Concert recording 2017-10-18a

[Track 1]. Caprice, op. 80 / Jean Baptiste Singelée -- [Track 2]. Syrinx / Claude Debussy translated by J. Rulli -- [Track 3]. Dialogue / Jean-Marie Depelsenaire -- [Tracks 4-8]. Pieces of sanity / Stacy Garrop -- [Tracks 9-13]. Five Ozark folk songs / Travis Herd

Concert recording 2013-04-06a

[Track 01]. Concerto por alto saxophone et orchestre. Andante et allegro ; [Track 02]. Giration-final: Allegro / Henri Tomasi -- [Track 03]. Concerto for alto saxophone and wind ensemble. Interlude: Bright window, your night is full of stars / David Maslanka -- [Track 04]. Phoenix (Fushicho) / Ryo Noda -- [Track 05]. Elegie et rondeau / Karel Husa -- [Track 06]. Naima / John Coltrane -- [Track 07]. Work song / Nat Adderley

Sensitization to gliadin induces moderate enteropathy and insulitis in nonobese diabetic-DQ8 mice

Celiac disease (CD) is frequently diagnosed in patients with type 1 diabetes (T1D), and T1D patients can exhibit Abs against tissue transglutaminase, the auto-antigen in CD. Thus, gliadin, the trigger in CD, has been suggested to have a role in T1D pathogenesis. The objective of this study was to investigate whether gliadin contributes to enteropathy and insulitis in NOD-DQ8 mice, an animal model that does not spontaneously develop T1D. Gliadin-sensitized NOD-DQ8 mice developed moderate enteropathy, intraepithelial lymphocytosis, and barrier dysfunction, but not insulitis. Administration of anti-CD25 mAbs before gliadin-sensitization induced partial depletion of CD25+Foxp3+ T cells and led to severe insulitis, but did not exacerbate mucosal dysfunction. CD4+T cells isolated from pancreatic lymph nodes of mice that developed insulitis showed increased proliferation and proinflammatory cytokines after incubation with gliadin but not with BSA. CD4+ T cells isolated from nonsensitized controls did not response to gliadin or BSA. In conclusion, gliadin sensitization induced moderate enteropathy in NOD-DQ8 mice. However, insulitis development required gliadin-sensitization and partial systemic depletion of CD25+Foxp3+ T cells. This humanized murine model provides a mechanistic link to explain how the mucosal intolerance to a dietary protein can lead to insulitis in the presence of partial regulatory T cell deficiency.Facultad de Ciencias Exacta

Sensitization to gliadin induces moderate enteropathy and insulitis in nonobese diabetic-DQ8 mice

Celiac disease (CD) is frequently diagnosed in patients with type 1 diabetes (T1D), and T1D patients can exhibit Abs against tissue transglutaminase, the auto-antigen in CD. Thus, gliadin, the trigger in CD, has been suggested to have a role in T1D pathogenesis. The objective of this study was to investigate whether gliadin contributes to enteropathy and insulitis in NOD-DQ8 mice, an animal model that does not spontaneously develop T1D. Gliadin-sensitized NOD-DQ8 mice developed moderate enteropathy, intraepithelial lymphocytosis, and barrier dysfunction, but not insulitis. Administration of anti-CD25 mAbs before gliadin-sensitization induced partial depletion of CD25+Foxp3+ T cells and led to severe insulitis, but did not exacerbate mucosal dysfunction. CD4+T cells isolated from pancreatic lymph nodes of mice that developed insulitis showed increased proliferation and proinflammatory cytokines after incubation with gliadin but not with BSA. CD4+ T cells isolated from nonsensitized controls did not response to gliadin or BSA. In conclusion, gliadin sensitization induced moderate enteropathy in NOD-DQ8 mice. However, insulitis development required gliadin-sensitization and partial systemic depletion of CD25+Foxp3+ T cells. This humanized murine model provides a mechanistic link to explain how the mucosal intolerance to a dietary protein can lead to insulitis in the presence of partial regulatory T cell deficiency.Facultad de Ciencias Exacta

