The Lantern Vol. 37, No. 1, Fall 1970

• Circumstance • Advice • For What You Do For Me • Blink • Love • Love II • Magic • To Be a Child • A Year Later • A Poem in February • The Crystal Brick Road • Ephemera • Life • Whiskers • Thoughts On Being Sick • A Non-Poem • A Gruk Anthology • Moon • A Thought • Dwarf in an Existential Dawn • Corridors To My Mind • Sadness • The Enzyme Song • Creatures of Sandhttps://digitalcommons.ursinus.edu/lantern/1098/thumbnail.jp

The Ursinus Weekly, October 26, 1972

Union and Bomberger renovation progress • Twenty-four degrees presented on successful Founder\u27s Day • SFARC starts year; Discusses women\u27s rules • Powell crowned Homecoming queen • Pre-med Society cleans cobwebbed constitution • Editorials: To voters; Do unto others • Faculty portrait: Dr. Joyce Henry • Up to New York from down on the farm; or the Fine Arts class sees the Met • WRUC radio revives; Moves to T-G Gym • Dormitory decorations trophy kept for good (show) by Shreiner • Campus once again united by sorority songs, traditions • Bear eleven rips Swarthmore; Whatley\u27s warriors win 35-21 as Ursinus\u27 offense dominates • Bearettes crunch G-burg • What ever happened to Eleanor Frost Snell? • Garnet booters trip Bears • Sports buffs\u27 cornerhttps://digitalcommons.ursinus.edu/weekly/1089/thumbnail.jp

A genetic modifier suggests that endurance exercise exacerbates Huntington's disease.

Polyglutamine expansions in the huntingtin gene cause Huntington's disease (HD). Huntingtin is ubiquitously expressed, leading to pathological alterations also in peripheral organs. Variations in the length of the polyglutamine tract explain up to 70% of the age-at-onset variance, with the rest of the variance attributed to genetic and environmental modifiers. To identify novel disease modifiers, we performed an unbiased mutagenesis screen on an HD mouse model, identifying a mutation in the skeletal muscle voltage-gated sodium channel (Scn4a, termed 'draggen' mutation) as a novel disease enhancer. Double mutant mice (HD; Scn4aDgn/+) had decreased survival, weight loss and muscle atrophy. Expression patterns show that the main tissue affected is skeletal muscle. Intriguingly, muscles from HD; Scn4aDgn/+ mice showed adaptive changes similar to those found in endurance exercise, including AMPK activation, fibre type switching and upregulation of mitochondrial biogenesis. Therefore, we evaluated the effects of endurance training on HD mice. Crucially, this training regime also led to detrimental effects on HD mice. Overall, these results reveal a novel role for skeletal muscle in modulating systemic HD pathogenesis, suggesting that some forms of physical exercise could be deleterious in neurodegeneration

The Lantern Vol. 38, No. 2, Spring 1972

• Summer II • For a True Romantic • The Lyre Neglected • Hands • To a Friend • Sleep • The Wind\u27s Confusing Sounds • The Garden • The Child Has Come Among Us • The River and the Sea • The Ice • La Lamentation de la Fleur • Nous Sommes • Upon Becoming • See! • Feeling November • Transience • Clear • Isotopes of Reality • Just Yesterday • Emergence • Push • The Way Love Starts • Poetic Prosy • An Agreement • Spring 1930 • The Summers of \u2759, \u2760, \u2761 • Ode to Optometry • The Easter Bunny - Noble Beasthttps://digitalcommons.ursinus.edu/lantern/1100/thumbnail.jp

Minimal methylation classifier (MIMIC): A novel method for derivation and rapid diagnostic detection of disease-associated DNA methylation signatures

Rapid and reliable detection of disease-associated DNA methylation patterns has major potential to advance molecular diagnostics and underpin research investigations. We describe the development and validation of minimal methylation classifier (MIMIC), combining CpG signature design from genome-wide datasets, multiplex-PCR and detection by single-base extension and MALDI-TOF mass spectrometry, in a novel method to assess multi-locus DNA methylation profiles within routine clinically-applicable assays. We illustrate the application of MIMIC to successfully identify the methylation-dependent diagnostic molecular subgroups of medulloblastoma (the most common malignant childhood brain tumour), using scant/low-quality samples remaining from the most recently completed pan-European medulloblastoma clinical trial, refractory to analysis by conventional genome-wide DNA methylation analysis. Using this approach, we identify critical DNA methylation patterns from previously inaccessible cohorts, and reveal novel survival differences between the medulloblastoma disease subgroups with significant potential for clinical exploitation

