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  • 451.
    Vrasdonk, Emke
    et al.
    Chalmers University of Technology.
    Palme, Ulrika
    Chalmers University of Technology.
    Lennartsson, Tommy
    Swedish University of Agricultural Sciences, Uppsala.
    Antonelli, Alexandre
    University of Gothenburg.
    Berg, Sofia
    University of Skövde, School of Bioscience. University of Skövde, The Systems Biology Research Centre.
    Jonsson, Annie
    University of Skövde, School of Bioscience. University of Skövde, The Systems Biology Research Centre.
    Cederberg, Christel
    Chalmers University of Technology.
    Defining the reference situation for biodiversity in Life Cycle Assessments: Review and recommendations2016Conference paper (Refereed)
  • 452.
    Walleczek, Jan
    et al.
    Phenoscience Laboratories, Berlin, Germany.
    Grössing, Gerhard
    Austrian Institute for Nonlinear Studies, Akademiehof, Austria.
    Pylkkänen, Paavo
    University of Skövde, School of Bioscience. University of Skövde, The Systems Biology Research Centre. Department of Philosophy, History, and Art Studies, University of Helsinki, Helsinki, Finland.
    Hiley, Basil
    Department of Physics and Astronomy, University College London, London, United Kingdom.
    Emergent quantum mechanics: David Bohm Centennial perspectives2019In: Entropy, ISSN 1099-4300, E-ISSN 1099-4300, Vol. 21, no 2, article id 113Article in journal (Refereed)
    Abstract [en]

    Emergent quantum mechanics (EmQM) explores the possibility of an ontology for quantum mechanics. The resurgence of interest in realist approaches to quantum mechanics challenges the standard textbook view, which represents an operationalist approach. The possibility of an ontological, i.e., realist, quantum mechanics was first introduced with the original de Broglie-Bohm theory, which has also been developed in another context as Bohmian mechanics. This Editorial introduces a Special Issue featuring contributions which were invited as part of the David Bohm Centennial symposium of the EmQM conference series (www.emqm17.org). Questions directing the EmQM research agenda are: Is reality intrinsically random or fundamentally interconnected? Is the universe local or nonlocal? Might a radically new conception of reality include a form of quantum causality or quantum ontology? What is the role of the experimenter agent in ontological quantum mechanics? The Special Issue also includes research examining ontological propositions that are not based on the Bohm-type nonlocality. These include, for example, local, yet time-symmetric, ontologies, such as quantum models based upon retrocausality. This Editorial provides topical overviews of thirty-one contributions which are organized into seven categories to provide orientation. 

  • 453.
    Walleczek, Jan
    et al.
    Phenoscience Laboratories, Berlin, Germany.
    Grössing, GerhardAustrian Institute for Nonlinear Studies, Vienna, Austria.Pylkkänen, PaavoUniversity of Skövde, School of Bioscience. University of Skövde, The Systems Biology Research Centre. Department of Philosophy, History, and Art Studies, University of Helsinki, Helsinki, Finland.Hiley, BasilUniversity College of London, UK.
    Emergent Quantum Mechanics: David Bohm Centennial Perspectives2019Collection (editor) (Refereed)
  • 454.
    Wallenhammar, Ann-Charlotte
    et al.
    HS Konsult AB, Örebro, Sweden.
    Algerin, Maria
    University of Skövde, School of Bioscience. University of Skövde, The Systems Biology Research Centre.
    Tilevik, Diana
    University of Skövde, School of Bioscience. University of Skövde, The Systems Biology Research Centre.
    Ny metod bedömer risk för bomullsmögel2017In: Arvensis, ISSN 2000-0871, no 3Article in journal (Other academic)
  • 455.
    Wallner, Fredrik K.
    et al.
    University of Skövde, School of Bioscience. University of Skövde, The Systems Biology Research Centre. Redoxis AB/ProNoxis AB, Lund, Sweden / Wallner Medicinal Chemistry AB, Göteborg, Sweden.
    Hultquist Hopkins, Malin
    Redoxis AB/ProNoxis AB, Lund, Sweden.
    Woodworth, Nina
    Redoxis AB/ProNoxis AB, Lund, Sweden.
    Lindvall Bark, Therese
    Redoxis AB/ProNoxis AB, Lund, Sweden.
    Olofsson, Peter
    Redoxis AB/ProNoxis AB, Lund, Sweden.
    Tilevik, Andreas
    University of Skövde, School of Bioscience. University of Skövde, The Systems Biology Research Centre.
    Correlation and cluster analysis of immunomodulatory drugs based on cytokine profiles2018In: Pharmacological Research, ISSN 1043-6618, E-ISSN 1096-1186, Vol. 128, p. 244-251Article in journal (Refereed)
    Abstract [en]

    Drug discovery is a constant struggle to overcome hurdles posed by the complexity of biological systems. One of these hurdles is to find and understand the molecular target and the biological mechanism of action. Although the molecular target has been determined, the true biological effect may be unforeseen also for well-established drugs. Hence, there is a need for novel ways to increase the knowledge of the biological effects of drugs in the developmental process. In this study, we have determined cytokine profiles for 26 non-biological immunomodulatory drugs or drug candidates and used these profiles to cluster the compounds according to their effect in a preclinical ex vivo culture model of arthritis. This allows for prediction of functions and drug target of a novel drug candidate based on profiles obtained in this study. Results from the study showed that the JAK inhibitors tofacitinib and ruxolitinib formed a robust cluster and were found to have a distinct cytokine profile compared to the other drugs. Another robust cluster included the calcineurin inhibitors cyclosporine A and tacrolimus and the protein kinase inhibitors fostamatinib disodium and sotrastaurin acetate, which caused a strong overall inhibition of the cytokine production. The results of this methodology indicate that cytokine profiles can be used to provide a fingerprint-like identification of a drug as a tool to benchmark novel drugs and to improve descriptions of mode of action.

