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1

The impact of neuraminidase on apoptosis in cultures of blood lymphocytes isolated from rats bearing Morris hepatoma

100%
Gasiorowski K., Steciwko A., Grata-Borkowska U., Drobnik J.
Cellular and Molecular Biology Letters
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2004
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tom 09
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nr 2
Lymphocytes were obtained by heart-punction from rats bearing Morris hepatoma. In the short term, 18-hour cultures of these lymphocytes exhibited a significantly higher amount of apoptotic cells than lymphocyte cultures from the healthy, control animals. Neuraminidase, injected into the caudal vein of the rats with Morris hepatoma, caused a marked lowering in the amount of apoptotic blood-lymphocytes and an elevation of the amount of viable cells. The possible mechanism of neuraminidase preventing the apoptosis of blood-circulating lymphocytes in tumour hosts is discussed herein.
2

Influenza A viruses of avian origin circulating in pigs and other mammals

86%
Urbaniak K., Kowalczyk A., Markowska-Daniel I.
Acta Biochimica Polonica
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2014
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tom 61
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nr 3
3

Studies on the adaptation of influenza virus replicated at low temperature. V. Isoelectric focusing studies

72%
Brydak L.
Acta Microbiologica Polonica
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1993
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tom 42
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nr 1
4

How influenza's neuraminidase promotes virulence and creates localized lung mucosa immunodeficiency

72%
Bhatia A., Kast R. E.
Cellular and Molecular Biology Letters
|
2007
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tom 12
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nr 1
Neuraminidase (NA) is an enzyme coded for by the genome of influenza critical for its pathogenicity and survival. Three currently accepted roles for this NA in promoting influenza virulence are: 1. NA cleaves newly formed virus particles from the host cell membrane. Without NA, newly formed virus would remain attached to the cell within which it was produced. 2. NA prevents newly released virus particles from aggregating to each other, preventing clumping that would reduce dissemination. 3. NA promotes viral penetration of sialic acid-rich mucin that bathes and protects respiratory epithelium through which the virus must spread and replicate. We outline here previous research evidence of two further, albeit hypothetical, functions of NA that together could cause disruption the mucosa-IgA axis, creating localized partial immunosuppressed state, enhancing both influenza infection itself and secondary bacterial pneumonia: 4. IgA provides primary immunoglobulin defense of mucosal surfaces. The hinge region of IgA is normally sialylated. IgA denuded of sialic acid is recognized, bound, and cleared by hepatic asialoglycoprotein receptor (ASGPR). Thus, IgA exposed to free NA would be so denuded and have increased hepatic clearance. 5. NA removes sialic acid moieties from mucosa-residing gamma/delta T cells or IgA producing B cells. Previous work indicates desialylation of these lymphocytes' outer cell membrane results in altered homing, to bone marrow, away from mucosa. Currently marketed NA inhibitors oseltamivir (Tamiflu) and zanamivir (Relenza) are FDA approved in USA for influenza prophylaxis and treatment. These NA inhibitors lower incidence of secondary bacterial infection in cases where an influenza infection occurs despite their use. Moreover, they are ameliorative in patients with secondary bacterial infections treated with antibiotics, a benefit that surpasses the treatment of antibiotics alone. We interpret these last two points as indicating our ascription of localized immunosuppression to influenza's NA could be correct and lead to new treatments of infections generally.
5

Effect of neuraminidase on adherence of Pseudomonas aeruginosa to human buccal epithelial cells. Inhibition of adhesion by monosaccharides

72%
Wolska K., Zabielska K., Jakubczak A.
Polish Journal of Microbiology
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2006
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tom 55
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nr 1
The aim of this study was to evaluate the action of Clostridium perfringens neuraminidase on the adherence of 28 strains of Pseudomonas aeruginosa which were isolated from humans, different animals and environment to human buccal epithelial cells (BECs). Two reference strains - NCTC 6749 and ATCC 27853 were also examined. Incubation of cells with the enzyme significantly increased bacterial adherence (a mean number of bacteria adhering to cells amounted 19.62 ±9.20, for controls - 7.54 ±5.86). The reference strains of Pseudomonas aeruginosa showed the following adherence: NCTC 6749-43.04 (control 20.83) and ATCC 27853-22.21 (control 5.51). This study demonstrates that asialogangliosides function as receptors on buccal epithelial cells for P. aeruginosa strains. Monosaccharides inhibition studies showed an inhibition of adhesion of P. aeruginosa (two reference strains - NCTC 6749 and ATCC 27853, two hospital strains - 80/85 and 351) to normal BECs in the presence of N-acetylneuraminic acid and N-acetylgalactosamine. D-galactose is the best inhibitor of bacterial adhesion to neuraminized BECs. All monosaccharides used had a significant effect on P. aeruginosa adherence to trypsinized BECs. These data suggest a difference in the receptors on the three types of BECs.
6
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Effects of neuraminidase on apoptosis of blood lymphocytes in rats with implanted Morris tumor

58%
Grata-Borkowska U., Steciwko A., Pokorski M., Drobnik J., Gasiorowski K., Pirogowicz I., Cieslar-Marczak E.
Journal of Physiology and Pharmacology. Supplement
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2007
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tom 58
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nr 5
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