Westland/Hallmark: 2008 Beef Recall; A Case Study by The Food Industry Center

A Humane Society video, made secretly at the Westland/Hallmark plant in late 2007 and released in early 2008, led to the recall of 143 million pounds of beef. This case study illustrates the complexity of the food industry and the food recall process. Although ultimately, the incident had more to do with animal welfare than food safety — no sicknesses were tied to the recalled beef, it resulted in changes to the nation’s food safety procedures. The 2008 Westland/Hallmark beef recall, the largest beef recall in U.S. history, is a stepping-off point to examine the beef supply chain generally and the ground beef supply chain specifically.Agribusiness, Food Consumption/Nutrition/Food Safety, Livestock Production/Industries,

National Memorial for the First Twenty

The Trans Atlantic Slave Trade was responsible for the enslavement and displacement of many Africans of different ages, genders, and cultures. The memorial presents the diversity in a line of African men, women, and children trudging down a pier in chains, the last figure looking back across the ocean to Africa’s western coast. The Port of Hampton Roads in Chesapeake, Virginia is the location in which the first enslaved Africans arrived in North America in 1619. Only about 20 of the 60 Africans survived the voyage and departed.https://csuepress.columbusstate.edu/historyfrombelow/1008/thumbnail.jp

Detecting short-term change and variation in health-related quality of life: within- and between-person factor structure of the SF-36 health survey.

BackgroundA major goal of much aging-related research and geriatric medicine is to identify early changes in health and functioning before serious limitations develop. To this end, regular collection of patient-reported outcome measure (PROMs) in a clinical setting may be useful to identify and monitor these changes. However, existing PROMs were not designed for repeated administration and are more commonly used as one-time screening tools; as such, their ability to detect variation and measurement properties when administered repeatedly remain unknown. In this study we evaluated the potential of the RAND SF-36 Health Survey as a repeated-use PROM by examining its measurement properties when modified for administration over multiple occasions.MethodsTo distinguish between-person (i.e., average) from within-person (i.e., occasion) levels, the SF-36 Health Survey was completed by a sample of older adults (N = 122, M age  = 66.28 years) daily for seven consecutive days. Multilevel confirmatory factor analysis (CFA) was employed to investigate the factor structure at both levels for two- and eight-factor solutions.ResultsMultilevel CFA models revealed that the correlated eight-factor solution provided better model fit than the two-factor solution at both the between-person and within-person levels. Overall model fit for the SF-36 Health Survey administered daily was not substantially different from standard survey administration, though both were below optimal levels as reported in the literature. However, individual subscales did demonstrate good reliability.ConclusionsMany of the subscales of the modified SF-36 for repeated daily assessment were found to be sufficiently reliable for use in repeated measurement designs incorporating PROMs, though the overall scale may not be optimal. We encourage future work to investigate the utility of the subscales in specific contexts, as well as the measurement properties of other existing PROMs when administered in a repeated measures design. The development and integration of new measures for this purpose may ultimately be necessary

Growing old and being old: Emotional well-being across adulthood.

The present study examines change in reports of daily, weekly, and monthly psychological distress over 20 years, and of negative and positive affect over 10 years, using data from the Midlife in the United States study. The study includes three waves of data collection on adults ranging from 22 to 95 years old. Cross-sectional findings reveal that older age is related to lower levels of psychological distress and negative affect and to higher levels of positive affect across each successive age group. Yet, longitudinal findings vary across younger, middle-aged, and older adults. Psychological distress decreases over time among younger adults (although only until age 33 for weekly reports), remains stable in midlife, and is stable (monthly) or slightly increases (daily and weekly) among older adults. For negative affect, levels decrease over time for younger and middle-aged adults, and only increase for the oldest adults for daily and monthly affect. Positive affect is stable over time among younger adults, but decreases in midlife starting in the mid-fifties. In conclusion, overall patterns of findings suggest that being old (assessed cross-sectionally) is related to higher levels of emotional well-being. Growing old (assessed longitudinally) is related to improvements in emotional well-being across younger and early middle adulthood, which mirrors cross-sectional findings. There is relative stability in later midlife, however, and continued stability or slight declines across older age. (PsycInfo Database Record (c) 2023 APA, all rights reserved)

Mind the Gap:New types of innovation habitats to help startups grow and scale faster: The Digital Catapult Centres in UK

This developmental paper makes an analogy with the much known British expression “Mind the Gap”, considering innovation habitats as instruments that can mitigate the gaps in the system and catalyse the innovation process, especially the relationships among startups and other actors in the system. These habitats represent a new form of innovation support, distinct from established instruments like technology parks and incubators, operating at a lower level of investment with activities that are typically co-produced with their participants. In the literature, and in empirical studies, we may find a range of innovation habitats, with their own remits and definitions. This paper begins with an exploration of such issues, focusing on an innovative policy initiative supported by Innovate UK (formerly UK Technology Strategy Board): the Digital Catapult Centres. The overall research objective is to understand the critical factors behind the implementation and operation of these Centres. The research also aims to obtain a better understanding of public policies to support them and the results generated by such Centres

