Elucidation of the Structure of Solanoeclepin A, a Natural Hatching Factor of Potato and Tomato Cyst Nematodes, by Single-crystal X-ray Diffraction

Potato crops can be severely damaged by potato cyst nematodes Globodera rostochiensis and Globodera pallida, nematodes highly specific to potatoes and some other Solanaceae. Hatching of juveniles is controlled by agents excreted by the roots of some Solanaceae species. Over seventy years much effort has been expended by many groups to isolate these agents and to determine their structures. However, all attempts have failed. We report here the structure determination of a hatching factor excreted from potato and tomato roots. The hatching factor bears some resemblance to Glycinoeclepins as found by Masamune et al.2-5 and is hence designated as Solanoeclepin A.1 C27H30O9.3H2O, Mr = 498.5, monoclinic, P21, a = 11.289(2), b = 20.644(4), c = 11.632(12) Å, β = 90.81(4), V = 2711(3) Å3, Z = 4, Dx = 1.35 g cm–3, λ(Cu-K&alpha ) = 1.5418 Å, μ(Cu-Kα ) = 9.0 cm–1, F(000) = 1176, –60 °C. Final R = 0.117 for 3721 observed reflections

Platelet-Associated CD40/CD154 Mediates Remote Tissue Damage after Mesenteric Ischemia/Reperfusion Injury

Several innate and adaptive immune cell types participate in ischemia/reperfusion induced tissue injury. Amongst them, platelets have received little attention as contributors in the process of tissue damage after ischemia reperfusion (I/R) injury. It is currently unknown whether platelets participate through the immunologically important molecules including, CD40 and when activated, CD154 (CD40L), in the pathogenesis of I/R injury. We hypothesized that constitutive expression of CD40 and activation-induced expression of CD154 on platelets mediate local mesenteric and remote lung tissue damage after I/R injury. Wild type (WT; C57BL/6J), CD40 and CD154 deficient mice underwent mesenteric ischemia for 30 minutes followed by reperfusion for 3 hours. WT mice subjected to mesenteric I/R injury displayed both local intestinal and remote lung damage. In contrast, there was significantly less intestinal damage and no remote lung injury in CD40 and CD154 deficient mice when compared to WT mice. Platelet-depleted WT mice transfused with platelets from CD40 or CD154 deficient mice failed to reconstitute remote lung damage. In contrast, when CD40 or CD154 deficient mice were transfused with WT platelets lung tissue damage was re-established. Together, these findings suggest that multiple mechanisms are involved in local and remote tissue injury and also identify platelet-expressed CD40 and/or CD154 as mediators of remote tissue damage

Decreasing incidence of adenotonsillar problems in Dutch general practice: real or artefact?

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