  • 456.
    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.

  • 457.
    Warzecha, Tomasz
    et al.
    University of Agriculture, Kraków, Poland.
    Lundh, Dan
    University of Skövde, School of Life Sciences. University of Skövde, The Systems Biology Research Centre.
    Mandal, Abul
    University of Skövde, School of Life Sciences. University of Skövde, The Systems Biology Research Centre.
    Effect of Fusarium culmorum infection on survivability of a T-DNA tagged mutant of Arabidopsis thaliana harboring a mutation in the peptide transporter gene At5g460502011In: Biotechnologia: Journal of Biotechnology, Computational Biology and Bionanotechnology, ISSN 0860-7796, Vol. 92, no 1, p. 77-84Article in journal (Refereed)
    Abstract [en]

    Previously, we have reported a T-DNA tagged mutant (TAG_009) of Arabidopsis thaliana exhibiting a significant sensitivity to biotic stresses. We have also cloned and analyzed the tagged gene At5g46050. Based on bioinformatic and molecular characterization, we proposed that At5g46050 is involved in the transport of peptides participating in plant defense against biotic stresses. To provide further evidence for supporting our proposal, this time we exposed this mutant to Fusarium culmorum, a potential fungal pathogen. Besides TAG_009 line, in our investigations we included two SALK insertion mutants (SALK_003119 and SALK_145209), two wild-type ecotypes (WT_C24 and WT_Col-0) and an additional T-DNA tagged mutant (TAG_197-6) of A. thaliana. We have found that the highest degree of leaf damage was exhibited by TAG_009 line (damage score 4.37), whereas the lowest was observed in WT_Col-0 ecotype (damage score 3.43). The highest rate of mortality after eight weeks of inoculation with F. culmorum was also observed in TAG_009 line (85.24%), while the lowest was in WT_Col-0 line (37.22%). We have also found that plants of SALK_145209 line, despite being infected with Fusarium, produced the highest number of leaves (average 14.17 leaves per plant), whereas the lowest number of leaves was produced by plants of TAG_197-6 line ( average 9.5 leaves per plant). Statistical analyses showed that the differences between the T-DNA tagged line TAG_009 and WT_Col-0 were significant, whereas in comparison with wild-type control plants WT_C24, they were insignificant. Based on these results, we can conclude that the gene we have tagged by using T-DNA-mediated in vivo gene fusion is indeed involved in the plant defense against Fusarium infection.

  • 458.
    Wegman, Pia
    et al.
    Department of Clinical Medicine, School of Health and Medical Sciences, Örebro University, 701 85 Örebro, Sweden.
    Göthlin Eremo, Anna
    Department of Clinical Medicine, School of Health and Medical Sciences, Örebro University, 701 85 Örebro, Sweden.
    Lindlöf, Angelica
    University of Skövde, School of Life Sciences. University of Skövde, The Systems Biology Research Centre.
    Karlsson, Mats
    Department of Pathology, School of Health and Medical Sciences, Örebro University Hospital, 701 85 Örebro, Sweden.
    Stål, Olle
    Department of Clinical and Experimental Medicine/Oncology, Faculty of Health Sciences, Linköping University, 581 85 Linköping, Sweden.
    Wingren, Sten
    Department of Clinical Medicine, School of Health and Medical Sciences, Örebro University, 701 85 Örebro, Sweden.
    Expression of the forkhead transcription factor FOXL2 correlates with good prognosis in breast cancer patients treated with tamoxifen2011In: International Journal of Oncology, ISSN 1019-6439, Vol. 38, no 4, p. 1145-1151Article in journal (Refereed)
    Abstract [en]

    Aromatase is an important enzyme in the local synthesis of oestrogens and its expression has been shown to be increased in breast cancer through the activation of multiple promoters. However, the mechanisms behind this are not yet fully understood. A novel candidate in this context is the transcription factor forkhead box L2 (FOXL2), which has been recognised to be co-expressed with aromatase and transcriptionally active promoter II in developing goat and chicken ovaries. We propose that FOXL2 could be involved in the increased expression of aromatase in breast cancer. We examined FOXL2 and its relation to aromatase in 132 post-menopausal breast cancer patients by immunohistochemistry. Using in silico analysis, we further searched for FOXL2 binding-elements in the aromatase gene promoters. The results demonstrate that FOXL2 is expressed in breast cancer and influences clinical outcome with improved recurrence-free survival in cases with nuclear expression. In a multivariate Cox model, nuclear FOXL2 was a significant prognostic factor in ER-positive patients treated with tamoxifen (HR=0.18, 95% confidence interval (CI)=0.04-0.81, P=0.03). Tumours expressing nuclear FOXL2 were also more likely positive for stromal and/or cytoplasmic aromatase (P=0.03 and P=0.008, respectively). In silico analyses revealed binding elements of FOXL2 in promoters I.3, II and I.7 of the aromatase gene of which promoter I.7 was most significant. In conclusion, this is the first study to report that FOXL2 is expressed in breast cancer and correlates with aromatase as well as with clinical outcome. The results further strengthen a possible binding of FOXL2 to aromatase promoter I.7. Nevertheless, whether FOXL2 is a direct activator of aromatase requires further investigation.

