Uncles ex Machina: Familial Epiphany in Euripides' Electra

At the close of Euripides’ Electra, the Dioscuri suddenly appear ‘on high’ to their distraught niece and nephew, who have just killed their mother, the divine twins’ mortal sister. This is in fact the second longest extant deus ex machina (after the final scene in Hippolytus), and the only scene in which a tragedian attempts to resolve directly the aftermath of the matricide. In this article, I argue that Castor's and Polydeuces’ sudden apparition to Orestes and Electra constitutes a specialised point of intersection between the mortal and immortal realms in Greek tragedy: familial epiphany, an appearance by a god who has an especially intimate relationship with those on stage. Euripides’ focus on the familial divine as a category accentuates various contradictions inherent to both ancient Greek theology and dramaturgy. The Dioscuri are a living paradox, ambiguously traversing the space between dead heroes and gods, managing at the same time to occupy both. They oscillate uniquely between the mortal and immortal worlds, as different sources assign different fathers to each brother, and others speak of each one possessing divinity on alternate days. As I propose, the epiphany of these ambiguous brothers crystallises the problem of the gods’ physical presence in drama. Tragedy is the arena in which gods burst suddenly into the mortal realm, decisively and irrevocably altering human action. The physical divine thus tends to be both marginal and directorial, tasked with reining in the plot or directing its future course. The appearance of the familial divine, on the other hand, can in fact obscure the resolution and future direction of a play, undermining the authority of the tragic gods. In the specific case of Electra, I contend that the involvement of the Dioscuri, who are Electra's and Orestes’ maternal uncles, produces a sense of claustrophobia at the close of the play, which simultaneously denies the resolution that is expected from a deus ex machina while also revealing the pessimistic nature of what is typically considered a reassuringly ‘domestic’ and character driven drama

The potential clinical impact of the release of two drafts of the human proteome

<p>The authors have carried out an investigation of the two “draft maps of the human proteome” published in 2014 in <i>Nature</i>. The findings include an abundance of poor spectra, low-scoring peptide-spectrum matches and incorrectly identified proteins in both these studies, highlighting clear issues with the application of false discovery rates. This noise means that the claims made by the two papers – the identification of high numbers of protein coding genes, the detection of novel coding regions and the draft tissue maps themselves – should be treated with considerable caution. The authors recommend that clinicians and researchers do not use the unfiltered data from these studies. Despite this these studies will inspire further investigation into tissue-based proteomics. As long as this future work has proper quality controls, it could help produce a consensus map of the human proteome and improve our understanding of the processes that underlie health and disease.</p

Mn-L1 inhibits LPS cellular signaling in macrophages through the MAP kinase pathway.

<p>Effects of Mn-L1 on the LPS-induced phosphorilation of MAPK kinases. THP-1 macrophages were incubated with Mn-L1 for 3 hours at the concetrations indicated in the figure and then challenged with 500 ng/ml of LPS for 1 hour. The phosphorylated and total ERK, JNK and p38 proteins were determined by Western blotting. ß-actin was used as loading control. Representative blots. (A) Representative blots and (B) densitometric evaluation (n = 3) *P < 0.01 compared to LPS-treated group.</p

Mn-L1 and Mn-L2-inhibited LPS-induced pro-inflammatory gene expression in THP1 human macrophages.

<p><b>(A) Inhibition of pro-inflammatory gene expression in macrophages by Mn-L1 and Mn-L2</b>. THP-1 macrophages were treated for 3 hours with 25 μmol/L of Mn-L1 or Mn-L2, the medium was removed and the cells were incubated one hour with fresh medium containing 100 ng/ml LPS. The mRNA levels were determined by quantitative real time PCR. The values are represented as percentages of the only LPS-stimulated control group. LPS 100% values (mean ± SE) were 5.5 ± 0.9; 63.58 ± 3.7; 74.12 ± 4.4; 13.83 ± 7.7.42 ± 5; and 13.15 ± 4 for GRP78, TNF-α, IL-6, Il-1ß, IL-8 and PTGS2 respectively. <b>(B) Inhibition of the production of pro-inflamatory TNF-α and IL-6 in macrophages by Mn-L1 and Mn-L2</b>. THP-1 macrophages were treated for 3 hours as explained in the figure. After 16 hours’ incubation with 500 ng/ml LPS, TNF-α, and IL-6 protein expression was determined in the cell culture medium. The data of three separate experiments performed in duplicate are shown. * P < 0.01 compared with LPS-treated group.</p

Mn-L1 and Mn-L2 anti-inflammatory activity in whole mice.

<p><b>(A) Mn-L1 protected mice from a lethal endotoxemic dose of LPS</b>. Survival data (%) were analyzed by using the Kaplan-Meier method and log rank test. * P < 0.05 versus the LPS-treated group. <b>(B) Inhibition of LPS induction of TNF-α and IL-6 concentration in serum</b>. The graphs show the serum levels of TNF-α (right panel) and IL-6 (left panel) after the different treatments with LPS, Mn-L1 or Mn-L2 as explained under the ordinate axis. Data are presented as mean ± SEM. <b>(C) Mn-L1 attenuates Kupffer cell LPS activation</b>. The panels show the immunohistochemistry for F4/80 and the graph the quantification of positive macrophage area. *P values < 0.05. Data are represented as mean ± SEM. <b>(D) Mn-L1 effect in LPS liver injury</b>. Liver injury was determined by histological examination on H&E-stained sections. Control untreated mice; LPS (mice treated with LPS alone) and LPS + Mn-L1 (mice treated with LPS and Mn-L1).</p

Differentially expressed peptides.

<p>Differentially expressed peptides between NSCLC and normal lung samples identified using SIEVE 1.2 software. Peptides presenting different m/z values have been identified with various charge states.</p

PTRF/cavin-1 and MIF label-free expression values by SIEVE.

<p>Boxplots represent mean and 25th–75th percentile; whiskers represent minimun and maximun. Measurements were obtained from five different samples in each condition. Kruskall-Wallis test p-values are shown. AC: Adenocarcinoma; SC: Squamous cell carcinoma; NL: Normal lung.</p

Analysis of differences in GO Pathways between NSCLC and normal lung.

<p>Comparison of number of proteins assigned to each GO pathway category. Normal tissue sample categories are represented as fold-change in relation to this category. Statistical significance is tested using the binomial test. Only significant categories (p<0.05) are shown.</p

Validation of PTRF/cavin-1 and MIF expression changes using IHC and western blot.

<p>a) Western blot of total protein extracted from indicated samples, using anti-MIF and anti-PTRF/cavin-1 primary antibodies. b) Densitometric analyses of western blot. ImageJ 1.38e software was employed to measure the intensity of bands. All values in arbitrary units. c) Immunohistochemistry of indicated samples, using anti-MIF and anti-PTRF/cavin-1 primary antibodies. AC: Adenocarcinoma; SC: Squamous cell carcinoma; NL: Normal lung.</p

Validation of PTRF/cavin-1 and MIF expression changes by western blot using a new cohort.

<p>Box-Plot graphs showing PTRF and MIF western blot quantification using ImageJ 1.38e software. All values in arbitrary units. Each Box includes values from nine different samples. Differences between normal and tumoral samples were p<0.005 in both cases (Kruskall-Wallis test).</p