The Legal Qualification of Ethnic Cleansing

Fees ScholarshipThough commonly used in public international law, ethnic cleansing is a term which has not, as yet, been formally classified, either by international tribunals or conventions. Consequently, the notion has existed in a grey area since its coinage in the 1990s. With fresh instances of destruction and expulsion of civilian groups continually emerging, it is vital that efforts are made to redress this situation. With this in mind, the present thesis aims to formulate a classification of ethnic cleansing within the public international law order that reflects its specific characteristics and conditions. Previously, attempts to address the issue of ethnic cleansing (in UN resolutions, scholarly work and jurisprudence) have aligned it against the standards of international humanitarian law, war crimes, genocide and crimes against humanity. A similar methodological principle shall be adopted here, beginning with a detailed assessment of the validity of Security Council resolutions qualifying the practice as a violation of international humanitarian law – a verdict which has not been re-affirmed by the International Criminal Tribunal for the Former Yugoslavia or any other tribunal, and thus lacks binding legal effect. Following this, a theoretical evaluation of all relevant case law will be used to examine ethnic cleansing against other international crimes – war crimes, genocide and crimes against humanity – focussing not only on the parallels but also the crucial disparities between them. Via close analysis of conditions and limitations, it shall here be shown how the current qualification fails to provide an efficient instrument for identification. Having its own particular characteristics, ethnic cleansing ought to be classified as a specific independent crime: one whose mental element is similar to that of crimes against humanity, and which does not only target human groups, and can, in fact, be perpetrated against populations, both in the context of armed conflict and during peacetime.School of Law, University of Exete

Law, Literature and Genocide: Rupert Bazambanza’s Smile Through the Tears

Proceeding from the view that international criminal law remains a neglected area of study within law-and-literature scholarship, this article undertakes a critical reading of Rupert Bazambanza’s 2004 graphic novel Smile Through the Tears, set during the Rwandan genocide. It argues that Bazambanza’s text not only provides a powerful rendering of the subjective experience of the victims of genocide, but also reveals to the reader a number of the conditioning factors that catalysed the violence. Reading the novel alongside case law and academic literature, the article ventures an analysis of how, by exposing such factors, the text might also aid in furthering awareness and understanding of core issues relating to the legal framework of genocide

Law, Narrative and Critique in Contemporary Verbatim Theatre

The present article undertakes an interdisciplinary inquiry into contemporary British verbatim theatre as a site of interplay between law, art and politics. Focusing on the example of Matt Woodhead and Richard Norton-Taylor’s 2016 play Chilcot, documenting the public inquiry into the UK’s role in the 2003 Iraq war, the authors explore the work as a space of legal and political critique, and ask how the specific theatrical and narrative affordances of the verbatim form shape its critical substance

Endothelin-1 directs airway remodeling and hyper-reactivity in a murine asthma model

BACKGROUND: The current paradigm describing asthma pathogenesis recognizes the central role of abnormal epithelial function in the generation and maintenance of the disease. However, the mechanisms responsible for the initiation of airway remodeling, which contributes to decreased lung function, remain elusive. Therefore, we aimed to determine the role of altered pulmonary gene expression in disease inception and identify proremodeling mediators. METHODS: Using an adenoviral vector, we generated mice overexpressing smad2, a TGF-β and activin A signaling molecule, in the lung. Animals were exposed to intranasal ovalbumin (OVA) without systemic sensitization. RESULTS: Control mice exposed to inhaled OVA showed no evidence of pulmonary inflammation, indices of remodeling, or airway hyper-reactivity. In contrast, local smad2 overexpression provoked airway hyper-reactivity in OVA-treated mice, concomitant with increased airway smooth muscle mass and peribronchial collagen deposition. Pulmonary eosinophilic inflammation was not evident, and there was no change in serum IgE or IgG1 levels. The profound remodeling changes were not mediated by classical pro-inflammatory Th2 cytokines. However, uric acid and interleukin-1β levels in the lung were increased. Epithelial-derived endothelin-1 and fibroblast growth factor were also augmented in smad2-expressing mice. Blocking endothelin-1 prevented these phenotypic changes. CONCLUSIONS: Innate epithelial-derived mediators are sufficient to drive airway hyper-reactivity and remodeling in response to environmental insults in the absence of overt Th2-type inflammation in a model of noneosinophilic, noninflammed types of asthma. Targeting potential asthma therapies to epithelial cell function and modulation of locally released mediators may represent an effective avenue for therapeutic design

