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  • 1.
    Eriksson, Cecilia
    et al.
    Göteborgs universitet.
    Lausmaa, Jukka
    SP Swedish National Testing and Research Institute, Boras.
    Nygren, Håkan
    Göteborgs universitet.
    Interactions between human whole blood and modified TiO2-surfaces: Influence of surface topography and oxide thickness on leukocyte adhesion and activation2001In: Biomaterials, ISSN 0142-9612, E-ISSN 1878-5905, Vol. 22, no 14, p. 1987-1996Article in journal (Refereed)
    Abstract [en]

    An in vitro model (Nygren et al., J Lab Clin Med 129 (1997) 35-46) was used to investigate interactions between leukocytes and four modified TiO2-surfaces. Surface topography was measured using scanning electron microscopy and optical profilometry while Auger electron spectroscopy was used to determine surface composition and oxide thickness. The surfaces were either smooth or rough with either thin or thick oxides. All surfaces consisted of TiO2 covered by a carbonaceous layer. The surfaces were incubated with capillary blood for time periods of between 8 min and 32h. Immunofluorescence techniques together with computer aided image analysis and chemiluminescence technique were used to detect cell adhesion, expression of adhesion receptors and the zymosan-stimulated respiratory burst response. Leukocyte adhesion to the surfaces increased during the first hours of blood-material contact and then decreased. Polymorphonuclear granulocytes were the dominating leukocytes on all surfaces followed by monocytes. Cells adhering to rough surfaces had higher normalized expression of adhesive receptors than cells on smooth surfaces. Maximum respiratory burst response occurred earlier on the smooth than on the rough surfaces. In conclusion, topography had a greater impact than oxide thickness on most cellular reactions investigated, but the latter often had a dampening effect on the responses. (C) 2001 Elsevier Science Ltd. All rights reserved.

  • 2.
    Prakash, Mansi
    et al.
    Dr. D. Y Patil Biotechnology and Bioinformatics Institute, Dr. D. Y. Patil Vidyapeeth, Tathawade, Pune, India.
    Bodas, Manish
    Dr. D. Y Patil Biotechnology and Bioinformatics Institute, Dr. D. Y. Patil Vidyapeeth, Tathawade, Pune, India.
    Prakash, Divya
    Dr. D. Y Patil Biotechnology and Bioinformatics Institute, Dr. D. Y. Patil Vidyapeeth, Tathawade, Pune, India.
    Nawani, Neelu
    Dr. D. Y Patil Biotechnology and Bioinformatics Institute, Dr. D. Y. Patil Vidyapeeth, Tathawade, Pune, India.
    Khetmalas, Madhukar
    Dr. D. Y Patil Biotechnology and Bioinformatics Institute, Dr. D. Y. Patil Vidyapeeth, Tathawade, Pune, India.
    Mandal, Abul
    University of Skövde, School of Life Sciences. University of Skövde, The Systems Biology Research Centre.
    Eriksson, Cecilia
    University of Skövde, School of Life Sciences. University of Skövde, The Systems Biology Research Centre.
    Diverse pathological implications of YKL-40: Answers may lie in 'outside-in' signaling2013In: Cellular Signalling, ISSN 0898-6568, E-ISSN 1873-3913, Vol. 25, no 7, p. 1567-1573Article, review/survey (Refereed)
    Abstract [en]

