Dressing and addressing the mental patient: the uses of clothing in the admission, care and employment of residents in English provincial mental hospitals, c. 1860–1960

Scholars of insanity and its historical antecedents have paid very little attention to personal and institutional clothing. Such dress, distributed to patients in mental institutions, has always been inscribed with the conflicting narratives of the period in which it was made and worn. The language of civil and medical authority is more evident than personal choice in the shape and address of the attire. This article examines clothing worn by patients in three Devon mental hospitals during the century before 1960. We consider the ways in which institutional clothing formed part of a hospital regimen of overt control, as well as suiting considerations of economy and employment that figured in these institutions

British employers and the development of industrial welfare, c. 1880-1920: An industrial and regional comparison

There has been no systematic study of the welfare provisions made by British employers for their workers in the decades, I880-I920. Research suggests that such an omission leaves an important gap in both economic and social history, and that welfare activities were of considerable significance in the- development of British industry. One of the most fundamental problems concerns the discovery of an appropriate definition and method of analysis of this form of welfare. Industrial welfare is seen principally as a relationship between the employer and his employees. The major formative influences on its development within industry were the production and market conditions in which firms operated, and the industrial relations which emerged in particular trades and industries. The comparison of firms within one sector, and of different sectors within a regional economy demonstrate the extensive experience of welfare activities in these years. Comparison of regions illustrates both the complexity of factors affecting the development of welfare services - influencing their qualitative character as well as quantitative scope - and the common themes which appear in quite distinct occupations. This pattern is confirmed by an examination of welfare in its broader social and political context. The agencies of growth and administration varied from the heterogeneous mass of friendly societies to the highly specific and tightly-organised employers' associations. Their welfare commitments tended to reflect the more general functions and priorities of the organisations concerned. The social context of much welfare investment is revealed by an examination of local community relations, and the ways in which welfare reinforced the images as well as material substance of local life. Such images form only part of the diverse and fluid ideology of industrial welfare, which was carried by currents ranging from scientific management and technical expertise to political philosophy and religious belief. All of these forces are evident in the interaction of employers' welfare and state social policy, with private provisions shaping both employers ' attitudes and government legislation during these decades of rapid economic change and shifting social relations. It is in this light that we must locate the development of industrial welfare over the period

The Molloy Student Literary Magazine Volume 10

The Molloy Student Literary Magazine, sponsored by Molloy College’s Office of Student Affairs, is devoted to publishing the best previously unpublished works of prose, poetry, drama, literary review, criticism, and other literary genres, that the Molloy student community has to offer. The journal welcomes submissions, for possible publication, from currently enrolled Molloy students at all levels. All submitted work will undergo a review process initiated by the Managing Editor prior to a decision being made regarding publication of said work. Given sufficient content, The Molloy Student Literary Magazine is published twice annually in Spring and Fall. Interested contributors from the currently enrolled Molloy student community should send work via e-mail attachment and brief cover letter (including a two-sentence biographical statement) to: Dr. Damian Ward Hey, Managing Editor, The Molloy Student Literary Magazine: [email protected]. Enrolled students who are interested in becoming members of The Molloy Student Literary Magazine staff may e-mail letters of inquiry. Excelsior!https://digitalcommons.molloy.edu/eng_litmag/1002/thumbnail.jp

Genetic mechanisms of critical illness in COVID-19.

Host-mediated lung inflammation is present1, and drives mortality2, in the critical illness caused by coronavirus disease 2019 (COVID-19). Host genetic variants associated with critical illness may identify mechanistic targets for therapeutic development3. Here we report the results of the GenOMICC (Genetics Of Mortality In Critical Care) genome-wide association study in 2,244 critically ill patients with COVID-19 from 208 UK intensive care units. We have identified and replicated the following new genome-wide significant associations: on chromosome 12q24.13 (rs10735079, P = 1.65 × 10-8) in a gene cluster that encodes antiviral restriction enzyme activators (OAS1, OAS2 and OAS3); on chromosome 19p13.2 (rs74956615, P = 2.3 × 10-8) near the gene that encodes tyrosine kinase 2 (TYK2); on chromosome 19p13.3 (rs2109069, P = 3.98 ×  10-12) within the gene that encodes dipeptidyl peptidase 9 (DPP9); and on chromosome 21q22.1 (rs2236757, P = 4.99 × 10-8) in the interferon receptor gene IFNAR2. We identified potential targets for repurposing of licensed medications: using Mendelian randomization, we found evidence that low expression of IFNAR2, or high expression of TYK2, are associated with life-threatening disease; and transcriptome-wide association in lung tissue revealed that high expression of the monocyte-macrophage chemotactic receptor CCR2 is associated with severe COVID-19. Our results identify robust genetic signals relating to key host antiviral defence mechanisms and mediators of inflammatory organ damage in COVID-19. Both mechanisms may be amenable to targeted treatment with existing drugs. However, large-scale randomized clinical trials will be essential before any change to clinical practice

IL-22BP controls the progression of liver metastasis in colorectal cancer

BackgroundThe immune system plays a pivotal role in cancer progression. Interleukin 22 binding protein (IL-22BP), a natural antagonist of the cytokine interleukin 22 (IL-22) has been shown to control the progression of colorectal cancer (CRC). However, the role of IL-22BP in the process of metastasis formation remains unknown.MethodsWe used two different murine in vivo metastasis models using the MC38 and LLC cancer cell lines and studied lung and liver metastasis formation after intracaecal or intrasplenic injection of cancer cells. Furthermore, IL22BP expression was measured in a clinical cohort of CRC patients and correlated with metastatic tumor stages.ResultsOur data indicate that low levels of IL-22BP are associated with advanced (metastatic) tumor stages in colorectal cancer. Using two different murine in vivo models we show that IL-22BP indeed controls the progression of liver but not lung metastasis in mice.ConclusionsWe here demonstrate a crucial role of IL-22BP in controlling metastasis progression. Thus, IL-22 might represent a future therapeutic target against the progression of metastatic CRC

Whole-genome sequencing reveals host factors underlying critical COVID-19

Critical COVID-19 is caused by immune-mediated inflammatory lung injury. Host genetic variation influences the development of illness requiring critical care1 or hospitalization2–4 after infection with SARS-CoV-2. The GenOMICC (Genetics of Mortality in Critical Care) study enables the comparison of genomes from individuals who are critically ill with those of population controls to find underlying disease mechanisms. Here we use whole-genome sequencing in 7,491 critically ill individuals compared with 48,400 controls to discover and replicate 23 independent variants that significantly predispose to critical COVID-19. We identify 16 new independent associations, including variants within genes that are involved in interferon signalling (IL10RB and PLSCR1), leucocyte differentiation (BCL11A) and blood-type antigen secretor status (FUT2). Using transcriptome-wide association and colocalization to infer the effect of gene expression on disease severity, we find evidence that implicates multiple genes—including reduced expression of a membrane flippase (ATP11A), and increased expression of a mucin (MUC1)—in critical disease. Mendelian randomization provides evidence in support of causal roles for myeloid cell adhesion molecules (SELE, ICAM5 and CD209) and the coagulation factor F8, all of which are potentially druggable targets. Our results are broadly consistent with a multi-component model of COVID-19 pathophysiology, in which at least two distinct mechanisms can predispose to life-threatening disease: failure to control viral replication; or an enhanced tendency towards pulmonary inflammation and intravascular coagulation. We show that comparison between cases of critical illness and population controls is highly efficient for the detection of therapeutically relevant mechanisms of disease