Dragonflies of (Anisoptera) Arkansas

Previous publications have recorded 69 species of dragonflies for Arkansas. Three of these are deleted, but state records for 21 new species are reported herein, bringing the list to 87 species. Based on lists from adjacent states, an additional nine species are listed as probably occurring in Arkansas. County records are given for both naiads and adults of each species, as well as first and last capture dates for adults. Specific location and capture date are given for new state records when such data are available. The most species (39) have been reported from Washington County. Twenty-nine counties list from 1-5 species, and six counties list no records

Naive and memory T cell trafficking in selectin ligand-deficient mice: the role of fucosyltransferase –IV and –VII in the differential migration of T cell populations

The correct and timely delivery of immune cells is critical for protection against foreign antigen. In order for cells to access most organs, there are requirements that must be met to facilitate exit from the blood into extravasculature. The initial requirement is selectin-selectin ligand interactions that mediate tethering and rolling to allow shear resistance. For proper selectin-selectin ligand interaction, glycoproteins must be modified by fucosyltransferases –IV and –VII, which adds fucose to an acceptor substrate to form the sialyl-LewisX moiety. Using fucosyltransferase –IV and –VII double knockout (FtDKO) mice, we made several novel observations. Our first observation showed increased numbers of naïve T cells in non-lymphoid organs. To support this observation, we blocked chemokine-mediated entry into lymph nodes (LNs) with pertussis toxin and L-selectin mediated entry with anti-CD62L antibody in WT mice. We also treated WT mice with the S1P1 agonist, FTY720, to retain lymphocytes in LNs. Our results suggested that when access to LN is perturbed, lymphocytes accumulate in non-lymphoid organs. Our second observation showed an enrichment of effector/memory T cells in FtDKO LNs. To determine if effector/memory CD8 T cells were retained in LNs, we transferred naïve and memory CD8 T cells into WT mice then treated the recipient mice with anti-CD62L. We found that LN exit rates of naïve and memory CD8 T cells were similar, but slowed as T cell density decreased. To understand if memory CD8 T cells were using selectin ligand independent mechanisms, we transferred naïve and memory CD8 T cells into WT or FtDKO mice. We found reduced numbers of memory CD8 T cells in LNs, however, their frequency was increased. We explored this result by transferring CFSE labeled memory CD8 T cells. We found that memory CD8 T cells divide more in FtDKO mice compared to WT. These experiments suggested that selectin ligand deficiencies cause increased frequency of effector/memory T cells in LNs due to low density and increased emptiness induced proliferation. Taken together, these findings reveal how selectin ligand deficiencies contribute to T cell accumulation in non-lymphoid organs and elucidate mechanisms of retention in LNs

Incorporation of host fatty acids promotes tolerance to membrane stressors by modifying the lipid content of \u3ci\u3eEnterococcus faecalis\u3c/i\u3e

Enterococcus faecalis is a Gram-positive commensal bacterium that resides in the human gastrointestinal tract. Unfortunately, E. faecalis can also cause infections in humans and is notoriously difficult to treat due to drug resistance. One treatment that is used to treat enterococcal infections is the cell membrane targeting lipopeptide antibiotic, daptomycin. However, daptomycin resistant strains of E. faecalis have been isolated. Studies aimed at understanding these resistant strains show that mutations in genes associated with membrane homeostasis are involved. E faecalis can also incorporate exogenous fatty acids from environments in which it thrives, bile (GI tract) and serum (wounds), which cause increased physiological tolerance to daptomycin. The host fatty acids, oleic acid (C18:1 cis 9) and linoleic acid (C18:2 cis 9, 12), that are prevalent in serum and bile, are the major factors that contribute to this induction of daptomycin tolerance. Within this work, I determined that the cis bond at the 9th carbon of oleic acid is critical for increased tolerance. Moreover, I found that when the carboxyl group of oleic acid or linoleic acid was replaced with an amide group, tolerance was lost. To assess if increased tolerance induced by these host fatty acids was a consequence of a membrane stress response, I examined a strain of E. faecalis which lacks the response regulator of the LiaFSR three-component system and concluded that host fatty acid induced tolerance was not mediated by LiaFSR. Finally, I investigated whether or not supplementation with host fatty acids was altering the membrane phospholipid composition leading to increased tolerance. After mass spectrometry analysis, I discovered alterations in the composition of the major phospholipids in E. faecalis. To test these alterations, I deleted genes responsible for production of lysyl-phosphatidylglycerol (mprF2) and cardiolipin (cls1 and cls2). After supplementation with oleic acid and linoleic acid, I still observed increased tolerance to daptomycin. However, long term exposure to daptomycin resulted in no recovery even after supplementation with host fatty acids. These data suggest that oleic acid and linoleic acid can induce lipid alterations, but alteration in the composition of L-PG and CL are not responsible for acute daptomycin tolerance

