Assistants, Guides, Collaborators, Friends: The Concealed Figures of Conflict Research

Recent scholarship has demonstrated an increasing awareness of the need for more grounded, empirical research into the micro-level dynamics of violent contexts. Research in these difficult, dangerous, and potentially violent conflict or post-conflict settings necessitates the formation of new relationships of dependency, and assistants, friends, collaborators, and guides become central figures in the field. However, all too often, these figures are written out of academic accounts and silenced in our analyses. This not only does them a significant disservice, but it also obscures potential biases, complexities, and ethical dilemmas that emerge in the way in which such research is carried out. Drawing upon fieldwork exploring the 2007–2008 Kenyan postelection violence, this paper argues that reliance upon insider-assistants is essential in conflict settings and explores the challenges inherent in these relationships. As researchers become increasingly engaged in micro-level studies of violent contexts, we must interrogate the realities of how our knowledge has been produced and engage in more open and honest discussions of the methodological and ethical challenges of conflict research

Knockout of MAPK Phosphatase-1 Exaggerates Type I IFN Response during Systemic Escherichia coli Infection.

We have previously shown that Mkp-1-deficient mice produce elevated TNF-α, IL-6, and IL-10 following systemic Escherichia coli infection, and they exhibited increased mortality, elevated bacterial burden, and profound metabolic alterations. To understand the function of Mkp-1 during bacterial infection, we performed RNA-sequencing analysis to compare the global gene expression between E. coli-infected wild-type and Mkp-1 -/- mice. A large number of IFN-stimulated genes were more robustly expressed in E. coli-infected Mkp-1 -/- mice than in wild-type mice. Multiplex analysis of the serum cytokine levels revealed profound increases in IFN-β, IFN-γ, TNF-α, IL-1α and β, IL-6, IL-10, IL-17A, IL-27, and GMSF levels in E. coli-infected Mkp-1 -/- mice relative to wild-type mice. Administration of a neutralizing Ab against the receptor for type I IFN to Mkp-1 -/- mice prior to E. coli infection augmented mortality and disease severity. Mkp-1 -/- bone marrow-derived macrophages (BMDM) produced higher levels of IFN-β mRNA and protein than did wild-type BMDM upon treatment with LPS, E. coli, polyinosinic:polycytidylic acid, and herring sperm DNA. Augmented IFN-β induction in Mkp-1 -/- BMDM was blocked by a p38 inhibitor but not by an JNK inhibitor. Enhanced Mkp-1 expression abolished IFN-β induction by both LPS and E. coli but had little effect on the IFN-β promoter activity in LPS-stimulated RAW264.7 cells. Mkp-1 deficiency did not have an overt effect on IRF3/7 phosphorylation or IKK activation but modestly enhanced IFN-β mRNA stability in LPS-stimulated BMDM. Our results suggest that Mkp-1 regulates IFN-β production primarily through a p38-mediated mechanism and that IFN-β plays a beneficial role in E. coli-induced sepsis

Structurally defined zincated and aluminated complexes of ferrocene made by alkali-metal-synergistic syntheses

Reaction of ferrocene with 1 or 2 molar equiv of the synergistic-operative bimetallic sodium zincate base TMEDA·Na(μ-TMP)(μ-tBu)Zn(tBu) yields mainly mono- or dizincated complexes TMEDA·Na(μ-TMP)[μ-(C5H4)Fe(C5H5)]ZntBu (1) and [TMEDA·Na(μ-TMP)Zn(tBu)]2(C5H4)2Fe (2). Likewise, the separated pairing of Li(TMP) and (TMP)AliBu2 in the presence of THF can mono- or dimetalate ferrocene in a synergistic two-step lithiation/trans-metal-trapping protocol to give THF·Li(μ-TMP)[μ-(C5H4)Fe(C5H5)]Al(iBu)2 (4) or [THF·Li(μ-TMP)Al(iBu)2]2(C5H4)2Fe (5). In the absence of Lewis donating cosolvents, a 4-fold excess of the sodium zincate appears to produce an unprecedented 4-fold zincated ferrocene of formula Na4(TMP)4Zn4(tBu)4[(C5H3)2Fe] (3), whereas when donor solvent is withheld from the lithium/aluminum pairing, only dimetalation of ferrocene is possible. Tetrametalation seems to be inhibited by the in situ generation of TMP(H) via amido basicity, which then acts as a Lewis donor toward lithium, preventing inverse-crown formation and preferentially forming the Lewis acid–Lewis base adduct [TMP(H)·Li(μ-TMP)Al(iBu)2]2(C5H4)2Fe (6). With the exception of 3, all aforementioned complexes have been characterized by X-ray crystallography, while 1–6 have also been studied by solution NMR spectroscopic studies