  • 459.
    Weishaupt, Holger
    et al.
    Department of Immunology, Genetics and Pathology, Science for Life Laboratory, Rudbeck Laboratory, Uppsala University, Uppsala, Sweden.
    Johansson, Patrik
    Department of Immunology, Genetics and Pathology, Science for Life Laboratory, Rudbeck Laboratory, Uppsala University, Uppsala, Sweden.
    Sundström, Anders
    Department of Immunology, Genetics and Pathology, Science for Life Laboratory, Rudbeck Laboratory, Uppsala University, Uppsala, Sweden.
    Lubovac-Pilav, Zelmina
    University of Skövde, School of Bioscience. University of Skövde, The Systems Biology Research Centre.
    Olsson, Björn
    University of Skövde, School of Bioscience. University of Skövde, The Systems Biology Research Centre.
    Nelander, Sven
    Department of Immunology, Genetics and Pathology, Science for Life Laboratory, Rudbeck Laboratory, Uppsala University, Uppsala, Sweden.
    Swartling, Fredrik J.
    Department of Immunology, Genetics and Pathology, Science for Life Laboratory, Rudbeck Laboratory, Uppsala University, Uppsala, Sweden.
    Batch-normalization of cerebellar and medulloblastoma gene expression datasets utilizing empirically defined negative control genes2019In: Bioinformatics, ISSN 1367-4803, E-ISSN 1367-4811, Vol. 35, no 18, p. 3357-3364Article in journal (Refereed)
    Abstract [en]

    Motivation: Medulloblastoma (MB) is a brain cancer predominantly arising in children. Roughly 70% of patients are cured today, but survivors often suffer from severe sequelae. MB has been extensively studied by molecular profiling, but often in small and scattered cohorts. To improve cure rates and reduce treatment side effects, accurate integration of such data to increase analytical power will be important, if not essential.

    Results: We have integrated 23 transcription datasets, spanning 1350 MB and 291 normal brain samples. To remove batch effects, we combined the Removal of Unwanted Variation (RUV) method with a novel pipeline for determining empirical negative control genes and a panel of metrics to evaluate normalization performance. The documented approach enabled the removal of a majority of batch effects, producing a large-scale, integrative dataset of MB and cerebellar expression data. The proposed strategy will be broadly applicable for accurate integration of data and incorporation of normal reference samples for studies of various diseases. We hope that the integrated dataset will improve current research in the field of MB by allowing more large-scale gene expression analyses.

  • 460.
    Westerberg, J.
    et al.
    Vrinnevi Hosp, Dept Otorhinolaryngol, S-60182 Norrköping, Sweden.
    Harder, H.
    Linköping Univ Hosp, Dept Otolaryngol, Linköping, Sweden.
    Magnuson, B.
    Linköping Univ Hosp, Dept Otolaryngol, Linköping, Sweden.
    Westerberg, Lars
    University of Skövde, School of Life Sciences. University of Skövde, The Systems Biology Research Centre.
    Hydén, D.
    Linköping Univ Hosp, Dept Otolaryngol, Linköping, Sweden.
    Ten-year myringoplasty series: does the cause of perforation affect the success rate?2011In: Journal of Laryngology and Otology, ISSN 0022-2151, E-ISSN 1748-5460, Vol. 125, no 2, p. 126-132Article in journal (Refereed)
    Abstract [en]

    Objective:  To  present  the  results  of  primary  myringoplasty  procedures  together  with  the  perforation  cause, perforation size and site, surgeon’s experience, and surgical method, and to investigate how these factors relate to graft ‘take’ rates. Study design: Retrospective chart review of 243 consecutive patients undergoing primary myringoplasty with temporalis fascia underlay over a 10-year period from 1994 to 2004. Results: The overall graft take rate was 95 per cent. The retroauricular approach resulted in a 97 per cent graft take rate, whereas a significantly lower rate (77 per cent) was seen for surgery conducted via the endaural approach, or via an ear speculum. There was no relationship between other factors and tympanic membrane healing. Conclusion: No association was found between perforation cause and graft take rate. The underlay technique is safe and reliable, and the retroauricular approach is preferable as it enables good surgical access and has better results.

  • 461.
    Yan, Bao-Yong
    et al.
    Hebei Medical University, Shijiazhuang.
    Wang, Da-Wei
    Hebei Medical University, Shijiazhuang.
    Zhu, Zhen-Long
    Hebei Medical University, Shijiazhuang.
    Yang, Yan-Hong
    Hebei Medical University, Shijiazhuang.
    Wang, Ming-Wei
    Hebei Medical University, Shijiazhuang.
    Cui, Dong-Sheng
    Hebei Medical University, Shijiazhuang.
    Zhang, Hong
    University of Skövde, The Systems Biology Research Centre. University of Skövde, School of Life Sciences.
    Sun, Xiao-Feng
    University of Linköping.
    Overexpression of MAC30 in the Cytoplasm of Oral Squamous Cell Carcinoma Predicts Nodal Metastasis and Poor Differentiation2010In: Chemotherapy, ISSN 0009-3157, E-ISSN 1421-9794, Vol. 56, no 6, p. 424-428Article in journal (Refereed)
    Abstract [en]

    Background: Expression of the meningioma-associated protein (MAC30) was increased in several types of tumors, including esophageal, gastric and colon tumors, compared to normal tissue. MAC30 expression levels gradually increased from normal colorectal mucosa to primary colorectal cancer and colorectal cancer spreading to the lymph nodes. MAC30 expression was related to survival in patients with colorectal cancer. However, there is no study on MAC30 in oral squamous cell carcinoma (OSCC). Methods: Therefore, MAC30 expression in OSCC was investigated and possible associations of MAC30 expression with clinicopathological variables in OSCC have been analyzed. MAC30 expression was immunohistochemically examined in 20 normal oral mucosa and 43 OSCC specimens. Results: Expression levels of MAC30 in the cytoplasm markedly increased from normal oral epithelial cells to primary OSCC. Strong cytoplasmic staining was significantly higher in primary OSCC compared to normal oral mucosa samples (51 vs. 20%, p = 0.019). Furthermore, MAC30 expression levels in primary tumors of patients with lymph node metastasis exceeded levels in those without metastasis (65 vs. 35%, p = 0.048), and MAC30 expression in poorly differentiated tumors was higher than in well-differentiated ones (90 vs. 39%, p = 0.005). Conclusion: Overexpression of MAC30 in the cytoplasm of OSCC may predict nodal metastasis and poor differentiation.

