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Sökning: WFRF:(Persson J) > Malmö universitet

  • Resultat 1-10 av 14
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1.
  • Buhlin, K., et al. (författare)
  • Periodontal treatment influences risk markers for atherosclerosis in patients with severe periodontitis
  • 2009
  • Ingår i: Atherosclerosis. - : Elsevier. - 0021-9150 .- 1879-1484. ; 206:2, s. 518-522
  • Tidskriftsartikel (refereegranskat)abstract
    • This study investigated the effect of mechanical infection control for periodontitis and periodontal surgery on the prevalence of well-established risk factors for atherosclerosis, and plasma levels of cytokines, antibodies against heat shock proteins and markers of systemic inflammation. Sixty-eight patients between 39 and 73 years of age with severe periodontitis who had been referred to four specialist periodontology clinics in Sweden were investigated. A fasting venous blood sample was taken at baseline and additional samples were collected after 3 and 12 months. A total of 54 patients underwent periodontal treatment. The periodontal treatment was successful, as pathogenic gingival pockets decreased significantly. Plasma glucose, lipids and markers of systemic inflammation were not significantly altered after 3 months. One year after the initial treatment, HDL-C concentrations were significantly increased (Δ0.08 mmol/L) whereas LDL-C concentrations decreased (Δ0.23 mmol/L). Haptoglobin concentrations were also lower. Interleukin-18 and interferon-γ levels were also lower after 12 months (60 ng/L (-23%) and 11 ng/L (-97%) respectively). Treatment had no effect on plasma levels of IgA, IgG1, IgG2 antibodies against heat shock proteins. In conclusion, this study indicates that standard treatment for periodontal disease induces systemic changes in several biochemical markers that reflect the risk for atherosclerosis. 
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2.
  • Fabijan, Aleksander, et al. (författare)
  • Competitive Online Clique Clustering
  • 2013
  • Ingår i: Proceedings of the 8th International Conference on Algorithms and Complexity;8. - Berlin, Heidelberg : Springer. ; , s. 221-233
  • Konferensbidrag (refereegranskat)abstract
    • Clique clustering is the problem of partitioning a graph into cliques so that some objective function is optimized. In online clustering, the input graph is given one vertex at a time, and any vertices that have previously been clustered together are not allowed to be separated. The objective here is to maintain a clustering the never deviates too far in the objective function compared to the optimal solution. We give a constant competitive upper bound for online clique clustering, where the objective function is to maximize the number of edges inside the clusters. We also give almost matching upper and lower bounds on the competitive ratio for online clique clustering, where we want to minimize the number of edges between clusters. In addition, we prove that the greedy method only gives linear competitive ratio for these problems.
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3.
  • Haigh, Daisy B., et al. (författare)
  • The METTL3 RNA Methyltransferase Regulates Transcriptional Networks in Prostate Cancer
  • 2022
  • Ingår i: Cancers. - : MDPI. - 2072-6694. ; 14:20
  • Tidskriftsartikel (refereegranskat)abstract
    • Prostate cancer (PCa) is a leading cause of cancer-related deaths and is driven by aberrant androgen receptor (AR) signalling. For this reason, androgen deprivation therapies (ADTs) that suppress androgen-induced PCa progression either by preventing androgen biosynthesis or via AR signalling inhibition (ARSi) are common treatments. The N6-methyladenosine (m6A) RNA modification is involved in regulating mRNA expression, translation, and alternative splicing, and through these mechanisms has been implicated in cancer development and progression. RNA-m6A is dynamically regulated by the METTL3 RNA methyltransferase complex and the FTO and ALKBH5 demethylases. While there is evidence supporting a role for aberrant METTL3 in many cancer types, including localised PCa, the wider contribution of METTL3, and by inference m6A, in androgen signalling in PCa remains poorly understood. Therefore, the aim of this study was to investigate the expression of METTL3 in PCa patients and study the clinical and functional relevance of METTL3 in PCa. It was found that METTL3 is aberrantly expressed in PCa patient samples and that siRNA-mediated METTL3 knockdown or METTL3-pharmacological inhibition significantly alters the basal and androgen-regulated transcriptome in PCa, which supports targeting m6A as a novel approach to modulate androgen signalling in PCa.
