scholarly journals Persistence of Mating Suppression of the Indian Meal Moth Plodia Interpunctella in the Presence and Absence of Commercial Mating Disruption Dispensers

Insects ◽  
2020 ◽  
Vol 11 (10) ◽  
pp. 701 ◽  
Author(s):  
Leanage K. W. Wijayaratne ◽  
Charles S. Burks
Keyword(s):  
Mating Disruption ◽  
Direct Interaction ◽  
Plodia Interpunctella ◽  
Dependent Manner ◽  
High Concentration ◽  
Concentration Dependent Manner ◽  
Indian Meal Moth ◽  
Indian Meal ◽  
Assay Chamber ◽  
High Concentrations

The Indian meal moth Plodia interpunctella (Hübner) (Lepidoptera: Pyralidae), is controlled by commercial mating disruption dispensers using passive release to emit high concentrations (relative to females or monitoring lures) of their principal sex pheromone component, (9Z,12E)-tetradecadienyl acetate. Since P. interpunctella is sexually active throughout the scotophase, an assay system was developed to determine the importance of direct interaction of the male with the dispenser, and whether exposure to mating disruption early in the night is sufficient to suppress mating throughout the night. Exposure to mating disruption dispensers in the mating assay chamber for the first two hours of a 10-h scotophase significantly reduced mating when females were introduced four hours later. Mating was also reduced to a lesser degree in a concentration-dependent manner based solely on re-emission of pheromone, and when males were exposed outside the mating assay chamber. These results indicate that the commercial mating disruption dispensers can suppress mating throughout the night based on interaction with the dispenser early in the night. Desensitization resulting from attraction to a high-concentration pheromone source is important to this suppression, but other factors such as re-emission from the environment may also have a role. These observations imply a non-competitive mechanism for P. interpunctella with the product studied, and suggest that effectiveness of the mating disruption dispenser might be augmented by using them in conjunction with another formulation such as an aerosol or micro-encapsulated product.

scholarly journals Beclin1-mediated ferroptosis activation is associated with isoflurane-induced toxicity in SH-SY5Y neuroblastoma cells

2019 ◽  
Author(s):  
Ruizhu Liu ◽  
Xuefeng Li ◽  
Guoqing Zhao
Keyword(s):  
Cell Death ◽  
Cell Damage ◽  
Neuroblastoma Cells ◽  
Underlying Mechanism ◽  
Dependent Manner ◽  
High Concentration ◽  
Concentration Dependent Manner ◽  
Regulated Cell Death ◽  
Deferoxamine Mesylate ◽  
High Concentrations

Abstract The widely used inhalation anesthetic, isoflurane, potentially induces neuronal injury in clinical practice. Previous studies showed multiple forms of cell death that resulted from isoflurane-induced cytotoxicity, but the precise underlying mechanism remains poorly understood. Ferroptosis has recently been identified as a non-apoptotic form of regulated cell death. Here, we found that ferroptosis inhibitors, ferrostatin-1 and deferoxamine mesylate (DFOM), showed great efficiency in maintaining cell viability in SH-SY5Y neuroblastoma cells exposed to a high concentration of isoflurane for 24 h. We also observed that cellular chelatable iron and lipid peroxidation were increased in a concentration-dependent manner in response to isoflurane. In addition, isoflurane upregulated Beclin1 phosphorylation, followed by the formation of a Beclin1-solute carrier family 7 member 11 (SLC7A11) complex, which affected the activity of cystine/glutamate antipoter and further regulated ferroptotic cell death. Accordingly, Beclin1 overexpression aggravated isoflurane-induced cell damage by upregulating ferroptosis. This phenomenon was significantly attenuated by silencing of Beclin1 in SH-SY5Y cells. These findings indicate that Beclin1 may regulate ferroptosis in a manner involving inhibition of glutamate exchange activity of system xc(−), which is implicated in isoflurane-induced toxicity. In particular, when isoflurane is administrated at high concentrations and for an extended duration, ferroptosis is more likely to play a crucial role in isoflurane-induced toxicity.

