Using Server-Side Include Commands for Subject Web-Page Management: An Alternative to Database-Driven Technologies for the Smaller Academic Library

Frustrated by the time-consuming process of updating subject Web pages, librarians at Samford University Library (SUL) developed a process for streamlining updates using Server-Side Include (SST) commands. They created text files on the library server that corresponded to each of 143 online resources. Include commands within the HTML document for each subject page refer to these text files, which are pulled into the page as it loads on the user's browser. For the user, the process is seamless. For librarians, time spent in updating Web pages is greatly reduced; changes to text files on the server result in simultaneous changes to the edited resources across the library's Web site. For small libraries with limited online resources, this process may provide an elegant solution to an ongoing problem

A survey of Samford University students regarding plagiarism and academic misconduct

The purpose of this study was to obtain students' attitudes and opinions at Samford University regarding plagiarism and academic misconduct by means of an internetbased survey system composed of yes/no questions and Likert-type rating scales. Data from 681 of approximately 4,500 Samford University students (15% return rate) were analysed. Research indicates that plagiarism and other incidents of academic misconduct are on the rise for a variety of reasons. Students seemingly have the notion that internet information is public knowledge and is thus free from intellectual property rights; therefore, they do not seem to think internet information needs to be cited for academic purposes. The vast majority of Samford students agreed that if one submits a paper written by someone else, this would constitute plagiarism; and that it was unacceptable to copy/paste information from the internet without proper citations. Slightly less than a majority of students disagreed that cheating was widespread at Samford; and a majority indicated that faculty should clarify their expectations regarding academic integrity. The results are somewhat similar to other plagiarism and academic misconduct studies

Prevalence of disease-causing mutations in families with autosomal dominant retinitis pigmentosa : A screen of known genes in 200 families

PURPOSE: To survey families with clinical evidence of autosomal dominant retinitis pigmentosa (adRP) for mutations in genes known to cause adRP. METHODS: Two hundred adRP families, drawn from a cohort of more than 400 potential families, were selected by analysis of pedigrees. Minimum criteria for inclusion in the adRP cohort included either evidence of at least three generations of affected individuals or two generations with evidence of male-to-male transmission. Probands from each family were screened for mutations in 13 genes known to cause adRP: CA4, CRX, FSCN2, IMPDH1, NRL, PRPF3 (RP18), PRPF8 (RP13), PRPF31 (RP11), RDS, RHO, ROM1, RP1, and RP9. Families without mutations in autosomal genes and in which an X-linked mode of inheritance could not be excluded were tested for mutations in ORF 15 of X-linked RPGR. Potentially pathogenic variants were evaluated based on a variety of genetic and computational criteria, to confirm or exclude pathogenicity. RESULTS: A total of 82 distinct, rare (nonpolymorphic) variants were detected among the genes tested. Of these, 57 are clearly pathogenic based on multiple criteria, 10 are probably pathogenic, and 15 are probably benign. In the cohort of 200 families, 94 (47%) have one of the clearly pathogenic variants and 10 (5%) have one of the probably pathogenic variants. One family (0.5%) has digenic RDS-ROM1 mutations. Two families (1%) have a pathogenic RPGR mutation, indicating that families with apparent autosomal transmission of RP may actually have X-linked genetic disease. Thus, 107 families (53.5%) have mutations in known genes, leaving 93 whose underlying cause is still unknown. CONCLUSIONS: Together, the known adRP genes account for retinal disease in approximately half of the families in this survey, mostly Americans of European origin. Among the adRP genes, IMPDH1, PRPF8, PRPF31, RDS, RHO, and RP1 each accounts for more than 2% of the total; CRX, PRPF3, and RPGR each accounts for roughly 1%. Disease-causing mutations were not found in CA4, FSCN2, NRL, or RP9. Because some mutations are frequent and some regions are more likely to harbor mutations than others, more than two thirds of the detected mutations can be found by screening less than 10% of the total gene sequences. Among the remaining families, mutations may lie in regions of known genes that were not tested, mutations may not be detectable by PCR-based sequencing, or other loci may be involved