Accreditation, Affordability, and Accessibility of New Non-Profit Colleges in the United States

Time-series data analysis demonstrates that the number of new colleges has dropped off gradually since its peak in the 1960s, and precipitously after the 1990s. The total number of new colleges is severely depressed, and among new colleges, religious, for-profit, and public colleges have started at a rate of 5x the number of private, secular, and non-profit ones. Interviews with contemporary secular, non-profit college founders and accreditation experts suggest that accreditation is the primary barrier to starting a new college. If we view higher education as an oligopoly or “cold cartel,” it explains the gradually falling quality and precipitously rising costs of higher education in the last seventy years. The economic theory of oligopolies suggests that lowering the barriers to entry for non-profit colleges would be an effective solution for solving the crises of quality, affordability, and accessibility facing higher education. Using the theoretical framework of organized irresponsibility, the researcher develops an explanation for legacy colleges’ and accreditors’ lack of responsibility and leadership, resistance to reform, and allegiance to the degrading status quo. The researcher uncovers three ways to remove the barriers to qualified professionals starting new colleges: 1) accreditor reform, 2) removing private accreditation from their gatekeeper role for federal Title IV funding and promoting state licensing in its place, or 3) founding new accreditors who will accredit new entrants. Findings suggest that the rigor of state licensing has improved over the last 40 years removing the original impetus to have accreditation in the first place

Art Therapy in the Time of COVID-19

We are fighting two invisible enemies: COVID-19 and mental health challenges due to unmitigated stress and trauma as we follow directions to avoid the spread of the virus. To address the mental health challenges, art therapy is offered as a tool to support individuals during periods of isolation. Art therapy is a wonderful self-care activity that can benefit individuals throughout the life span

On the ignorance of group-level effects – The tragedy of personnel evaluation?

In social-dilemma situations (e.g., public-good games), people may pursue their local self- interests, thereby lowering the overall payoff of their group and, paradoxically, even their individual payoffs as a result. Likewise, in inner-individual dilemmas, even without conflict of interest between persons, people may pursue local goals at the expense of overall utility. Our experiments investigate such dissociations of individual and group-level effects in the context of personnel evaluation and selection. Participants were given the role of human resource managers selecting workers to optimize the overall payoff for the company. We investigated contexts where the individually best/worst ‘employees’ systematically caused the worst/best group performance. When workers in a team could substantially increase or decrease co-workers’ performance, most participants (albeit not all) tended to focus solely on individual performance without considering their overall contribution even when instructed to maximize group performance. This undue focus on individual information meant that employees who enhanced team performance the most often received the most negative evaluations. This may result in a ‘tragedy of personnel evaluation’ relevant to maladaptive incentive structures (personnel evaluation), job offers (personnel selection), and a substantially negative impact on organizational effectiveness. At the same time, the results suggest ways this problem may be overcome

A process independent of the anaphase-promoting complex contributes to instability of the yeast S phase cyclin Clb5

Proteolytic destruction of many cyclins is induced by a multi-subunit ubiquitin ligase termed the anaphase promoting complex/ cyclosome (APC/C). In the budding yeast Saccharomyces cerevisiae, the S phase cyclin Clb5 and the mitotic cyclins Clb1-4 are known as substrates of this complex. The relevance of APC/C in proteolysis of Clb5 is still under debate. Importantly, a deletion of the Clb5 destruction box has little influence on cell cycle progression. To understand Clb5 degradation in more detail, we applied in vivo pulse labeling to determine the half-life of Clb5 at different cell cycle stages and in the presence or absence of APC/C activity. Clb5 is significantly unstable, with a half-life of ∼8-10 min, at cell cycle periods when APC/C is inactive and in mutants impaired in APC/C function. A Clb5 version lacking its cyclin destruction box is similarly unstable. The half-life of Clb5 is further decreased in a destruction box-dependent manner to 3-5 min in mitotic or G 1 cells with active APC/C. Clb5 instability is highly dependent on the function of the proteasome. We conclude that Clb5 proteolysis involves two different modes for targeting of Clb5 to the proteasome, an APC/C-dependent and an APC/C-independent mechanism. These different modes apparently have overlapping functions in restricting Clb5 levels in a normal cell cycle, but APC/C function is essential in the presence of abnormally high Clb5 levels. © 2007 by The American Society for Biochemistry and Molecular Biology, Inc

