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  • 1
    ISSN: 0248-4900
    Keywords: amphibia ; band 3 ; flask cells ; immunocytochemistry ; mitochondria-rich cells ; peanut lectin
    Source: Elsevier Journal Backfiles on ScienceDirect 1907 - 2002
    Topics: Biology
    Type of Medium: Electronic Resource
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  • 2
    ISSN: 0248-4900
    Keywords: Band 3 ; amphibian skin ; anion exchange ; chloride permeability ; mitochondria-rich cells
    Source: Elsevier Journal Backfiles on ScienceDirect 1907 - 2002
    Topics: Biology
    Type of Medium: Electronic Resource
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  • 3
    ISSN: 1432-1106
    Keywords: Hydrocephalus ; Kaolin blockage ; Borna disease virus infection ; Subcommissural organ ; Reissner's fiber ; Immunocytochemistry ; Rat
    Source: Springer Online Journal Archives 1860-2000
    Topics: Medicine
    Notes: Summary The subcommissural organ (SCO)-Reissner's fiber (RF) complex of rats suffering from postnatal hydrocephalus was investigated immunocytochemically (peroxidase-antiperoxidase technique) by use of an antiserum against bovine RF. Hydrocephalus was induced by injecting kaolin into the cisterna magna or by intracerebral infection with Borna disease virus. The kaolin-injected, hydrocephalie male rats were divided into two groups: (1) possessing an open communication between the fourth ventricle and the central canal of the spinal cord; (2) enduring an obliteration of this communication. In the latter group of rats the dilation of the ventricular cavities was far greater than in the former group. The Borna disease virus-infected female rats developed a severe hydrocephalus although in these animals all ventricular cavities and the central canal were in fully open communication. All rats belonging to the above-mentioned three groups displayed essentially the same alterations of their SCO-RF complex: (i) A reduction in the size of SCO and in the height of the ependymal secretory cells. (ii) A progressive disappearance of the immunoreactive hypendymal cells. (iii) The amount of AFRU-immunoreactive secretory material located in the rough endoplasmic reticulum was reduced. (iv) In contrast, the amount, location and immunoreactivity of the apical secretory granules did not undergo variations in comparison to sham-operated rats. (v) In the area of the SCO the layer of pre-RF material was thin or missing and a RF was not formed, and thus the central canal was also free of such secretory products. (vi) Clusters of AFRU-immunoreactive material were found attached to the wall of the Sylvian aqueduct. It is concluded that in the presented types of hydrocephalus: (i) the secretory material stored in the SCO is partially depleted, thus indicating a probably increased turnover of this material; (ii) the SCO continues to secrete into the ventricle; and (iii) unknown factors prevent the assembly of the released secretory material into the characteristic thread-like structure of the RF.
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  • 4
    ISSN: 1432-8798
    Source: Springer Online Journal Archives 1860-2000
    Topics: Medicine
    Notes: Summary.  Mutations in the fusion, F, protein of Sendai virus resulting in increased cleavability by ubiquitous host protease(s), and mutations in the matrix, M, protein resulting in bipolar budding, are both important determinants for the systemic infection in mice caused by the protease activating pantropic mutant, F1-R. Several mutants of Sendai virus (BY, BF, and KD-M) with phenotypes of bipolar budding and/or increased cleavability of F protein were isolated. Genomic RNA sequence analysis of the F and M genes of the mutants revealed that several deduced amino acids in the F and M proteins were different from those of F1-R, T-5 (a revertant of F1-R), and wild-type viruses. The BF and KD-M mutants that budded bipolarly and were also activated by ubiquitous proteases were examined for replication in tissue culture cells and in mice. All of the mutants exhibited multiple-step replication in MDCK, MDBK, and LLC-MK2 cells without trypsin, but formed plaques only in MDCK cells. One of the mutants, designated KD-52M, was similar to F1-R in that it formed plaques in all three cell lines without addition of exogenous protease. However, none of the mutant viruses, including KD-52M, caused a systemic infection in mice. The mutated M protein of F1-R enhances the disruption of microtubles. However, none of the mutants with a bipolar budding phenotype (BY, BF, and KD-M), disrupted the microtubules to the same extent as F1-R. All of these mutants had mutations in the M protein that were different from those found in F1-R. Taken together, these results suggest that mutations at Ser115 to Pro in the F protein and at Asp 128 to Gly and Ile210 to Thr in the M protein of F1-R are the mutations specifically required for the systemic infection caused by F1-R.