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4.
  • Hammar, Mikael, et al. (författare)
  • Competitive Exploration of Rectilinear Polygons
  • 2006
  • Ingår i: Theoretical Computer Science. - : Elsevier. - 0304-3975 .- 1879-2294. ; 354:3, s. 367-378
  • Tidskriftsartikel (refereegranskat)abstract
    • Exploring a polygon with robots, when the robots do not have knowledge of the surroundings can be viewed as an online problem. Typical for online problems is that decisions must be made based on past events without complete information about the future. In our case the robots do not have complete information about the environment. Competitive analysis can be used to measure the performance of methods solving online problems. The competitive ratio of such a method is the ratio between the method's performance and the performance of the best method having full knowledge of the future. We are interested in obtaining good bounds on the competitive ratio of exploring polygons and prove constant competitive strategies and lower bounds for exploring a simple rectilinear polygon in the $L_1$ metric.
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5.
  • Hammar, Mikael, et al. (författare)
  • The Online Freeze-Tag Problem
  • 2006
  • Ingår i: LATIN 2006: Theoretical Informatics. - Berlin, Heidelberg : Encyclopedia of Global Archaeology/Springer Verlag. ; , s. 569-579
  • Konferensbidrag (refereegranskat)abstract
    • We consider the following problem from swarm robotics: given one or more “awake” robots in some metric space M, wake up a set of “asleep” robots. A robot awakens a sleeping robot by moving to the sleeping robot’s position. When a robot awakens, it is available to assist in awakening other slumbering robots. We investigate offline and online versions of this problem and give a 2-competitive strategy and a lower bound of 2 in the case when M is discrete and the objective is to minimize the total movement cost. We also study the case when M is continuous and show a lower bound of 7/3 when the objective is to minimize the time when the last robot awakens.
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6.
  • Harris, Anna E., et al. (författare)
  • Exploring anti-androgen therapies in hormone dependent prostate cancer and new therapeutic routes for castration resistant prostate cancer
  • 2022
  • Ingår i: Frontiers in Endocrinology. - : Frontiers Media S.A.. - 1664-2392. ; 13
  • Forskningsöversikt (refereegranskat)abstract
    • Androgen deprivation therapies (ADTs) are important treatments which inhibit androgen-induced prostate cancer (PCa) progression by either preventing androgen biosynthesis (e.g. abiraterone) or by antagonizing androgen receptor (AR) function (e.g. bicalutamide, enzalutamide, darolutamide). A major limitation of current ADTs is they often remain effective for limited durations after which patients commonly progress to a lethal and incurable form of PCa, called castration-resistant prostate cancer (CRPC) where the AR continues to orchestrate pro-oncogenic signalling. Indeed, the increasing numbers of ADT-related treatment-emergent neuroendocrine-like prostate cancers (NePC), which lack AR and are thus insensitive to ADT, represents a major therapeutic challenge. There is therefore an urgent need to better understand the mechanisms of AR action in hormone dependent disease and the progression to CRPC, to enable the development of new approaches to prevent, reverse or delay ADT-resistance. Interestingly the AR regulates distinct transcriptional networks in hormone dependent and CRPC, and this appears to be related to the aberrant function of key AR-epigenetic coregulator enzymes including the lysine demethylase 1 (LSD1/KDM1A). In this review we summarize the current best status of anti-androgen clinical trials, the potential for novel combination therapies and we explore recent advances in the development of novel epigenetic targeted therapies that may be relevant to prevent or reverse disease progression in patients with advanced CRPC.
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9.
  • Magnusson, Martin, et al. (författare)
  • Low Plasma Level of Atrial Natriuretic Peptide Predicts Development of Diabetes: The Prospective Malmo Diet and Cancer Study.