Concert recording 2013-03-28

[Track 01]. Fanfares liturgiques. Procession du Vendredi-Saint / Henri Tomasi -- [Track 02]. The good soldier Schweik suite. Overture / Robert Kurka -- [Track 03]. The good soldier Schweik suite. Lament / Robert Kurka -- [Track 04]. The good soldier Schweik suite. March / Robert Kurka -- [Track 05]. The good soldier Schweik suite. War Dance / Robert Kurka -- [Track 06]. The good soldier Schweik suite. Pastoral / Robert Kurka -- [Track 07]. The good soldier Schweik suite. Finale / Robert Kurka -- [Track 08]. Serenade no. 11 in E flat major, KV 375. Allegro maestoso / Wolfgang Amadeus Mozart -- [Track 09]. Prelude, fugue and riffs / Leonard Bernstein

Rescuing the Duty to Rescue

Clinicians and health researchers frequently encounter opportunities to rescue people. Rescue cases can generate a moral duty to aid those in peril. As such, bioethicists have leveraged a duty to rescue for a variety of purposes. Yet, despite its broad application, the duty to rescue is under-analyzed. In this paper, we assess the state of theorizing about the duty to rescue. There are large gaps in bioethicists’ understanding of the force, scope, and justification of the two most cited duties to rescue—the individual duty of easy rescue and the institutional rule of rescue. We argue that the duty of easy rescue faces unresolved challenges regarding its force and scope, and the rule of rescue is indefensible. If the duty to rescue is to help solve ethical problems, these theoretical gaps must be addressed. We identify two further conceptions of the duty to rescue that have received less attention—an institutional duty of easy rescue and the professional duty to rescue. Both provide guidance in addressing force and scope concerns and, thereby, traction in answering the outstanding problems with the duty to rescue. We conclude by proposing and propose research priorities for developing accounts of duties to rescue in bioethic

SARS-CoV-2 Variant Tracking and Mitigation During In-Person Learning at a Midwestern University in the 2020-2021 School Year

Importance: The COVID-19 pandemic led many higher education institutions to close campuses during the 2020-2021 academic year. As campuses prepared for a return to in-person education, many institutions were mandating vaccines for students and considering the same for faculty and staff. Objective: To determine the association between vaccination coverage and the levels and spread of SARS-CoV-2, even in the presence of highly-transmissible variants and congregate living, at a midsized university in the US. Design, Setting, and Participants: This case series was conducted at a midsized Midwestern university during the spring 2021 semester. The university developed a saliva-based surveillance program capable of high-throughput SARS-CoV-2 polymerase chain reaction testing and genomic sequencing with the capacity to deliver results in less than 24 hours. On April 7, 2021, the university announced a vaccine requirement for all students for the fall 2021 semester and announced the same requirement for faculty and staff on May 20, 2021. The university hosted an onsite mass vaccination clinic using the 2-dose Pfizer-BioNTech vaccine during April 8 to 15 and April 29 to May 6, 2021. Data were analyzed for 14 894 individuals from the university population who were tested for COVID-19 on campus from January 6 to May 20, 2021. Main Outcomes and Measures: Positive SARS-CoV-2 diagnosis was confirmed by quantitative reverse transcription–polymerase chain reaction of saliva specimens, and variant identity was assessed by quantitative reverse transcription–polymerase chain reaction and next-generation sequencing of viral genomes. Results: Between January 6 and May 20, 2021, the university conducted 196 185 COVID-19 tests for 14 894 individuals and identified 1603 positive cases. Within those positive cases, 950 individuals (59.3%) were male, 644 (40.2%) were female, 1426 (89.0%) were students, and 1265 (78.9%) were aged 17 to 22 years. Among the 1603 positive cases, 687 were identified via polymerase chain reaction of saliva specimens. The Alpha (B.1.1.7) variant constituted 218 of the 446 total positives sequenced (48.9%). By May 20, 2021, 10 068 of 11 091 students (90.8%), 814 of 883 faculty (92.2%), and 2081 of 2890 staff (72.0%) were vaccinated. The 7-day rolling average of positive cases peaked at 37 cases on February 17 but declined to zero by May 14, 2021. The 7-day moving average of positive cases was inversely associated with cumulative vaccination coverage, with a statistically significant Pearson correlation coefficient of −0.57 (95% CI, −0.68 to −0.44). Conclusions and Relevance: This case series study elucidated the association of a robust vaccination program with a statistically significant decrease in positive COVID-19 cases among the study population even in the presence of highly transmissible variants and congregate living

