(The) rise and influence of third parties in the United States since 1865

Thesis (M.A.)--Boston University, 1931. This item was digitized by the Internet Archive

Traumatic dislocation of the knee joint

Of the three main etiological factors which may give rise to Dislocation of the Knee, viz: - Congenital abnormalities, Disepce: Traumatism; I intend to limit myself to that of "Traumatism," which, although rare, is, in modern practice, probably more frequently met with than either of the other two.With regard to Traumatic Dislocation itself, the literature on the subject is not very extensive, only some 114 cases having been collected by Stimson in 1901. Since his work appeared, I have been able to obtain particulars of five other cases in addition to the three which came under my own observation during the period I acted as House Surgeon at the David Lewis Northern Hospital, Liverpool.So far as I have been able to ascertain, no previous research has been conducted upon this particular subject. That little I have been enabled to carry out is by no means complete, a misfortune due entirely to the véry great difficulties experienced in endeavouring to obtain material upon which to work.I have been enabled to experiment upon six bodies in all, and the results of this work will be indicated in detail at a later stage.During the process of dissection, careful notes were made, not only of the position and relations of the structures which were displayed upon the photographic plate, but also of the various structures which, from their anatomical situation, were unable to be represented owing to their deep seated aid therefore concealed position. These notes will be considered in detail when the different forms of dislocation are studied seriatim

Curiosity Killed the M-Cat: an Examination of Illicit Drugs and Media

Using mainstream media communication theories, this article outlines different mechanisms by which media can impact on public perceptions of drugs and crime. The media can set the agenda and define public interest; frame issues through selection and salience; indirectly shape individual and community attitudes towards risk and norms; and feed into political debate and decision making. We demonstrate how the media can fulfill each of these roles by examining the so-called Miaow Miaow (Mephedrone) legal high ‘epidemic’, as reported in the United Kingdom news media from 2009-2010. In doing so we illustrate that by contributing to hysteria, exerting pressure for policy change and increasing curiosity in drug use, the media can have a potentially powerful impact on demand for drugs and public perceptions of illicit drugs and drugs policy.Sydney Institute of Criminology; School of Social Sciences at the University of Western Sydne

Are there functional consequences of a reduction in selenium intake in UK subjects?

Dietary Se levels in the UK have fallen over the last 20 years and recent surveys indicate that average Se intakes are 30-40 microg/d, which is well below the current UK reference nutrient intake for adult men (75 microg/d) or women (60 microg/d). Functional consequences of this decline have not been recognised, although epidemiological data suggest it may contribute to increased risk of infections and incidence of some cancers. Previous data have indicated that biochemical changes in Se-dependent proteins occur in otherwise healthy UK subjects given small Se supplements. The current studies have focused on the effect of small Se supplements on the immune response since there is evidence of specific interactions between Se intake and viral replication, and since the potential anti-cancer effects of Se may be mediated by non-antioxidant effects of Se such as changes in immune function. Data indicate that subjects given small Se supplements (50 or 100 microg Se/d) have changes in the activity of Se-dependent enzymes and evidence of improved immune function and clearance of an administered live attenuated virus in the form of poliovirus vaccine. Responses of individual subjects to Se supplements are variable, and current work is evaluating potential explanations for this variability, including genetic variability and pre-existing Se status

Induction of a chemoattractant transcriptional response by a Campylobacter jejuni boiled cell extract in colonocytes

<p>Abstract</p> <p>Background</p> <p><it>Campylobacter jejuni</it>, the commonest cause of bacterial diarrhoea worldwide, can also induce colonic inflammation. To understand how a previously identified heat stable component contributes to pro-inflammatory responses we used microarray and real-time quantitative PCR to investigate the transcriptional response to a boiled cell extract of <it>Campylobacter jejuni </it>NCTC 11168.</p> <p>Results</p> <p>RNA was extracted from the human colonocyte line HCA-7 (clone 29) after incubation for 6 hours with <it>Campylobacter jejuni </it>boiled cell extract and was used to probe the Affymetrix Human Genome U133A array. Genes differentially affected by <it>Campylobacter jejuni </it>boiled cell extract were identified using the Significance Score algorithm of the Bioconductor software suite and further analyzed using the Ingenuity Pathway Analysis program. The chemokines CCL20, CXCL3, CXCL2, Interleukin 8, CXCL1 and CXCL6 comprised 6 of the 10 most highly up-regulated genes, all with Significance Scores ≥ 10. Members of the Tumor Necrosis Factor α/Nuclear Factor-κB super-family were also significantly up-regulated and involved in the most significantly regulated signalling pathways (Death receptor, Interleukin 6, Interleukin 10, Toll like receptor, Peroxisome Proliferator Activated Receptor-γ and apoptosis). Ingenuity Pathway Analysis also identified the most affected functional gene networks such as cell movement, gene expression and cell death. In contrast, down-regulated genes were predominantly concerned with structural and metabolic functions.</p> <p>Conclusion</p> <p>A boiled cell extract of <it>Campylobacter jejuni </it>has components that can directly switch the phenotype of colonic epithelial cells from one of resting metabolism to a pro-inflammatory one, particularly characterized by increased expression of genes for leukocyte chemoattractant molecules.</p