    The developing paradigms about YKL-40, a member of the "mammalian chitinase-like proteins", from across the globe, project it as a vital parameter for the detection of disease onset and progression. It is expressed and secreted by cancer cells of different origins along with a variety of non-malignant cells including inflammatory and structural cells. Numerous studies demonstrate that YKL-40 over-expression is associated with increased patient mortality though the cellular receptors responsible for mediating these effects have not yet been identified. The putative YKL-40 ligands are thought to be carbohydrate structures, since it is capable of binding chitin, chito-oligosaccharides and heparin. Binding of collagen to YKL-40, identified it as the only non-carbohydrate extracellular matrix (ECM) ligand for YKL-40. Our broad understanding of YKL-40 as a versatile biomarker and its involvement in activating several signaling pathways make us anticipate that its specific receptors/binding partners may exist on the cell surface also. The cell surface heparan sulfate (HS) moieties seem to be the potential candidates for this role, suggesting that it could interact with HS-proteoglycans. It is recommended to clearly delineate YKL-40-mediated signaling mechanisms before promoting the YKL-40 know-how for translational research, in both diagnostic and therapeutic applications. The present review provides an overview of YKL-40 as a versatile biomarker, discussing the related pathological mechanisms and aims to reassess and unify the already proposed diverse hypotheses in YKL-40-regulated signaling mechanisms. (c) 2013 Elsevier Inc. All rights reserved.

  • 3.
    Salgaonkar, Neeta A.
    et al.
    Microbial Diversity Research Centre, Dr D Y Patil Biotechnology and Bioinformatics Institute, Dr D Y Patil Vidyapeeth, Pune, India.
    Thakare, Prasad M.
    Microbial Diversity Research Centre, Dr D Y Patil Biotechnology and Bioinformatics Institute, Dr D Y Patil Vidyapeeth, Pune, India.
    Junnarkar, Manisha V.
    Microbial Diversity Research Centre, Dr D Y Patil Biotechnology and Bioinformatics Institute, Dr D Y Patil Vidyapeeth, Pune, India.
    Kapadnis, Balasaheb P.
    Department of Microbiology, Savitribai Phule University of Pune, Pune, India.
    Mandal, Abul
    University of Skövde, School of Bioscience. University of Skövde, The Systems Biology Research Centre.
    Eriksson, Cecilia
    University of Skövde, School of Health and Education. University of Skövde, Health and Education.
    Neelu, Nawani N.
    Microbial Diversity Research Centre, Dr D Y Patil Biotechnology and Bioinformatics Institute, Dr D Y Patil Vidyapeeth, Pune, India.
    Use of N,N-diacetylchitobiose in decreasing toxic effects of indoor air pollution by preventing oxidative DNA damage2016In: Biologia (Bratislava), ISSN 0006-3088, E-ISSN 1336-9563, Vol. 71, no 5, p. 505-515Article in journal (Refereed)
    Abstract [en]

    Indoor air pollution occurs due to hazardous pollutants, such as tobacco smoke, pesticides and carbon oxides, sulphur oxides and nitrogen oxides arising from combustion of biomass fuels. Exposure to these pollutants results in respiratory conditions like asthma, chronic obstructive pulmonary disease, lung cancer, pneumonia and other lower respiratory infections. Several of these infections are a result of inflammation and oxidative stress. Here we demonstrate the ability of N,N-diacetylchitobiose in preventing oxidative DNA damage in peripheral blood mononuclear cells exposed to biomass smoke extracts and cigarette smoke extract. The cytotoxic effect of these pollutants was determined by trypan blue exclusion assay in peripheral blood mononuclear cells, where cytotoxicity in decreasing order was  garette > wood > sawdust > cowdung. Cytotoxicity could be due to single- and double-strand breaks in the DNA as a result of oxidative stress. Comet assay measures the extent of DNA damage in the cells exposed to toxic agents. When mononuclear cells were treated with N,N-diacetylchitobiose and later exposed to smoke extracts, the extent of DNA damage decreased by 44.5% and 57.5% as compared to untreated cells. The protection offered by N,N-diacetylchitobiose towards oxidative DNA damage was at par with quercetin, a popular herbal medicine. Glutathione-S-transferase activity was determined in mononuclear cells exposed to smoke extracts, where oxidative stress in cells exposed to cigarette smoke extract was maximum. The present study demonstrates for the first time the ability of N,N -diacetylchitobiose to alleviate the harmful effects of indoor air pollutants.

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