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  • 1
    ISSN: 1573-0832
    Keywords: Chick embryo ; Embryopathology ; Fumonisin ; Fusarium proliferatum ; Moniliformin
    Source: Springer Online Journal Archives 1860-2000
    Topics: Biology , Medicine
    Notes: Abstract One hundred eight fertile eggs (Columbia × New Hampshire) were assigned to 10 groups of 10 eggs each (2 control groups had 14 eggs each). Five groups of eggs were inoculated on day 1 of incubation, while the other 5 groups were inoculated on day 10. The inoculum of the 4 treatment groups on both day 1 and 10 consisted of 1,10, or 100 µM purified fumonisin B1 (FB1) or a culture material extract (CME) ofFusarium proliferatum, having known amounts of FB1, FB2 and moniliformin (FB1 20 µM; FB2 4 µM and moniliformin 7 µM). Inoculum consisted of the respective toxin(s) dissolved in 100 µl double distilled, autoclaved water (diluent). Control eggs were inoculated with diluent only. Mortality was both dose- and time-responsive in all treatments. Eggs inoculated on day 1 with 1 µM FB1 had 50% mortality; 10 µM FB1 had 70% mortality; 100 µM FB1 had 100% mortality; and CME had 100% mortality. Eggs inoculated on day 10 with 1,10 or 100 µM FB1 or CME had 30, 60, 90 and 80% mortality, respectively. Normal chicks were hatched from all control eggs. The median death times (MDT50) were inversely dose-responsive in all treatments, ranging from 3.0 to 7.4 days in embryos exposed on day 1 and from 3.2 to 9.0 days in those exposed on day 10. Early embryonic changes in exposed embryos included hydrocephalus, enlarged beaks and elongated necks. Pathologic changes were noted in liver, kidneys, heart, lungs, musculoskeletal system, intestines, testes and brain toxin-exposed embryos.
    Type of Medium: Electronic Resource
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  • 2
    ISSN: 1573-0832
    Keywords: Chicken ; Fumonisin ; Fusarium moniliforme ; Fusarium proliferatum ; Moniliformin ; Mycotoxin
    Source: Springer Online Journal Archives 1860-2000
    Topics: Biology , Medicine
    Notes: Abstract Two hundred twenty-eight male chicks (Columbia × New Hampshire) were given feed amended with autoclaved culture material (CM) ofFusarium proliferatum Containing fumonisin B1 (FB1), fumonisin B2 (FB2) and moniliformin in 3 separate feeding trials. Purified FB1 and moniliformin were given separately and in combination in a fourth feeding trial. Birds were given amended rations at day 1 (Trial 1 and 4), day 7 (Trial 2), and day 21 (Trial 3) and their respective ration was given for 28 days (Trial 1), 21 days (Trial 2), 7 days (Trial 3), and 14 days (Trial 4). FB1 concentrations were 546, 193, and 61 ppm; FB2 were 98, 38 and 14 ppm; and moniliformin were 367, 193, and 66 ppm in the first 3 feeding trial regimens. Chicks in Trial 4 were given dietary concentrations of purified FB1 at 274 and 125 ppm, and moniliformin at 154 and 27 ppm. FB1 and moniliformin, both alone and in combination, produced dose-responsive clinical signs, reduced weight gains and mortality in chicks. Age of birds given amended feeds had little difference in the clinical response; however, those given the rations from days 7 or 21 were slightly less susceptible than those given rations beginning at 1 day of age. Additive effects were noted when the toxins were given in combination. When toxins were given separately, adverse effects took longer to occur. A system to monitor pattern and rate of defecation (RD) was developed for assessing the chicks' approach to feed, water and heat source as illness progressed. Our results indicate that chicks fed corn heavily infected withF. proliferatum under field conditions could suffer acute death similar to that described for ‘spiking mortality syndrome’ during the first 3 weeks of age.
    Type of Medium: Electronic Resource
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  • 3
    ISSN: 1432-0878
    Keywords: Jejunum ; Glycoproteins ; Radioautography ; Nocodazole ; Colchicine ; Mouse
    Source: Springer Online Journal Archives 1860-2000
    Topics: Biology , Medicine
    Notes: Summary Explants from mouse jejunum were cultured for 3–7 h in the absence (control) or presence of colchicine (100 gm/ml) or nocodazole (10 μg/ml). In recovery experiments, expiants were cultured in fresh medium for an additional period. To label glycoproteins, 3H-fucose was added during the last 3 or 6 h of the initial culture or recovery period. Subcellular fractionation studies revealed that colchicine and nocodazole inhibited migration of labelled glycoproteins to the brush border (P2) by 40–45%. Radioautographic studies of absorptive cells showed that colchicine and nocodazole inhibited labelling of the microvillous border by 67% and 87%, while labelling of the basolateral plasma membrane increased by 114% and 275%. Immunocytochemical studies revealed that both colchicine and nocodazole caused the virtual disappearance of the microtubular network in the absorptive cells. It is possible that some glycoproteins normally destined for the microvillous border are rerouted to the basolateral membrane. The observed loss of microtubules after drug treatment suggests that microtubules may play a role in the intracellular migration of membrane glycoproteins. Additional support for this concept is provided by the fact that in recovery experiments the distribution of label returned to control values after the microtubular network became re-established.
    Type of Medium: Electronic Resource
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  • 4
    ISSN: 1432-0878
    Keywords: Jejunum ; Organ culture ; Glycoproteins ; Monensin ; Radioautography ; Mouse
    Source: Springer Online Journal Archives 1860-2000
    Topics: Biology , Medicine
    Notes: Summary Expiants from adult mouse jejunum were cultured for 3 h in a medium which contained both 3H-fucose (10 or 25 μCi/ml) and monensin (100 μM) or 3H-fucose only (control). Radiochemical analysis of cell fractions showed that 3H-fucose labelling of the brush border fraction decreased 42% in monensin-treated expiants, suggesting that in absorptive cells the intracellular transport of newly synthesized glycoproteins to the apical plasma membrane had been inhibited. Electron-microscopic examination of treated expiants revealed a variation in response to the drug from region to region. In some areas, both absorptive and goblet cells exhibited little alteration. In others, the Golgi cisternae of both absorptive and goblet cells were entirely replaced by large vacuoles, and in the latter cell type, the cisternae of the rough endoplasmic reticulum were greatly distended. Electron-microscopic radioautographic analysis showed that in absorptive and goblet cells exhibiting little morphological change, intracellular transport of newly synthesized glycoproteins was similar to that in controls. In regions where absorptive cells exhibited extensive Golgi modifications, intracellular transport remained normal in some cases; more often-however, there was a marked inhibition (over 70%) of transport of labelled glycoproteins to the apical surface. Transport to the basolateral membrane was never affected. In goblet cells exhibiting modifications of the Golgi apparatus and rough endoplasmic reticulum, no incorporation of 3H-fucose label in the Golgi apparatus occurred, suggesting a block of intracellular transport proximal to the site at which 3H-fucose is added. In absorptive cells, this does not appear to be the case, since the level of 3H-fucose incorporation in all treated cells remained similar to that in controls.
    Type of Medium: Electronic Resource
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