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Carex roanensis is a globally rare species endemic in moderate to high elevation forests in the southern Appalachian Mountains. All known collections were reviewed, including previously unpublished records from Pennsylvania, West Virginia, Virginia, North Carolina, and Tennessee, and an annotated distribution map is presented. A preliminary assessment of its ecological affinities is provided, especially with respect to the closely related C. aestivalis and C. virescens.

1. Many physiologically important activities of oligodendrocyte progenitor cells (O-2A cells), including proliferation, migration and differentiation, are regulated by cytosolic Ca2+ signals. However, little is known concerning the mechanisms of Ca2+ signalling in this cell type. We have studied the interactions between Ca2+ entry, Ca2+ release from endoplasmic reticulum and Ca2+ regulation by mitochondria in influencing cytosolic Ca2+ responses in O-2A cells. 2. Methacholine (MCh; 100 microM) activated Ca2+ waves that propagated from several initiation sites along O-2A processes. 3. During a Ca2+ wave evoked by MCh, mitochondrial membrane potential was often either depolarized (21 % of mitochondria) or hyperpolarized (20 % of mitochondria), as measured by changes in the fluorescence of 5,5',6,6'-tetrachloro-1,1',3, 3'-tetraethylbenzimidazole carbocyanine iodide (JC-1). 4. Stimulation with kainate (100 microM) evoked a slowly rising, sustained cytosolic Ca2+ elevation in O-2A cells. This also, in some cases, resulted in either a depolarization (15 % of mitochondria) or hyperpolarization (12 % of mitochondria) of mitochondrial membrane potential. 5. Simultaneous measurement of cytosolic (fluo-3 AM) and mitochondrial (rhod-2 AM) Ca2+ responses revealed that Ca2+ elevations in the cytosol evoked by either MCh or kainate were translated into long-lasting Ca2+ elevations in subpopulations of mitochondria. In some mitochondria, Ca2+ signals appeared to activate Ca2+ release into the cytosol. 6. Inhibition of the mitochondrial Na+-Ca2+ exchanger by CGP-37157 (25 microM) decreased kainate Ca2+ response amplitude and increased the rate of return of the response to basal Ca2+ levels. 7. Thus, both ionotropic and metabotropic stimulation evoke changes in mitochondrial membrane potential and Ca2+ levels in O-2A cells. Ca2+ uptake into some mitochondria is activated by Ca2+ entry into cells or release from stores. Mitochondrial Ca2+ release appears to play a key role in shaping kainate-evoked Ca2+ responses.

The purpose of this study was to detect and confirm PI dairy cattle, research the dam's location during the first trimester of gestation, and genetically sequence a portion of the 5' untranslated (UTR) region of viral RNA to determine the prevalence of different genotypes of BVDV PI dairy cattle in the upper midwestern United States., American Association of Bovine Practitioners Proceedings of the Annual Conference, 2010

BRD produces disease with morbidity peaking in 1-3 weeks and mortality peaking in 2-4 weeks after entering the feedlot.1,4 When an epidemic curve for BRD is constructed using fatal disease onset rather than mortality as the parameter, it can be seen that calves dying from BRD become ill within the first 2 weeks of entering the feedlot.4 The fact that calves become ill so quickly after entering the feedlot obviously puts great emphasis on the type of animal and its recent history. This will be important in determining the morbidity and mortality which may occur. Fall placed calves going into feedlots in Canada and the northern United States will have higher morbidity and mortality than older calves. The morbidity and mortality of fall placed calves in the northern United States will be similar to that seen in stocker calves in southern United States. Both types of calves are young, multiorigin, long haul sale barn calves whose age and handling result in higher BRD morbidity and mortality.5 Antimicrobial agents can be used in the feedlot in the traditional manner to control mortality and improve performance in sick calves experiencing BRD as well as prophylactically on arrival to limit both BRD morbidity and mortality., American Association of Bovine Practitioners Proceedings of the Annual Conference, 1994

The effect of bovine respiratory syncytial virus (BRSV) upon alveolar macrophage (AM) function was investigated using an in vivo calf inoculation model. Alveolar macrophages were collected sequentially from live calves at multiple time points during the 14 day period following viral inoculation. Alveolar macrophages from bronchoalveolar lavage fluids were purified by density gradient centrifugation (> 95% AM) prior to in vitro evaluation of cell functions. There were significant but variable and inconsistent differences in the functions of AM from the BRSV inoculated calves compared to the control calves. Fc-receptor mediated phagocytosis was either increased or unchanged by BRSV inoculation. Nonopsonized phagocytosis was decreased during the early postinoculation period and later increased. There was a variable effect on AM phagosome lysosome fusion with increased fusion activity on postinoculation days 2 through 5, 7 and 12 but reduced activity on days 6 and 10. The AM respiratory burst, as measured by nitroblue tetrazolium dye reduction, was essentially unaffected with a reduction in activity on day 10 only. In this model, BRSV inoculation of calves primarily resulted in an alteration of the membrane associated phagocytic functions of the alveolar macrophages (p < 0.05).

Pasteurella haemolytica biotype A, serotype 1 (Al) has been established as the primary agent responsible for the clinical disease and pathophysiologic events leading to acute lobar fibrinonecrotizing pneumonia associated with bovine pneumonic pasteurellosis(1,2,3). The bacteria produces several potential virulent factors, of which the leukotoxin (LKT) has received the most attention(4). The LKT is a heat-labile proteinaceous exotoxin, that is oxygen-stable, non-dialyzable, water soluble, and is produced in high concentrations by P.haemolytica during the logarithmic phase of growth(5). The genes that code for the synthesis and secretion of this LKT have been cloned(6). All 15 serotypes of P. haemolytica produce LKT(7). It has a molecular weight of 101-105kDa when determined by sodium dodecyl sulfate-polyacrylamide gel electrophoretic analysis(8). Attempts to purify the LKT has been futile because it is tightly bound to the LPS and there is no efficient way to remove the LPS without inactivating the LKT. It is one of a family of RTX(repeat toxins)-pore forming cytolysin which has a unique specificity, in that it is only cytocidal to ruminant leukocytes(9). This cytotoxicity is caused by the formation of pores in the cell membrane which allows the influx of calcium and results in a sequence of cell-damaging events(lO). Since this organism produces disease only in ruminants, this would support the role of LKT as a virulence factor. Indeed, several observations point to the central role that LKT has in the pathogenesis of pneumonic pasteurellosis. For example, in experimental pasteurellosis, the clinical and pathophysiologic events are dose-dependently reproduced by the intatracheal administration of live logarithmic phase P. haemolytica and not by stationary phase organisms(ll). This enhanced pathogenicity may be related to the amount of LKT produced by these different populations. Indeed, we (5) and others(12)* have shown that the logarithmic phase cells produce far greater amounts of this LKT than stationary cells. In other studies, cattle with high LKT neutralizing antibody titers have higher survival rates in the natural disease and experimental pasteurellosis than animals with low antibody titers(13). Although advances have been made in describing the cytolytic properties of the P.haemolytica LKT, the mechanisms by which it brings about lung injury in cattle are poorly understood. Our laboratory has long been interested in elucidating the contributions and mechanisms by which the LKT induce this acute lung injury in pneumonic pasteurellosis. Three experiments were designed to study if the LKT contributed in the genesis of lung injury in pneumonic pasteurellosis., American Association of Bovine Practitioners Proceedings of the Annual Conference, 1992: Volume 3