Relationship Between Nursing and Nurse Practitioner Instructors’ Online Teaching Self-Efficacy and Their Students’ Online Academic Self-Efficacy

AbstractTo meet the high demand for nurses and nurse practitioners (NPs) and address the national shortage of these professionals, nursing and NP schools are rapidly moving courses online. With this trend, and with the COVID-19 pandemic, many universities across the United States have been conducting classes in the online environment. The rapid transition from brick-and-mortar classes to online education has been a challenge for underprepared educators. The purpose of this correlational study was to investigate whether a relationship existed between potentially underprepared instructors’ online teaching self-efficacy and their students’ online academic self-efficacy. Bandura’s self-efficacy theory served as the theoretical framework. The research questions addressed the relationship of the instructors’ online teaching self-efficacy and the number of classes previously taught online, the online academic self-efficacy of students and the number of classes previously taken online, and the instructors’ and students’ respective self-efficacies in the online academic environment. Undergraduate and graduate nursing students (N = 211) and their instructors were recruited from one university. The instructors and students were given an online survey at the beginning of the course; students also completed a survey at the end of the course. Multiple regression was used to analyze the data. The number of classes previously taught predicted R2 = 0.58 of the variance in teachers’ online self-efficacy (β = -0.56, p = .000). The results of this study may contribute to positive social change by providing universities with data that can be used to inform decision making on what is important and not important for instructor and student self-efficacy and for promoting the graduation of more nurses and NPs who can enter the field

CD43-independent augmentation of mouse T-cell function by glycoprotein cleaving enzymes

Previous work has shown that the function of mouse CD4 + T cells can be augmented by an enzyme, O -sialoglycoprotein endopeptidase (OSGE), which cleaves surface CD43, suggesting the idea that the high levels of glycosylated CD43 found on T cells from aged mice may contribute to immune senescence. New results now show that OSGE improves T-cell function even in mice lacking CD43, showing that other glycoproteins must contribute to the OSGE effect on function. Evaluation of other enzymes found two whose ability to stimulate CD4 activation was higher in aged than in young T cells. One of these, PNGase F, is a glycosidase specific for N-linked glycans, and the other, ST-Siase(2,3) from Salmonella typhimurium , is specific for α2,3-linked terminal sialic acid residues. Parallel lectin-binding experiments showed that removal of α2,3-linked sialic acid residues vulnerable to PNGase F and ST-Siase(2,3) was also greater in old than in young T cells. The preferential ability of PNGase F and ST-Siase(2,3) to improve the function of T cells from aged mice may involve cleavage of glycoproteins containing α2,3-linked sialic acid residues on N-linked or O-linked glycans or both.Peer Reviewedhttp://deepblue.lib.umich.edu/bitstream/2027.42/75621/1/j.1365-2567.2006.02419.x.pd

Direct comparison of methionine restriction with leucine restriction on the metabolic health of C57BL/6J mice

EKL was the recipient of a BBSRC postgraduate studentship. This work was funded by Tenovus Scotland project grant to MD and NM (G13/07) and BBSRC DTG. MD is also supported by the British Heart Foundation (PG/09/048/27675, PG/11/8/28703 and PG/14/43/30889) and Diabetes UK (14/0004853). NM is funded by British Heart Foundation (PG/16/90/32518).Peer reviewedPublisher PD

Identification and Validation of Novel Cerebrospinal Fluid Biomarkers for Staging Early Alzheimer's Disease

Ideally, disease modifying therapies for Alzheimer disease (AD) will be applied during the 'preclinical' stage (pathology present with cognition intact) before severe neuronal damage occurs, or upon recognizing very mild cognitive impairment. Developing and judiciously administering such therapies will require biomarker panels to identify early AD pathology, classify disease stage, monitor pathological progression, and predict cognitive decline. To discover such biomarkers, we measured AD-associated changes in the cerebrospinal fluid (CSF) proteome.CSF samples from individuals with mild AD (Clinical Dementia Rating [CDR] 1) (n = 24) and cognitively normal controls (CDR 0) (n = 24) were subjected to two-dimensional difference-in-gel electrophoresis. Within 119 differentially-abundant gel features, mass spectrometry (LC-MS/MS) identified 47 proteins. For validation, eleven proteins were re-evaluated by enzyme-linked immunosorbent assays (ELISA). Six of these assays (NrCAM, YKL-40, chromogranin A, carnosinase I, transthyretin, cystatin C) distinguished CDR 1 and CDR 0 groups and were subsequently applied (with tau, p-tau181 and Aβ42 ELISAs) to a larger independent cohort (n = 292) that included individuals with very mild dementia (CDR 0.5). Receiver-operating characteristic curve analyses using stepwise logistic regression yielded optimal biomarker combinations to distinguish CDR 0 from CDR>0 (tau, YKL-40, NrCAM) and CDR 1 from CDR<1 (tau, chromogranin A, carnosinase I) with areas under the curve of 0.90 (0.85-0.94 95% confidence interval [CI]) and 0.88 (0.81-0.94 CI), respectively.Four novel CSF biomarkers for AD (NrCAM, YKL-40, chromogranin A, carnosinase I) can improve the diagnostic accuracy of Aβ42 and tau. Together, these six markers describe six clinicopathological stages from cognitive normalcy to mild dementia, including stages defined by increased risk of cognitive decline. Such a panel might improve clinical trial efficiency by guiding subject enrollment and monitoring disease progression. Further studies will be required to validate this panel and evaluate its potential for distinguishing AD from other dementing conditions