The Geography of Conflict and Death in Belfast, Northern Ireland

The conflict known as the oTroubleso in Northern Ireland began during the late 1960s and is defined by political and ethno-sectarian violence between state, pro-state, and anti-state forces. Reasons for the conflict are contested and complicated by social, religious, political, and cultural disputes, with much of the debate concerning the victims of violence hardened by competing propaganda-conditioning perspectives. This article introduces a database holding information on the location of individual fatalities connected with the contemporary Irish conflict. For each victim, it includes a demographic profile, home address, manner of death, and the organization responsible. Employing geographic information system (GIS) techniques, the database is used to measure, map, and analyze the spatial distribution of conflict-related deaths between 1966 and 2007 across Belfast, the capital city of Northern Ireland, with respect to levels of segregation, social and economic deprivation, and interfacing. The GIS analysis includes a kernel density estimator designed to generate smooth intensity surfaces of the conflict-related deaths by both incident and home locations. Neighborhoods with high-intensity surfaces of deaths were those with the highest levels of segregation ( 90 percent Catholic or Protestant) and deprivation, and they were located near physical barriers, the so-called peacelines, between predominantly Catholic and predominantly Protestant communities. Finally, despite the onset of peace and the formation of a power-sharing and devolved administration (the Northern Ireland Assembly), disagreements remain over the responsibility and ocommemorationo of victims, sentiments that still uphold division and atavistic attitudes between spatially divided Catholic and Protestant populations.

A Functional Variant of Elafin With Improved Anti-inflammatory Activity for Pulmonary Inflammation

Elafin is a serine protease inhibitor produced by epithelial and immune cells with anti-inflammatory properties. Research has shown that dysregulated protease activity may elicit proteolytic cleavage of elafin, thereby impairing the innate immune function of the protein. The aim of this study was to generate variants of elafin (GG- and QQ-elafin) that exhibit increased protease resistance while retaining the biological properties of wild-type (WT) elafin. Similar to WT-elafin, GG- and QQ-elafin variants retained antiprotease activity and susceptibility to transglutaminase-mediated fibronectin cross-linking. However, in contrast to WT-elafin, GG- and QQ-elafin displayed significantly enhanced resistance to degradation when incubated with bronchoalveolar lavage fluid from patients with cystic fibrosis. Intriguingly, both variants, particularly GG-elafin, demonstrated improved lipopolysaccharide (LPS) neutralization properties in vitro. In addition, GG-elafin showed improved anti-inflammatory activity in a mouse model of LPS-induced acute lung inflammation. Inflammatory cell infiltration into the lung was reduced in lungs of mice treated with GG-elafin, predominantly neutrophilic infiltration. A reduction in MCP-1 levels in GG-elafin treated mice compared to the LPS alone treatment group was also demonstrated. GG-elafin showed increased functionality when compared to WT-elafin and may be of future therapeutic relevance in the treatment of lung diseases characterized by a protease burden.

Religion, anti-slavery, and identity: Irish Presbyterians, the United States, and transatlantic evangelicalism, c. 1820-1914

Scholars have devoted much attention to the causes and consequences of Presbyterian emigration from Ulster to the thirteen colonies before 1776. This article moves beyond the eighteenth century to examine the continued religious links between Presbyterians in Ireland and the United States in the nineteenth century. It begins with an examination of the influence of evangelicalism on both sides of the Atlantic and how this promoted unity in denominational identity, missionary activity to convert Catholics, and revivalist religion during the first half of the century. Though Irish Presbyterians had great affection for their American co-religionists, they were not uncritical, and significant tensions did develop over slavery. The article then examines the religious character of Scotch-Irish or Ulster-Scots identity in the late nineteenth century, which was articulated in response to the alleged demoralising influence of large-scale Irish immigration during and after the Famine of the 1840s, the so-called Romanisation of Catholicism, and the threat of Home Rule in Ireland. The importance of identity politics should not obscure religious developments, and the article ends with a consideration of the origins and character of fundamentalism, perhaps one of the most important cultural connections between Protestants in Northern Ireland and the United States in the twentieth century.

Favorable effect on acute and chronic graft-versus-host disease with cyclophosphamide and in vivo anti-CD52 monoclonal antibodies for marrow transplantation from HLA-identical sibling donors for acquired aplastic anemia

Between August 1989 and November 2003, 33 patients at our center with acquired aplastic anemia underwent bone marrow transplantation (BMT) from HLA-identical sibling donors with cyclophosphamide and in vivo anti-CD52 monoclonal antibodies (MoAb) for conditioning. The median age at BMT was 17 years (range, 4-46 years). Before BMT, 58% were heavily transfused (>50 transfusions), and 42% had previously experienced treatment failure with antithymocyte globulin-based immunosuppressive therapy. Unmanipulated bone marrow was used as the source of stem cells in all patients except 1. Graft-versus-host disease (GVHD) prophylaxis was with cyclosporine alone in 19 (58%) patients; 14 received anti-CD52 MoAb in addition to cyclosporine. The conditioning regimen was well tolerated without significant acute toxicity. Graft failure was seen in 8 patients (primary, n = 4; secondary, n = 4). Of those whose grafts failed, 4 survived long-term (complete autologous recovery, n = 2; rescue with previously stored marrow, n = 1; second allograft, n = 1). The cumulative incidence of graft failure and grade II to IV acute and chronic GVHD was 24%, 14%, and 4%, respectively. None developed extensive chronic GVHD. With a median follow-up of 59 months, the 5-year survival was 81% (95% confidence interval, 68%-96%). No unexpected early or late infectious or noninfectious complications were observed. We conclude that the conditioning regimen containing cyclophosphamide and anti-CD52 MoAb is well tolerated and effective for acquired aplastic anemia with HLA-matched sibling donors. The favorable effect on the incidence and severity of GVHD is noteworthy in this study and warrants further investigation.

Nonsteroidal Anti-Inflammatory Drug Use is Not Associated With Reduced Risk of Barrett’s Esophagus

OBJECTIVES: Regular use of nonsteroidal anti-inflammatory drugs (NSAIDs) is associated with a reduced risk of esophageal adenocarcinoma. Epidemiological studies examining the association between NSAID use and the risk of the precursor lesion, Barrett’s esophagus, have been inconclusive.

METHODS: We analyzed pooled individual-level participant data from six case-control studies of Barrett’s esophagus in the Barrett’s and Esophageal Adenocarcinoma Consortium (BEACON). We compared medication use from 1474 patients with Barrett’s esophagus separately with two control groups: 2256 population-based controls and 2018 gastroesophageal reflux disease (GERD) controls. Study-specific odds ratios (OR) and 95% confidence intervals (CI) were estimated using multivariable logistic regression models and were combined using a random effects meta-analytic model.

RESULTS: Regular (at least once weekly) use of any NSAIDs was not associated with the risk of Barrett’s esophagus (vs. population-based controls, adjusted OR = 1.00, 95% CI = 0.76–1.32; I2=61%; vs. GERD controls, adjusted OR = 0.99, 95% CI = 0.82–1.19; I2=19%). Similar null findings were observed among individuals who took aspirin or non-aspirin NSAIDs. We also found no association with highest levels of frequency (at least daily use) and duration (≥5 years) of NSAID use. There was evidence of moderate between-study heterogeneity; however, associations with NSAID use remained non-significant in “leave-one-out” sensitivity analyses.

CONCLUSIONS: Use of NSAIDs was not associated with the risk of Barrett’s esophagus. The previously reported inverse association between NSAID use and esophageal adenocarcinoma may be through reducing the risk of neoplastic progression in patients with Barrett’s esophagus.