  • 2012
  • Ingår i: The Journal of clinical endocrinology and metabolism. - : The Endocrine Society. - 1945-7197 .- 0021-972X. ; 97:2, s. 638-645
  • Tidskriftsartikel (refereegranskat)abstract
    • Context:The cardiac natriuretic peptides are involved in blood pressure regulation, and large cross-sectional studies have shown lower plasma levels of N-terminal pro-natriuretic peptide levels [N-terminal atrial natriuretic peptide (N-ANP) and N-terminal brain natriuretic peptide (N-BNP)] in patients with insulin resistance, obesity, and diabetes.Objective:In this study, we prospectively tested whether plasma levels of mid-regional ANP (MR-ANP) and N-BNP predict new-onset diabetes and long-term glucose progression.Design, Setting, and Patients:MR-ANP and N-BNP were measured in 1828 nondiabetic individuals of the Malmö Diet and Cancer cohort (mean age 60 yr; 61% women) who subsequently underwent a follow-up exam including an oral glucose tolerance test after a median follow-up time of 16 yr. Logistic regression was used to adjust for covariates.Results:During follow-up, 301 subjects developed new-onset diabetes. After full multivariate adjustment, MR-ANP was significantly inversely associated with incident diabetes (OR = 0.85; 95% CI = 0.73-0.99; P = 0.034) but not N-BNP (OR = 0.92; 95% CI = 0.80-1.06; P = 0.262). In fully adjusted linear regression models, the progression of fasting glucose during follow-up was significantly inversely related to baseline levels of MR-ANP (P = 0.004) but not N-BNP (P = 0.129). Quartile analyses revealed that the overall association was mainly accounted for by excess risk of incident diabetes in subjects belonging to the lowest quartile of MR-ANP. After full adjustment, the odds ratio for incident diabetes in the bottom compared with the top quartile of MR-ANP was 1.65 (OR = 1.08-2.51, P = 0.019) and 1.43 (OR = 1.04-1.96, P = 0.027) compared with all other subjects.Conclusion:Low plasma levels of MR-ANP predict development of future diabetes and glucose progression over time, suggesting a causal role of ANP deficiency in diabetes development.
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10.
  • Metzler, Veronika M., et al. (författare)
  • The KDM5B and KDM1A lysine demethylases cooperate in regulating androgen receptor expression and signalling in prostate cancer
  • 2023
  • Ingår i: Frontiers in Cell and Developmental Biology. - : Frontiers Media S.A.. - 2296-634X. ; 11
  • Tidskriftsartikel (refereegranskat)abstract
    • Histone H3 lysine 4 (H3K4) methylation is key epigenetic mark associated with active transcription and is a substrate for the KDM1A/LSD1 and KDM5B/JARID1B lysine demethylases. Increased expression of KDM1A and KDM5B is implicated in many cancer types, including prostate cancer (PCa). Both KDM1A and KDM5B interact with AR and promote androgen regulated gene expression. For this reason, there is great interested in the development of new therapies targeting KDM1A and KDM5B, particularly in the context of castrate resistant PCa (CRPC), where conventional androgen deprivation therapies and androgen receptor signalling inhibitors are no longer effective. As there is no curative therapy for CRPC, new approaches are urgently required to suppress androgen signalling that prevent, delay or reverse progression to the castrate resistant state. While the contribution of KDM1A to PCa is well established, the exact contribution of KDM5B to PCa is less well understood. However, there is evidence that KDM5B is implicated in numerous pro-oncogenic mechanisms in many different types of cancer, including the hypoxic response, immune evasion and PI3/AKT signalling. Here we elucidate the individual and cooperative functions of KDM1A and KDM5B in PCa. We show that KDM5B mRNA and protein expression is elevated in localised and advanced PCa. We show that the KDM5 inhibitor, CPI-455, impairs androgen regulated transcription and alternative splicing. Consistent with the established role of KDM1A and KDM5B as AR coregulators, we found that individual pharmacologic inhibition of KDM1A and KDM5 by namoline and CPI-455 respectively, impairs androgen regulated transcription. Notably, combined inhibition of KDM1A and KDM5 downregulates AR expression in CRPC cells. Furthermore, combined KDM1A and KDM5 inhibition impairs PCa cell proliferation and invasion more than individual inhibition of KDM1A and KDM5B. Collectively our study has identified individual and cooperative mechanisms involving KDM1A and KDM5 in androgen signalling in PCa. Our findings support the further development of KDM1A and KDM5B inhibitors to treat advanced PCa. Further work is now required to confirm the therapeutic feasibility of combined inhibition of KDM1A and KDM5B as a novel therapeutic strategy for targeting AR positive CRPC.
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