Neutrophil Elastase Potentiates Cathepsin G-lnduced Platelet Activation

1992 ◽  
Vol 68 (05) ◽  
pp. 570-576 ◽  
Author(s):  
Mary A Selak
Keyword(s):  
Neutrophil Elastase ◽  
Cell Activation ◽  
Thromboxane A2 ◽  
Creatine Phosphate ◽  
Dense Granule ◽  
Cathepsin G ◽  
Dependent Manner ◽  
Concentration Dependent Manner ◽  
Low Concentrations ◽  
High Concentrations

SummaryWe have previously demonstrated that human neutrophil cathepsin G is a strong platelet agonist that binds to a specific receptor. This work describes the effect of neutrophil elastase on cathepsin G-induced platelet responses. While platelets were not activated by high concentrations of neutrophil elastase by itself, elastase enhanced aggregation, secretion and calcium mobilization induced by low concentrations of cathepsin G. Platelet aggregation and secretion were potentiated in a concentration-dependent manner by neutrophil elastase with maximal responses observable at 200 nM. Enhancement was observed when elastase was preincubated with platelets for time intervals of 10–60 s prior to addition of a low concentration of cathepsin G and required catalytically-active elastase since phenylmethanesulphonyl fluoride-inhibited enzyme failed to potentiate cell activation. Neutrophil elastase potentiation of platelet responses induced by low concentrations of cathepsin G was markedly inhibited by creatine phosphate/creatine phosphokinase and/or indomethacin, indicating that the synergism between elastase and cathepsin G required the participation of ADP and thromboxane A2. On the other hand, platelet responses were not attenuated by the PAF antagonist BN 52021, signifying that PAF-acether did not play a role in elastase potentiation. At higher concentrations porcine pancreatic elastase exhibits similar effects to neutrophil elastase, demonstrating that the effect of elastase was not unique to the neutrophil protease. While neutrophil elastase failed to alter the ability of cathepsin G to hydrolyze a synthetic chromogenic substrate, preincubation of platelets with elastase increased the apparent affinity of cathepsin G binding to platelets. In contrast to their effect on cathepsin G-induced platelet responses, neither neutrophil nor pancreatic elasatse potentiated aggregation or dense granule release initiated by ADP, PAF-acether, arachidonic acid or U46619, a thromboxane A2 mimetic. Moreover, unlike its effect on cathepsin G, neutrophil elastase inhibited thrombin-induced responses. The current observations demonstrate that elastase can potentiate platelet responses mediated by low concentrations of cathepsin G, suggesting that both enzymes may function synergistically to activate platelets under conditions where neutrophil degranulation occurs.

scholarly journals Methyl Benzoate Is Superior to Other Natural Fumigants for Controlling the Indian Meal Moth (Plodia interpunctella)

Insects ◽  
2020 ◽  
Vol 12 (1) ◽  
pp. 23
Author(s):  
Md Munir Mostafiz ◽  
Errol Hassan ◽  
Rajendra Acharya ◽  
Jae-Kyoung Shim ◽  
Kyeong-Yeoll Lee
Keyword(s):  
Insect Pests ◽  
Insect Pest ◽  
Plodia Interpunctella ◽  
Methyl Benzoate ◽  
Management Tool ◽  
Contact Toxicity ◽  
Fumigant Toxicity ◽  
Indian Meal Moth ◽  
Indian Meal ◽  
Food Commodities

The Indian meal moth, Plodia interpunctella (Hübner) (Lepidoptera: Pyralidae), is an insect pest that commonly affects stored and postharvest agricultural products. For the control of insect pests and mites, methyl benzoate (MBe) is lethal as a fumigant and also causes contact toxicity; although it has already been established as a food-safe natural product, the fumigation toxicity of MBe has yet to be demonstrated in P. interpunctella. Herein, we evaluated MBe as a potential fumigant for controlling adults of P. interpunctella in two bioassays. Compared to the monoterpenes examined under laboratory conditions, MBe demonstrated high fumigant activity using a 1-L glass bottle at 1 μL/L air within 4 h of exposure. The median lethal concentration (LC50) of MBe was 0.1 μL/L air; the median lethal time (LT50) of MBe at 0.1, 0.3, 0.5, and 1 μL/L air was 3.8, 3.3, 2.8, and 2.0 h, respectively. Compared with commercially available monoterpene compounds used in pest control, MBe showed the highest fumigant toxicity (toxicity order as follows): MBe > citronellal > linalool > 1,8 cineole > limonene. Moreover, in a larger space assay, MBe caused 100% mortality of P. interpunctella at 0.01 μL/cm3 of air after 24 h of exposure. Therefore, MBe can be recommended for use in food security programs as an ecofriendly alternative fumigant. Specifically, it provides another management tool for curtailing the loss of stored food commodities due to P. interpunctella infestation.