  • 462.
    Yang, L.
    et al.
    Linköping University.
    Olsson, B.
    Linköping University.
    Pfeifer, D.
    Linköping University.
    Jönsson, J.-I.
    Linköping University.
    Zhou, Z.-G.
    Sichuan University.
    Jiang, X.
    Sichuan University.
    Fredriksson, B.-A.
    Linköping University.
    Zhang, Hong
    University of Skövde, School of Life Sciences. University of Skövde, The Systems Biology Research Centre.
    Sun, X.-F.
    Linköping University.
    Knockdown of peroxisome proliferator-activated receptor-β induces less differentiation and enhances cell-fibronectinadhesion of colon cancer cells2010In: Oncogene, ISSN 0950-9232, E-ISSN 1476-5594, Vol. 29, no 4, p. 516-526Article in journal (Refereed)
    Abstract [en]

    The role of peroxisome proliferator-activated receptor-/ (PPAR-/) in the pathogenesis of colon cancer remains highly controversial. This study specifically silenced the PPAR- expression in three colon cancer cell lines with different metastatic potentials. Although PPAR-knockdown resulted in more malignant morphological changes, bigger colony sizes and lower carcinoembryonic antigen (CEA) secretion, and enhanced the cell-fibronectin adhesion, cell invasion and migration were unaffected. These effects were stronger in poorly metastatic cell lines compared with highly metastatic ones. Simultaneously, PPAR-knockdown decreased the mRNAs encoding adipocyte differentiation-related protein and liver fatty acid binding protein, and increased the mRNA of ILK, whereas the mRNAs encoding integrin-1 and angiopoietin-like 4 were unchanged. Using immunohistochemistry, we determined that the intensity of PPAR- expression was stronger in rectal cancers with better differentiation than in those with poor differentiation, and was stronger in early-stage tumors than in advanced ones. Together, these findings consistently indicate that PPAR- may facilitate differentiation and inhibit the cell-fibronectin adhesion of colon cancer, having a role as an inhibitor in the carcinogenesis and progression of colorectal cancer. Interestingly PPAR- seems to have a more important role in poorly metastatic cells than in highly metastatic ones.

  • 463.
    Yang, Lie
    et al.
    Sichuan Univ, W China Hosp, Inst Digest Surg, Chengdu 610064, Sichuan Prov, Peoples R China / Sichuan Univ, W China Hosp, State Key Lab Biotherapy, Chengdu 610064, Sichuan Prov, Peoples R China / Linkoping Univ, Dept Oncol & Clin & Expt Med, SE-58185 Linkoping, Sweden .
    Zhang, Hong
    University of Skövde, The Systems Biology Research Centre. University of Skövde, School of Life Sciences.
    Zhou, Zong-Guang
    Sichuan Univ, W China Hosp, Inst Digest Surg, Chengdu 610064, Sichuan Prov, Peoples R China / Sichuan Univ, W China Hosp, State Key Lab Biotherapy, Chengdu 610064, Sichuan Prov, Peoples R China .
    Yan, Hui
    Sichuan Univ, W China Hosp, Inst Digest Surg, Chengdu 610064, Sichuan Prov, Peoples R China / Sichuan Univ, W China Hosp, State Key Lab Biotherapy, Chengdu 610064, Sichuan Prov, Peoples R China .
    Adell, Gunnar
    Karolinska Univ Hosp, Dept Oncol, Stockholm, Sweden.
    Sun, Xiao-Feng
    Sichuan Univ, W China Hosp, Inst Digest Surg, Chengdu 610064, Sichuan Prov, Peoples R China / Sichuan Univ, W China Hosp, State Key Lab Biotherapy, Chengdu 610064, Sichuan Prov, Peoples R China / Linkoping Univ, Dept Oncol & Clin & Expt Med, SE-58185 Linkoping, Sweden .
    Biological Function and Prognostic Significance of Peroxisome Proliferator-Activated Receptor delta in Rectal Cancer2011In: Clinical Cancer Research, ISSN 1078-0432, E-ISSN 1557-3265, Vol. 17, no 11, p. 3760-3770Article in journal (Refereed)
    Abstract [en]

    Purpose: To investigate the expression significance of PPAR beta/delta in relation to radiotherapy (RT), clinicopathologic, and prognostic variables of rectal cancer patients. Experimental Design: We included 141 primary rectal cancer patients who participated in a Swedish clinical trial of preoperative RT. Tissue microarray samples from the excised rectal cancers and the adjacent or distant normal mucosa and lymph node metastases were stained with PPAR delta antibody. Survival probability was computed by the Kaplan-Meier method and Cox regression model. The proliferation of colon cancer cell lines KM12C, KM12SM, and KM12L4a was assayed after PPAR delta knockdown. Results: PPAR delta was increased from adjacent or distant normal mucosa to primary cancers, whereas it decreased from primary cancers to lymph node metastases. After RT, PPAR delta was increased in normal mucosa, whereas it decreased in primary cancers and lymph node metastases. In primary cancers, the high expression of PPAR delta was related to higher frequency of stage I cases, lower lymph node metastasis rate, and low expression of Ki-67 in the unirradiated cases, and related to favorable survival in the cases either with or without RT. The proliferation of the KM12C, KM12SM, or KM12L4a cells was significantly accelerated after PPAR delta knockdown. Conclusions: RT decreases the PPAR delta expression in primary rectal cancers and lymph node metastases. PPAR delta is related to the early development of rectal cancer and inhibits the proliferation of colorectal cancer cells. Increase of PPAR delta predicts favorable survival in the rectal cancer patients either with or without preoperative RT. Clin Cancer Res; 17(11); 3760-70. (C)2011 AACR.

