The Reason(s) Small, Private Schools Start Football Programs

The number of college football programs in the United States currently totals 774, which is an all-time high. It’s clear there is a demand for football as there are 128 schools in 10 conferences at the highest level FBS and 125 schools participating at the second highest level, FCS. Both of these subdivisions are required to provide scholarships for players, making these two levels the most expensive for universities to offer (NCAA.com, ND). There are a number of reasons that schools establish and fund football programs. At the highest level, there is a lot of money through media rights and merchandising. Many of these larger programs also have high attendance at their games, which is another source of revenue. Football, at most levels, means exposure for the schools. And football, for many, is part of a culture and just plain fun. All of these reasons seem important functions of a university, especially at the highest levels. But what’s in it for smaller universities and colleges that won’t see a windfall from media rights, merchandising and attendance? This paper examines the reasons students and alumni gave to why they wanted to see football established at Mercer University. The findings of this study are beneficial to any small university that is considering founding a football program on its campus. First, students clearly expect a level of enjoyment out of going to the game. While the negative relationship between expected enjoyment and donation may seem surprising, the finding can be easily supported by literature. It is clear that individuals would find going to the game enjoyable but only those who truly consider potential development of a football program to be important to the university as a whole would actually go beyond the consumption by donating money to the program and the school. Only small effect of football fan identity on consumption is surprising from theoretical perspective

Birth prevalence of anorectal malformations in England and 5-year survival: a national birth cohort study

OBJECTIVE: To determine the birth prevalence, maternal risk factors and 5-year survival for isolated and complex anorectal malformations. DESIGN: National birth cohort using hospital admission data and death records. SETTING: All National Health Service England hospitals. PATIENTS: Live-born singletons delivered from 2002 through 2018, with evidence in the first year of life of a diagnosis of an anorectal malformation and repair during a hospital admission, or anorectal malformation recorded on the death certificate. Cases were further classified as isolated or complex depending on the presence of additional anomalies. MAIN OUTCOME MEASURES: Birth prevalence of anorectal malformations per 10 000 live births, risk ratios for isolated and complex anorectal malformation by maternal, infant and birth characteristics, and 5-year survival. RESULTS: We identified 3325 infants with anorectal malformations among 9 474 147 live-born singletons; 61.7% (n=2050) of cases were complex. Birth prevalence was 3.5 per 10 000 live births (95% CI 3.4 to 3.6). Complex anorectal malformations were associated with maternal age extremes after accounting for other sociodemographic factors. Compared with maternal ages 25-34 years, the risk of complex anorectal malformations was 31% higher for ≥35 years (95% CI 17 to 48) and 13% higher for ≤24 years (95% CI 0 to 27). Among 2376 anorectal malformation cases (n=1450 complex) born from 2002 through 2014, 5-year survival was lower for complex (86.9%; 95% CI 85.1% to 88.5%) than isolated anorectal malformations (98.2%; 95% CI 97.1% to 98.9%). Preterm infants with complex anorectal malformations had the lowest survival (73.4%; 95% CI 68.1% to 78.0%). CONCLUSIONS: Differences in maternal risk factors for isolated and complex anorectal malformations may reflect different underlying mechanisms for occurrence. Five-year survival is high but lowest for preterm children with complex anorectal malformations

Mesoscopic persistent currents in a strong magnetic field

Recent precision measurements of mesoscopic persistent currents in normal-metal rings rely on the interaction between the magnetic moment generated by the current and a large applied magnetic field. Motivated by this technique, we extend the theory of mesoscopic persistent currents to include the effect of the finite thickness of the ring and the resulting penetration of the large magnetic field. We discuss both the sample-specific typical current and the ensemble-averaged current which is dominated by the effects of electron-electron interactions. We find that the magnetic field strongly suppresses the interaction-induced persistent current and so provides direct access to the independent-electron contribution. Moreover, the technique allows for measurements of the entire distribution function of the persistent current. We also discuss the consequences of the Zeeman splitting and spin-orbit scattering, and include a detailed and quantitative comparison of our theoretical results to experimental data.Comment: 12 pages, 7 figure

The administration of chitosan-tripolyphosphate-DNA nanoparticles to express exogenous SREBP1a enhances conversion of dietary carbohydrates into lipids in the liver of Sparus aurata