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  • 5
    ISSN: 1432-8798
    Source: Springer Online Journal Archives 1860-2000
    Topics: Medicine
    Notes: Summary Hemagglutinating and acetylesterase functions as well as the 124 kDa glycoprotein were present in the highly cell-culture adapted, avirulent bovine coronavirus strain BCV-L9, in the Norden vaccine strain derived from it, and in 5 wild-type, virulent strains that multiplied in HRT-18 cells but were restricted in several types of cultured bovine cells. The BCV-L9 and the wild-type strain BCV-LY-138 agglutinated chicken and mouse erythrocytes. The acetylesterase facilitated break-down of the BCV-erythrocyte complex with chicken but only to a minimal extent with mouse erythrocytes in the receptor-destroying enzyme test. Purified preparations of the vaccine and the wild-type strains agglutinated chicken erythrocytes at low titers and mouse erythrocytes at 128 to 256 times higher titers whereas receptor destroying enzyme activity was detectable only with chicken erythrocytes. When wild-type strains were propagated in HRT cells at low passage levels, they produced 5×105 to 4.5×106 plaque forming units per 50 µl which agglutinated erythrocytes from mice but not from chickens. Diisopropylfluoro-phosphate moderately increased the hemagglutination titers, but completely inhibited the receptor destroying enzyme of purified virus of all strains. It had virtually no influence on the plaque-forming infectivity of the different BCV strains. The acetylesterase of strain BCV-L9 reacting in the receptor-destroying enzyme test was stable for 3h at 37 and 42°C. It was inactivated within 30 min at 56°C while the hemagglutinin function of this strain was stable for 3 h at 37, 42, and 56°C, but it was inactivated at 65°C within 1 h.
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  • 6
    ISSN: 1432-8798
    Source: Springer Online Journal Archives 1860-2000
    Topics: Medicine
    Notes: Summary Selective damage of the optic nerve of 14 rabbits without interfering with the choroidal blood flow which supplies the retina and without altering the autonomic nerve supply was successfully achieved by Xenon coagulation. This procedure interrupted the axonal pathway between the brain and the eye. After experimental infection with Borna disease virus the typical disease could be induced. The pathognomonic retinopathy as well as characteristic perivascular choroidal infiltrates, however, did not appear in eyes with coagulated nerve heads. In general virus-specific antigen or infectious virus were not present in the retinas of such damaged eyes. These results permit the conclusion that the ocular expression of Borna disease is a consequence of virus transport via the optic nerve.
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  • 7
    ISSN: 1432-8798
    Source: Springer Online Journal Archives 1860-2000
    Topics: Medicine
    Notes: Summary Influenza virus A/turkey/Ontario/7732/66 (H 5 N 9), which is highly pathogenic to chickens, is nonpathogenic to quails. After intratracheal or intramuscular inoculation of quails, virus replication was limited to the respiratory tract, genital organs, and pancreas. However, aggravation of the pathogenicity was achieved through adaptation only by several passages of lung homogenates in quails. The adapted virus caused a fatal generalized infection in quails as well as in chickens. The pathogenic change of the virus could not be explained by a change in the proteolytic cleavability of the hemagglutinin, because no difference was found in the cleavability between the original and the adapted viruses. The adapted virus formed larger plaques and grew a little faster than the original one in both chicken embryo and quail embryo cells. The faster multiplication of the adapted virus at the site of infection might be the reason for its change in pathogenicity. The original virus could circulate among quails by a direct contact transmission without causing disease. The shed virus, however, caused a fatal infection in chickens when they were kept in contact with the infected quails. The epidemiological significance of this observation is discussed.
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  • 8
    ISSN: 1432-8798
    Source: Springer Online Journal Archives 1860-2000
    Topics: Medicine
    Notes: Summary During October of 1984 an influenza epidemic occurred on mink farms in the coastal region of South Sweden. Six strains of an influenza A virus were isolated. All six isolates were of the H10 subtype in combination with N4. The H10 subtype in combination with various N subtypes was hitherto only known to occur in avian strains, the prototype being the A/chicken/Germany/N/49 (H10N7) virus.
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  • 9
    ISSN: 1432-8798
    Source: Springer Online Journal Archives 1860-2000
    Topics: Medicine
    Notes: Summary Increases in infectiousness, neurotropism and virulence were found in a laboratory variant of influenza A/Seal/Massachussets/1/80 (H7N7) virus having a highly cleavable hemagglutinin. Sequential passage from host to host further increased pathogenicity of the H7N7 virus in mice, ferrets and rats.
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  • 10
    ISSN: 1432-8798
    Source: Springer Online Journal Archives 1860-2000
    Topics: Medicine
    Notes: Summary Disulfiram at concentrations between 0.1 and 0.3 mM inhibits the multiplication of Semliki Forest virus (SFV), fowl plague virus (FPV), Newcastle disease virus (NDV), vesicular stomatitis virus (VSV), and pseudorabies virus (PRV), when administered 1 hour before and during adsorption. There is, however, no inhibition of virus multiplication, when the drug is added after adsorption onto chick embryo cells. Disulfiram interferes neither with the receptors of the virus nor of erythrocytes, and it does not prevent virus adsorption. Possibly an early step in virus multiplication is affected by disulfiram. Infected cells once treated with the drug recover after some time of incubation in an inhibitor-free medium. The inhibitory state can be maintained, however, if relatively low doses of disulfiram are present in the culture medium also after adsorption. Disulfiram has no effect on macromolecular synthesis of the host cells. It has, however, a marked effect on membrane function. While virus multiplication is readily inhibited by disulfiram when chick embryo or BHK cells were investigated, virus multiplication in HeLa cells is almost resistant against the action of disulfiram.
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