Crop Updates 2002 - Cereals

This session covers thirty one papers from different authors: VARIETIES AND BREEDING 1. Agronomic evaluation of wheat and barley in the central wheatbelt of Western Australia, Peter Burgess1and Gary Fawell2, 1Agritech and 2Farmanco Management 2. Evaluating stress tolerance to terminal drought by Western Australian wheats, Dean Diepeveen and Dr Tim Setter, Department of Agriculture 3. Broadscale wheat variety comparisons featuring Wyalkatchem, Jeff Russell, Department of Agriculture 4. Australian crop accreditation system variety selector, Tony Seymour, Australian Crop Accreditation System 5. Future wheat varieties, Robin Wilson, Iain Barclay,Robyn McLean, Robert Loughman, Jenny Garlinge, Bill Lambe, Neil Venn and Peter Clarke, Department of Agriculture AGRONOMY 6. Beware of wheat variety interactions with row spacing and seed rate, Mohammad Amjad and Wal Anderson, Department of Agriculture 7. Yield and falling numbers of wheat varieties on the South Coast, Mohammad Amjad and Wal Anderson, Department of Agriculture 8. Maximising wheat variety performance through agronomic management, Wal Anderson, Raffaele Del Cima, James Bee, Darshan Sharma, Sheena Lyon, Melaine Kupsch, Mohammad Amjad, Pam Burgess, Veronika Reck, Brenda Shackley, Ray Tugwell, BindiWebb and Steve Penny Jr, Department of Agriculture 9. High impact of soil type and seasonal rainfall on optimum wheat seed rate , Raffaele Del Cima and Wal Anderson Department of Agriculture 10. 101 seasons in one day: Using the ‘WA Wheat’ database to predict wheat yield, James Fisher1, Bill Bowden1, Craig Scanlan1, Senthold Asseng2and Michael Robertson2 1Department of Agriculture, 2CSIRO 11. Economics of improving compact soils, M.A. Hamza1, G. McConnell2and W.K. Anderson1, 1Department of Agriculture, 2Planfarm 12. Reducing the risks in producing durum wheat in Western Australia, Md Shahajahan Miyan and Wal Anderson, Department of Agriculture 13. Taking the Why out of Wyalkatchem – the new widely adopted wheat variety, Steve Penny, Department of Agriculture 14. Influence of nutrition and environmental factors on seed vigour in wheat, Darshan Sharma, Wal Anderson and Daya Patabendige, Department of Agriculture NUTRITION 15. N and K are important for oat yield and quality, Patrick Gethin, Stephen Loss, Tim O’Dea, Ryan Guthrie and Lisa Leaver, CSBP Futurefarm 16. Effects of nitrogen and phosphorus on the grain yield and quality of noodle wheat, Tyrone Henning1, Lionel Martin1and Wal Anderson2 1Muresk Institute of Agriculture, 2Department of Agriculture 17. Assessment of a high input fertiliser regime on the yield and quality of Gairdner barley, Narelle Hill1, Simon Wallwork2and Laurence Carslake2 1Department of Agriculture, 2Wesfarmers Landmark 18. The use of Flexi-N to achieve high yielding, high protein wheat, Darren Hughes1, Lionel Martin1, Wal Anderson2and Stephen Loss3 1Muresk Institute of Agriculture, 2Department of Agriculture, 3CSBP Futurefarm 19. Are liquid phosphorus fertilisers more efficient than solid fertilisers in Western Australia?Stephen Loss, Lisa Leaver, Ryan Guthrie, Patrick Gethin and Tim O’Dea, CSBP Futurefarm 20. Oats respond to phosphorus and potassium, Glenn McDonald, Department of Agriculture PESTS AND DISEASES 21. Cereal disease diagnostics and rust monitoring, Nichole Burges and Dominie Wright, Department of Agriculture 22. Distribution and incidence of aphids and barley yellow dwarf virus in over-summering grasses in the Western Australian wheatbelt, Jenny Hawkes and Roger Jones, Centre for Legumes in Mediterranean Agriculture and Department of Agriculture 23. Spring sprays for powdery mildew control in cereals, Kith Jayasena1, Kazue Tanaka1, Vanessa Johnson1, Robert Loughman1and Josh Jury2 1Department of Agriculture, 2Wesfarmers Landmark 24. Impact of root lesion nematodes on wheat and triticale in Western Australia, Sean Kelly and Shashi Sharma, Department of Agriculture 25. Cropping options for the management of root lesion nematodes in Western Australia, Sean Kelly, Shashi Sharma and Robert Loughman, Department of Agriculture 26. Cereal rust update 2002 – new stem rust on Camm wheat, Robert Loughman1and Robert Park2 1Department of Agriculture, 2University of Sydney 27. Cereal aphids and direct feeding damage to cereals, Phil Michael, Department of Agriculture 28. A decision support system for control of aphids and BYDV in cereal crops, Debbie Thackray, Jenny Hawkes and Roger Jones, Department of Agriculture and Centre for Legumes in Mediterranean Agriculture STORAGE 29. Aeration – opportunity for profit, Christopher Newman, Department of Agriculture CLIMATE 30. Financial impact of frost on the Western Australian grains industry, Garren Knell and Kim Povey, ConsultAg 31. Summary of 2001 weather and seasonal prospects for 2002, David Stephens, Department of Agricultur

