RSS 1.0Welcome to the SUNY Open Access Repository
The SUNY Open Access Repository (SOAR) is a centrally managed online digital repository that stores, indexes, and makes available scholarly and creative works of SUNY faculty, students, and staff across SUNY campuses. SOAR serves as an open access platform for those SUNY campuses that do not have their own open access repository environments.
Access to SUNY campus communities in SOAR are available below under SUNY sectors and also listed alphabetically under the Campus Communities in SOAR on the navigation bar on the left.
Additional information includes
- Approved SUNY Campus Open Access Policies (clicking on this link will take you out of SOAR)
- Links to additional SUNY repositories
- SOAR guidelines
Communities in SUNY Open Access Repository
Select a community to browse its collections.
Recently Added
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Black Campus LifeAn in-depth ethnography of Black engineering students at a historically White institution, Black Campus Life examines the intersection of two crises, up close: the limited number of college graduates in science, technology, engineering, and math (STEM) fields, and the state of race relations in higher education. Antar Tichavakunda takes readers across campus, from study groups to parties and beyond as these students work hard, have fun, skip class, fundraise, and, at times, find themselves in tense racialized encounters. By consistently centering their perspectives and demonstrating how different campus communities, or social worlds, shape their experiences, Tichavakunda challenges assumptions about not only Black STEM majors but also Black students and the “racial climate” on college campuses more generally. Most fundamentally, Black Campus Life argues that Black collegians are more than the racism they endure. By studying and appreciating the everyday richness and complexity of their experiences, we all—faculty, administrators, parents, policymakers, and the broader public—might learn how to better support them.
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Virtual Connectedness: Working Together to Create a Companion Site for Spanish Phonetics & PhonologyThe creation of a resource for students who are struggling or who simply want to practice their skills, that is accessible to all, is crucial, especially during the current times of virtual learning. We have created a companion site for the Spanish Phonetics & Phonology course for all SUNY students to use, as there is no resource of its kind, that is in the target language (Spanish) and is free of cost for all students and faculty. This will be a long-lasting tool that will allow for clarification of concepts, practice with engaging virtual exercises, and many opportunities to exercise skills and learning. After students learn concepts in class, they can access the companion site to further reinforce the comprehension of content, test what they know, see diagrams, practice, and get tips from other students who have already taken the course. We use h5p plugins in order to create different types of interactive activities for students in each module, which enhance the practice and learning experience. Each module in the site follows the same structure: 1) objectives of the module, 2) a short pre-reading quiz, 3) the content of the module, used to review concepts covered in class with examples and diagrams, 4) a “tips from other students” section so that students can learn from other students who already took the course and remember some tricks that will help them when preparing for exams, 5) a section for activities and practice, and 6) a summary of what was covered in the module. Two key resources that have been crucial to the creation of the companion site are Pressbooks and Monday.com. Pressbooks is the site used to create content and interactive activities. Monday.com is a site that allows for task management, progress tracking, making comments, and for student-faculty accountability. This companion site is an Open Educational Resource (OER) and is ADA-compliant, so that all students- regardless of income and potential disability- can access it for free. This resource also falls into the category of Open Pedagogy, with our companion site being one of the few Open Pedagogy projects across the SUNY system, where content is planned and created by students under faculty supervision.
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Meta-Analysis of Alzheimer's Disease Risk with Obesity, Diabetes, and Related DisordersBackground: Late-onset Alzheimer’s disease (AD) is a multifactorial and heterogeneous disorder with major risk factors including advanced age, presence of an apolipoprotein E 4 (APOE4) allele, and family history of AD. Other risk factors may be obesity and diabetes and related disorders, which are highly prevalent. Methods: We reviewed longitudinal epidemiological studies of body mass, diabetes, metabolic syndrome, and glucose and insulin levels on risk for AD. We conducted meta-analyses of the results from these studies. Results: For obesity assessed by body mass index, the pooled effect size for AD was 1.59 (95% confidence interval [CI] 1.02–2.5; z 2.0; p .042), and for diabetes, the pooled effect size for AD was 1.54 (95% CI 1.33–1.79; z 5.7; p .001). Egger’s test did not find significant evidence for publication bias in the meta-analysis for obesity (t 1.4, p .21) or for diabetes (t .86, p .42). Since these disorders are highly comorbid, we conducted a meta-analysis combining all studies of obesity, diabetes, and abnormal glucose or insulin levels, which yielded a highly significant pooled effect size for AD of 1.63 (95% CI 1.39 –1.92; z 5.9; p .001). Conclusions: Obesity and diabetes significantly and independently increase risk for AD. Though the level of risk is less than that with the APOE4 allele, the high prevalence of these disorders may result in substantial increases in future incidence of AD. Physiological changes common to obesity and diabetes plausibly promote AD.