Rooted and grounded in love : cultivating the Christian heart through dispositional spiritual formation-in-common

https://place.asburyseminary.edu/ecommonsatsdissertations/1808/thumbnail.jp

Naïve T Cells Re-Distribute to the Lungs of Selectin Ligand Deficient Mice

Background: Selectin mediated tethering represents one of the earliest steps in T cell extravasation into lymph nodes via high endothelial venules and is dependent on the biosynthesis of sialyl Lewis X (sLe x) ligands by several glycosyltransferases, including two fucosyltransferases, fucosyltransferase-IV and –VII. Selectin mediated binding also plays a key role in T cell entry to inflamed organs. Methodology/Principal Findings: To understand how loss of selectin ligands (sLe x) influences T cell migration to the lung, we examined fucosyltransferase-IV and –VII double knockout (FtDKO) mice. We discovered that FtDKO mice showed significant increases (,5-fold) in numbers of naïve T cells in non-inflamed lung parenchyma with no evidence of induced bronchusassociated lymphoid tissue. In contrast, activated T cells were reduced in inflamed lungs of FtDKO mice following viral infection, consistent with the established role of selectin mediated T cell extravasation into inflamed lung. Adoptive transfer of T cells into FtDKO mice revealed impaired T cell entry to lymph nodes, but selective accumulation in non-lymphoid organs. Moreover, inhibition of T cell entry to the lymph nodes by blockade of L-selectin, or treatment of T cells with pertussis toxin to inhibit chemokine dependent G-coupled receptor signaling, also resulted in increased T cells in non-lymphoid organs. Conversely, inhibition of T cell egress from lymph nodes using FTY720 agonism of S1P1 impaired T cell migration into non-lymphoid organs. Conclusions/Significance: Taken together, our results suggest that impaired T cell entry into lymph nodes via hig

B cells are capable of independently eliciting rapid reactivation of encephalitogenic CD4 T cells in a murine model of multiple sclerosis

<div><p>Recent success with B cell depletion therapies has revitalized efforts to understand the pathogenic role of B cells in Multiple Sclerosis (MS). Using the adoptive transfer system of experimental autoimmune encephalomyelitis (EAE), a murine model of MS, we have previously shown that mice in which B cells are the only MHCII-expressing antigen presenting cell (APC) are susceptible to EAE. However, a reproducible delay in the day of onset of disease driven by exclusive B cell antigen presentation suggests that B cells require optimal conditions to function as APCs in EAE. In this study, we utilize an <i>in vivo</i> genetic system to conditionally and temporally regulate expression of MHCII to test the hypothesis that B cell APCs mediate attenuated and delayed neuroinflammatory T cell responses during EAE. Remarkably, induction of MHCII on B cells following the transfer of encephalitogenic CD4 T cells induced a rapid and robust form of EAE, while no change in the time to disease onset occurred for recipient mice in which MHCII is induced on a normal complement of APC subsets. Changes in CD4 T cell activation over time did not account for more rapid onset of EAE symptoms in this new B cell-mediated EAE model. Our system represents a novel model to study how the timing of pathogenic cognate interactions between lymphocytes facilitates the development of autoimmune attacks within the CNS.</p></div

New Distributional Records for Freshwater Mussels in the Ouachita River, Arkansas

Two freshwater mussel species thought to have been extirpated from Arkansas have recently been rediscovered in the Ouachita River in the vicinity of Camden. Prior to this survey, Wheeler (1918) last reported Arkansia wheeleri Ortmann and Walker, the Ouachita rock-pocketbook, and Cumberlandia monodonta (Say), the spectaclecase, from the Ouachita River near Arkadelphia. Quadrula apiculata (Lea), the southern mapleleaf, has been reported from Arkansas on two occasions, but due to taxonomic uncertainty, it has not been recognized in recent compilations of Arkansas freshwater mussels. During this survey, the southern mapleleaf was collected from the Ouachita River which verifies its occurrence within Arkansas. Quadrula fragosa (Conrad), the winged mapleleaf, is reported as a new state record. Arkansia wheeleri and Quadrula fragosa are listed as threatened and endangered species, respectively, by the U.S. Fish and Wildlife Service