Sensitization to gliadin induces moderate enteropathy and insulitis in nonobese Diabetic-DQ8 mice

Celiac Disease (CD) is frequently diagnosed in patients with type 1 diabetes (T1D), and T1D patients can exhibit antibodies against tissue transglutaminase, the auto-antigen in CD. Thus, gliadin, the trigger in CD, has been suggested to play a role in T1D pathogenesis. The objective of this study was to investigate whether gliadin contributes to enteropathy and insulitis in NOD-DQ8 mice, an animal model that does not spontaneously develop T1D. Gliadin-sensitized NOD-DQ8 mice developed mucosal dysfunction, but no insulitis. Administration of anti-CD25 mAbs before sensitization induced partial depletion of CD25+Foxp3+ T-cells and led to insulitis. Mice that developed insulitis had increased pro-inflammatory cytokines in the mesenteric (MLN) and pancreatic lymph nodes (PLN). CD4+ T-cells isolated from PLN of mice that developed insulitis showed increased proliferation and proinflammatory cytokines after incubations with gliadin but not, with bovine serum albumin (BSA). In control mice, CD4+ T-cells from PLN did not proliferate in response to gliadin. In conclusion, gliadin sensitization induced moderate enteropathy in NOD-DQ8 mice but insulitis development required gliadin-sensitization and partial systemic depletion of CD25+Foxp3+ T-cells. This animal model provides a mechanistic link through which the dietary antigen gliadin, which triggers CD, modulates the onset of insulitis in the presence of partial regulatory T cell deficiency. Both innate and adaptive immune mechanisms related to gluten intolerance can be investigated in NOD-DQ8 mice.Fil: Galipeau, Heather J.. McMaster University Medical Centre; CanadáFil: Rulli, Nestor Ezequiel. Universidad Nacional de La Plata. Facultad de Ciencias Exactas. Departamento de Ciencias Biológicas. Laboratorio de Investigaciones del Sistema Inmune; Argentina. Consejo Nacional de Investigaciones Científicas y Técnicas. Centro Científico Tecnológico Conicet - La Plata; ArgentinaFil: Jury, Jennifer. McMaster University Medical Centre; CanadáFil: Huang, Xianxi. McMaster University Medical Centre; CanadáFil: Araya, Romina Elizabeth. Universidad Nacional de La Plata. Facultad de Ciencias Exactas. Departamento de Ciencias Biológicas. Laboratorio de Investigaciones del Sistema Inmune; Argentina. Consejo Nacional de Investigaciones Científicas y Técnicas. Centro Científico Tecnológico Conicet - La Plata; ArgentinaFil: Murray, Joseph A.. Mayo Clinic Cancer Center; Estados UnidosFil: David, Chella S.. Mayo Clinic Cancer Center; Estados UnidosFil: Chirdo, Fernando Gabriel. Universidad Nacional de La Plata. Facultad de Ciencias Exactas. Departamento de Ciencias Biológicas. Laboratorio de Investigaciones del Sistema Inmune; Argentina. Consejo Nacional de Investigaciones Científicas y Técnicas. Centro Científico Tecnológico Conicet - La Plata; ArgentinaFil: McCoy, Kathy D.. McMaster University Medical Centre; CanadáFil: Verdu, Elena F.. McMaster University Medical Centre; Canad