A New Pathway to University Retention? Identity Fusion With University Predicts Retention Independently of Grades.
Ontology highlight
ABSTRACT:
SUBMITTER: Talaifar S
PROVIDER: S-EPMC8009486 | biostudies-literature |
REPOSITORIES: biostudies-literature
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Project description:Math anxiety is widely considered a potential barrier to success in STEM. Current thinking holds that math anxiety is directly linked to avoidance of and underperformance in STEM domains. However, past evidence supporting these claims is limited in important ways. Perhaps most crucially, it is possible that math anxiety predicts STEM outcomes merely as a proxy for poor math skills. Here, we tested the link between math anxiety and subsequent STEM outcomes by measuring math anxiety, math ability, and several covariates in 183 first-semester university students. We then tracked students' STEM avoidance and achievement through four years at university via official academic transcripts. Results showed that math anxiety predicted both a reduction in how many STEM courses students took and, separately (i.e., controlling for one another), lower STEM grades. Crucially, these associations held after controlling for math ability (and other covariates). That math anxiety predicts math-related academic achievement independently of Math Ability suggests that, contrary to current thinking, math anxiety's effects on academic performance likely operate via mechanisms other than negatively affecting math ability. Beyond this, we show evidence that math anxiety can account for associations between math ability and STEM outcomes, suggesting that past links between math ability and real-world outcomes may, in fact, be at least partially explainable by attitudes toward math. These findings provide clear impetus for developing and testing interventions that target math anxiety specifically and suggest that focusing on math ability without additional attention to math anxiety may fail to optimally boost STEM outcomes.
| S-EPMC8203776 | biostudies-literature
Project description:BackgroundObesity, typically quantified in terms of Body Mass Index (BMI) exceeding threshold values, is considered a leading cause of premature death worldwide. For given body size (BMI), it is recognized that risk is also affected by body shape, particularly as a marker of abdominal fat deposits. Waist circumference (WC) is used as a risk indicator supplementary to BMI, but the high correlation of WC with BMI makes it hard to isolate the added value of WC.Methods and findingsWe considered a USA population sample of 14,105 non-pregnant adults (age ≥ 18) from the National Health and Nutrition Examination Survey (NHANES) 1999-2004 with follow-up for mortality averaging 5 yr (828 deaths). We developed A Body Shape Index (ABSI) based on WC adjusted for height and weight: ABSI ≡ WC/(BMI(2/3)height(1/2)). ABSI had little correlation with height, weight, or BMI. Death rates increased approximately exponentially with above average baseline ABSI (overall regression coefficient of +33% per standard deviation of ABSI [95% confidence interval: +20%-+48%), whereas elevated death rates were found for both high and low values of BMI and WC. 22% (8%-41%) of the population mortality hazard was attributable to high ABSI, compared to 15% (3%-30%) for BMI and 15% (4%-29%) for WC. The association of death rate with ABSI held even when adjusted for other known risk factors including smoking, diabetes, blood pressure, and serum cholesterol. ABSI correlation with mortality hazard held across the range of age, sex, and BMI, and for both white and black ethnicities (but not for Mexican ethnicity), and was not weakened by excluding deaths from the first 3 yr of follow-up.ConclusionsBody shape, as measured by ABSI, appears to be a substantial risk factor for premature mortality in the general population derivable from basic clinical measurements. ABSI expresses the excess risk from high WC in a convenient form that is complementary to BMI and to other known risk factors.