  • 464.
    Yewale, Priti Prabhakar
    et al.
    Microbial Diversity Research Centre, Dr. D. Y. Patil Biotechnology and Bioinformatics Institute, Dr. D. Y. Patil Vidyapeeth, Pune, India.
    Lokhande, Kiran Bharat
    Bioinformatics Research Laboratory, Dr. D. Y. Patil Biotechnology and Bioinformatics Institute, Dr. D. Y. Patil Vidyapeeth, Pune, India.
    Sridhar, Aishwarya
    Microbial Diversity Research Centre, Dr. D. Y. Patil Biotechnology and Bioinformatics Institute, Dr. D. Y. Patil Vidyapeeth, Pune, India.
    Vaishnav, Monika
    Microbial Diversity Research Centre, Dr. D. Y. Patil Biotechnology and Bioinformatics Institute, Dr. D. Y. Patil Vidyapeeth, Pune, India.
    Khan, Faisal Ahmad
    The Life Science Centre-Biology, School of Science and Technology, Örebro University, Sweden.
    Mandal, Abul
    University of Skövde, School of Bioscience. University of Skövde, The Systems Biology Research Centre.
    Swamy, Kakumani Venkateswara
    Bioinformatics Research Laboratory, Dr. D. Y. Patil Biotechnology and Bioinformatics Institute, Dr. D. Y. Patil Vidyapeeth, Pune, India.
    Jass, Jana
    The Life Science Centre-Biology, School of Science and Technology, Örebro University, Sweden.
    Nawani, Neelu
    Microbial Diversity Research Centre, Dr. D. Y. Patil Biotechnology and Bioinformatics Institute, Dr. D. Y. Patil Vidyapeeth, Pune, India.
    Molecular profiling of multidrug-resistant river water isolates: insights into resistance mechanism and potential inhibitors2019In: Environmental science and pollution research international, ISSN 0944-1344, E-ISSN 1614-7499Article in journal (Refereed)
    Abstract [en]

    Polluted waters are an important reservoir for antibiotic resistance genes and multidrug-resistant bacteria. This report describes the microbial community, antibiotic resistance genes, and the genetic profile of extended spectrum β-lactamase strains isolated from rivers at, Pune, India. ESBL-producing bacteria isolated from diverse river water catchments running through Pune City were characterized for their antibiotic resistance. The microbial community and types of genes which confer antibiotic resistance were identified followed by the isolation of antibiotic-resistant bacteria on selective media and their genome analysis. Four representative isolates were sequenced using next generation sequencing for genomic analysis. They were identified as Pseudomonas aeruginosa, Escherichia coli, and two isolates were Enterobacter cloacae. The genes associated with the multidrug efflux pumps, such as tolC, macA, macB, adeL, and rosB, were detected in the isolates. As MacAB-TolC is an ABC type efflux pump responsible for conferring resistance in bacteria to several antibiotics, potential efflux pump inhibitors were identified by molecular docking. The homology model of their MacB protein with that from Escherichia coli K12 demonstrated structural changes in different motifs of MacB. Molecular docking of reported efflux pump inhibitors revealed the highest binding affinity of compound MC207-110 against MacB. It also details the potential efflux pump inhibitors that can serve as possible drug targets in drug development and discovery. 

  • 465.
    Yewale, Priti Prabhakar
    et al.
    Microbial Diversity Research Centre, Dr. D. Y. Patil Biotechnology and Bioinformatics Institute, Dr. D. Y. Patil Vidyapeeth, Maharashtra, Pune, India.
    Rahman, Aminur
    University of Skövde, School of Bioscience. University of Skövde, The Systems Biology Research Centre.
    Nahar, Noor
    University of Skövde, School of Bioscience. University of Skövde, The Systems Biology Research Centre.
    Saha, Anandakumar
    Department of Zoology, University of Rajshahi, Rajshahi, Bangladesh.
    Jass, Jana
    The Life Science Center, The School of Science and Technology, Örebro University, Örebro, Sweden.
    Mandal, Abul
    University of Skövde, School of Bioscience. University of Skövde, The Systems Biology Research Centre.
    Nawani, Neelu N.
    Microbial Diversity Research Centre, Dr. D. Y. Patil Biotechnology and Bioinformatics Institute, Dr. D. Y. Patil Vidyapeeth, Pune, Maharashtra, India.
    Sources of Metal Pollution, Global Status, and Conventional Bioremediation Practices2017In: Handbook of Metal–Microbe Interactions and Bioremediation / [ed] Surajit Das, Hirak Ranjan Dash, Boca Raton, FL: CRC Press, 2017, p. 25-40Chapter in book (Refereed)
    Abstract [en]

    Pollution control has become a priority task for global regulatory authorities. The framing of regulations, guidelines, and implementation of pollution awareness and control programs has begun at a massive scale. Heavy metals that are one of the most challenging pollutants that affect humans, animals, plants, and the ecosystem health. The sources of different metals and their toxicities are described. Current approaches in bioremediation are addressed along with the challenges posed by them. Furthermore, recent developments in biotechnology that offer novel ways to recover metals from contaminated sites are discussed.

