his.sePublications
Change search
Refine search result
1 - 7 of 7
CiteExportLink to result list
Permanent link
Cite
Citation style
  • apa
  • harvard1
  • ieee
  • modern-language-association-8th-edition
  • vancouver
  • Other style
More styles
Language
  • de-DE
  • en-GB
  • en-US
  • fi-FI
  • nn-NO
  • nn-NB
  • sv-SE
  • Other locale
More languages
Output format
  • html
  • text
  • asciidoc
  • rtf
Rows per page
  • 5
  • 10
  • 20
  • 50
  • 100
  • 250
Sort
  • Standard (Relevance)
  • Author A-Ö
  • Author Ö-A
  • Title A-Ö
  • Title Ö-A
  • Publication type A-Ö
  • Publication type Ö-A
  • Issued (Oldest first)
  • Issued (Newest first)
  • Created (Oldest first)
  • Created (Newest first)
  • Last updated (Oldest first)
  • Last updated (Newest first)
  • Disputation date (earliest first)
  • Disputation date (latest first)
  • Standard (Relevance)
  • Author A-Ö
  • Author Ö-A
  • Title A-Ö
  • Title Ö-A
  • Publication type A-Ö
  • Publication type Ö-A
  • Issued (Oldest first)
  • Issued (Newest first)
  • Created (Oldest first)
  • Created (Newest first)
  • Last updated (Oldest first)
  • Last updated (Newest first)
  • Disputation date (earliest first)
  • Disputation date (latest first)
Select
The maximal number of hits you can export is 250. When you want to export more records please use the Create feeds function.
  • 1.
    Eriksson, Katarina
    et al.
    Alands Cent Sjukhus, Dept Obstet & Gynecol, Mariehamn, Finland / Linkoping Univ, Dept Clin & Expt Med, Linkoping, Sweden .
    Larsson, Per-Göran
    University of Skövde, School of Life Sciences.
    Nilsson, Maud
    Linkoping Univ, Dept Clin & Expt Med, Linkoping, Sweden .
    Forsum, Urban
    Linkoping Univ, Dept Clin & Expt Med, Linkoping, Sweden .
    Vaginal retention of locally administered clindamycin2011In: Acta Pathologica, Microbiologica et Immunologica Scandinavica (APMIS), ISSN 0903-4641, E-ISSN 1600-0463, Vol. 119, no 6, p. 373-376Article in journal (Refereed)
    Abstract [en]

    Since bacterial vaginosis (BV) is characterized by a lack of, or very few, lactobacilli and high numbers of small, mostly anaerobic bacteria, an obvious treatment modality would be eradication of the BV-associated bacterial flora followed by reintroduction of lactobacilli vaginally. As probiotic treatment with lactobacilli is one tool for improving the cure rate when treating BV, it is necessary to know the length of time after treatment that clindamycin can be found in the vagina and if this could interfere with the growth of the probiotic lactobacilli. We evaluated the vaginal concentration of clindamycin in 12 women for 8 days to obtain data on the concentration of clindamycin in the vagina after intravaginal treatment with the drug. The participants were examined five times between two menstrual periods: before treatment, the day after treatment was finished, and 3, 5 and 8 days post-treatment. The first day post-treatment clindamycin 0.46 x 10-3 to 8.4 x 10-3 g/g vaginal fluid (median 2.87 x 10-3) was found. Thereafter, the concentration of clindamycin decreased rapidly. In 10 patients clindamycin was found after 3 days. A very low concentration was still present 5 days after treatment in four patients. After 8 days no clindamycin was found. Clindamycin is rapidly eliminated from the vagina, within 3-8 days, after local administration. Our results indicate that treatment with probiotic lactobacilli could be problematic if carried out within 5 days after cessation of clindamycin treatment.