PREDICT identifies precipitating events associated with the clinical course of acutely decompensated cirrhosis

Background & Aims: Acute decompensation (AD) of cirrhosis may present without acute-on-chronic liver failure (ACLF) (ADNo ACLF), or with ACLF (AD-ACLF), defined by organ failure(s). Herein, we aimed to analyze and characterize the precipitants leading to both of these AD phenotypes. Methods: The multicenter, prospective, observational PREDICT study (NCT03056612) included 1,273 non-electively hospitalized patients with AD (No ACLF = 1,071; ACLF = 202). Medical history, clinical data and laboratory data were collected at enrolment and during 90-day follow-up, with particular attention given to the following characteristics of precipitants: induction of organ dysfunction or failure, systemic inflammation, chronology, intensity, and relationship to outcome. Results: Among various clinical events, 4 distinct events were precipitants consistently related to AD: proven bacterial infections, severe alcoholic hepatitis, gastrointestinal bleeding with shock and toxic encephalopathy. Among patients with precipitants in the AD-No ACLF cohort and the AD-ACLF cohort (38% and 71%, respectively), almost all (96% and 97%, respectively) showed proven bacterial infection and severe alcoholic hepatitis, either alone or in combination with other events. Survival was similar in patients with proven bacterial infections or severe alcoholic hepatitis in both AD phenotypes. The number of precipitants was associated with significantly increased 90day mortality and was paralleled by increasing levels of surrogates for systemic inflammation. Importantly, adequate first-line antibiotic treatment of proven bacterial infections was associated with a lower ACLF development rate and lower 90-day mortality. Conclusions: This study identified precipitants that are significantly associated with a distinct clinical course and prognosis in patients with AD. Specific preventive and therapeutic strategies targeting these events may improve outcomes in patients with decompensated cirrhosis. Lay summary: Acute decompensation (AD) of cirrhosis is characterized by a rapid deterioration in patient health. Herein, we aimed to analyze the precipitating events that cause AD in patients with cirrhosis. Proven bacterial infections and severe alcoholic hepatitis, either alone or in combination, accounted for almost all (96-97%) cases of AD and acute-on-chronic liver failure. Whilst the type of precipitant was not associated with mortality, the number of precipitant(s) was. This study identified precipitants that are significantly associated with a distinct clinical course and prognosis of patients with AD. Specific preventive and therapeutic strategies targeting these events may improve patient outcomes. (c) 2020 European Association for the Study of the Liver. Published by Elsevier B.V. This is an open access article under the CC BY-NC-ND license (http://creativecommons.org/licenses/by-nc-nd/4.0/)

