Abstract:Insects in the order Hymenoptera defend themselves, attack prey and regulate hosts using toxins that are effective in small quantities. In this study, advances in the researches on parasitic hymenopteran toxins are summarized in terms of the production, categories, components, properties, ecological functions and mechanisms. The glands that produce venoms derive from the ectoderm tissue and evolve from the accessory glands of the reproductive system. Venoms are excreted by the poison gland or acid gland of mat… Show more
“…Since ectoparasitoids develop on the body surface of host where they are not fully exposed to circulating host hemolymph‐associated immune responses like endoparasitoids, venoms of them often are believed to cause permanent host paralysis and developmental arrest other than the suppression of the hosts immune response for favoring successful development of their offsprings (Hu et al., ; Moreau & Asgari, ; Wang & Yang, ). Interestingly, it was notably found in this study that S. guani venom has subtly virulent effects on cellular defense of T. molitor .…”
Venom is a prominently maternal virulent factor utilized by parasitoids to overcome hosts immune defense. With respect to roles of this toxic mixture involved in manipulating hosts immunity, great interest has been mostly restricted to Ichneumonoidea parasitoids associated with polydnavirus (PDV), of which venom is usually considered as a helper component to enhance the role of PDV, and limited Chalcidoidea species. In contrast, little information is available in other parasitoids, especially ectoparasitic species not carrying PDV. The ectoparasitoid Scleroderma guani injects venom into its host, Tenebrio molitor, implying its venom was involved in suppression of hosts immune response for successful parasitism. Thus, we investigated the effects of parasitism and venom of this parasitoid on counteracting the cellular immunity of its host by examining changes of hemocyte counts, and hemocyte spreading and encapsulation ability. Total hemocyte counts were elevated in parasitized and venom-injected pupae. The spreading behavior of both granulocytes and plasmatocytes was impaired by parasitization and venom. High concentration of venom led to more severely increased hemocyte counts and suppression of hemocyte spreading. The ability of hemocyte encapsulation was inhibited by venom in vitro. In addition to immediate effects observed, venom showed persistent interference in hosts cellular immunity. These results indicate that venom alone from S. guani plays a pivotal role in blocking hosts cellular immune response, serving as a regulator that guarantees the successful development of its progenies. The findings provide a foundation for further investigation of the underlying mechanisms in immune inhibitory action of S. guani venom.
“…Since ectoparasitoids develop on the body surface of host where they are not fully exposed to circulating host hemolymph‐associated immune responses like endoparasitoids, venoms of them often are believed to cause permanent host paralysis and developmental arrest other than the suppression of the hosts immune response for favoring successful development of their offsprings (Hu et al., ; Moreau & Asgari, ; Wang & Yang, ). Interestingly, it was notably found in this study that S. guani venom has subtly virulent effects on cellular defense of T. molitor .…”
Venom is a prominently maternal virulent factor utilized by parasitoids to overcome hosts immune defense. With respect to roles of this toxic mixture involved in manipulating hosts immunity, great interest has been mostly restricted to Ichneumonoidea parasitoids associated with polydnavirus (PDV), of which venom is usually considered as a helper component to enhance the role of PDV, and limited Chalcidoidea species. In contrast, little information is available in other parasitoids, especially ectoparasitic species not carrying PDV. The ectoparasitoid Scleroderma guani injects venom into its host, Tenebrio molitor, implying its venom was involved in suppression of hosts immune response for successful parasitism. Thus, we investigated the effects of parasitism and venom of this parasitoid on counteracting the cellular immunity of its host by examining changes of hemocyte counts, and hemocyte spreading and encapsulation ability. Total hemocyte counts were elevated in parasitized and venom-injected pupae. The spreading behavior of both granulocytes and plasmatocytes was impaired by parasitization and venom. High concentration of venom led to more severely increased hemocyte counts and suppression of hemocyte spreading. The ability of hemocyte encapsulation was inhibited by venom in vitro. In addition to immediate effects observed, venom showed persistent interference in hosts cellular immunity. These results indicate that venom alone from S. guani plays a pivotal role in blocking hosts cellular immune response, serving as a regulator that guarantees the successful development of its progenies. The findings provide a foundation for further investigation of the underlying mechanisms in immune inhibitory action of S. guani venom.
Abstract:A graph G = (V , E) is called (k, k )-total weight choosable if the following holds: For any total list assignment L which assigns to each vertex x a set L(x) of k real numbers, and assigns to each edge e a set L(e) of k real numbers, there is a mapping f : V ∪E → R such that f (y) ∈ L(y) for any y ∈ V ∪E and for any two adjacent vertices x, x , e∈E(x) f (e)+f (x) = e∈E(x ) f (e)+f (x ). We conjecture that every graph is (2, 2)-total weight choosable and every graph without isolated edges is (1, 3)-total weight choosable. It follows from results in [7] that complete graphs, complete bipartite graphs, trees other than K 2 are (1, 3)-total weight choosable. Also a graph G obtained from an arbitrary graph H by subdividing each edge with at least three vertices is (1, 3)-total weight choosable. This article proves that complete graphs, trees, generalized theta graphs are (2, 2)-total weight choosable. We also prove that for any graph H, a graph G obtained from H by subdividing each edge with at least two vertices is (2, 2)-total weight
Let c be a proper edge coloring of a graph G=(V,E) with integers 1,2,…,k. Then k≥Δ(G), while Vizing's theorem guarantees that we can take k≤Δ(G)+1. On the course of investigating irregularities in graphs, it has been conjectured that with only slightly larger k, that is, k=Δ(G)+2, we could enforce an additional strong feature of c, namely that it attributes distinct sums of incident colors to adjacent vertices in G if only this graph has no isolated edges and is not isomorphic to C5. We prove the conjecture is valid for planar graphs of sufficiently large maximum degree. In fact an even stronger statement holds, as the necessary number of colors stemming from the result of Vizing is proved to be sufficient for this family of graphs. Specifically, our main result states that every planar graph G of maximum degree at least 28, which contains no isolated edges admits a proper edge coloring c:E→{1,2,…,Δ(G)+1} such that ∑e∋ucfalse(efalse)≠∑e∋vcfalse(efalse) for every edge uv of G.
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