In addition to being essential for the transcription of genes involved in cellular lipogenesis, increasing evidence associates sterol regulatory element binding proteins (SREBPs) with the transcriptional control of carbohydrate metabolism. The aim of this study was to assess the effect of overexpression SREBP1a, a potent activator of all SREBP-responsive genes, on the intermediary metabolism of Sparus aurata, a glucose-intolerant carnivorous fish. Administration of chitosan-tripolyphosphate nanoparticles complexed with a plasmid driving expression of the N-terminal transactivation domain of SREBP1a significantly increased SREBP1a mRNA and protein in the liver of S. aurata. Overexpression of SREBP1a enhanced the hepatic expression of key genes in glycolysis-gluconeogenesis (glucokinase and 6-phosphofructo-2-kinase/fructose-2,6-bisphosphatase), fatty acid synthesis (acetyl-CoA carboxylase 1 and acetyl-CoA carboxylase 2), elongation (elongation of very long chain fatty acids protein 5) and desaturation (fatty acid desaturase 2) as well as reduced nicotinamide adenine dinucleotide phosphate production (glucose-6-phosphate 1-dehydrogenase) and cholesterol synthesis (3-hydroxy-3-methylglutaryl-coenzyme A reductase), leading to increased blood triglycerides and cholesterol levels. Beyond reporting the first study addressing in vivo effects of exogenous SREBP1a in a glucose-intolerant model, our findings support that SREBP1a overexpression caused multigenic effects that favoured hepatic glycolysis and lipogenesis and thus enabled protein sparing by improving dietary carbohydrate conversion into fatty acids and cholesterolPeer ReviewedPostprint (published version

Metformin counteracts glucose-dependent lipogenesis and impairs transdeamination in the liver of gilthead sea bream (Sparus aurata)

Metformin is an anti-diabetic drug with a major impact on regulating blood glucose levels by decreasing hepatic gluconeogenesis but also affecting other pathways, including glucose transport and energy/lipid metabolism. Carnivorous fish are considered glucose intolerant, as they exhibit poor ability to using dietary carbohydrates. To increase the current knowledge about the molecular mechanisms by which metformin can improve glucose homeostasis in carnivorous fish, we addressed the effect of intraperitoneal administration of metformin, in the presence or absence of a glucose load, on metabolic rate-limiting enzymes and lipogenic factors in the liver of gilthead sea bream (Sparus aurata). Hyperglycemia markedly up-regulated the expression of glycolytic enzymes (glucokinase and 6-phosphofructo-1-kinase, PFK1) 5 h following glucose administration, while at 24 h post-treatment it increased isocitrate dehydrogenase (IDH) activity, a key enzyme of the tricarboxylic acid cycle, and the expression of lipogenic factors (PGC1b, Lpin1 and SREBP1). Metformin counteracted glucose-dependent effects, and down-regulated glutamate dehydrogenase, alanine aminotransferase and mTOR 5 h post-treatment in the absence of a glucose load, leading to decreased long-term activity of PFK1 and IDH. The results of the present study suggest that hyperglycemia enhances lipogenesis in the liver of S. aurata, and that metformin may exert specific metabolic effects in fish by decreasing hepatic transdeamination and supressing the use of amino acids as gluconeogenic substrates. Our findings highlight the role of amino acid metabolism in the glucose-intolerant carnivorous fish model. KEYWORDS: Glutamate dehydrogenase; Lipogenesis; Liver; Metformin; Sparus aurat

Fischer indole reaction in batch and flow employing a sulfonic acid resin: synthesis of pyrido[2,3-a]carbazoles

An Amberlite IR 120 H-promoted one-pot Fischer indolization from a cis-decahydroquinoline using a range of phenylhydrazines led to compounds with the pyrido[2,3-a]carbazole scaffold. The process may be conducted either in batch mode or in a continuous manner in a flow reactor. The stereochemical course of the Fischer indole reaction changed in going from using free phenylhydrazine to the corresponding hydrochloride in batch conditions, whereas, with the short reaction times in continuous flow, no changes due to isomerization processes were observed. Keywords: Fischer indole synthesis, one-pot synthesis, continuous-flow synthesis, sulfonic acid resin, immobilized reagents, pyrido[2,3-a]carbazole

Response to First Course of Intensified Immunosuppression in Genetically-Stratified Steroid Resistant Nephrotic Syndrome