Philosophy of Law in the Arctic

This is rather the first book with a title Philosophy of Law in the Arctic in the literature. This philosophy of law is a very wide and cross-disciplinary area of research: between law, philosophy, anthropology, history, cultural ecology or environmental studies. I have no doubts that we have done such kind of philosophy in the academia so far, not using this term, but keeping up with the concept, the idea. The book is a result of research conducted by many members of the Sub-group of Philosophy of Law in the Arctic (the University of the Arctic). This team seems a very interdisciplinary academic group. Our cooperation bears fruit. The aim of the book is to define and systematise Arctic legal philosophy problems. In this book, there are five thematic parts. Each part consists of two-five short articles (we can call them also chapters or papers). These are the sixteen short articles all together. Each article consists of between six and fourteen pages. So going further, what we see in the book then is, in fact, a set of both theoretical and practical papers. The topics of these papers (chapters) are different as the authors are different while representing a wide-ranging scope of academic disciplines or specialisations. Each paper is followed by a relevant bibliography, which might be helpful for other scholars interested in the field. The seventeen writers come from such countries as Finland (4), Norway (1), Canada (3), Poland (3), Japan (2), Austria (1), Ireland (1), and England (2). Some of them have Arctic indigenous roots (3). In the end of the book, there is a very original attachment - the map of Arctic Canada.https://digitalcommons.schulichlaw.dal.ca/faculty_books/1052/thumbnail.jp

Acute effects of active breaks during prolonged sitting on subcutaneous adipose tissue gene expression: an ancillary analysis of a randomised controlled trial.

Active breaks in prolonged sitting has beneficial impacts on cardiometabolic risk biomarkers. The molecular mechanisms include regulation of skeletal muscle gene and protein expression controlling metabolic, inflammatory and cell development pathways. An active communication network exists between adipose and muscle tissue, but the effect of active breaks in prolonged sitting on adipose tissue have not been investigated. This study characterized the acute transcriptional events induced in adipose tissue by regular active breaks during prolonged sitting. We studied 8 overweight/obese adults participating in an acute randomized three-intervention crossover trial. Interventions were performed in the postprandial state and included: (i) prolonged uninterrupted sitting; or prolonged sitting interrupted with 2-minute bouts of (ii) light- or (iii) moderate-intensity treadmill walking every 20 minutes. Subcutaneous adipose tissue biopsies were obtained after each condition. Microarrays identified 36 differentially expressed genes between the three conditions (fold change ≥0.5 in either direction; p < 0.05). Pathway analysis indicated that breaking up of prolonged sitting led to differential regulation of adipose tissue metabolic networks and inflammatory pathways, increased insulin signaling, modulation of adipocyte cell cycle, and facilitated cross-talk between adipose tissue and other organs. This study provides preliminary insight into the adipose tissue regulatory systems that may contribute to the physiological effects of interrupting prolonged sitting

1,4-dihydroxy quininib activates ferroptosis pathways in metastatic uveal melanoma and reveals a novel prognostic biomarker signature

Uveal melanoma (UM) is an ocular cancer, with propensity for lethal liver metastases. When metastatic UM (MUM) occurs, as few as 8% of patients survive beyond two years. Efficacious treatments for MUM are urgently needed. 1,4-dihydroxy quininib, a cysteinyl leukotriene receptor 1 (CysLT1) antagonist, alters UM cancer hallmarks in vitro, ex vivo and in vivo. Here, we investigated the 1,4-dihydroxy quininib mechanism of action and its translational potential in MUM. Proteomic profiling of OMM2.5 cells identified proteins differentially expressed after 1,4-dihydroxy quininib treatment. Glutathione peroxidase 4 (GPX4), glutamate-cysteine ligase modifier subunit (GCLM), heme oxygenase 1 (HO-1) and 4 hydroxynonenal (4-HNE) expression were assessed by immunoblots. Biliverdin, glutathione and lipid hydroperoxide were measured biochemically. Association between the expression of a specific ferroptosis signature and UM patient survival was performed using public databases. Our data revealed that 1,4-dihydroxy quininib modulates the expression of ferroptosis markers in OMM2.5 cells. Biochemical assays validated that GPX4, biliverdin, GCLM, glutathione and lipid hydroperoxide were significantly altered. HO-1 and 4-HNE levels were significantly increased in MUM tumor explants from orthotopic patient-derived xenografts (OPDX). Expression of genes inhibiting ferroptosis is significantly increased in UM patients with chromosome 3 monosomy. We identified IFerr, a novel ferroptosis signature correlating with UM patient survival. Altogether, we demontrated that in MUM cells and tissues, 1,4-dihydroxy quininib modulates key markers that induce ferroptosis, a relatively new type of cell death driven by iron-dependent peroxidation of phospholipids. Furthermore, we showed that high expression of specific genes inhibiting ferroptosis is associated with a worse UM prognosis, thus, the IFerr signature is a potential prognosticator for which patients develop MUM. All in all, ferroptosis has potential as a clinical biomarker and therapeutic target for MUM