Effect of constant and fluctuating temperature on the circadian foraging rhythm of the red imported fire ant,Solenopsis invicta Buren (Hymenoptera: Formicidae)

Understanding circadian foraging rhythms activity of the red imported fire ant, Solenopsis invicta Buren (Hymenoptera: Formicidae) foragers at different temperatures is an important step towards developing control measures in Integrated Pest Management (IPM) programs. In this study, the circadian foraging rhythm activities of S. invicta foragersat different temperature were investigated under laboratory and field conditions. Results indicated that the foraging activity increased after sunrise, and maximum foraging occurred at 14:00 (foraging rate was 69.22 ± 0.57 and 72.58 ± 1.15 foragers/min in the first and second year, respectively) in the tea fields of Guangzhou during autumn. Furthermore, foragers demonstrated circadian rhythms and exhibited a unimodal after 24 h. A significant correlation was found between foraging activity and temperature. S. invicta colonies were active at moderate soil temperatures (approximately 26.65 °C to 29.24 °C). The preferred temperature of the colonies was 26 °C, followed by 22 °C and 18 °C in the laboratory. The individual S. invicta activity was maximum at 17:00 (18.67 ± 1.66 times /10 min) and minimum at 5:00 (8.33 ± 2.51 times/10 min) at 26 °C. The fluctuating temperature had a significant impact on individual locomotor activity (r = 0.8979, P < 0.01) but did not alter the rhythm activity. Our results demonstrated that temperature might play an important role in circadian foraging rhythms activity of S. invicta. These results may have implications for the development of more effective fire ant management strategies.     

Relative Changes from Prior Reward Contingencies Can Constrain Brain Correlates of Outcome Monitoring

It is well-known that the affective value of an environment can be relative to whether it reflects an improvement or a worsening from a previous state. A potential explanation for this phenomenon suggests that relative changes from previous reward contingencies can constrain how brain monitoring systems form predictions about future events. In support of this idea, we found that changes per se relative to previous states of learned reward contingencies modulated the Feedback-Related Negativity (FRN), a human brain potential known to index discrepancies between predictions and affective outcomes. Specifically, we observed that environments with a 50% reward probability yielded different FRN patterns according to whether they reflected an improvement or a worsening from a previous environment. Further, we also found that this pattern of results was driven mainly by variations in the amplitude of ERPs to positive outcomes. Overall, these results suggest that relative changes in reward probability from previous learned environments can constrain how neural systems of outcome monitoring formulate predictions about the likelihood of future rewards and nonrewards.     

Induction of uPA gene expression by the blockage of E-cadherin via Src- and Shc-dependent Erk signaling

Loss of E-cadherin-mediated cell-cell adhesion and expression of proteolytic enzymes characterize the transition from benign lesions to invasive, metastatic tumor, a rate-limiting step in the progression from adenoma to carcinoma in vivo. A soluble E-cadherin fragment found recently in the serum and urine of cancer patients has been shown to disrupt cell-cell adhesion and to drive cell invasion in a dominant-interfering manner. Physical disruption of cell-cell adhesion can be mimicked by the function-blocking antibody Decma. We have shown previously in MCF7 and T47D cells that urokinase-type plasminogen activator (uPA) activity is up-regulated upon disruption of E-cadherin-dependent cell-cell adhesion. We explored the underlying molecular mechanisms and found that blockage of E-cadherin by Decma elicits a signaling pathway downstream of E-cadherin that leads to Src-dependent Shc and extracellular regulated kinase (Erk) activation and results in uPAgene activation. siRNA-mediated knockdown of endogenous Src-homology collagen protein (Shc) and subsequent expression of single Shc isoforms revealed that p46(Shc) and p52(Shc) but not p66(Shc) were able to mediate Erk activation. A parallel pathway involving PI3K contributed partially to Decma-induced Erk activation. This report describes that disruption of E-cadherin-dependent cell-cell adhesion induces intracellular signaling with the potential to enhance tumorigenesis and, thus, offers new insights into the pathophysiological mechanisms of tumor development.     

Analysis of extracellular proteins of two Perkinsus spp. isolated from the softshell clam Mya arenaria in vitro

Biochemical characterization of the extracellular proteins (ECP) of two softshell clam Perkinsus spp. cloned isolates, Perkinsus chesapeaki isolate G-117 and Perkinsus marinus H-49, was performed and compared to that of the oyster-derived P. marinus isolate P-1. G-117 and H-49 demonstrated distinct differences in enzyme activities; however, all three isolates shared common bands. Substrate-impregnated gels showed H-49 to possess proteolytic activities while G-117 did not. Inhibition studies revealed that H-49 ECP contain serine proteases similar to those described for P-1. The G-117 ECP lacked proteolytic activity but showed a higher production of lipolytic enzymes than H-49 or P-1. Optimal in vitro growth temperatures for the two clam isolates were generally lower than those for P-1. G-117 showed faster growth at lower salinities than either H-49 or P-1. Clam Perkinsus spp. isolates appear to be better adapted to lower salinities and temperatures than the P. marinus isolate of the eastern oyster.     