BACKGROUND AND OBJECTIVES: Intensified immunosuppression in steroid-resistant nephrotic syndrome is broadly applied, with disparate outcomes. This review of patients from the United Kingdom National Study of Nephrotic Syndrome cohort aimed to improve disease stratification by determining, in comprehensively genetically screened patients with steroid-resistant nephrotic syndrome, if there is an association between response to initial intensified immunosuppression and disease progression and/or post-transplant recurrence. DESIGN, SETTING, PARTICIPANTS, & MEASUREMENTS: Pediatric patients with steroid-resistant nephrotic syndrome were recruited via the UK National Registry of Rare Kidney Diseases. All patients were whole-genome sequenced, whole-exome sequenced, or steroid-resistant nephrotic syndrome gene-panel sequenced. Complete response or partial response within 6 months of starting intensified immunosuppression was ascertained using laboratory data. Response to intensified immunosuppression and outcomes were analyzed according to genetic testing results, pattern of steroid resistance, and first biopsy findings. RESULTS: Of 271 patients, 178 (92 males, median onset age 4.7 years) received intensified immunosuppression with response available. A total of 4% of patients with monogenic disease showed complete response, compared with 25% of genetic-testing-negative patients (P=0.02). None of the former recurred post-transplantation. In genetic-testing-negative patients, 97% with complete response to first intensified immunosuppression did not progress, whereas 44% of nonresponders developed kidney failure with 73% recurrence post-transplant. Secondary steroid resistance had a higher complete response rate than primary/presumed resistance (43% versus 23%; P=0.001). The highest complete response rate in secondary steroid resistance was to rituximab (64%). Biopsy results showed no correlation with intensified immunosuppression response or outcome. CONCLUSIONS: Patients with monogenic steroid-resistant nephrotic syndrome had a poor therapeutic response and no post-transplant recurrence. In genetic-testing-negative patients, there was an association between response to first intensified immunosuppression and long-term outcome. Patients with complete response rarely progressed to kidney failure, whereas nonresponders had poor kidney survival and a high post-transplant recurrence rate. Patients with secondary steroid resistance were more likely to respond, particularly to rituximab

Gene markers of dietary macronutrient composition and growth in the skeletal muscle of gilthead sea bream (Sparus aurata)

To increase our current knowledge on the nutritional regulation of growth and gene expression pattern in fish skeletal muscle, the effect of dietary macronutrient composition was assessed on digestibility, nutrient retention, growth performance, and the mRNA levels of key genes involved in functionality, growth and development of the skeletal muscle in gilthead sea bream (Sparus aurata). Long-term starvation decreased the expression of myogenic regulatory factors such as Myod2, Myf5, myogenin (Myog) and Myf6 in the skeletal muscle of S. aurata. The supply of high or medium protein, low carbohydrate diets enhanced growth parameters, feed efficiency ratio, feed conversion ratio and significantly upregulated myod2. However, the supply of low protein, high carbohydrate diets restricted growth and stimulated the mRNA levels of myostatin, while downregulated follistatin (fst), igf1, mtor and rps6. Microarray analysis revealed igfals, tnni2, and gadd45a as gene markers upregulated by diets enriched with protein, lipids and carbohydrates, respectively. The results of the present study show that in addition to myod2, fst, igf1, mtor and rps6, the expression levels of igfals, tnni2 and remarkably gadd45a in the skeletal muscle can be used as markers to evaluate the effect of dietary macronutrient changes on fish growth and muscle development in S. aurata

Towards Becoming an Ecology of Care

Thinking about care in the organization of an ecology is central to the interdisciplinary research group Care Ecologies; found during a lockdown in the spring of 2021 and hosted by ARIAS Platform for Research Through the Arts and Sciences in Amsterdam. In Towards Becoming an Ecology of Care group members Valentina Curandi, Inte Gloerich, Ania Molenda, Maaike Muntinga, Natalia Sanchez Querubin, Nienke Scholts and Marloeke van der Vlugt, offer an initial articulation on their approaches and principles – performative practices, reflection, speculations - of what an ecology of care could be. While each bringing in different understandings of care, staying with those differences shaped the ways in which the agenda of the research group has been (un)settled. To exchange knowledge and experiences, the group uses various on- and off-line frameworks, like presentations and practice sessions. Exploring how activities that sustain a research group – coordinating, meeting, writing and documenting – may be done with care, this paper attempts to present a speculative proposition for functioning as a research ecology on and around care. Bringing into focus what care can do, while being attentive to what is neglected. This is not only done in writing but also becomes visible in the accompanying images compiled of material and immaterial memories. It is an ongoing process, for which the writing of this paper became a catalyst for reflection. While not aiming for clear answers the authors invite themselves and others to become more aware, devising and testing work strategies for care-based practices