  • 466.
    Zhang, Hong
    et al.
    University of Skövde, School of Life Sciences. University of Skövde, The Systems Biology Research Centre.
    Wang, Da-Wei
    University of Skövde, School of Life Sciences. University of Skövde, The Systems Biology Research Centre. Department of Stomatology, The Third Hospital of Hebei Medical University, Hebei, China.
    Adell, Gunnar
    Department of Oncology, Karolinska University Hospital, Karolinska, Sweden.
    Sun, Xiao-Feng
    Division of Oncology, Department of Clinical and Experimental Medicine, Faculty of Heath Science, Linköping University, Sweden .
    WRAP53 is an independent prognostic factor in rectal cancer- a study of Swedish clinical trial of preoperative radiotherapy in rectal cancer patients2012In: BMC Cancer, ISSN 1471-2407, E-ISSN 1471-2407, Vol. 12, p. 294-Article in journal (Refereed)
    Abstract [en]

    Background: Expression of WRAP53 protein has oncogenic properties and it is up regulated in several types of tumors. Methods: We examined expression of WRAP53 protein in rectal cancers and analyzed its relationship to the response to preoperative radiotherapy and patient survival. The WRAP53 protein was examined by immunohistochemistry in normal mucosa, primary tumors and lymph node metastases from 143 rectal cancer patients participated in a Swedish clinical trial of preoperative radiotherapy. Results: Frequency of WRAP53 protein expression was increased in primary rectal cancer compared to the normal mucosa (p < 0.05). In non-radiotherapy group positive WRAP53 in primary tumors (p = 0.03, RR, 3.73, 95% CI, 1.13-11.89) or metastases (p = 0.01, RR, 4.11, 95% CI, 1.25-13.14), was associated with poor prognosis independently of stages and differentiations. In radiotherapy group, positive WRAP53 in the metastasis correlated with better survival (p = 0.04). An interaction analysis showed that the correlations of WRAP53 with the prognostic significance with and without radiotherapy in the metastasis differed (p = 0.01). In the radiotherapy group, expression of WRAP53 in metastases gave a better outcome (p = 0.02, RR, 0.32, 95% CI, 0.13-0.84), and an interaction analysis showed significance between the two groups (p = 0.01). Conclusion: WRAP53 may be a new biomarker used to predict prognosis and to select suitable patients for preoperative radiotherapy.

  • 467.
    Zhang, Hong
    et al.
    University of Skövde, School of Life Sciences. University of Skövde, The Systems Biology Research Centre.
    Widegren, Emma
    Linkoping Univ, Dept Oncol, Inst Clin & Expt Med, Linkoping, Sweden .
    Wang, Da-Wei
    Hebei Med Univ, Hosp 3, Dept Stomatol, Shijiazhuang, Peoples R China.
    Sun, Xiao-Feng
    Linkoping Univ, Dept Oncol, Inst Clin & Expt Med, Linkoping, Sweden .
    SPARCL1: a potential molecule associated with tumor diagnosis, progression and prognosis of colorectal cancer2011In: Tumor Biology, ISSN 1010-4283, E-ISSN 1423-0380, Vol. 32, no 6, p. 1225-1231Article in journal (Refereed)
    Abstract [en]

    We investigated whether SPARCL1 played an essential role in tumor initiation, formation and progression of colorectal carcinomas. In this study, we examined expression of SPARCL1 protein in the normal colorectal mucosa, adjacent normal mucosa and primary and lymph node metastases from colorectal cancer patients. In matched patients, we found that SPARCL1 was negative in the distant normal colorectal mucosa, weakly expressed in the adjacent normal mucosa, strongly expressed in primary colorectal adenocarcinomas and slightly expressed in their lymph node metastases. A similar pattern was observed in the SPARCL1 expression from our series of non-matched colorectal cancer patients. The strongest expression and highest frequency of the SPARCL1 protein were found in the primary cancers. Interestingly, in the primary tumors, the frequency of SPARCL1 expression was significantly increased from the Dukes' A to Dukes' B tumors and then decreased gradually from the Dukes' B to C and D tumors. There was no difference in the intensity of SPARCL1 expression between the central areas and invasion margins of the primary tumors. Moreover, the SPARCL1 protein was more strongly expressed in the highly differentiated tumors than the lower differentiated ones. The patients with positive expression of SPARCL1 in their tumors had worse prognosis than the patients with SPARCL1-negative ones, even after the analyses by Multivariate and Interaction method. Expression of SPARCL1 protein might be a valuable biomarker for early diagnosis in colorectal cancers and further predicting patients' prognosis.

  • 468.
    Zhang, Zhi-Yong
    et al.
    Linkoping Univ, Inst Clin & Expt Med, Dept Oncol, S-58185 Linkoping, Sweden / Tangshan Gongren Hosp, Dept Pathol, Tangshan, Peoples R China / Hebei Med Univ, Hosp 1, Lab Ctr, Shijiazhuang, Peoples R China.
    Zhang, Hong
    University of Skövde, School of Life Sciences. University of Skövde, The Systems Biology Research Centre.
    Adell, Gunnar
    Karolinska Univ Hosp, Dept Oncol, Stockholm, Sweden.
    Sun, Xiao-Feng
    Linkoping Univ, Inst Clin & Expt Med, Dept Oncol, S-58185 Linkoping, Sweden.
    Endosialin expression in relation to clinicopathological and biological variables in rectal cancers with a Swedish clinical trial of preoperative radiotherapy2011In: BMC Cancer, ISSN 1471-2407, E-ISSN 1471-2407, Vol. 11, p. Artikelnr 89-Article in journal (Refereed)
    Abstract [en]

    Background: The importance of changes in tumour-associated stroma for tumour initiation and progression has been established. Endosialin is expressed in fibroblasts and pericytes of blood vessels in several types of tumours, and is involved in the progression of colorectal cancer. In order to see whether endosialin was related to radiotherapy (RT) response, and clinicopathological and biological variables, we investigated endosialin expression in rectal cancers from the patients who participated in a Swedish clinical trial of preoperative RT. Methods: Endosialin was immunohistochemically examined in normal mucosa, including distant (n = 72) and adjacent (n = 112) normal mucosa, and primary tumours (n = 135). Seventy-three of 135 patients received surgery alone and 62 received additional preoperative RT. Results: Endosialin expression in the stroma increased from normal mucosa to tumour (p < 0.0001) both in RT and non-RT group. In the RT group, endosialin expression in the stroma was positively associated with expression of cyclooxygenase-2 (Cox-2) (p = 0.03), p73 (p = 0.01) and phosphates of regenerating liver (PRL) (p = 0.002). Endosialin expression in the tumour cells of both in the RT group (p = 0.01) and the non-RT group (p = 0.06) was observed more often in tumours with an infiltrative growth pattern than in tumours with an expansive growth pattern. In the RT group, endosialin expression in tumour cells was positively related to PRL expression (p = 0.02), whereas in the non-RT group, endosialin expression in tumour cells was positively related to p73 expression (p = 0.01). Conclusions: Endosialin expression may be involved in the progression of rectal cancers, and was related to Cox-2, p73 and PRL expression. However, a direct relationship between endosialin expression and RT responses in patients was not found.