Direct interaction of the tau 1 transactivation domain of the human glucocorticoid receptor with the basal transcriptional machinery

1993 ◽  
Vol 13 (1) ◽  
pp. 399-407
Author(s):  
I J McEwan ◽  
A P Wright ◽  
K Dahlman-Wright ◽  
J Carlstedt-Duke ◽  
J A Gustafsson
Keyword(s):  
Glucocorticoid Receptor ◽  
Protein Interactions ◽  
Core Promoter ◽  
Specific Interaction ◽  
Direct Interaction ◽  
Dependent Manner ◽  
Transactivation Domain ◽  
Yeast Saccharomyces Cerevisiae ◽  
Concentration Dependent Manner

We have used a yeast (Saccharomyces cerevisiae) cell free transcription system to study protein-protein interactions involving the tau 1 transactivation domain of the human glucocorticoid receptor that are important for transcriptional transactivation by the receptor. Purified tau 1 specifically inhibited transcription from a basal promoter derived from the CYC1 gene and from the adenovirus 2 major late core promoter in a concentration-dependent manner. This inhibition or squelching was correlated with the transactivation activity of tau 1. Recombinant yeast TATA-binding protein (yTFIID), although active in vitro, did not specifically reverse the inhibitory effect of tau 1. In addition, no specific interaction between tau 1 and yTFIID could be shown in vitro by affinity chromatography. Taken together, these results indicate that the tau 1 transactivation domain of the human glucocorticoid receptor interacts directly with the general transcriptional apparatus through some target protein(s) that is distinct from the TATA-binding factor. Furthermore, this assay can be used to identify interacting factors, since after phosphocellulose chromatography of a whole-cell yeast extract, a fraction that contained an activity which selectively counteracted the squelching effect of tau 1 was found.

scholarly journals Efficacy of essential oils to control the Indian meal moth, Plodia interpunctella (Hübner) (Lepidoptera: Pyralidae)

2017 ◽  
Vol 20 (4) ◽  
pp. 1122-1129 ◽  
Author(s):  
Emiliano Nicolás Jesser ◽  
Jorge Omar Werdin-González ◽  
Ana Paula Murray ◽  
Adriana Alicia Ferrero
Keyword(s):  
Essential Oils ◽  
Plodia Interpunctella ◽  
Indian Meal Moth ◽  
Indian Meal ◽  
Lepidoptera Pyralidae

Endothelium and mechanical responses of isolated monkey pulmonary veins to histamine

1990 ◽  
Vol 259 (4) ◽  
pp. H1032-H1037 ◽  
Author(s):  
T. Matsuki ◽  
T. Ohhashi
Keyword(s):  
Pulmonary Veins ◽  
Dependent Manner ◽  
High Concentration ◽  
Concentration Dependent Manner ◽  
Mechanical Responses ◽  
Relaxing Factor ◽  
Prostaglandin F2 Alpha ◽  
H2 Receptors ◽  
Endothelium Derived Relaxing Factor ◽  
Stimulation Of

Ring strips of monkey pulmonary veins precontracted with a high concentration of prostaglandin F2 alpha (PGF2 alpha) relaxed in a concentration-dependent manner in response to histamine. Treatment with mepyramine and/or famotidine attenuated the relaxation. 2-Pyridylethylamine (2PEA) and dimaprit caused relaxations in the precontracted preparations, which were inhibited by pretreatment with mepyramine and famotidine, respectively. Removal of endothelium reversed the histamine- and 2PEA-induced relaxations to dose-related contractions. On the other hand, the removal had no effect on the dimaprit-induced relaxations, which were significantly reduced by pretreatment with famotidine. Histamine-induced relaxations in the precontracted strips with endothelium in the presence and absence of famotidine were suppressed or abolished by treatment with methylene blue or hemoglobin but were unaffected by aspirin. It may be concluded that histamine-induced relaxation in monkey pulmonary veins precontracted with PGF2 alpha is mediated by H2-receptors in smooth muscle and H1-receptors in endothelium. Also, stimulation of the endothelial H1-receptors liberates an endothelium-derived relaxing factor.

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