Whole genome expression analysis within the angiotensin II-apolipoprotein E deficient mouse model of abdominal aortic aneurysm

Abstract\ud Background: An animal model commonly used to investigate pathways and potential therapeutic\ud interventions relevant to abdominal aortic aneurysm (AAA) involves subcutaneous infusion of\ud angiotensin II within the apolipoprotein E deficient mouse. The aim of this study was to investigate\ud genes differentially expressed in aneurysms forming within this mouse model in order to assess the\ud relevance of this model to human AAA.\ud Results: Using microarrays we identified genes relevant to aneurysm formation within\ud apolipoprotein E deficient mice. Firstly we investigated genes differentially expressed in the\ud aneurysm prone segment of the suprarenal aorta in these mice. Secondly we investigated genes that\ud were differentially expressed in the aortas of mice developing aneurysms relative to those that did\ud not develop aneurysms in response to angiotensin II infusion. Our findings suggest that a host of\ud inflammation and extracellular matrix remodelling pathways are upregulated within the aorta in\ud mice developing aneurysms. Kyoto Encyclopedia of Genes and Genome categories enriched in the\ud aortas of mice with aneurysms included cytokine-cytokine receptor interaction, leukocyte\ud transendothelial migration, natural killer cell mediated cytotoxicity and hematopoietic cell lineage.\ud Genes associated with extracellular matrix remodelling, such as a range of matrix\ud metalloproteinases were also differentially expressed in relation to aneurysm formation.\ud Conclusion: This study is the first report describing whole genome expression arrays in the\ud apolipoprotein E deficient mice in relation to aneurysm formation. The findings suggest that the\ud pathways believed to be critical in human AAA are also relevant to aneurysm formation in this\ud mouse model. The findings therefore support the value of this model to investigate interventions\ud and mechanisms of human AAA

Urocortin 2 inhibits human aortic smooth muscle cell proliferation via corticotrophin releasing hormone receptor-2 in abdominal aortic aneurysm

Introduction: A key feature of abdominal aortic aneurysm is the loss of proliferation and paucity of vascular smooth muscle cells, the major cells within the aortic tunica media. It has been suggested that urocortin 2 (UCN2), a selective ligand for corticotrophin releasing factor receptor 2 (CRFR2) may play a beneficial role in various cardiovascular diseases. However, the role of this peptide in abdominal aortic aneurysm has not been studied in detail. Here we assessed the hypothesis that urocortin 2 promotes an aneurysm phenotype in human aortic smooth muscles in vitro via CRFR2. Experimental Procedure: We assessed the release of UCN2 from explants of human tissue biopsies in vitro (Aortic aneurysm thrombus, n = 14; aortic aneurysm body, n = 11; femoral atheroma control, n = 6) using ELISA. We investigated the effect of incubating human aortic smooth muscle cells with recombinant UCN2 or aneurysm thrombus explants secretions at a UCN2 dose of 0, 10 and 100 nM for 24 and 48 hours (n = 6 per group x 3 experiments). Cell proliferation was determined by the alamarBlue® cell viability reagent. Results were analyzed and presented as mean ± SEM relative to the control. We also investigated the impact of blocking CRFR2 on UCN2 induced changes on these cells. Results: Secretion of UCN2 was significantly higher from aneurysm thrombus (n = 14, p = 0.0020) and aneurysm body (n = 11, p = 0.0104) compared to femoral atheroma. Human aortic smooth muscle cells proliferation was dose dependently inhibited by recombinant UCN2 (p = 0.0172) and aortic aneurysm thrombus conditioned medium (p = 0.0273) after 24 hours. This effect of recombinant UCN2 was abrogated significantly by prior incubation with the CRFR2 blocker Astressin-2B (p = 0.0043). Similar effects were seen on incubating cells for 48 hours. Conclusion: UCN2 is released in high concentrations by aortic aneurysm thrombus. UCN2 inhibits aortic vascular smooth muscle cell proliferation in vitro via CRFR2. This effect may be relevant to the pathogenesis of abdominal aortic aneurysm

Urocortin 2 inhibits human aortic smooth muscle cell proliferation via corticotrophin releasing hormone receptor-2 in abdominal aortic aneurysm