The orexigenic effect of ghrelin is mediated through central activation of the endogenous cannabinoid system

Introduction

Ghrelin and cannabinoids stimulate appetite, this effect possibly being mediated by the activation of hypothalamic AMP-activated protein kinase (AMPK), a key enzyme in appetite and metabolism regulation. The cannabinoid receptor type 1 (CB1) antagonist rimonabant can block the orexigenic effect of ghrelin. In this study, we have elucidated the mechanism of the putative ghrelin-cannabinoid interaction.

Methods

The effects of ghrelin and CB1 antagonist rimonabant in wild-type mice, and the effect of ghrelin in CB1-knockout animals, were studied on food intake, hypothalamic AMPK activity and endogenous cannabinoid content. In patch-clamp electrophysiology experiments the effect of ghrelin was assessed on the synaptic inputs in parvocellular neurons of the hypothalamic paraventricular nucleus, with or without the pre-administration of a CB1 antagonist or of cannabinoid synthesis inhibitors.

Results and Conclusions

Ghrelin did not induce an orexigenic effect in CB1-knockout mice. Correspondingly, both the genetic lack of CB1 and the pharmacological blockade of CB1 inhibited the effect of ghrelin on AMPK activity. Ghrelin increased the endocannabinoid content of the hypothalamus in wild-type mice and this effect was abolished by rimonabant pre-treatment, while no effect was observed in CB1-KO animals. Electrophysiology studies showed that ghrelin can inhibit the excitatory inputs on the parvocellular neurons of the paraventricular nucleus, and that this effect is abolished by administration of a CB1 antagonist or an inhibitor of the DAG lipase, the enzyme responsible for 2-AG synthesis. The effect is also lost in the presence of BAPTA, an intracellular calcium chelator, which inhibits endocannabinoid synthesis in the recorded parvocellular neuron and therefore blocks the retrograde signaling exerted by endocannabinoids. In summary, an intact cannabinoid signaling pathway is necessary for the stimulatory effects of ghrelin on AMPK activity and food intake, and for the inhibitory effect of ghrelin on paraventricular neurons.     

Modulation of Activation-Induced Cytidine Deaminase by Curcumin in Helicobacter pylori-Infected Gastric Epithelial Cells

Background: Anomalous expression of activation‐induced cytidine deaminase (AID) in Helicobacter pylori‐infected gastric epithelial cells has been postulated as one of the key mechanisms in the development of gastric cancer. AID is overexpressed in the cells through nuclear factor (NF)‐κB activation by H. pylori and hence, inhibition of NF‐κB pathway can downregulate the expression of AID. Curcumin, a spice‐derived polyphenol, is known for its anti‐inflammatory activity via NF‐κB inhibition. Therefore, it was hypothesized that curcumin might suppress AID overexpression via NF‐κB inhibitory activity in H. pylori‐infected gastric epithelial cells. Materials and Methods: MKN‐28 or MKN‐45 cells and H. pylori strain 193C isolated from gastric cancer patient were used for co‐culture experiments. Cells were pretreated with or without nonbactericidal concentrations of curcumin. Apoptosis was determined by DNA fragmentation assay. Enzyme‐linked immunosorbent assay was performed to evaluate the anti‐adhesion activity of curcumin. Real‐time polymerase chain reaction was employed to evaluate the expression of AID mRNA. Immunoblot assay was performed for the analysis of AID, NF‐κB, inhibitors of NF‐κB (IκB), and IκB kinase (IKK) complex regulation with or without curcumin. Results: The adhesion of H. pylori to gastric epithelial cells was not inhibited by curcumin pretreatment at nonbactericidal concentrations (≤10 μmol/L). Pretreatment with nonbactericidal concentration of curcumin downregulated the expression of AID induced by H. pylori. Similarly, NF‐κB activation inhibitor (SN‐50) and proteasome inhibitor (MG‐132) also downregulated the mRNA expression of AID. Moreover, curcumin (≤10 μmol/L) has suppressed H. pylori‐induced NF‐κB activation via inhibition of IKK activation and IκB degradation. Conclusion: Nonbactericidal concentrations of curcumin downregulated H. pylori‐induced AID expression in gastric epithelial cells, probably via the inhibition of NF‐κB pathway. Hence, curcumin can be considered as a potential chemopreventive candidate against H. pylori‐related gastric carcinogenesis.     

