Emergency endovascular repair of acute descending thoracic aortic dissection

Muhammad Anees Sharif, Mark Edward O’Donnell, Paul Henry Blair, Peter KennedyDepartment of Vascular and Endovascular Surgery, Royal Victoria Hospital, Grosvenor Road, Belfast, BT12 6BA, United KingdomBackground: Acute descending thoracic aortic dissection is a life-threatening emergency. It is not often considered as the initial diagnosis in patients presenting with epigastric pain and could easily be missed in a busy casualty department.Aim: This case report is aimed to highlight the feasibility of the technique and the need for long-term surveillance following endovascular repair of acute thoracic aortic dissection.Results: The patient presented with epigastric pain radiating to the interscapular region with a stable hemodynamic status. A computerized tomography (CT) scan demonstrated type B thoracic aortic dissection of the proximal descending thoracic aorta. A successful endovascular repair was carried out with uneventful recovery and follow-up CT scan six years after stent-grafting shows satisfactory position of the stent-graft, patent false lumen in the abdominal aorta perfusing the right kidney, and progressively enlarging diameter of the abdominal aorta.Conclusion: Thoracic aortic dissection should be considered as a differential diagnosis in patients presenting with epigastric and interscapular chest pain. Emergency endovascular repair of acute thoracic aortic dissection is feasible and relatively safe. Regular follow-up with CT scan is required to evaluate the long-term effi cacy and identify the need for re-intervention.Keywords: aortic, dissection, endovascular, thoraci

Ariel - Volume 11 Number 1

Executive Editors Ellen Feldman Leonardo S. Nasca, Jr. Business Managers Barbara L. Davies Martin B. Getzow News Editor Aaron D. Bleznak Features Editor Dave Van Wagoner CAHS Editor Joan M. Greco Editorial Page Editor Samuel Markind Photography Editor Leonardo S. Nasca, Jr. Sports Editor Paul F. Mansfiel

Parent-progeny relationships and genotype X environment effects for factors associated with grass tetany and forage quality in Russian Wildrye

Grass tetany (hypomagnesemia) has caused severe economic losses in ruminant animals grazing cool-season grasses, including Russian wildrye [Psathyrostachys juncea (Fisch.) Nevski]. The malady has been associated with deficiencies in Mg, Ca, and carbohydrates, and high levels of K. The K/(Ca + Mg) ratio (KRAT), expressed as moles of charge, is often used to express the grass tetany potential of forage. Development and use of new cultivars with an improved balance of the associated minerals would be an economical approach to reduce the incidence of grass tetany. Objectives of this study were to characterize the genetic variability, genotype by environment interactions, and intercharacter relationships for P, K, Ca, Mg, KRAT, crude protein (CP), neutral detergent fiber (NDF), and in vitro dry matter digestibility (IVDMD), among 21 clonal lines of Russian wildrye and their polycross progenies. Evaluations were made for 2 yr at three diverse locations in the USA and Canada. The clonal lines were derived from cultivars and plant introductions. Although the clone x location interaction was usually significant, differences among the clonal lines were significant for K, Ca, Mg, and KRAT, and three forage quality estimates of CP, NDF, and true IVDMD. Although the magnitude of the genetic variability among the progenies was substantially less than that found among the clonal lines, we conclude that the grass tetany potential, CP, NDF, IVDMD, and P concentration of this breeding population can be altered through breeding. Opportunities for genetic improvement in forage quality were particularly favorable for CP. Genetic correlations among the clonal lines suggested that selection for higher levels of CP would be accompanied by increased K, Ca, Mg, and IVDMD and reduced KR AT and NDF

Ernst Freund as Precursor of the Rational Study of Corporate Law

Gindis, David, Ernst Freund as Precursor of the Rational Study of Corporate Law (October 27, 2017). Journal of Institutional Economics, Forthcoming. Available at SSRN: https://ssrn.com/abstract=2905547, doi: https://dx.doi.org/10.2139/ssrn.2905547The rise of large business corporations in the late 19th century compelled many American observers to admit that the nature of the corporation had yet to be understood. Published in this context, Ernst Freund's little-known The Legal Nature of Corporations (1897) was an original attempt to come to terms with a new legal and economic reality. But it can also be described, to paraphrase Oliver Wendell Holmes, as the earliest example of the rational study of corporate law. The paper shows that Freund had the intuitions of an institutional economist, and engaged in what today would be called comparative institutional analysis. Remarkably, his argument that the corporate form secures property against insider defection and against outsiders anticipated recent work on entity shielding and capital lock-in, and can be read as an early contribution to what today would be called the theory of the firm.Peer reviewe

Risk estimation of distant metastasis in node-negative, estrogen receptor-positive breast cancer patients using an RT-PCR based prognostic expression signature