  • 2.
    Fernandes, Ricardo A.
    et al.
    Radcliffe Department of Medicine, John Radcliffe Hospital, University of Oxford, United Kingdom / Medical Research Council Human Immunology Unit, John Radcliffe Hospital, University of Oxford, United Kingdom / Department of Molecular and Cellular Physiology, Department of Structural Biology, Stanford University, United States.
    Ganzinger, Kristina A.
    Department of Chemistry, University of Cambridge, United Kingdom / Living Matter Department, Physics of Cellular Interactions Group, AMOLF, Amsterdam, Netherlands.
    Tzou, Justin C.
    Department of Applied and Computational Mathematics and Statistics, University of Notre Dame, United States.
    Jönsson, Peter
    Department of Chemistry, University of Cambridge, United Kingdom / Department of Chemistry, Lund University, Sweden.
    Lee, Steven F.
    Department of Chemistry, University of Cambridge, United Kingdom.
    Palayret, Matthieu
    Department of Chemistry, University of Cambridge, United Kingdom.
    Santos, Ana Mafalda
    Radcliffe Department of Medicine, John Radcliffe Hospital, University of Oxford, United Kingdom / Medical Research Council Human Immunology Unit, John Radcliffe Hospital, University of Oxford, United Kingdom.
    Carr, Alexander R.
    Department of Chemistry, University of Cambridge, United Kingdom.
    Ponjavic, Aleks
    Department of Chemistry, University of Cambridge, United Kingdom.
    Chang, Veronica T.
    Radcliffe Department of Medicine, John Radcliffe Hospital, University of Oxford, United Kingdom / Medical Research Council Human Immunology Unit, John Radcliffe Hospital, University of Oxford, United Kingdom / Neurobiology Division, Medical Research Council Laboratory of Molecular Biology, Cambridge, United Kingdom.
    Macleod, Charlotte
    Department of Chemistry, University of Cambridge, United Kingdom.
    Lagerholm, B. Christoffer
    Radcliffe Department of Medicine, John Radcliffe Hospital, University of Oxford, United Kingdom.
    Lindsay, Alan E.
    Mathematics Department, University of British Columbia, Vancouver, Canada.
    Dushek, Omer
    Sir William Dunn School of Pathology, University of Oxford, United Kingdom / Wolfson Centre for Mathematical Biology, University of Oxford, United Kingdom.
    Tilevik, Andreas
    University of Skövde, School of Bioscience. University of Skövde, The Systems Biology Research Centre. School of Bioscience, University of Skövde, Sweden.
    Davis, Simon J.
    Radcliffe Department of Medicine, John Radcliffe Hospital, University of Oxford, United Kingdom / Medical Research Council Human Immunology Unit, John Radcliffe Hospital, University of Oxford, United Kingdom.
    Klenerman, David
    Department of Chemistry, University of Cambridge, United Kingdom.
    A cell topography-based mechanism for ligand discrimination by the T cell receptor2019In: Proceedings of the National Academy of Sciences of the United States of America, ISSN 0027-8424, E-ISSN 1091-6490, Vol. 116, no 28, p. 14002-14010Article in journal (Refereed)
    Abstract [en]

    The T cell receptor (TCR) initiates the elimination of pathogens and tumors by T cells. To avoid damage to the host, the receptor must be capable of discriminating between wild-type and mutated self and nonself peptide ligands presented by host cells. Exactly how the TCR does this is unknown. In resting T cells, the TCR is largely unphosphorylated due to the dominance of phosphatases over the kinases expressed at the cell surface. However, when agonist peptides are presented to the TCR by major histocompatibility complex proteins expressed by antigen-presenting cells (APCs), very fast receptor triggering, i.e., TCR phosphorylation, occurs. Recent work suggests that this depends on the local exclusion of the phosphatases from regions of contact of the T cells with the APCs. Here, we developed and tested a quantitative treatment of receptor triggering reliant only on TCR dwell time in phosphatase-depleted cell contacts constrained in area by cell topography. Using the model and experimentally derived parameters, we found that ligand discrimination likely depends crucially on individual contacts being ∼200 nm in radius, matching the dimensions of the surface protrusions used by T cells to interrogate their targets. The model not only correctly predicted the relative signaling potencies of known agonists and nonagonists but also achieved this in the absence of kinetic proofreading. Our work provides a simple, quantitative, and predictive molecular framework for understanding why TCR triggering is so selective and fast and reveals that, for some receptors, cell topography likely influences signaling outcomes. 