  • 469.
    Zichner, Thomas
    et al.
    University of Skövde, The Systems Biology Research Centre. University of Skövde, School of Life Sciences.
    Lubovac, Zelmina
    University of Skövde, The Systems Biology Research Centre. University of Skövde, School of Life Sciences.
    Olsson, Björn
    University of Skövde, The Systems Biology Research Centre. University of Skövde, School of Life Sciences.
    Temporal analysis of oncogenesis using microRNA expression data2008In: Proc. Ger. Conf. Bioinformatics, GCB, Bonn: Gesellschaft für Informatik , 2008, p. 128-137Conference paper (Refereed)
    Abstract [en]

    MicroRNAs (miRNAs) have rapidly become the focus of many cancer research studies. These small non-coding RNAs have been shown to play important roles in the regulation of oncogenes and tumor suppressors. It has also been demonstrated that miRNA expression profiles differ significantly between normal and cancerous cells, which indicates the possibility of using miRNAs as markers for cancer diagnosis and prognosis. However, not much is known about the regulation of miRNA expression. One of the issues worth investigating is whether deregulations of miRNA expression in cancer cells occur according to some pattern or in a random order. We therefore selected two approaches, previously used to derive graph models of oncogenesis using chromosomal imbalance data, and adapted them to miRNA expression data. Applying the adapted algorithms to a breast cancer data set, we obtained results indicating the temporal order of miRNA deregulations during tumor development. When analyzing the specific deregulations appearing at different time points in the derived model, we found that several of the deregulations identified as early events could be supported through literature studies.

  • 470.
    Ziemke, Tom
    et al.
    University of Skövde, School of Humanities and Informatics. University of Skövde, The Systems Biology Research Centre.
    Bickhard, Mark
    Department of Philosophy, Lehigh University, 15 University Drive, Bethlehem, PA 18015, United States.
    Cognitive robotics: Introduction to the special issue2011In: New ideas in psychology, ISSN 0732-118X, E-ISSN 1873-3522, Vol. 29, no 3, p. 201-202Article in journal (Other (popular science, discussion, etc.))
  • 471.
    Östensson, Malin
    et al.
    Department of Mathematical Sciences, Chalmers University of Technology, Gothenburg, Sweden.
    Montén, Caroline
    Diabetes and Celiac Disease Unit, Department of Clinical Sciences, Lund University, Malmö, Sweden.
    Bacelis, Jonas
    Institute of Biomedicine, Department of Medical and Clinical Genetics, Sahlgrenska Academy at the University of Gothenburg, Gothenburg, Sweden.
    Gudjonsdottir, Audur H.
    Queen Silvia Children’s Hospital, Sahlgrenska Academy at the University of Gothenburg, Department of Pediatrics, Gothenburg, Sweden.
    Adamovic, Svetlana
    Institute of Biomedicine, Department of Medical and Clinical Genetics, Sahlgrenska Academy at the University of Gothenburg, Gothenburg, Sweden.
    Ek, Johan
    Buskerud Central Hospital, Department of Pediatrics, Drammen, Norway.
    Ascher, Henry
    Sahlgrenska Academy at the University of Gothenburg, Department of Public Health and Community Medicine, Unit of Social Medicine, Gothenburg, Sweden.
    Pollak, Elisabet
    Institute of Biomedicine, Department of Medical and Clinical Genetics, Sahlgrenska Academy at the University of Gothenburg, Gothenburg, Sweden.
    Arnell, Henrik
    Department of Pediatric Gastroenterology, Hepatology and Nutrition, Karolinska University Hospital and Division of Pediatrics, CLINTEC, Karolinska Institutet, Stockholm, Sweden.
    Browaldh, Lars
    Department of Clinical Science and Education, Karolinska Institutet Södersjukhuset, Stockholm, Sweden.
    Agardh, Daniel
    Diabetes and Celiac Disease Unit, Department of Clinical Sciences, Lund University, Malmö, Sweden.
    Wahlström, Jan
    Institute of Biomedicine, Department of Medical and Clinical Genetics, Sahlgrenska Academy at the University of Gothenburg, Gothenburg, Sweden.
    Nilsson, Staffan
    Department of Mathematical Sciences, Chalmers University of Technology, Gothenburg, Sweden.
    Torinsson-Naluai, Åsa
    University of Skövde, School of Life Sciences. University of Skövde, The Systems Biology Research Centre. Institute of Biomedicine, Department of Medical and Clinical Genetics, Sahlgrenska Academy at the University of Gothenburg, Gothenburg, Sweden.
    A Possible Mechanism behind Autoimmune Disorders Discovered By Genome-Wide Linkage and Association Analysis in Celiac Disease2013In: PLoS ONE, ISSN 1932-6203, E-ISSN 1932-6203, Vol. 8, no 8, article id e70174Article in journal (Refereed)
    Abstract [en]