Draft Genome Sequence of the Phenazine-Producing \u3ci\u3ePseudomonas fluorescens\u3c/i\u3e Strain 2-79

Pseudomonas fluorescens strain 2-79, a natural isolate of the rhizosphere of wheat (Triticum aestivum L.), possesses antagonistic potential toward several fungal pathogens. We report the draft genome sequnce of strain 2-79, which comprises 5,674 protein-coding sequences

Zum Sudden Acquired Retinal Degeneration Syndrome (SARDS) beim Hund

The subject of the study was to investigate the aetiology of SARDS. Following an initial literature review, patient data and clinical findings from 39 Patients were collected and analysed. One specific observation was that one third of all patients comprised Dachshunds and that 51.3 % of affected animals were female neutered. The average age of SARDS patients was found to be 8.8 years (range 3 months to 13 years). The ophthalmoscopic appearance of the fundus of SARDS patients was documented at different stages of the disease during serial examinations with the help of fundus photography. This revealed degenerative retinal changes which were found to progress linear following the onset of SARDS, finally resembling dogs with severe generalised progressive retinal degeneration. In the second part of the study, the hypothesis that SARD is an autoimmune disease, was tested with the help of autoantibody screening. In a first step, serum from 24 SARDS patients and 14 normal controls were assessed for autoantibodies to the purified autoantigens S-Antigen and CRALBP with the help of a western blot. No difference in the incidence of autoantibodies could be found between SARDS patients and healthy controls while testing the well known autoantigens S-antigen and CRALBP. In a second step, an attempt was made to identify new autoantigens by testing the entire retinal proteom as an autoantigenic source, again using Western blot techniques. Following the initial detection of a reaction against a specific protein found almost exclusively in SARDS patients, it was possible to identify this protein with the help of mass spectrometry (MALDI/TOF/TOF) as NSE. These findings were verified by the binding of IgG antibodies to purified NSE in 25% of the SARDS patients and 0% of the normal control dogs. The results of this study suggest that an autoimmune aetiology of SARDS involving autoantibodies against NSE is possible. However, it is unclear whether these play a causative role in SARDS or whether they are the result of retinal destruction by another mechanism. Further investigations into a possible autoimmune aetiology of SARDS are therefore indicated and the role of NSE as an autoantigen must be further assessed

Zum Sudden Acquired Retinal Degeneration Syndrome (SARDS) beim Hund

The subject of the study was to investigate the aetiology of SARDS. Following an initial literature review, patient data and clinical findings from 39 Patients were collected and analysed. One specific observation was that one third of all patients comprised Dachshunds and that 51.3 % of affected animals were female neutered. The average age of SARDS patients was found to be 8.8 years (range 3 months to 13 years). The ophthalmoscopic appearance of the fundus of SARDS patients was documented at different stages of the disease during serial examinations with the help of fundus photography. This revealed degenerative retinal changes which were found to progress linear following the onset of SARDS, finally resembling dogs with severe generalised progressive retinal degeneration. In the second part of the study, the hypothesis that SARD is an autoimmune disease, was tested with the help of autoantibody screening. In a first step, serum from 24 SARDS patients and 14 normal controls were assessed for autoantibodies to the purified autoantigens S-Antigen and CRALBP with the help of a western blot. No difference in the incidence of autoantibodies could be found between SARDS patients and healthy controls while testing the well known autoantigens S-antigen and CRALBP. In a second step, an attempt was made to identify new autoantigens by testing the entire retinal proteom as an autoantigenic source, again using Western blot techniques. Following the initial detection of a reaction against a specific protein found almost exclusively in SARDS patients, it was possible to identify this protein with the help of mass spectrometry (MALDI/TOF/TOF) as NSE. These findings were verified by the binding of IgG antibodies to purified NSE in 25% of the SARDS patients and 0% of the normal control dogs. The results of this study suggest that an autoimmune aetiology of SARDS involving autoantibodies against NSE is possible. However, it is unclear whether these play a causative role in SARDS or whether they are the result of retinal destruction by another mechanism. Further investigations into a possible autoimmune aetiology of SARDS are therefore indicated and the role of NSE as an autoantigen must be further assessed