Data to Decisions: Shared Print Retention in Maine

Shared print initiatives are gaining visibility across the country. While the majority of programs up to this point, such as the West Storage Trust and the CIC, have focused on journals, a growing number of these cooperative ventures are exploring regional retention of both monographs and journals. The Maine Shared Collection Strategy is one such initiative. All of a sudden, libraries seem have too much print in their stacks, much of it unused, if statistics are to be believed. The usual solution is judicious de-accessioning, aka weeding, based on various factors such as circulation, age, duplication across formats, and collection policies. This may be fine for individual libraries, but what if you are part of group of libraries, interdependent and connected by a shared discovery catalog and delivery service? What if no one kept enough copies of stuff to supply users with needed books and journals in the future? And aren’t we all really parts of a larger library group? Learn how nine institutions in Maine—including public, university, and college libraries, the state library, and the statewide collaborative system—are deciding what to keep, rather than what to discard. At last year’s Charleston Conference, the Maine Shared Collections Strategy grant, funded by the Institute of Museum and Library Services, presented as part of the Shared Print Archiving: Making It Work preconference. We have made great progress since then. Deb Rollins (Collection Services, University of Maine) and Becky Albitz (Collection Management, Bates College) will discuss the review and analysis of collections data for a collective three million monographs, OCLC shared print symbols and retention disclosure from local to national levels, HathiTrust and Internet Archive digital copies and their effect on decisions, implications of a multitype library group on what we are keeping, policy issues, and more

Koinonia

Azusa 1988; Azusa Conference Report Balancing Love and Discipline, Forgiveness and Consequence, R.A. Rollins From the President AIDS Update: Calvin College and Seminary Lessons on Leadership from the Trenches, R. Hestenes AIDS and Adolescents-Threat Greater than Statistics Indicate A Time and a Place, Deb Laceyhttps://pillars.taylor.edu/acsd_koinonia/1056/thumbnail.jp

Application of In Vivo Induced Antigen Technology (IVIAT) to Bacillus anthracis

In vivo induced antigen technology (IVIAT) is an immuno-screening technique that identifies bacterial antigens expressed during infection and not during standard in vitro culturing conditions. We applied IVIAT to Bacillus anthracis and identified PagA, seven members of a N-acetylmuramoyl-L-alanine amidase autolysin family, three P60 family lipoproteins, two transporters, spore cortex lytic protein SleB, a penicillin binding protein, a putative prophage holin, respiratory nitrate reductase NarG, and three proteins of unknown function. Using quantitative real-time PCR comparing RNA isolated from in vitro cultured B. anthracis to RNA isolated from BALB/c mice infected with virulent Ames strain B. anthracis, we confirmed induced expression in vivo for a subset of B. anthracis genes identified by IVIAT, including L-alanine amidases BA3767, BA4073, and amiA (pXO2-42); the bacteriophage holin gene BA4074; and pagA (pXO1-110). The exogenous addition of two purified putative autolysins identified by IVIAT, N-acetylmuramoyl-L-alanine amidases BA0485 and BA2446, to vegetative B. anthracis cell suspensions induced a species-specific change in bacterial morphology and reduction in viable bacterial cells. Many of the proteins identified in our screen are predicted to affect peptidoglycan re-modeling, and our results support significant cell wall structural remodeling activity during B. anthracis infection. Identification of L-alanine amidases with B. anthracis specificity may suggest new potential therapeutic targets

Identification of In Vivo-Induced Antigens Including an RTX Family Exoprotein Required for Uropathogenic Escherichia coli Virulence ▿

Uncomplicated urinary tract infections (UTI) are caused most commonly by uropathogenic Escherichia coli (UPEC). Whole-genome screening approaches, including transcriptomic, proteomic, and signature-tagged mutagenesis, have shown that UPEC highly expresses or requires genes for translational machinery, capsule, lipopolysaccharide, type 1 fimbriae, and iron acquisition systems during UTI. To identify additional genes expressed by UPEC during UTI, an immunoscreening approach termed in vivo-induced antigen technology (IVIAT) was employed to identify antigens produced during experimental infection that are not produced during in vitro culture. An inducible protein expression library, constructed from genomic DNA isolated from UPEC strain CFT073, was screened using exhaustively adsorbed pooled sera from 20 chronically infected female CBA/J mice. Using this approach, we identified 93 antigens induced by UPEC in vivo. A representative subset of these genes was tested by quantitative PCR for expression by CFT073 in vivo and during growth in human urine or LB medium in vitro; proWX, narJI, lolA, lolD, tosA (upxA), c2432, katG, ydhX, kpsS, and yddQ were poorly expressed in vitro but highly expressed in vivo. Of these, tosA, a gene encoding a predicted repeat-in-toxin family member, was expressed exclusively during UTI. Deletion of tosA in UPEC strain CFT073 resulted in significant attenuation in bladder and kidney infections during ascending UTI. By screening for in vivo-induced antigens, we identified a novel UPEC virulence factor and additional proteins that could be useful as potential vaccine targets