaneous apoptosis. GC-MSCs induced the activation of neutrophils to highly express IL-8, CCL2, TNFα, and oncostatin M (OSM), leading to the increase of gastric cancer cell migration and angiogenesis in vitro. GC-MSCs exerted this effect through the IL-6–STAT3–ERK1/2 signaling axis, and blockade of the IL-6–IL-6R interaction or pharmacological inhibition of STAT3 and ERK1/2 activation abrogated this role. In turn, GC-MSCs-activated neutrophils could trigger the CAF differentiation of normal MSCs. Therefore, these results establish a bi-directional interaction between GC-MSCs and neutrophils that may be critically involved in the progression of gastric cancer.     

Effects of the maize C<Subscript>4</Subscript> phosphoenolpyruvate carboxylase (<Emphasis Type="Italic">ZmPEPC</Emphasis>) gene on nitrogen assimilation in transgenic wheat

Nitrogen (N) is the primary limiting factor for crop growth, development, and productivity. Transgenic technology is a straightforward strategy for improving N assimilation in crops. The present study assessed the effects of maize C₄ phosphoenolpyruvate carboxylase (ZmPEPC) gene overexpression on N assimilation in three independent transgenic lines and wild-type (WT) wheat (Triticum aestivum L.). The transgenic wheat lines depicted ZmPEPC overexpression and higher PEPC enzyme activity relative to that in the WT. The leaves of the transgenic wheat lines subjected to low N treatment showed an increase in ribulose-1,5-bisphosphate carboxylase/oxygenase (RuBisCO) expression, content, and carboxylase activity. The transgenic wheat lines also depicted an upregulation of genes associated with the anaplerotic pathway for the TCA cycle, suggesting that more carbon (C) skeleton material is being allocated for N assimilation under low N conditions. Furthermore, ZmPEPC expression in transgenic wheat lines induced the upregulated of genes associated primary N metabolism, including TaNR, TaGS2, TaGOGAT, TaAspAT, and TaASN1. The average total free amino acid content in the transgenic wheat lines was 48.18% higher than that in the WT, and asparagine (Asn), glutamine (Gln), aspartic acid (Asp), and serine (Ser) were also markedly enhanced. In addition, elementary analysis showed that N and C content, and the biomass of the transgenic wheat lines increased with low N treatment. Yield trait analysis indicated that ZmPEPC overexpression improved grain yield by increasing 1000-grain weight. In conclusion, ZmPEPC overexpression in wheat could modulate C metabolism, significantly improve N assimilation, enhances growth, and improves yield under low N conditions.