| S-EPMC3399847 | biostudies-literature
Project description:IntroductionThe management of spinal neoplasia consists of surgical, radiation, and systemic options. Little data exist to guide management based on overall health status, which is particularly challenging when patients who could benefit from surgery may be too frail for it. This study's objective was to evaluate the 5-Item Modified Frailty Index (mFI-5) as a predictor of 30-day morbidity in patients undergoing instrumented resection for metastatic extradural spinal tumors.MethodsAdults undergoing extradural tumor resection from the 2011 to 2019 National Surgical Quality Improvement Program datasets were identified by Current Procedural Terminology codes 63275-63278 with an adjunct instrumentation code (22840-22843). Patients were classified into frailty levels 0, 1, or 2+ based on mFI-5 scores of 0, 1, or 2-5, respectively. The primary outcome was morbidity. Secondary outcomes were readmission and reoperation. Multivariate modeling was utilized to analyze mFI-5 as a predictor of outcomes. The Akaike information criterion (AIC) was used to compare relative-model-fit based on frailty versus individual comorbidity variables to determine the optimal model. Chi-squared and Fisher's exact tests were used to establish significance between individual complications and frailty.ResultsThere were 874 patients. Readmission, reoperation, and morbidity rates were 19.5%, 5.0%, 52.3%, respectively. In multivariate analyses, mFI-5=1 (OR: 1.45, SE: 0.31, p=0.036), mFI-5=2+ (OR: 1.41, SE: 0.40, p=0.036), operative time (OR: 1.18, SE: 0.03, p≤0.001), and chronic steroid use (OR: 1.56, SE: 0.42, p=0.037) independently predicted morbidity. Elective surgery (OR: 0.61) was protective. Frailty did not predict readmission or reoperation. Frailty was found to be significantly associated with respiratory complications, urinary tract infections, cardiac events, and sepsis/septic shock specifically.ConclusionsmFI-5=1 independently predicted 45% increased odds of morbidity. mFI-5=2+ independently predicted 41% increased odds of morbidity. Further, every 30 additional minutes of operative time predicted 18% increased odds of morbidity, suggesting an increased risk of site-related complication events. Taken together, the mFI-5 serves as a valid predictor of morbidity in patients with extradural tumor undergoing instrumented excision.
| S-EPMC9931415 | biostudies-literature
Project description:The most frequent genetic alteration identified in pediatric pilocytic astrocytomas and pilomyxoid variant is the KIAA1549-BRAF fusion, which typically results from a 2.0 Mb tandem duplication in chromosome band 7q34. Less frequent abnormalities include fusion genes,BRAF, FGFR, KRAS, and NF1 point mutations, and whole chromosome gains. To correlate genetic alterations with clinical course data, we retrospectively analyzed the tumors with pilocytic and pilomyxoid histology of a cohort of 116 pediatric patients, aged 5 months to 23 years. Gross total resection was associated with a decreased risk of recurrence (p = 0.001), supporting previous findings that complete tumor excision correlates with long-term and disease-free survival. We found no significant association between recurrence rate and the presence of the KIAA1549-BRAF fusion or BRAF mutation (p = 0.167). Interestingly, gain of whole chromosome 7 (WC7) was associated with a 4.7-fold increased risk of tumor recurrence, even after adjusting for surgical status (p = 0.025), and other genetic alterations. Using fluorescence in situ hybridization, we demonstrated that when WC7 gain accompanies the KIAA1549-BRAF fusion, the fusion likely arises first. This study highlights the utility of genetic studies for risk assessment of pilocytic and pilomyxoid astrocytomas, which may impact treatment selections.
| S-EPMC5009478 | biostudies-literature
Project description:ObjectiveTo explore university students' experience of retention and identify potential barriers and facilitators to long-term adherence.DesignCross-sectional qualitative study using virtual focus groups.SettingUniversity of Leeds.ParticipantsDental and non-dental students from the University of Leeds, who had previously undergone orthodontic treatment and had received removable retainers.MethodsStudents were invited to participate via email. Virtual focus groups were undertaken using Microsoft Teams. A topic guide was used to explore the experience of orthodontic retention including factors that influence long-term retainer wear. Focus groups were recorded and analysed using an inductive thematic approach.ResultsIn total, 23 students participated in four focus groups, including 13 dental students. The period since the end of orthodontic treatment varied from 9 months to 10 years. Of the 23 participants, 8 (35%) were no longer wearing their retainers. Four themes were identified: (1) experience of orthodontic treatment including knowledge of relapse; (2) experience of retainer wear, including motivators and barriers; (3) role of others; and (4) increasing adherence. Key factors influencing use of retainers were the importance placed on maintaining treatment outcomes, awareness of unwanted tooth movement and understanding of the role of the retainer, access to replacement retainers, and ongoing support to encourage retainer wear. Greater knowledge and dental awareness reported by dental students did not necessarily increase adherence.ConclusionAdherence to removable retainer wear is an important aspect of orthodontic treatment but it is recognised that long-term retainer wear is highly variable. The understanding of relapse and retention is variable. Challenges in gaining access to replacement retainers are a common cause of cessation of retainer wear. Dental professionals are perceived to be important in encouraging and supporting retainer wear and individuals reported they would like more follow-up.
