Pictures on the wall of my life : photographs to life writing to fiction, an ekphrastic journey

This study investigates the practice of writing a novel with its starting point in family photographs. It consists of the novel itself in latest draft form as well as a theoretical commentary on the writing of it. The particular focus for discussion is how the visual informs the written text and how the visual and verbal together become ‘imagetext’.1 The novel is narrated in the first person by Lily Adams who learns from the many ancestral portraits in black and white that line the halls of her childhood home that what they embody is not visually representative of a past she has been encouraged to believe in, but rather of one she is now forced to question as the pictures speak to her, in their own voices, of a world re-focused through their own lens. A critical commentary follows in three chapters: a chapter on ‘punctum’ discusses motivation and photography as a technical and creative driver for this work, and the following one on ‘ekphrasis’ makes literary connections between two main drafts, one in third person (see Appendix) and the other (latest) in first person, looking in detail at the way ‘ekphrasis’ or visual to verbal translation has developed in these two versions. The growth of the idea from earlier beginnings is traced and related to the notion of ekphrasis as it has shaped the later drafts. The concluding chapter on ‘ekphrastic realism’ draws these strands together by making an attempt to situate my novel within the canonical intersection of ekphrasis and magical realism. These make a contribution to an understanding of the concept of ekphrasis by way of ekphrastic writing, known merely as an obscure literary genre

Pictures on the wall of my life: photographs to life writing to fiction, an ekphrastic journey

This study investigates the practice of writing a novel with its starting point in family photographs. It consists of the novel itself in latest draft form as well as a theoretical commentary on the writing of it. The particular focus for discussion is how the visual informs the written text and how the visual and verbal together become ‘imagetext’.1 The novel is narrated in the first person by Lily Adams who learns from the many ancestral portraits in black and white that line the halls of her childhood home that what they embody is not visually representative of a past she has been encouraged to believe in, but rather of one she is now forced to question as the pictures speak to her, in their own voices, of a world re-focused through their own lens. A critical commentary follows in three chapters: a chapter on ‘punctum’ discusses motivation and photography as a technical and creative driver for this work, and the following one on ‘ekphrasis’ makes literary connections between two main drafts, one in third person (see Appendix) and the other (latest) in first person, looking in detail at the way ‘ekphrasis’ or visual to verbal translation has developed in these two versions. The growth of the idea from earlier beginnings is traced and related to the notion of ekphrasis as it has shaped the later drafts. The concluding chapter on ‘ekphrastic realism’ draws these strands together by making an attempt to situate my novel within the canonical intersection of ekphrasis and magical realism. These make a contribution to an understanding of the concept of ekphrasis by way of ekphrastic writing, known merely as an obscure literary genre

The Ursinus Weekly, January 11, 1965

Football players receive awards at banquet: Tony Motto gets All-ECAC • Ursinus to send delegation to Model UN • Weekly names Sam Walker sports editor • Faculty Forum to present concert, lecture recital: 20th century American music, subject • Three placed in teaching positions • Pre-meds to hear two Sacred Heart pathologists • World\u27s Fair invites college talent to perform • Pi Nu Epsilon, music fraternity, initiates eight • Norristown man named to vacancy in Treas. Office • Good band, decorations add to great TG dance • The best TV show in the world • Editorial: Our large small college • Bob Dylan: Alone and indifferent • J. D. Salinger writes for The Ursinus Weekly • Anthem, a warning to society • The Doanes report on teaching in the South • Bears drop two, F&M-Swarthmore; Troster\u27s thirty points rock PMC • Matmen drop opener to Del. • Soccer team puts three on All-MAC • Y Commission sponsors film on discrimination • Greek gleanings • Letters to the editor • Kaffee Klatsch debates Negro block bustinghttps://digitalcommons.ursinus.edu/weekly/1238/thumbnail.jp

The Ursinus Weekly, October 12, 1964

Thespians choose Blore & Rodimer, Fall cast leads: Write me a murder heads into first stage of production • Pledging begins as sororities end last week of rushing: 61 women sign bids • Queen Jeanne Dawson, grid triumph, flavor weekend fun: Returning alumni enjoy cold day\u27s festivities • Lancaster theologian speaking tonight on Vatican Council II • Pre-meds hear members, list season speakers • Peace Corps worker to speak here • Y adds new concept to traditional retreat format: Fernbrook site of weekend\u27s activities • Editorial: Apathy or futility • Green poncho raincoats become UC fetish • UC students see touring Goldwater • Democrats meet the candidates • Young Republicans hold first caucus • Kaffee Klatch drafts variety • Human Relations Club begins work • Bears eat-up Blue Jays 38-22, exciting second half: Degenhardt wins Walker Memorial • Beta Sig, Seals lead leagues • Soccer team ties East Baptist, 2-2 • UC soccer team outplays alumni • J.V. hockey team victorious in first two season games: Crush Gwynedd 6-1, line scores at will; Defense stalwart defeat tough Penn • Answers and questions • Dear Ursala: advice column • Greek gleaningshttps://digitalcommons.ursinus.edu/weekly/1229/thumbnail.jp

