A Model for the Development of the Rhizobial and Arbuscular Mycorrhizal Symbioses in Legumes and Its Use to Understand the Roles of Ethylene in the Establishment of these two Symbioses

We propose a model depicting the development of nodulation and arbuscular mycorrhizae. Both processes are dissected into many steps, using Pisum sativum L. nodulation mutants as a guideline. For nodulation, we distinguish two main developmental programs, one epidermal and one cortical. Whereas Nod factors alone affect the cortical program, bacteria are required to trigger the epidermal events. We propose that the two programs of the rhizobial symbiosis evolved separately and that, over time, they came to function together. The distinction between these two programs does not exist for arbuscular mycorrhizae development despite events occurring in both root tissues. Mutations that affect both symbioses are restricted to the epidermal program. We propose here sites of action and potential roles for ethylene during the formation of the two symbioses with a specific hypothesis for nodule organogenesis. Assuming the epidermis does not make ethylene, the microsymbionts probably first encounter a regulatory level of ethylene at the epidermis–outermost cortical cell layer interface. Depending on the hormone concentrations there, infection will either progress or be blocked. In the former case, ethylene affects the cortex cytoskeleton, allowing reorganization that facilitates infection; in the latter case, ethylene acts on several enzymes that interfere with infection thread growth, causing it to abort. Throughout this review, the difficulty of generalizing the roles of ethylene is emphasized and numerous examples are given to demonstrate the diversity that exists in plants

Nickel and cobalt trigger NF-κB activation, which is not inhibited by lipid IVa.

<p>(A, B) Dose-dependent activation of human TLR4/MD-2 by nickel and cobalt. HEK293/hTLR4 cells were transfected with plasmid encoding hMD-2 and luciferase reporter plasmids. Cells were stimulated with LPS (0, 1, 5, 10, 100 ng/ml) and nickel (A) or cobalt (B) (0.10, 0.25, 0.50, 0.75, 1.0, 2.0, 4.0 mM) for 6 hours, lysed and tested for luciferase activity. (C) Copper and cadmium do not activate human TLR4/MD-2 receptor complex at low, non-toxic concentrations. (D) Tetraacylated lipid IVa (compound 406) does not inhibit human TLR4 activation by nickel or cobalt ions. #p≥0,01 (not significant); *p<0,01; ***p<0,0001 (t-test, compared to the unstimulated control unless indicated otherwise by brackets).</p

The impact of cultural differences in self-representation on the neural substrates of posttraumatic stress disorder

A significant body of literature documents the neural mechanisms involved in the development and maintenance of posttraumatic stress disorder (PTSD). However, there is very little empirical work considering the influence of culture on these underlying mechanisms. Accumulating cultural neuroscience research clearly indicates that cultural differences in self-representation modulate many of the same neural processes proposed to be aberrant in PTSD. The objective of this review paper is to consider how culture may impact on the neural mechanisms underlying PTSD. We first outline five key affective and cognitive functions and their underlying neural correlates that have been identified as being disrupted in PTSD: (1) fear dysregulation; (2) attentional biases to threat; (3) emotion and autobiographical memory; (4) self-referential processing; and (5) attachment and interpersonal processing. Second, we consider prominent cultural theories and review the empirical research that has demonstrated the influence of cultural variations in self-representation on the neural substrates of these same five affective and cognitive functions. Finally, we propose a conceptual model that suggests that these five processes have major relevance to considering how culture may influence the neural processes underpinning PTSD. Highlights of the article