Preparation of Oligomeric β-amyloid1-42 and Induction of Synaptic Plasticity Impairment on Hippocampal Slices

Impairment of synaptic connections is likely to underlie the subtle amnesic changes occurring at the early stages of Alzheimer s Disease (AD). β-amyloid (Aβ), a peptide produced in high amounts in AD, is known to reduce Long-Term Potentiation (LTP), a cellular correlate of learning and memory. Indeed, LTP impairment caused by Aβ is a useful experimental paradigm for studying synaptic dysfunctions in AD models and for screening drugs capable of mitigating or reverting such synaptic impairments. Studies have shown that Aβ produces the LTP disruption preferentially via its oligomeric form. Here we provide a detailed protocol for impairing LTP by perfusion of oligomerized synthetic Aβ1-42 peptide onto acute hippocampal slices. In this video, we outline a step-by-step procedure for the preparation of oligomeric Aβ_1-42. Then, we follow an individual experiment in which LTP is reduced in hippocampal slices exposed to oligomerized Aβ_1-42 compared to slices in a control experiment where no Aβ_1-42 exposure had occurred.Download video file.^{(55M, mp4)}     

Toxic potential of some indigenous plant oils against the rice weevil,Sitophilus oryzae (Linnaeus)

The present study was conducted to evaluate the toxic potential of five indigenous plant oils: black pepper (Piper nigrum), Chinese cinnamon (Cinnamomum cassia), garlic (Allium sativum), river red gum (Eucalyptus camaldulensis), and yellow oleander (Thevetia peruviana), against laboratory reared Sitophilus oryzae adults. The bioassays were done by the diet incorporation method with concentrations ranging from 50 ppm to 500 ppm. Based on lethal concentrations to kill 50% (LC₅₀) of the subjected weevils, T. peruviana proved to be the most toxic having the lowest LC₅₀ values, 414.58, 201.94, and 129.52 ppm, after 7, 14, and 21 days of exposure, respectively, followed by E. camaldulensis (475.51, 366.65, and 251.28 ppm, respectively). The rest of the plant oils also showed toxic potential, but these were less toxic compared with T. peruviana and E. camaldulensis. With respect to the time taken to cause 50% mortality (LT₅₀) of the exposed weevils, T. peruviana had LT₅₀ at 14.54 days followed by P. nigrum (22.09 days), E. camaldulensis (24.29 days), and C. cassia (28.71 days). Whereas, A. sativum took the longest time (44.47 days) to cause 50% mortality of the exposed weevils. In conclusion, the result revealed toxic potential of tested plant oils, and suggests further studies under simulated‐field conditions should be included in the management plan for S. oryzae.     

Isolation of Aeromonas salmonicida from sea lamprey (Petromyzon marinus) with furuncle-like lesions in Lake Ontario

For the past six decades, parasitic sea lampreys (Petromyzon marinus) have caused devastating losses to salmonid fisheries in the Great Lakes. To reduce the number of sea lampreys, the Great Lakes Fishery Commission began a large-scale program based on trapping male sea lampreys, sterilizing them, and releasing sterile males back into streams to compete with fertile males for spawning females. The transfer of lampreys among lakes can potentially lead to the transfer of various pathogens, and this has raised major concerns regarding the possibility of resident fish populations becoming infected by introduced pathogens. During a health inspection of sea lampreys collected from Lake Ontario, lampreys with obvious furuncle-like lesions (1-2 cm in diameter) were noticed. Most of the furuncles occupied the dorso-lateral musculature, and Aeromonas salmonicida subsp. salmonicida was isolated from the kidneys. This bacterium was cultured from kidneys of 2.5% of the sea lampreys collected from two locations within the Lake Ontario watershed in 2004. The identity of bacterial colonies was presumptively verified with biochemical reactions and confirmed with polymerase chain reaction. This is the first report of A. salmonicida infection in sea lamprey in the Great Lakes basin associated with furunculosis.     

Zygosity at the major histocompatibility class IIB locus predicts susceptibility to Renibacterium salmoninarum in Atlantic salmon (Salmo salar L.)

Major histocompatibility (MH) class II genes play an important role in the vertebrate immune response. Here, we investigate the relationship between Atlantic salmon (Salmo salar) MH class IIB zygosity and susceptibility to Renibacterium salmoninarum, the causal agent of bacterial kidney disease. By combining DNA sequences from the salmon MH class IIB gene with quantitative ELISA data on R. salmoninarum antigen levels, we found that MH class IIB homozygotes were significantly more susceptible to R. salmoninarum than heterozygotes. These findings are discussed in the context of current evolutionary theory.