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It is challenging to design a routing scheme that can successfully operate in the presence of adversarial environment in mobile ad hoc network (MANET), where several types of severe routing security threats can be easily employed against normal routing. Among them, active black hole attack is a typical one. Most existing defense schemes postulated that active black hole attackers have no knowledge about the internal prevention mechanisms of MANETs. However, due to the open and self-organized nature of MANET, it is necessary to assume that all nodes, including attackers, know how the security mechanism works. In this paper, we propose a distributed self-checking scheme that can effectively prevent various forms of active black hole attackers. Even the internal attackers who know the security mechanism cannot get any benefit to launch those attacks. Simulation results affirm that our proposed solution is robust and able to improve the packet delivery ratio significantly in an adversarial MANET environment as compared with other routing schemes. Copyright © 2015 John Wiley & Sons, Ltd.

Aphis glycines Matsumura is an important pest of soybean in Asia and North America. Hymenoptera parasitoids play a key role in the control of the soybean aphid. The correct identification of parasitoids is a critical step that precedes the assessment of their potential biological control agents. Accurate identification of the majority of the species attacking the soybean aphid often requires elaborate specimen preparation and expert taxonomic knowledge. In this study, we facilitated the identification of soybean aphid parasitoids by applying a DNA barcoding approach following a preliminary morphological identification. We generated DNA sequence data from the mitochondrial COI gene and the D2 region of 28S rDNA to assess the genetic variation within and between parasitoid species emerging from the soybean aphid in China. Fifteen Hymenoptera parasitoid species belonging to 10 genera of five families were identified with little intra-specific variation (0.09% ± 0.06% for 28S and 0.36% ± 0.18% for COI) and large inter-specific divergence (30.46% ± 3.42% for 28S and 20.4% ± 1.20% for COI).

Lung carcinogenesis is a complex process in an unregulated inflammatory environment. Curcumin has been extensively investigated as a multi‐target anti‐tumor and anti‐inflammation compound. In this paper, we demonstrate a novel inflammation‐related mechanism for curcumin‐induced inhibition of lung tumor growth. We found that neutrophil elastase, an important regulator of inflammatory processes, directly triggered tumor cell proliferation in human lung adenocarcinoma A549 cells, and curcumin could completely suppress the excess tumor proliferation induced by neutrophil elastase. α1‐antitrypsin is synthesized by tumor cells and is the natural inhibitor of neutrophil elastase. We found that curcumin counteracted the decrease of α1‐antitrypsin induced by neutrophil elastase by inducing the promoter activity of α1‐antitrypsin and promoting its expression in A549 cells. The inhibition of neutrophil elastase‐induced proliferation by curcumin was dependent on the PI3K/Akt pathway. Knockdown of α1‐antitrypsin by siRNA further enhanced the tumor cell proliferation induced by neutrophil elastase and significantly blocked the anti‐proliferation effect of curcumin against neutrophil elastase. Curcumin remarkably inhibited the primary tumor growth of Lewis lung carcinoma (LLC) in C57BL/6 mice. We further showed that curcumin upregulated the level of α1‐antitrypsin in primary tumor tissue by promoting its local expression, and the protein level of neutrophil elastase in tumor tissue was obviously decreased in mice treated with curcumin. Overall, our results suggest that neutrophil elastase and α1‐antitrypsin play important roles in modulating lung tumor proliferation in inflammatory microenvironment and curcumin inhibits neutrophil elastase‐induced tumor proliferation via upregulating α1‐antitrypsin expression in vitro and in vivo.

Antiglucocorticoid therapy in depressed patients is effective, which indicates that glucocorticoids play a key role in the occurrence of depression. Our previous work demonstrated the efficacy of curcumin in treating depression in rat and mouse models. We characterized the protective effects of curcumin against corticosterone-induced cytotoxicity in PC12 cells and explored the mechanisms of these protective effects in association with the phosphorylation and expression of ERK1/2 in PC12 cells. MTT assay showed that curcumin significantly protected PC12 cells from corticosterone-induced cytotoxicity. Curcumin at concentrations from 10(-8) to 10(-6) M rescued PC12 cells from corticosterone-induced cytotoxicity. Cell viability was increased more than 20% with curcumin treatment. Western blot analysis showed that corticosterone increased ERK1/2 phosphorylation in PC12 cells and curcumin 10(-9) M to 10(-6) M significantly inhibited corticosterone-induced ERK1/2 phosphorylation in PC12 cells in a dose-dependent manner. These results suggest that curcumin is able to protect PC12 cells which may be associated with inhibition of ERK phosphorylation.