Eosinophils Are Important for Protection, Immunoregulation and Pathology during Infection with Nematode Microfilariae

Eosinophil responses typify both allergic and parasitic helminth disease. In helminthic disease, the role of eosinophils can be both protective in immune responses and destructive in pathological responses. To investigate whether eosinophils are involved in both protection and pathology during filarial nematode infection, we explored the role of eosinophils and their granule proteins, eosinophil peroxidase (EPO) and major basic protein-1 (MBP-1), during infection with Brugia malayi microfilariae. Using eosinophil-deficient mice (PHIL), we further clarify the role of eosinophils in clearance of microfilariae during primary, but not challenge infection in vivo. Deletion of EPO or MBP-1 alone was insufficient to abrogate parasite clearance suggesting that either these molecules are redundant or eosinophils act indirectly in parasite clearance via augmentation of other protective responses. Absence of eosinophils increased mast cell recruitment, but not other cell types, into the broncho-alveolar lavage fluid during challenge infection. In addition absence of eosinophils or EPO alone, augmented parasite-induced IgE responses, as measured by ELISA, demonstrating that eosinophils are involved in regulation of IgE. Whole body plethysmography indicated that nematode-induced changes in airway physiology were reduced in challenge infection in the absence of eosinophils and also during primary infection in the absence of EPO alone. However lack of eosinophils or MBP-1 actually increased goblet cell mucus production. We did not find any major differences in cytokine responses in the absence of eosinophils, EPO or MBP-1. These results reveal that eosinophils actively participate in regulation of IgE and goblet cell mucus production via granule secretion during nematode-induced pathology and highlight their importance both as effector cells, as damage-inducing cells and as supervisory cells that shape both innate and adaptive immunity

Long Lasting Microvascular Tone Alteration in Rat Offspring Exposed In Utero to Maternal Hyperglycaemia

Epidemiologic studies have demonstrated that cardiovascular risk is not only determined by conventional risk factors in adulthood, but also by early life events which may reprogram vascular function. To evaluate the effect of maternal diabetes on fetal programming of vascular tone in offspring and its evolution during adulthood, we investigated vascular reactivity of third order mesenteric arteries from diabetic mother offspring (DMO) and control mother offspring (CMO) aged 3 and 18 months. In arteries isolated from DMO the relaxation induced by prostacyclin analogues was reduced in both 3- and 18-month old animals although endothelium (acetylcholine)-mediated relaxation was reduced in 18-month old DMO only. Endothelium-independent (sodium nitroprusside) relaxation was not affected. Pressure-induced myogenic tone, which controls local blood flow, was reduced in 18-month old CMO compared to 3-month old CMO. Interestingly, myogenic tone was maintained at a high level in 18-month old DMO even though agonist-induced vasoconstriction was not altered. These perturbations, in 18-months old DMO rats, were associated with an increased pMLC/MLC, pPKA/PKA ratio and an activated RhoA protein. Thus, we highlighted perturbations in the reactivity of resistance mesenteric arteries in DMO, at as early as 3 months of age, followed by the maintenance of high myogenic tone in older rats. These modifications are in favour of excessive vasoconstrictor tone. These results evidenced a fetal programming of vascular functions of resistance arteries in adult rats exposed in utero to maternal diabetes, which could explain a re-setting of vascular functions and, at least in part, the occurrence of hypertension later in life

Exposure to Maternal Diabetes Induces Salt-Sensitive Hypertension and Impairs Renal Function in Adult Rat Offspring

OBJECTIVE—Epidemiological and experimental studies have led to the hypothesis of fetal origin of adult diseases, suggesting that some adult diseases might be determined before birth by altered fetal development. We have previously demonstrated in the rat that in utero exposure to maternal diabetes impairs renal development leading to a reduction in nephron number. Little is known on the long-term consequences of in utero exposure to maternal diabetes. The aim of the study was to assess, in the rat, long-term effects of in utero exposure to maternal diabetes on blood pressure and renal function in adulthood