  • 3.
    Hambardzumyan, Karen
    University of Skövde, School of Life Sciences.
    Bioengineered T cells for Leukaemia and Lymphoma2011Independent thesis Advanced level (degree of Master (One Year)), 20 credits / 30 HE creditsStudent thesis
    Abstract [en]

    Cancer immunotherapy is a promising tool for treatment of malignancies. However, there are still hindrances that need to be overcome. Chimeric antigen receptors have the ability to direct immune cytotoxic cells towards tumour-associated antigens in major histocompatibility complex-independent manner. In this study 2 generations of such receptor-bearing T cells, against the CD19 B-cell marker, were investigated for treatment of chronic lymphocytic leukaemia. The 2 nd generation   of this genetically engineered T cell contains CD3ζ  and CD28 intracellular domain, while the third generation has CD137 (4-1BB) in addition. Previous studies have demonstrated advantages of 2 nd  generation chimeric antigen receptor T cells  compared with 1 st generation. In this project the 2 nd and 3 rd generation T   cells  were compared for transduction efficiency, phenotype, proliferative capacity and cytotoxicity in response to antigen from a malignant B cell line. The analysis of transduction showed similar transduction efficiency for both types of chimeric  antigen receptor. However, the data from T cell phenotyping and cytotoxic analysis could not be used for drawing any conclusion, because of too little amount of samples and subsequently, lack of statistical analysis. Further, the proliferative capacity was similar between all transduced T-cell groups and did not give any   conclusive data. The next step will be to stimulate the 2 nd and 3 rd generation T cells with autologous target cells and follow them for a longer time since  allogeneic tumour cell lines trigger an alloreactivity that may mask the different activation states that may occur in the two T cell products.

  • 4.
    Li, Kaitao
    et al.
    Coulter Department of Biomedical Engineering, Georgia Institute of Technology, Atlanta, USA.
    Cheng, Xiaoxiao
    Radcliffe Department of Medicine and Medical Research Council Human Immunology Unit, University of Oxford, John Radcliffe Hospital, Headington, Oxford, United Kingdom.
    Tilevik, Andreas
    University of Skövde, School of Bioscience. University of Skövde, The Systems Biology Research Centre.
    Davis, Simon J.
    Radcliffe Department of Medicine and Medical Research Council Human Immunology Unit, University of Oxford, John Radcliffe Hospital, Headington, Oxford, United Kingdom.
    Zhu, Cheng
    Coulter Department of Biomedical Engineering, Woodruff School of Mechanical Engineering, Institute for Bioengineering and Bioscience, Georgia Institute of Technology, USA.
    In situ and in silico kinetic analyses of programmed cell death-1 (PD-1) receptor, programmed cell death ligands, and B7-1 protein interaction network2017In: Journal of Biological Chemistry, ISSN 0021-9258, E-ISSN 1083-351X, Vol. 292, no 16, p. 6799-6809Article in journal (Refereed)
    Abstract [en]

    Programmed cell death-1 (PD-1) is an inhibitory receptor with an essential role in maintaining peripheral tolerance and is among the most promising immunotherapeutic targets for treating cancer, autoimmunity, and infectious diseases. A complete understanding of the consequences of PD-1 engagement by its ligands, PD-L1 and PD-L2, and of PD-L1 binding to B7-1 requires quantitative analysis of their interactions at the cell surface. We present here the first complete in situ kinetic analysis of the PD-1/PD-ligands/B7-1 system. Consistent with previous solution measurements, we observed higher in situ affinities for human (h) than murine (m) PD-1 interactions, stronger binding of hPD-1 to hPD-L2 than hPD-L1, and comparable binding of mPD-1 to both ligands. However, in contrast to the relatively weak solution affinities, the in situ affinities of PD-1 are as high as those of the T cell receptor for agonist pMHC and of LFA-1 (lymphocyte function-associated antigen 1) for ICAM-1 (intercellular adhesion molecule 1) but significantly lower than that of the B7-1/CTLA-4 interaction, suggesting a distinct basis for PD-1- versus CTLA-4-mediated inhibition. Notably, the in situ interactions of PD-1 are much stronger than that of B7-1 with PD-L1. Overall, the in situ affinity ranking greatly depends on the on-rate instead of the off-rate. In silico simulations predict that PD-1/PD-L1 interactions dominate at interfaces between activated T cells and mature dendritic cells and that these interactions will be highly sensitive to the dynamics of PD-L1 and PD-L2 expression. Our results provide a kinetic framework for better understanding inhibitory PD-1 activity in health and disease.

