Programmatic Review Process Guide

The Grand Valley State University Libraries created a programmatic review process to review, realign, and renew its programmatic areas as the University faced changes and budget challenges. This programmatic review process guide details the Libraries’ guiding principles, prioritization approach, and decision-making criteria created to address the process by which library resources may be allocated. The Libraries were proactively reacting to the University’s projected budget shortfalls as a result of the continued demographic decline in college-aged individuals as well as the global pandemic. In this guide, University Libraries has clearly defined its mission for the coming years, the expectations and desired outcomes of mission fulfillment, an implementation timeline and a communication plan for the review process as well as templates for questions to be discussed, recommendations, and Executive Team rationale

Investigating the viability of genetic screening/testing for RA susceptibility using combinations of five confirmed risk loci

Objective. Five loci—the shared epitope (SE) of HLA-DRB1, the PTPN22 gene, a locus on 6q23, the STAT4 gene and a locus mapping to the TRAF1/C5 genetic region—have now been unequivocally confirmed as conferring susceptibility to RA. The largest single effect is conferred by SE. We hypothesized that combinations of susceptibility alleles may increase risk over and above that of any individual locus alone

Supergiant shells and molecular cloud formation in the large magellanic cloud

We investigate the influence of large-scale stellar feedback on the formation of molecular clouds in the Large Magellanic Cloud (LMC). Examining the relationship between Hi and 12CO(J=1–0) in supergiant shells (SGSs), we find that the molecular fraction in the total volume occupied by SGSs is not enhanced with respect to the rest of the LMC disk. However, the majority of objects (∼ 70% by mass) are more molecular than their local surroundings, implying that the presence of a supergiant shell does on average have a positive effect on the molecular gas fraction. Averaged over the full SGS sample, our results suggest that ∼ 12–25% of the molecular mass in supergiant shell systems was formed as a direct result of the stellar feedback that created the shells. This corresponds to ∼ 4–11% of the total molecular mass of the galaxy. These figures are an approximate lower limit to the total contribution of stellar feedback to molecular cloud formation in the LMC, and constitute one of the first quantitative measurements of feedback-triggered molecular cloud formation in a galactic syste

The diversity of the Chagas parasite, <i>Trypanosoma cruzi</i>, infecting the main Central American vector, <i>Triatoma dimidiata</i>, from Mexico to Colombia

<div><p>Little is known about the strains of <i>Trypanosoma cruzi</i> circulating in Central America and specifically in the most important vector in this region, <i>Triatoma dimidiata</i>. Approximately six million people are infected with <i>T</i>. <i>cruzi</i>, the causative agent of Chagas disease, which has the greatest negative economic impact and is responsible for ~12,000 deaths annually in Latin America. By international consensus, strains of <i>T</i>. <i>cruzi</i> are divided into six monophyletic clades called discrete typing units (DTUs TcI-VI) and a seventh DTU first identified in bats called TcBat. TcI shows the greatest geographic range and diversity. Identifying strains present and diversity within these strains is important as different strains and their genotypes may cause different pathologies and may circulate in different localities and transmission cycles, thus impacting control efforts, treatment and vaccine development. To determine parasite strains present in <i>T</i>. <i>dimidiata</i> across its geographic range from Mexico to Colombia, we isolated abdominal DNA from <i>T</i>. <i>dimidiata</i> and determined which specimens were infected with <i>T</i>. <i>cruzi</i> by PCR. Strains from infected insects were determined by comparing the sequence of the 18S rDNA and the spliced-leader intergenic region to typed strains in GenBank. Two DTUs were found: 94% of infected <i>T</i>. <i>dimidiata</i> contained TcI and 6% contained TcIV. TcI exhibited high genetic diversity. Geographic structure of TcI haplotypes was evident by Principal Component and Median-Joining Network analyses as well as a significant result in the Mantel test, indicating isolation by distance. There was little evidence of association with TcI haplotypes and host/vector or ecotope. This study provides new information about the strains circulating in the most important Chagas vector in Central America and reveals considerable variability within TcI as well as geographic structuring at this large geographic scale. The lack of association with particular vectors/hosts or ecotopes suggests the parasites are moving among vectors/hosts and ecotopes therefore a comprehensive approach, such as the Ecohealth approach that makes houses refractory to the vectors will be needed to successfully halt transmission of Chagas disease.</p></div

Median-Joining Network for the single nucleotide polymorphism region of the intergenic region of the spliced leader gene (SL-IR).