Contemporary Homozygous Familial Hypercholesterolemia in the United States: Insights From the CASCADE FH Registry

Erratum in: J Am Heart Assoc. 2023 Jun 6;12(11):e027706. doi: 10.1161/JAHA.122.027706. Epub 2023 Jun 1.Free PMC article: https://www.ncbi.nlm.nih.gov/pmc/articles/PMC10227232/Background: Homozygous familial hypercholesterolemia (HoFH) is a rare, treatment-resistant disorder characterized by earlyonset atherosclerotic and aortic valvular cardiovascular disease if left untreated. Contemporary information on HoFH in the United States is lacking, and the extent of underdiagnosis and undertreatment is uncertain. Methods and Results: Data were analyzed from 67 children and adults with clinically diagnosed HoFH from the CASCADE (Cascade Screening for Awareness and Detection) FH Registry. Genetic diagnosis was confirmed in 43 patients. We used the clinical characteristics of genetically confirmed patients with HoFH to query the Family Heart Database, a US anonymized payer health database, to estimate the number of patients with similar lipid profiles in a “real-world” setting. Untreated lowdensity lipoprotein cholesterol levels were lower in adults than children (533 versus 776mg/dL; P=0.001). At enrollment, atherosclerotic cardiovascular disease and supravalvular and aortic valve stenosis were present in 78.4% and 43.8% and 25.5% and 18.8% of adults and children, respectively. At most recent follow-up, despite multiple lipid-lowering treatment, low-density lipoprotein cholesterol goals were achieved in only a minority of adults and children. Query of the Family Heart Database identified 277 individuals with profiles similar to patients with genetically confirmed HoFH. Advanced lipid-lowering treatments were prescribed for 18%; 40% were on no lipid-lowering treatment; atherosclerotic cardiovascular disease was reported in 20%; familial hypercholesterolemia diagnosis was uncommon. Conclusions: Only patients with the most severe HoFH phenotypes are diagnosed early. HoFH remains challenging to treat. Results from the Family Heart Database indicate HoFH is systemically underdiagnosed and undertreated. Earlier screening, aggressive lipid-lowering treatments, and guideline implementation are required to reduce disease burden in HoFH.Dr Martin is supported by grants/contracts from the American Heart Association (20SFRN35380046, 20SFRN35490003, 878924, and 882415), Patient‐Centered Outcomes Research Institute (PCORI) (ME‐2019C1‐15328), National Institutes of Health (NIH) (R01AG071032 and P01 HL108800), the David and June Trone Family Foundation, Pollin Digital Health Innovation Fund, and Sandra and Larry Small; Dr Knowles is supported by the NIH through grants P30 DK116074 (to the Stanford Diabetes Research Center), R01 DK116750, R01 DK120565, and R01 DK106236; and by a grant from the Bilateral Science Foundation. Dr Linton is supported by NIH grants P01HL116263, HL148137, HL159487, and HL146134.info:eu-repo/semantics/publishedVersio

HEART UK statement on the management of homozygous familial hypercholesterolaemia in the United Kingdom

This consensus statement addresses the current three main modalities of treatment of homozygous familial hypercholesterolaemia (HoFH): pharmacotherapy, lipoprotein (Lp) apheresis and liver transplantation. HoFH may cause very premature atheromatous arterial disease and death, despite treatment with Lp apheresis combined with statin, ezetimibe and bile acid sequestrants. Two new classes of drug, effective in lowering cholesterol in HoFH, are now licensed in the United Kingdom. Lomitapide is restricted to use in HoFH but, may cause fatty liver and is very expensive. PCSK9 inhibitors are quite effective in receptor defective HoFH, are safe and are less expensive. Lower treatment targets for lipid lowering in HoFH, in line with those for the general FH population, have been proposed to improve cardiovascular outcomes. HEART UK presents a strategy combining Lp apheresis with pharmacological treatment to achieve these targets in the United Kingdom (UK). Improved provision of Lp apheresis by use of existing infrastructure for extracorporeal treatments such as renal dialysis is promoted. The clinical management of adults and children with HoFH including advice on pregnancy and contraception are addressed. A premise of the HEART UK strategy is that the risk of early use of drug treatments beyond their licensed age restriction may be balanced against risks of liver transplantation or ineffective treatment in severely affected patients. This may be of interest beyond the UK

