Reproductive and economic impact following controlled introduction of cattle persistently infected with bovine viral diarrhea virus into a naive group of heifers

The reproductive impact following controlled introduction of animals persistently infected (PI) with bovine viral diarrhea virus (BVDV) was evaluated in BVDV-naive heifers. Heifers were randomly allocated into two groups: an unexposed control herd (n = 34) and a herd exposed to five persistently infected (PI) animals for 7 mo, beginning 50 days before the breeding season (n = 34). Initiation of the BVDV-challenge was timed to mimic either direct contact with PI calves born in the previous calving season or accidental introduction of PI herd additions prior to the breeding season. The PI animals represented BVDV Types 1a (n = 3), 1b (n = 1) and 2 (n = 1). Two BVDV-free, seropositive bulls were used in each group for 78 days breeding seasons. In both groups, 33 of 34 heifers became pregnant, with similar distribution of fetal ages. Two heifers in each group aborted (etiology undetermined). In addition, one calf was born dead and one calf died 3 days post-partum in the BVDV-exposed group. One calf in the unexposed group died 4 mo post-partum. No calves, including the stillborn calf and the two calves that died prior to weaning, were persistently infected with BVDV. In summary, introduction of PI cattle to a group of BVDV-naive heifers 50 days prior to the breeding season did not negatively impact reproductive performance. To the contrary, the active immunity that developed following field exposure to BVDV provided effective reproductive and fetal protection during the breeding season and subsequent gestations, despite continuous exposure to PI animals until approximately midgestation. Although BVDV can have potentially devastating reproductive effects, timing of infection is a critical determinant in the outcome of a BVDV infection. A controlled breeding season with introduction of herd additions at less critical reproductive time points can mitigate the negative reproductive health consequences of BVDV.     

Imatinib and Dasatinib Inhibit Hemangiosarcoma and Implicate PDGFR-β and Src in Tumor Growth

Hemangiosarcoma, a natural model of human angiosarcoma, is an aggressive vascular tumor diagnosed commonly in dogs. The documented expression of several receptor tyrosine kinases (RTKs) by these tumors makes them attractive targets for therapeutic intervention using tyrosine kinase inhibitors (TKIs). However, we possess limited knowledge of the effects of TKIs on hemangiosarcoma as well as other soft tissue sarcomas. We report here on the use of the TKIs imatinib and dasatinib in canine hemangiosarcoma and their effects on platelet-derived growth factor receptor β (PDGFR-β) and Src inhibition. Both TKIs reduced cell viability, but dasatinib was markedly more potent in this regard, mediating cytotoxic effects orders of magnitude greater than imatinib. Dasatinib also inhibited the phosphorylation of the shared PDGFR-β target at a concentration approximately 1000 times less than that needed by imatinib and effectively blocked Src phosphorylation. Both inhibitors augmented the response to doxorubicin, suggesting that clinical responses likely will be improved using both drugs in combination; however, dasatinib was significantly (P < .05) more effective in this context. Despite the higher concentrations needed in cell-based assays, imatinib significantly inhibited tumor growth (P < .05) in a tumor xenograft model, highlighting that disruption of PDGFR-β/PDGF signaling may be important in targeting the angiogenic nature of these tumors. Treatment of a dog with spontaneously occurring hemangiosarcoma established that clinically achievable doses of dasatinib may be realized in dogs and provides a means to investigate the effect of TKIs on soft tissue sarcomas in a large animal model.     

Degradation of Atrazine by Hornwort in Aquatic Systems

Hornwort (Ceratophyllum deinersuin) incubated in the presence of 1 mg L^{-1 14}C atrazine in an aqueous nutrient solution became radioactive. Microscopic autoradiography was used to investigate the localization of ¹⁴C atrazine in a hornwort/epiphyte system. Radioactivity was present within the plant tissue (and also in the nutrient solution), with larger quantities in mature tissue, including stems compared with young tissue. An irregular distribution of black silver granules (which indicate radioactivity) was observable on the plant surface, suggesting the possible involvement of epiphytes (plant surface microorganisms) in the degradation process. Labeled compounds in the extracted plant included atrazine and a major metabolite that may have been an artrazine-glutathione connjugate. Concentrations of atrazine and the metabolite, and the fraction of the metabolite (based on total radioactivity), all in the extracted plant, were dependent on the initial atrazine concentration in the solution. The degradation process was light dependent and the analyses of the nutrient solution indicated that the first half-life of atrazine in the presence of hornwort was 5 days under day/night conditions, while only about 30% of initial atrazine disappeared after 3 weeks under complete dark. The major metabolite in the solution was identified as deethylatrazine.     

Iron (II) Activated Persulfate Oxidation of MGP Contaminated Soil

The persulfate anion (S₂O₈ ^2?) is a strong oxidant with a redox potential of 2.01 V. However, when mixed with iron (II), it is capable of forming the sulfate radical (SO₄ ^?.) that has an even higher redox potential (E ^o = 2.6 V). In these studies the sulfate radical was investigated to determine if it was a feasible oxidant for the destruction of BTEX and PAH compounds found in MGP contaminated soil. The sulfate radical was generated by either the sequential addition of iron (II) solutions or by a single addition of a citric acid chelated iron (II) solution. The sequentially added iron destroyed 86% of the total BTEX concentration and 56% of the total PAH concentration in the soil. The citric acid chelated iron destroyed 95% of the total BTEX concentration and 85% of the total PAH concentration. A second dose of persulfate and citric acid chelated iron (II) resulted in the destruction of 99% of the total BTEX concentration and 92% of the total PAH concentration. In both the sequential and chelated iron studies the lower molecular weight BTEX compounds were oxidized to a greater extent than the higher molecular weight BTEX compounds, whereas the oxidation of PAH compounds showed no preference to molecular weight.     

Isolation of oligomeric proanthocyanidins from flavonoid-producing cell cultures

Summary The extraction, fractionation, and chromatographic separation of a series of proanthocyanidin monomers and oligomers were facilitated using a flavonoid-rich cell culture of Vaccinium pahalae Skottsberg as the donor tissue. The cell cultures, after exposure to light, readily accumulated anthocyanin pigments and other flavonoids in relatively large amounts, with minimal concurrent production of pectins, enzymes, and complex sugars produced in field-grown Vaccinium berries. The absence of these interfering compounds greatly simplified the isolation and purification of proanthocyanidins and other phenolic compounds from cell cultures, primarily using vacuum chromatography. Subsequently, the structures and molecular weights of several individual compounds and the general composition of unresolved fractions were established with ¹H- and ¹³C-NMR and MS. The initial extract of V. pahalae cell cultures was readily fractionated on silica gel to yield a series of fractions containing proanthocyanidin B-2, a series of increasingly polar proanthocyanidin oligomers ranging from dimers to heptamers largely based on (−)-epicatechin structures (some with A-type linkages), a mixture of E- and Z-p-coumaric acid, the corresponding 4-O-glucoside, and other compounds containing E- and Z-p-coumaric acid moieties. Cell culture extracts demonstrated broad antioxidant capacity and significant ability to inhibit tumor promotion in vitro, as indicated in an ornithine decarboxylase assay.