<p>Networks were constructed with 89—SL-IR haplotypes and the size of each node proportional to the frequency of the haplotype. Small red circles (median vectors) represent hypothetical intermediate nodes. TcBat is the outgroup. The number of mutational steps ≥3 are shown. Clustering is examined by: (A) geographic origin, (B) vector or host, and (C) ecotope.</p

Genetic Polymorphism and Diversity of TcI isolates.

<p>Genetic Polymorphism and Diversity of TcI isolates.</p

<i>Trypanosoma cruzi</i> strains TcI and TcIV identified in <i>Triatoma dimidiata</i> from Mexico, Central America and Colombia as determined by 18S rDNA and SL-IR (spliced leader intergenic region) sequences.

<p>Size of the circles is proportional to the numbers of <i>T</i>. <i>dimidiata</i> specimens with a particular <i>T</i>. <i>cruzi</i> strain (TcI -dark gray or TcIV—light gray) in different countries. Political map was modified from: <a href="https://commons.wikimedia.org/wiki/Atlas_of_the_world#/media/File:BlankMap-World6.svg" target="_blank">https://commons.wikimedia.org/wiki/Atlas_of_the_world#/media/File:BlankMap-World6.svg</a> under public domain.</p

Principle component plots of variation in TcI isolates for the two markers by geographic region (A: 18S, B: SL-IR) and ecotope (C: 18S, D: SL-IR).

<p>Ellipses cover 50% of the variables. For geographic regions, both 18S and SL-IR are significantly different among regions. For ecotopes, the 18S sylvatic is significantly different from domestic, but for SL-IR, the differences are not statistically significant.</p

Th17-to-Tfh plasticity during periodontitis limits disease pathology

In autoinflammatory diseases Th17 cell plasticity has been shown to be crucial for development of disease pathology. Periodontitis is a prevalent inflammatory disease where Th17 cells mediate key pathological roles, yet whether they exhibit any functional diversification that contributes to pathology during periodontitis remains unexplored. Using an IL-17A fate reporter mouse we found that during periodontitis gingival IL-17 fate-mapped T cells still predominantly produce IL-17A, with little diversification of cytokine production. However, plasticity of IL-17 fate-mapped cells did occur during periodontitis, but in the lymph node draining the inflammatory site. Here some Th17 cells took on features of Tfh cells, a functional plasticity that was dependent on IL-6. Notably, we show that this Th17-to-Tfh diversification was important to limit periodontitis pathology. Preventing Th17-to-Tfh plasticity resulted in elevated periodontal bone loss which was not simply a result of increased proportions of conventional Th17 cells. Instead, loss of Th17-to-Tfh cells resulted in reduced IgG levels within the oral cavity and a failure to restrict the biomass of the oral commensal community. Thus, our data identify a novel protective function for a subset of otherwise pathogenic Th17 cells during periodontitis

Th17-to-Tfh plasticity during periodontitis limits disease pathology

Th17 cell plasticity is crucial for development of autoinflammatory disease pathology. Periodontitis is a prevalent inflammatory disease where Th17 cells mediate key pathological roles, yet whether they exhibit any functional plasticity remains unexplored. We found that during periodontitis, gingival IL-17 fate-mapped T cells still predominantly produce IL-17A, with little diversification of cytokine production. However, plasticity of IL-17 fate-mapped cells did occur during periodontitis, but in the gingiva draining lymph node. Here, some Th17 cells acquired features of Tfh cells, a functional plasticity that was dependent on IL-6. Notably, Th17-to-Tfh diversification was important to limit periodontitis pathology. Preventing Th17-to-Tfh plasticity resulted in elevated periodontal bone loss that was not simply due to increased proportions of conventional Th17 cells. Instead, loss of Th17-to-Tfh cells resulted in reduced IgG levels within the oral cavity and a failure to restrict the biomass of the oral commensal community. Thus, our data identify a novel protective function for a subset of otherwise pathogenic Th17 cells during periodontitis.</p