The PREDICT study uncovers three clinical courses of acutely decompensated cirrhosis that have distinct pathophysiology

Acute decompensation (AD) of cirrhosis is defined as the acute development of ascites, gastrointestinal hemorrhage, hepatic encephalopathy, infection or any combination thereof, requiring hospitalization. The presence of organ failure(s) in patients with AD defines acute-on-chronic liver failure (ACLF). The PREDICT study is a European, prospective, observational study, designed to characterize the clinical course of AD and to identify predictors of ACLF. A total of 1,071 patients with AD were enrolled. We collected detailed pre-specified information on the 3-month period prior to enrollment, and clinical and laboratory data at enrollment. Patients were then closely followed up for 3 months. Outcomes (liver transplantation and death) at 1 year were also recorded. Three groups of patients were identified. Pre-ACLF patients (n = 218) developed ACLF and had 3-month and 1-year mortality rates of 53.7% and 67.4%, respectively. Unstable decompensated cirrhosis (UDC) patients (n = 233) required ≥1 readmission but did not develop ACLF and had mortality rates of 21.0% and 35.6%, respectively. Stable decompensated cirrhosis (SDC) patients (n = 620) were not readmitted, did not develop ACLF and had a 1-year mortality rate of only 9.5%. The 3 groups differed significantly regarding the grade and course of systemic inflammation (high-grade at enrollment with aggravation during follow-up in pre-ACLF; low-grade at enrollment with subsequent steady-course in UDC; and low-grade at enrollment with subsequent improvement in SDC) and the prevalence of surrogates of severe portal hypertension throughout the study (high in UDC vs. low in pre-ACLF and SDC). Acute decompensation without ACLF is a heterogeneous condition with 3 different clinical courses and 2 major pathophysiological mechanisms: systemic inflammation and portal hypertension. Predicting the development of ACLF remains a major future challenge. ClinicalTrials.gov number: NCT03056612. Lay summary: Herein, we describe, for the first time, 3 different clinical courses of acute decompensation (AD) of cirrhosis after hospital admission. The first clinical course includes patients who develop acute-on-chronic liver failure (ACLF) and have a high short-term risk of death - termed pre-ACLF. The second clinical course (unstable decompensated cirrhosis) includes patients requiring frequent hospitalizations unrelated to ACLF and is associated with a lower mortality risk than pre-ACLF. Finally, the third clinical course (stable decompensated cirrhosis), includes two-thirds of all patients admitted to hospital with AD - patients in this group rarely require hospital admission and have a much lower 1-year mortality risk

The Early Growth Genetics (EGG) and EArly Genetics and Lifecourse Epidemiology (EAGLE) consortia : design, results and future prospects

The impact of many unfavorable childhood traits or diseases, such as low birth weight and mental disorders, is not limited to childhood and adolescence, as they are also associated with poor outcomes in adulthood, such as cardiovascular disease. Insight into the genetic etiology of childhood and adolescent traits and disorders may therefore provide new perspectives, not only on how to improve wellbeing during childhood, but also how to prevent later adverse outcomes. To achieve the sample sizes required for genetic research, the Early Growth Genetics (EGG) and EArly Genetics and Lifecourse Epidemiology (EAGLE) consortia were established. The majority of the participating cohorts are longitudinal population-based samples, but other cohorts with data on early childhood phenotypes are also involved. Cohorts often have a broad focus and collect(ed) data on various somatic and psychiatric traits as well as environmental factors. Genetic variants have been successfully identified for multiple traits, for example, birth weight, atopic dermatitis, childhood BMI, allergic sensitization, and pubertal growth. Furthermore, the results have shown that genetic factors also partly underlie the association with adult traits. As sample sizes are still increasing, it is expected that future analyses will identify additional variants. This, in combination with the development of innovative statistical methods, will provide detailed insight on the mechanisms underlying the transition from childhood to adult disorders. Both consortia welcome new collaborations. Policies and contact details are available from the corresponding authors of this manuscript and/or the consortium websites.Peer reviewe