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RASD2, MYH9, and CACNG2 Genes at Chromosome 22q12 Associated with the Subgroup of Schizophrenia with Non-Deficit in Sustained Attention and Executive FunctionBackground: In a previous linkage study of schizophrenia that included Taiwanese samples, the marker D22S278 (22q12.3) was significantly linked to schizophrenia (p .001). Methods: We conducted fine mapping of the implicated genomic region, with 47 validated single nucleotide polymorphism (SNP) markers around 1 Mb of D22S278, in a Taiwanese sample of 218 pedigrees with at least 2 siblings affected with schizophrenia. We examined the association of these SNPs and their haplotypes with schizophrenia and with subgroups defined by the presence and absence of deficits in sustained attention as assessed by undegraded and degraded continuous performance tests (CPTs). We also examined subgroups defined by deficits in categories achieved in the Wisconsin Card Sort Test (WCST). Results: Three of five candidate vulnerability genes (RASD2, APOL5, MYH9, EIF3S7, and CACNG2), which had marginally significant associations with schizophrenia, had significant associations with schizophrenic patients who did not have deficits in sustained attention on the undegraded CPT (RASD2 gene SNP rs736212; p .0008 with single locus analysis) and the degraded CPT (MYH9 gene haplotype 1-1-1-1 of SNP rs3752463 - rs1557540 - rs713839 - rs739097; p .0059 with haplotype analysis). We also found a significant association for patients who showed no deficits in executive function as measured by categories achieved in the WCST (CACNG2 gene haplotype 2-1-1-1 of SNP rs2267360 - rs140526 - rs1883987 - rs916269; p .0163 with haplotype analysis). Conclusions: The genes RASD2, MYH9, and CACNG2 might be vulnerability genes for neuropsychologically defined subgroups of schizophrenic patients.
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Advanced Paternal Age and Early Onset of Schizophrenia in Sporadic Cases: Not Confounded by Parental Polygenic Risk for SchizophreniaBACKGROUND:Whether paternal age effect on schizophrenia is a causation or just an association due to con-founding by selection into late parenthood is still debated. We investigated the association between paternal age andearly onset of schizophrenia in offspring, controlling for both paternal and maternal predisposition to schizophrenia asempirically estimated using polygenic risk score (PRS) derived from the Psychiatric Genomics Consortium.METHODS:Among 2923 sporadic schizophrenia cases selected from the Schizophrenia Trio Genomic Research inTaiwan project, 1649 had parents’genotyping data. The relationships of paternal schizophrenia PRS to paternal ageatfirst birth (AFB) and of maternal schizophrenia PRS to maternal AFB were examined. A logistic regression model ofpatients’early onset of schizophrenia (#18 years old) on paternal age was conducted.RESULTS:Advanced paternal age over 20 years exhibited a trend of an increasing proportion of early onset ofschizophrenia (odds ratio per 10-year increase in paternal age = 1.28,p= .007) after adjusting for maternal age, sex,and age. Older paternal AFB also exhibited an increasing trend of paternal schizophrenia PRS. Additionally, aU-shaped relationship between maternal AFB and maternal schizophrenia PRS was observed. After adjusting forboth paternal and maternal schizophrenia PRS, the association of paternal age with patients’early onset ofschizophrenia remained (odds ratio = 1.29,p= .04).CONCLUSIONS:The association between paternal age and early onset of schizophrenia was not confounded byparental PRS for schizophrenia, which partially captures parental genetic vulnerability to schizophrenia. Ourfindingssupport an independent role of paternal age per se in increased risk of early onset of schizophrenia in offspring