Introduction: A key feature of abdominal aortic aneurysm is the loss of proliferation and paucity of vascular smooth muscle cells, the major cells within the aortic tunica media. It has been suggested that urocortin 2 (UCN2), a selective ligand for corticotrophin releasing factor receptor 2 (CRFR2) may play a beneficial role in various cardiovascular diseases. However, the role of this peptide in abdominal aortic aneurysm has not been studied in detail. Here we assessed the hypothesis that urocortin 2 promotes an aneurysm phenotype in human aortic smooth muscles in vitro via CRFR2. Experimental Procedure: We assessed the release of UCN2 from explants of human tissue biopsies in vitro (Aortic aneurysm thrombus, n = 14; aortic aneurysm body, n = 11; femoral atheroma control, n = 6) using ELISA. We investigated the effect of incubating human aortic smooth muscle cells with recombinant UCN2 or aneurysm thrombus explants secretions at a UCN2 dose of 0, 10 and 100 nM for 24 and 48 hours (n = 6 per group x 3 experiments). Cell proliferation was determined by the alamarBlue® cell viability reagent. Results were analyzed and presented as mean ± SEM relative to the control. We also investigated the impact of blocking CRFR2 on UCN2 induced changes on these cells. Results: Secretion of UCN2 was significantly higher from aneurysm thrombus (n = 14, p = 0.0020) and aneurysm body (n = 11, p = 0.0104) compared to femoral atheroma. Human aortic smooth muscle cells proliferation was dose dependently inhibited by recombinant UCN2 (p = 0.0172) and aortic aneurysm thrombus conditioned medium (p = 0.0273) after 24 hours. This effect of recombinant UCN2 was abrogated significantly by prior incubation with the CRFR2 blocker Astressin-2B (p = 0.0043). Similar effects were seen on incubating cells for 48 hours. Conclusion: UCN2 is released in high concentrations by aortic aneurysm thrombus. UCN2 inhibits aortic vascular smooth muscle cell proliferation in vitro via CRFR2. This effect may be relevant to the pathogenesis of abdominal aortic aneurysm

Angiopoietin-2 attenuates angiotensin II-induced aortic aneurysm and atherosclerosis in apolipoprotein E-deficient mice

Angiogenesis and inflammation are implicated in aortic aneurysm and atherosclerosis and regulated by angiopoietin-2 (Angpt2). The effect of Angpt2 administration on experimental aortic aneurysm and atherosclerosis was examined. Six-month-old male apolipoprotein E deficient (ApoE⁻/⁻) mice were infused with angiotensin II (AngII) and administered subcutaneous human Fc-protein (control) or recombinant Angpt2 (rAngpt2) over 14 days. Administration of rAngpt2 significantly inhibited AngII-induced aortic dilatation and rupture of the suprarenal aorta (SRA), and development of atherosclerosis within the aortic arch. These effects were blood pressure and plasma lipoprotein independent and associated with Tie2 activation and down-regulation of monocyte chemotactic protein-1 (MCP-1) within the SRA. Plasma concentrations of MCP-1 and interleukin-6 were significantly lower in mice receiving rAngpt2. Immunostaining for the monocyte/macrophage marker MOMA-2 and the angiogenesis marker CD31 within the SRA were less in mice receiving rAngpt2 than controls. The percentage of inflammatory (Ly6Cʰⁱ) monocytes within the bone marrow was increased while that in peripheral blood was decreased by rAngpt2 administration. In conclusion, administration of rAngpt2 attenuated angiotensin II-induced aortic aneurysm and atherosclerosis in ApoE⁻/⁻ mice associated with reduced aortic inflammation and angiogenesis. Up-regulation of Angpt2 may have potential therapeutic value in patients with aortic aneurysm and atherosclerosis

Filanesib plus bortezomib and dexamethasone in relapsed/refractory t(11;14) and 1q21 gain multiple myeloma.

Filanesib is a first-in-class kinesin spindle protein inhibitor which demonstrated safety and encouraging activity in combination with bortezomib and dexamethasone in relapsed/refractory multiple myeloma in a preliminary analysis of dose-escalation phase results. This multicenter study included first a dose-escalation phase to determine maximum tolerated dose of two schedules of filanesib, bortezomib, and dexamethasone and a subsequent dose-expansion phase using the maximum tolerated doses. In the dose-expansion phase, 28 patients were evaluable for safety and efficacy. The most common grade ≥3 adverse events were neutropenia (21%) and anemia (18%), which were noncumulative and reversible, and hypertension (18%). The overall response rate was 43% with median duration of response not yet reached (range, 2.8-23.7+ months) with median follow-up of 6.3 months. A post hoc analysis incorporated 29 dose-escalation phase patients who received therapeutic filanesib doses, with an overall response rate of 39% and median duration of response of 18.0 months among the 57 total patients with median progression-free survival of 8.5 months. Notably, the PFS of high risk patients was comparable at 8.5 months, driven by the patients with 1q21 gain, characterized by increased MCL-1 expression, with a PFS of 9.1 months versus 3.5 months for the remainder of high risk patients. Patients with t(11;14) also had an encouraging PFS of 15.0 months. The combination of filanesib, bortezomib, and dexamethasone continues to show safety and encouraging activity in relapsed/refractory multiple myeloma, particularly in those patients with 1q21 gain and t(11;14)