Cells growing in high density were observed to undergo a variety of responses due to cell-cell contact, pericellular hypoxia, etc. In order to investigate the influence of cell density on cell proliferation and adhesion and to elucidate possible mechanisms, we tested the growth ability of human prostate tumour (PC-3M) cells in dense culture and the influences of density on cell adhesion. Our results demonstrate that increasing cell density exerted stress on PC-3M cells, which decreased cell proliferation in dense cultures, but tended to facilitate tumour metastasis since cell adhesion ability was elevated and the cells showed an increased growth rate after being moved to a favourable growth environment. We conclude that higher cell density-mediated pericellular hypoxia was an important factor inducing expression of the intrinsic hypoxia marker osteopontin, another mechanism contributing to cell adhesion enhancement in PC-3M cells. In addition, cell density enhanced adhesion ability due to the activation of p38 mitogen-activated protein kinase (p38 MAPK) and protein kinase C. Intracellular calcium also played positive roles at least partially through activating p38 MAPK.

Whether and how in-vitro-produced human neural precursors mature and integrate into the brain are crucial to the utility of human embryonic stem (hES) cells in treating neurological disorders. After transplantation into the ventricles of neonatal immune-deficient mice, hES-cell-derived neural precursors stopped expressing the cell division marker Ki67, except in neurogenic areas, and differentiated into neurons and then glia in a temporal course intrinsic to that of human cells regardless of location. The human cells located in the gray matter became neurons in the olfactory bulb and striatum, whereas those in the white matter produced exclusively glia. Importantly, the grafted human cells formed synapses. Thus, the in-vitro-produced human neural precursors follow their intrinsic temporal program to produce neurons and glia and, in response to environmental signals, generate cells appropriate to their target regions and integrate into the brain.

The effects of melatonin on the mitochondrial DNA (mtDNA) damage induced by 1-methyl-4-phenyl-1, 2, 3, 6-tetrahydropyridine (MPTP) and 1-methyl-4-phenylpyridine ion (MPP(+)) were investigated both in vivo and in vitro. MPTP (24 mg/kg, s.c.) induced a rapid increase in the immunoreactivity of 8-hydroxyguanine (8-oxoG), a common biomarker of DNA oxidative damage, in the cytoplasm of neurons in the Substantia Nigra Compact of mouse brain. Melatonin preinjection (7.5, 15 or 30 mg/kg, i.p.) dose-dependently prevented MPTP-induced DNA oxidative damage. In SH-SY5Y cells, MPP(+) (1 mm) increased the immunoreactivity of 8-oxoG in the mitochondria at 1 hr and in the nucleus at 3 hr after treatment. Melatonin (200 microm) preincubation significantly attenuated MPP(+)-induced mtDNA oxidative damage. Furthermore, MPP(+) time-dependently increased the accumulation of mitochondrial oxygen free radicals (mtOFR) from 1 to 24 hr and gradually decreased the mitochondrial membrane potential (Psim) from 18 to 36 hr after incubation. At 72 hr after incubation, MPP(+) caused cell death in 49% of the control. However, melatonin prevented MPP(+)-induced mtOFR generation and Psim collapse, and later cell death. The present results suggest that cytoprotection of melatonin against MPTP/MPP(+)-induced cell death may be associated with the attenuation of mtDNA oxidative damage via inhibition of mtOFR generation and the prevention of Psim collapse.

Aims/hypothesis Refractory wounds in diabetic patients constitute a serious complication that often leads to amputation with limited treatment regimens. The present study was designed to determine the role of FoxO1/iNOS pathway and effect of the soy isoflavone genistein on diabetic wound healing. Methods Streptozotocin (STZ)-induced type 1 diabetic mice with full-thickness excisional wounds given intragastrically 1 and 3 mg/kg/day of iNOS selective inhibitor (L-NIL) or received 0.2, 1 and 5 mg/kg/day of genistein via subcutaneous injection. Results In diabetic wound tissues, the inducible nitric oxide synthase (iNOS) was activated, silent information regulator 1 (SIRT1) and forkhead box O transcription factor 1 (FoxO1) were elevated. Genistein administration prevented increased iNOS activity and attenuated diabetic cutaneous SIRT1 and FoxO1 levels in a dose-dependent manner. Diabetic conditions significantly increased superoxide anion (O2.-) production, nitrotyrosine formation, and decreased nitrite level...

Acetazolamide (AZA), a prototype of carbonic anhydrase (CA) inhibitor, acts as a diuretic agent with its site of action on renal proximal tubules. These nephron segments also contain aquaporin-1 (A...