  • 5.
    Mohamed, Ahmed
    University of Skövde, School of Bioscience.
    Deciphering the ontogeny of unmutated and mutated subsets of Chronic Lymphocytic Leukemia2019Independent thesis Advanced level (degree of Master (Two Years)), 30 credits / 45 HE creditsStudent thesis
    Abstract [en]

    Chronic Lymphocytic Leukemia (CLL) is a type of cancer that affects the B cells of the immune system causing problems in the process of producing antibodies. It can be sorted into mutated and unmutated CLL based on the percentage of somatic mutations in the Immunoglobulin Heavy chain Variable region (IgHV). The B cells of healthy individuals can be sorted into three groups; CD27dull memory B cells (MBCs), CD27bright MBCs and naïve B cells. The hypothesis for the project was that the unmutated CLL subset originates from CD27dull MBCs and the mutated CLL subset originates from CD27bright MBCs. RNA-sequencing data from healthy individuals were acquired from a collaboration partner in Rome and CLL-patients were collected from public datasets available online. Several bioinformatic tools were used to analyze the data. First, the quality of the data files was checked, then adapter sequence from the sequencing process and low-quality bases were removed (trimming). Good quality of the files was confirmed after the trimming. Secondly, these files were mapped against the human reference genome (GRCh38/hg38) for alignment, then the resulted data was used to check for genes that showed differential expression between the different groups. Results were analyzed and visualized using Venn diagrams, Principal Component Analysis (PCA) and heatmap plots and random forest. A list of 85 genes was generated based on the different comparisons and was used in one PCA plot that showed clear separation between the different groups. The SWAP70 gene was analyzed for single nucleotide polymorphisms (SNPs). The study concluded five genes that could be used as biomarkers for CLL and the diagnosis of its subtypes where some of them were discussed in previous studies. Also, the mutated CLL subset showed a similar behavior to the healthy individuals and this could validate the original hypothesis and justifies the better disease prognosis for this subtype.

  • 6.
    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.

  • 7.
    Wallner, Fredrik K.
    et al.
    University of Skövde, School of Bioscience. University of Skövde, The Systems Biology Research Centre. Redoxis AB, Lund, Sweden.
    Hultqvist Hopkins, Malin
    Redoxis AB, Lund, Sweden.
    Lindvall, Therese
    Redoxis AB, Lund, Sweden.
    Olofsson, Peter
    Redoxis AB, Lund, Sweden.
    Tilevik, Andreas
    University of Skövde, School of Bioscience. University of Skövde, The Systems Biology Research Centre.
    Cytokine correlation analysis based on drug perturbation2017In: Cytokine, ISSN 1043-4666, E-ISSN 1096-0023, Vol. 90, p. 73-79Article in journal (Refereed)
    Abstract [en]

    Cytokines and chemokines play a crucial role in regulating the immune system. Understanding how these molecules are co-regulated is important to understand general immunology, and particularly their role in clinical applications such as development and evaluation of novel drug therapies. Cytokines are today widely used as therapeutic targets and as biomarkers to monitor effects of drug therapies and for prognosis and diagnosis of diseases. Therapies that target a specific cytokine are also likely to affect the production of other cytokines due to their cross-regulatory functions and because the cytokines are produced by common cell types. In this study, we have perturbated the production of 17 different cytokines in a preclinical rat model of autoimmune arthritis, using 55 commercially available immunomodulatory drugs and clinical candidates. The majority of the studied drugs was selected for their anti-inflammatory role and was confirmed to inhibit the production of IL-2 and IFN-γ in this model but was also found to increase the production of other cytokines compared to the untreated control. Correlation analysis identified 58 significant pairwise correlations between the cytokines. The strongest correlations found in this study were between IL-2 and IFN-γ (r=0.87) and between IL-18 and EPO (r=0.84). Cluster analysis identified two robust clusters: (1) IL-7, IL-18 and EPO, and (2) IL-2, IL-17 and IFN-γ. The results show that cytokines are highly co-regulated, which provide valuable information for how a therapeutic drug might affect clusters of cytokines. In addition, a cytokine that is used as a therapeutic biomarker could be combined with its related cytokines into a biomarker panel to improve diagnostic accuracy.

1 - 7 of 7
CiteExportLink to result list
Permanent link
Cite
Citation style
  • apa
  • harvard1
  • ieee
  • modern-language-association-8th-edition
  • vancouver
  • Other style
More styles
Language
  • de-DE
  • en-GB
  • en-US
  • fi-FI
  • nn-NO
  • nn-NB
  • sv-SE
  • Other locale
More languages
Output format
  • html
  • text
  • asciidoc
  • rtf