The Transactions of Mortal Coil: Hellenic Meaning in the Suffering of the Iliad and the Oresteia

The meaning of suffering is enigmatic. To grasp at it cosmologically, I examine both Archaic and Classical Greek views of suffering via their primary literature and culture. Homer’s Iliad reveals the transactionality of suffering as it is embedded in the heroic code through an analysis of the Glaucus-Diomedes exchange. An investigation of Achilles’ development portrays both the Homeric system that equates honor and suffering and the unquantifiable suffering that critiques said system. Meanwhile, a study of Aeschylus’ Oresteia exhibits the interrelation of suffering and learning in Zeus’ law. The progression of the trilogy displays an accruement of wisdom by means of the rectification of an inherited misunderstanding: that personal vengeance is Zeus’ justice. I conclude that the desire for wisdom concerning how to live the best life motivated the Hellenic evolution of suffering’s transaction from honor to knowledge

La Actividad Reciente Antes De La Corteinternacional De La Justicia: Tendencia 0 Ciclo

Siguiendo el rechazo de los Estados Unidos para participar en el caso de Nicaragua\u27, y su retiro subsiguiente de la Ilamada cldusula opcional, un gran ambiente de pesimismo rode6 el futuro de la Corte Internacional de Justici

Recent Activity Before The International Court Of Justice: Trend Or Cycle?

Following the United States refusal to participate in the Nicaragua case,\u27 and its subsequent withdrawal from the so-called optional clause, , a great deal of pessimism surrounded the future of the International Court of Justice.3 Less than a decade later, and only half way through the decade of international law, it would appear, to paraphrase Mark Twain, that reports of the court\u27s demise were greatly exaggerated

The Role of Extracellular Vesicles in the Progression of ALS and Their Potential as Biomarkers and Therapeutic Agents with Which to Combat the Disease

Amyotrophic lateral sclerosis (ALS) is a fatal neurodegenerative disease that impairs motor neuron function, leading to severe muscular atrophy. The non-cell autonomous and heterogeneous nature of the disease has so far hindered attempts to define ALS etiology, leaving the disease incurable and without effective treatments. Recent studies have focused on the pathologic role of intercellular communication between nerve cells to further our understanding of ALS pathophysiology. In this chapter, we summarize recent works investigating the role of extracellular vesicles (EVs) as a means of cellular crosstalk for ALS disease propagation, diagnosis, and treatment. There is growing evidence that EVs secreted by the majority of mammalian cells serve as effective biomolecule carriers to modulate recipient cell behavior. This underscores the need to understand the EV-mediated interplay that occurs within irreversibly degenerating nervous tissue in ALS patients. Additionally, we highlight current gaps in EV-ALS research, especially in terms of the pathologic role and responsibilities of specific EV cargos in diseased cells, specificity issues associated with the use of EVs in ALS diagnosis, and the efficacy of EV-mediated treatments for the restoration of diseased neuromuscular tissue. Finally, we provide suggestions for future EV-ALS research to better understand, diagnose, and cure this inveterate disease

Species-specific difference in expression and splice-site choice in Inpp5b, an inositol polyphosphate 5-phosphatase paralogous to the enzyme deficient in Lowe Syndrome

The oculocerebrorenal syndrome of Lowe (OCRL; MIM #309000) is an X-linked human disorder characterized by congenital cataracts, mental retardation, and renal proximal tubular dysfunction caused by loss-of-function mutations in the OCRL gene that encodes Ocrl, a type II phosphatidylinositol bisphosphate (PtdIns4,5P2) 5-phosphatase. In contrast, mice with complete loss-of-function of the highly homologous ortholog Ocrl have no detectable renal, ophthalmological, or central nervous system abnormalities. We inferred that the disparate phenotype between Ocrl-deficient humans and mice was likely due to differences in how the two species compensate for loss of the Ocrl enzyme. We therefore turned our attention to Inpp5b, another type II PtdIns4,5P2 5-phosphatase encoded by Inpp5b in mice and INPP5B in humans, as potential compensating genes in the two species, because Inpp5b/INPP5B are the most highly conserved paralogs to Ocrl/OCRL in the respective genomes of both species and Inpp5b demonstrates functional overlap with Ocrl in mice in vivo. We used in silico sequence analysis, reverse-transcription PCR, quantitative PCR, and transient transfection assays of promoter function to define splice-site usage and the function of an internal promoter in mouse Inpp5b versus human INPP5B. We found mouse Inpp5b and human INPP5B differ in their transcription, splicing, and primary amino acid sequence. These observations form the foundation for analyzing the functional basis for the difference in how Inpp5b and INPP5B compensate for loss of Ocrl function and, by providing insight into the cellular roles of Ocrl and Inpp5b, aid in the development of a model system in which to study Lowe syndrome

The development and evaluation of exercises for meaningful responses in reading in grade two

Research chapter for this study will be found in Ash, Dorothea: "Development and evaluation of silent reading exercises in grade one" Thesis (M.A.)--Boston Universit

ALMA constraints on the faint millimetre source number counts and their contribution to the cosmic infrared background

We have analysed 18 ALMA continuum maps in Bands 6 and 7, with rms down to 7.8$\mu$Jy, to derive differential number counts down to 60$\mu$Jy and 100$\mu$Jy at $\lambda=$1.3 mm and $\lambda=$1.1 mm, respectively. The area covered by the combined fields is $\rm 9.5\times10^{-4}deg^2$ at 1.1mm and $\rm 6.6\times10^{-4}deg^{2}$ at 1.3mm. We improved the source extraction method by requiring that the dimension of the detected sources be consistent with the beam size. This method enabled us to remove spurious detections that have plagued the purity of the catalogues in previous studies. We detected 50 faint sources with S/N$>$3.5 down to 60$\mu$Jy, hence improving the statistics by a factor of four relative to previous studies. The inferred differential number counts are $\rm dN/d(Log_{10}S)=1\times10^5~deg^2$ at a 1.1 mm flux $S_{\lambda = 1.1~mm} = 130~\mu$Jy, and $\rm dN/d(Log_{10}S)=1.1\times10^5~deg^2$ at a 1.3 mm flux $\rm S_{\lambda = 1.3~mm} = 60~\mu$Jy. At the faintest flux limits, i.e. 30$\mu$Jy and 40$\mu$Jy, we obtain upper limits on the differential number counts of $\rm dN/d(Log_{10}S) < 7\times10^5~deg^2$ and $\rm dN/d(Log_{10}S)<3\times10^5~deg^2$, respectively. Our results provide a new lower limit to CIB intensity of 17.2${\rm Jy\ deg^{-2}}$ at 1.1mm and of 12.9${\rm Jy\ deg^{-2}}$ at 1.3mm. Moreover, the flattening of the integrated number counts at faint fluxes strongly suggests that we are probably close to the CIB intensity. Our data imply that galaxies with SFR$<40~M_{\odot}/yr$ certainly contribute less than 50% to the CIB while more than 50% of the CIB must be produced by galaxies with $\rm SFR>40~M_{\odot}/yr$. The differential number counts are in nice agreement with recent semi-analytical models of galaxy formation even as low as our faint fluxes. Consequently, this supports the galaxy evolutionary scenarios and assumptions made in these models.Comment: 11 pages, 9 figures, A&A accepte