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 hospitalisation2-4 following SARS-CoV-2 infection. The GenOMICC (Genetics of Mortality in Critical Care) study enables the comparison of genomes from critically-ill cases with population controls in order to find underlying disease mechanisms. Here, we use whole genome sequencing in 7,491 critically-ill cases 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 involved in interferon signalling (IL10RB, PLSCR1), leucocyte differentiation (BCL11A), and blood type antigen secretor status (FUT2). Using transcriptome-wide association and colocalisation to infer the effect of gene expression on disease severity, we find evidence implicating multiple genes, including reduced expression of a membrane flippase (ATP11A), and increased mucin expression (MUC1), in critical disease. Mendelian randomisation provides evidence in support of causal roles for myeloid cell adhesion molecules (SELE, ICAM5, CD209) and 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 critically-ill cases and population controls is highly efficient for detection of therapeutically-relevant mechanisms of disease

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 care(1) or hospitalization(2-4) 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. © 2022, The Author(s)

Large-Scale Gene-Centric Meta-Analysis across 39 Studies Identifies Type 2 Diabetes Loci

To identify genetic factors contributing to type 2 diabetes (T2D), we performed large-scale meta-analyses by using a custom similar to 50,000 SNP genotyping array (the ITMAT-Broad-CARe array) with similar to 2000 candidate genes in 39 multiethnic population-based studies, case-control studies, and clinical trials totaling 17,418 cases and 70,298 controls. First, meta-analysis of 25 studies comprising 14,073 cases and 57,489 controls of European descent confirmed eight established T2D loci at genome-wide significance. In silico follow-up analysis of putative association signals found in independent genome-wide association studies (including 8,130 cases and 38,987 controls) performed by the DIAGRAM consortium identified a T2D locus at genome-wide significance (GATAD2A/CILP2/PBX4; p = 5.7 x 10(-9)) and two loci exceeding study-wide significance (SREBF1, and TH/INS; p <2.4 x 10(-6)). Second, meta-analyses of 1,986 cases and 7,695 controls from eight African-American studies identified study-wide-significant (p = 2.4 x 10(-7)) variants in HMGA2 and replicated variants in TCF7L2 (p = 5.1 x 10(-15)). Third, conditional analysis revealed multiple known and novel independent signals within five T2D-associated genes in samples of European ancestry and within HMGA2 in African-American samples. Fourth, a multiethnic meta-analysis of all 39 studies identified T2D-associated variants in BCL2 (p = 2.1 x 10(-8)). Finally, a composite genetic score of SNPs from new and established T2D signals was significantly associated with increased risk of diabetes in African-American, Hispanic, and Asian populations. In summary, large-scale meta-analysis involving a dense gene-centric approach has uncovered additional loci and variants that contribute to T2D risk and suggests substantial overlap of T2D association signals across multiple ethnic groups

Contemporary Homozygous Familial Hypercholesterolemia in the United States: Insights From the CASCADE FH Registry

Background Homozygous familial hypercholesterolemia (HoFH) is a rare, treatment‐resistant disorder characterized by early‐onset atherosclerotic and aortic valvular cardiovascular disease if left untreated. Contemporary information on HoFH in the United States is lacking, and the extent of underdiagnosis and undertreatment is uncertain. Methods and Results Data were analyzed from 67 children and adults with clinically diagnosed HoFH from the CASCADE (Cascade Screening for Awareness and Detection) FH Registry. Genetic diagnosis was confirmed in 43 patients. We used the clinical characteristics of genetically confirmed patients with HoFH to query the Family Heart Database, a US anonymized payer health database, to estimate the number of patients with similar lipid profiles in a “real‐world” setting. Untreated low‐density lipoprotein cholesterol levels were lower in adults than children (533 versus 776 mg/dL; P=0.001). At enrollment, atherosclerotic cardiovascular disease and supravalvular and aortic valve stenosis were present in 78.4% and 43.8% and 25.5% and 18.8% of adults and children, respectively. At most recent follow‐up, despite multiple lipid‐lowering treatment, low‐density lipoprotein cholesterol goals were achieved in only a minority of adults and children. Query of the Family Heart Database identified 277 individuals with profiles similar to patients with genetically confirmed HoFH. Advanced lipid‐lowering treatments were prescribed for 18%; 40% were on no lipid‐lowering treatment; atherosclerotic cardiovascular disease was reported in 20%; familial hypercholesterolemia diagnosis was uncommon. Conclusions Only patients with the most severe HoFH phenotypes are diagnosed early. HoFH remains challenging to treat. Results from the Family Heart Database indicate HoFH is systemically underdiagnosed and undertreated. Earlier screening, aggressive lipid‐lowering treatments, and guideline implementation are required to reduce disease burden in HoFH