| S-EPMC10225999 | biostudies-literature
Project description: Not available
| S-EPMC10642543 | biostudies-literature
Project description:Mitochondrial flashes mediated by optic atrophy 1 (OPA1) fusion protein are bioenergetic responses to stochastic drops in mitochondrial membrane potential (Δψm) whose origin is unclear. Using structurally distinct genetically encoded pH-sensitive probes, we confirm that flashes are matrix alkalinization transients, thereby establishing the pH nature of these events, which we renamed "mitopHlashes". Probes located in cristae or intermembrane space as verified by electron microscopy do not report pH changes during Δψm drops or respiratory chain inhibition. Opa1 ablation does not alter Δψm fluctuations but drastically decreases the efficiency of mitopHlash/Δψm coupling, which is restored by re-expressing fusion-deficient OPA1K301A and preserved in cells lacking the outer-membrane fusion proteins MFN1/2 or the OPA1 proteases OMA1 and YME1L, indicating that mitochondrial membrane fusion and OPA1 proteolytic processing are dispensable. pH/Δψm uncoupling occurs early during staurosporine-induced apoptosis and is mitigated by OPA1 overexpression, suggesting that OPA1 maintains mitopHlash competence during stress conditions. We propose that OPA1 stabilizes respiratory chain supercomplexes in a conformation that enables respiring mitochondria to compensate a drop in Δψm by an explosive matrix pH flash.
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Project description:Genetic and microscopic approaches using Saccharomyces cerevisiae have identified many proteins that play a role in mitochondrial dynamics, but it is possible that other proteins and pathways that play a role in mitochondrial division and fusion remain to be discovered. Mutants lacking mitochondrial fusion are characterized by rapid loss of mitochondrial DNA. We took advantage of a petite-negative mutant that is unable to survive mitochondrial DNA loss to select for mutations that allow cells with fusion-deficient mitochondria to maintain the mitochondrial genome on fermentable medium. Next-generation sequencing revealed that all identified suppressor mutations not associated with known mitochondrial division components were localized to PDR1 or PDR3, which encode transcription factors promoting drug resistance. Further studies revealed that at least one, if not all, of these suppressor mutations dominantly increases resistance to known substrates of the pleiotropic drug resistance pathway. Interestingly, hyperactivation of this pathway did not significantly affect mitochondrial shape, suggesting that mitochondrial division was not greatly affected. Our results reveal an intriguing genetic connection between pleiotropic drug resistance and mitochondrial dynamics.
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Project description:The Utrecht-Management of Identity Commitments Scale (U-MICS) has already been validated in nine languages and has had a major scientific impact. Thus, the aim of this study was to validate this instrument in its Spanish version, one of the most important languages in the world. We analyzed the psychometric properties of the scale, applied to a sample of 378 students of the Faculty of Education at the University of Cordoba. The scale consists of 13 items, divided into three dimensions of the process of identity: commitments, in-depth exploration, and reconsideration of the commitments. In this report, the factorial three-dimensional model of process identity is confirmed and shows that the instrument is reliable for measuring the educational, social or global identity of the individual.
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Project description:Pilocytic astrocytoma (PA) is the most common pediatric brain tumor. A recurrent feature of PA is deregulation of the mitogen activated protein kinase (MAPK) pathway most often through KIAA1549-BRAF fusion, but also by other BRAF- or RAF1-gene fusions and point mutations (e.g. BRAFV600E). These features may serve as diagnostic and prognostic markers, and also facilitate development of targeted therapy. The aims of this study were to characterize the genetic alterations underlying the development of PA in six tumor cases, and evaluate methods for fusion oncogene detection. Using a combined analysis of RNA sequencing and copy number variation data we identified a new BRAF fusion involving the 5' gene fusion partner GTF2I (7q11.23), not previously described in PA. The new GTF2I-BRAF 19-10 fusion was found in one case, while the other five cases harbored the frequent KIAA1549-BRAF 16-9 fusion gene. Similar to other BRAF fusions, the GTF2I-BRAF fusion retains an intact BRAF kinase domain while the inhibitory N-terminal domain is lost. Functional studies on GTF2I-BRAF showed elevated MAPK pathway activation compared to BRAFWT. Comparing fusion detection methods, we found Fluorescence in situ hybridization with BRAF break apart probe as the most sensitive method for detection of different BRAF rearrangements (GTF2I-BRAF and KIAA1549-BRAF). Our finding of a new BRAF fusion in PA further emphasis the important role of B-Raf in tumorigenesis of these tumor types. Moreover, the consistency and growing list of BRAF/RAF gene fusions suggests these rearrangements to be informative tumor markers in molecular diagnostics, which could guide future treatment strategies.
| S-EPMC5407815 | biostudies-literature