<p>Abstract</p> <p>Background</p> <p>Given the large number of genes purported to be prognostic for breast cancer, it would be optimal if the genes identified are not confounded by the continuously changing systemic therapies. The aim of this study was to discover and validate a breast cancer prognostic expression signature for distant metastasis in untreated, early stage, lymph node-negative (N-) estrogen receptor-positive (ER+) patients with extensive follow-up times.</p> <p>Methods</p> <p>197 genes previously associated with metastasis and ER status were profiled from 142 untreated breast cancer subjects. A "metastasis score" (MS) representing fourteen differentially expressed genes was developed and evaluated for its association with distant-metastasis-free survival (DMFS). Categorical risk classification was established from the continuous MS and further evaluated on an independent set of 279 untreated subjects. A third set of 45 subjects was tested to determine the prognostic performance of the MS in tamoxifen-treated women.</p> <p>Results</p> <p>A 14-gene signature was found to be significantly associated (p < 0.05) with distant metastasis in a training set and subsequently in an independent validation set. In the validation set, the hazard ratios (HR) of the high risk compared to low risk groups were 4.02 (95% CI 1.91–8.44) for the endpoint of DMFS and 1.97 (95% CI 1.28 to 3.04) for overall survival after adjustment for age, tumor size and grade. The low and high MS risk groups had 10-year estimates (95% CI) of 96% (90–99%) and 72% (64–78%) respectively, for DMFS and 91% (84–95%) and 68% (61–75%), respectively for overall survival. Performance characteristics of the signature in the two sets were similar. Ki-67 labeling index (LI) was predictive for recurrent disease in the training set, but lost significance after adjustment for the expression signature. In a study of tamoxifen-treated patients, the HR for DMFS in high compared to low risk groups was 3.61 (95% CI 0.86–15.14).</p> <p>Conclusion</p> <p>The 14-gene signature is significantly associated with risk of distant metastasis. The signature has a predominance of proliferation genes which have prognostic significance above that of Ki-67 LI and may aid in prioritizing future mechanistic studies and therapeutic interventions.</p

Applying new biotechnologies to the study of occupational cancer--a workshop summary.

As high-throughput technologies in genomics, transcriptomics, and proteomics evolve, questions arise about their use in the assessment of occupational cancers. To address these questions, the National Institute for Occupational Safety and Health, the National Cancer Institute, the National Institute of Environmental Health Sciences, and the American Chemistry Council sponsored a workshop 8-9 May 2002 in Washington, DC. The workshop brought together 80 international specialists whose objective was to identify the means for best exploiting new technologies to enhance methods for laboratory investigation, epidemiologic evaluation, risk assessment, and prevention of occupational cancer. The workshop focused on identifying and interpreting markers for early biologic effect and inherited modifiers of risk

Effects of antiplatelet therapy on stroke risk by brain imaging features of intracerebral haemorrhage and cerebral small vessel diseases: subgroup analyses of the RESTART randomised, open-label trial

Background Findings from the RESTART trial suggest that starting antiplatelet therapy might reduce the risk of recurrent symptomatic intracerebral haemorrhage compared with avoiding antiplatelet therapy. Brain imaging features of intracerebral haemorrhage and cerebral small vessel diseases (such as cerebral microbleeds) are associated with greater risks of recurrent intracerebral haemorrhage. We did subgroup analyses of the RESTART trial to explore whether these brain imaging features modify the effects of antiplatelet therapy

Targeted Genetic Screen in Amyotrophic Lateral Sclerosis Reveals Novel Genetic Variants with Synergistic Effect on Clinical Phenotype

Amyotrophic lateral sclerosis (ALS) is underpinned by an oligogenic rare variant architecture. Identified genetic variants of ALS include RNA-binding proteins containing prion-like domains (PrLDs). We hypothesized that screening genes encoding additional similar proteins will yield novel genetic causes of ALS. The most common genetic variant of ALS patients is a G4C2-repeat expansion within C9ORF72. We have shown that G4C2-repeat RNA sequesters RNA-binding proteins. A logical consequence of this is that loss-of-function mutations in G4C2-binding partners might contribute to ALS pathogenesis independently of and/or synergistically with C9ORF72 expansions. Targeted sequencing of genomic DNA encoding either RNA-binding proteins or known ALS genes (n = 274 genes) was performed in ALS patients to identify rare deleterious genetic variants and explore genotype-phenotype relationships. Genomic DNA was extracted from 103 ALS patients including 42 familial ALS patients and 61 young-onset (average age of onset 41 years) sporadic ALS patients; patients were chosen to maximize the probability of identifying genetic causes of ALS. Thirteen patients carried a G4C2-repeat expansion of C9ORF72. We identified 42 patients with rare deleterious variants; 6 patients carried more than one variant. Twelve mutations were discovered in known ALS genes which served as a validation of our strategy. Rare deleterious variants in RNA-binding proteins were significantly enriched in ALS patients compared to control frequencies (p = 5.31E-18). Nineteen patients featured at least one variant in a RNA-binding protein containing a PrLD. The number of variants per patient correlated with rate of disease progression (t-test, p = 0.033). We identified eighteen patients with a single variant in a G4C2-repeat binding protein. Patients with a G4C2-binding protein variant in combination with a C9ORF72 expansion had a significantly faster disease course (t-test, p = 0.025). Our data are consistent with an oligogenic model of ALS. We provide evidence for a number of entirely novel genetic variants of ALS caused by mutations in RNA-binding proteins. Moreover we show that these mutations act synergistically with each other and with C9ORF72 expansions to modify the clinical phenotype of ALS. A key finding is that this synergy is present only between functionally interacting variants. This work has significant implications for ALS therapy development