    Celiac disease is a common autoimmune disorder characterized by an intestinal inflammation triggered by gluten, a storage protein found in wheat, rye and barley. Similar to other autoimmune diseases such as type 1 diabetes, psoriasis and rheumatoid arthritis, celiac disease is the result of an immune response to self-antigens leading to tissue destruction and production of autoantibodies. Common diseases like celiac disease have a complex pattern of inheritance with inputs from both environmental as well as additive and non-additive genetic factors. In the past few years, Genome Wide Association Studies (GWAS) have been successful in finding genetic risk variants behind many common diseases and traits. To complement and add to the previous findings, we performed a GWAS including 206 trios from 97 nuclear Swedish and Norwegian families affected with celiac disease. By stratifying for HLA-DQ, we identified a new genome-wide significant risk locus covering the DUSP10 gene. To further investigate the associations from the GWAS we performed pathway analyses and two-locus interaction analyses. These analyses showed an over-representation of genes involved in type 2 diabetes and identified a set of candidate mechanisms and genes of which some were selected for mRNA expression analysis using small intestinal biopsies from 98 patients. Several genes were expressed differently in the small intestinal mucosa from patients with celiac autoimmunity compared to intestinal mucosa from control patients. From top-scoring regions we identified susceptibility genes in several categories: 1) polarity and epithelial cell functionality; 2) intestinal smooth muscle; 3) growth and energy homeostasis, including proline and glutamine metabolism; and finally 4) innate and adaptive immune system. These genes and pathways, including specific functions of DUSP10, together reveal a new potential biological mechanism that could influence the genesis of celiac disease, and possibly also other chronic disorders with an inflammatory component.

  • 472.
    Österberg, Lovisa
    et al.
    University of Gothenburg.
    Levan, Kristina
    University of Gothenburg.
    Partheen, Karolina
    University of Gothenburg.
    Dalle, Ulla
    University of Gothenburg.
    Olsson, Björn
    University of Skövde, The Systems Biology Research Centre. University of Skövde, School of Life Sciences.
    Sundfeldt, Karin
    University of Gothenburg.
    Horvath, György
    University of Gothenburg.
    Specific Copy Number Alterations Associated with Docetaxel/Carboplatin Response in Ovarian Carcinomas2010In: Anticancer Research, ISSN 0250-7005, E-ISSN 1791-7530, Vol. 30, no 11, p. 4451-4458Article in journal (Refereed)
    Abstract [en]

    Background: The continued high recurrence and mortality rate in ovarian cancer is a significant problem and the major obstacle in the treatment of ovarian cancer patients is chemotherapy resistance. Thus, finding predictive markers of chemoresistance and elucidating resistance mechanisms is crucial for individualising treatment and improving survival of ovarian cancer patients. Materials and Methods: Using array comparative genomic hybridisation (CGH), this pilot study analysed the tumour genomes of patients treated with docetaxel/carboplatin as first-line chemotherapy (6 resistant versus 24 sensitive cases). This is the first array CGH study of  such  material.  Results:  The  study  identified  genetic alterations specific to chemoresistant (gains in 9p13.2-13.1, 9q21.2-21.32,  9q21.33,  9q22.2-22.31,  9q22.32-22.33  and 9q33.1-34.11) and chemosensitive (losses in 8p23.3-23.1 and 8p22) disease. Additionally, when comparing the results to previously analysed tumour material from patients treated with paclitaxel/carboplatin, the two datasets identified different genetic  alteration  profiles.  Conclusion:  Specific  genetic alterations were identified and associated with chemotherapy response in ovarian cancer. It will be interesting to investigate these exciting data further in larger independent series of ovarian   tumours,   and   hopefully   will   contribute   to   the establishment of predictive markers.

  • 473.
    Österberg, Lovisa
    et al.
    University of Gothenburg.
    Levan, Kristina
    University of Gothenburg.
    Partheen, Karolina
    University of Gothenburg.
    Delle, Ulla
    University of Gothenburg.
    Olsson, Björn
    University of Skövde, The Systems Biology Research Centre. University of Skövde, School of Life Sciences.
    Horvath, Karin
    University of Gothenburg.
    Potential predictive markers of chemotherapy resistance ovarian serous carcinomas2009In: BMC Cancer, ISSN 1471-2407, E-ISSN 1471-2407, Vol. 9, p. 368-Article in journal (Refereed)
    Abstract [en]

    Background Chemotherapy resistance remains a major obstacle in the treatment of women with ovarian cancer. Establishing predictive markers of chemoresponse would help to individualize therapy and improve survival of ovarian cancer patients. Chemotherapy resistance in ovarian cancer has been studied thoroughly and several non-overlapping single genes, gene profiles and copy number alterations have been suggested as potential markers. The objective of this study was to explore genetic alterations behind chemotherapy resistance in ovarian cancer with the ultimate aim to find potential predictive markers.

    Methods To create the best opportunities for identifying genetic alterations of importance for resistance, we selected a homogenous tumor material concerning histology, stage and chemotherapy. Using high-resolution whole genome array comparative genomic hybridization (CGH), we analyzed the tumor genomes of 40 fresh-frozen stage III ovarian serous carcinomas, all uniformly treated with combination therapy paclitaxel/carboplatin. Fisher's exact test was used to identify significant differences. Subsequently, we examined four genes in the significant regions (EVI1, MDS1, SH3GL2, SH3KBP1) plus the ABCB1 gene with quantitative real-time polymerase chain reaction (QPCR) to evaluate the impact of DNA alterations on the transcriptional level.

    Results We identified gain in 3q26.2, and losses in 6q11.2-12, 9p22.3, 9p22.2-22.1, 9p22.1-21.3, Xp22.2-22.12, Xp22.11-11.3, and Xp11.23-11.1 to be significantly associated with chemotherapy resistance. In the gene expression analysis, EVI1 expression differed between samples with gain versus without gain, exhibiting higher expression in the gain group.

    Conclusion In conclusion, we detected specific genetic alterations associated with resistance, of which some might be potential predictive markers of chemotherapy resistance in advanced ovarian serous carcinomas. Thus, further studies are required to validate these findings in an independent ovarian tumor series.

78910 451 - 473 of 473
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