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Publications (10 of 13) Show all publications
Lundh, D., Hedelin, H., Jonsson, K., Gifford, M. & Larsson, D. (2013). Assessing chronic pelvic pain syndrome patients: Blood plasma factors and cortisol saliva. Scandinavian Journal of Urology, 47(6), 521-528
Open this publication in new window or tab >>Assessing chronic pelvic pain syndrome patients: Blood plasma factors and cortisol saliva
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2013 (English)In: Scandinavian Journal of Urology, ISSN 2168-1813, Vol. 47, no 6, p. 521-528Article in journal (Refereed) Published
Abstract [en]

Objective. The aim of this study was to identify changes in inflammatory molecules in the blood (plasma) of patients with chronic prostatitis/chronic pelvic syndrome (CP/CPPS) compared with controls. Altered levels indicate a systemic component by possible involvement of the prostate and/or the inner pelvic floor musculature. Material and methods. In 32 patients with CP/CPPS and 37 controls, blood plasma levels of testosterone, macrophage migration inhibitory factor (MIF), tumour necrosis factor-alpha (TNF-alpha), TNF-beta, interleukin-2 (IL-2) and IL-1 beta were measured by enzyme-linked immunosorbent assay. Cortisol in saliva samples was measured in the morning and late evening. All participants answered a questionnaire regarding their health profile. Results. Significantly higher levels of MIF (p = 0.012) were detected in patients. The testosterone level was, contrary to other studies, little lower in patients (p = 0.014; age adjusted). When controls with health issues and patients with a parallel disease were excluded, the MIF and TNF-alpha levels were higher in the patients (p = 0.007, p = 0.016, respectively) than in controls, and the testosterone was slightly lower in patients (p = 0.047). Conclusions. The findings show an immune response extending to the circulatory system, in which MIF makes a significant contribution to CP/CPPS. This study also indicates TNF-alpha as a circulatory component when excluding subjects with concomitant diseases. Both MIF and TNF-alpha have previously been highlighted for other diseases related to chronic pain and here also for CP/CPPS. These results provide further insights into the immunological basis of CP/CPPS.

Place, publisher, year, edition, pages
Informa Healthcare, 2013
National Category
Medical and Health Sciences
Research subject
Medical sciences
Identifiers
urn:nbn:se:his:diva-8783 (URN)10.3109/21681805.2013.769460 (DOI)000328899000013 ()23394140 (PubMedID)2-s2.0-84890518365 (Scopus ID)
Available from: 2014-02-14 Created: 2014-02-14 Last updated: 2017-11-27Bibliographically approved
Lundh, D., Hedelin, H. & Larsson, D. (2013). Chronic prostatitis/chronic pelvic pain syndrome: Interplay of inflammatory mediators, "Beyond the Abstract". UroToday International Journal
Open this publication in new window or tab >>Chronic prostatitis/chronic pelvic pain syndrome: Interplay of inflammatory mediators, "Beyond the Abstract"
2013 (English)In: UroToday International Journal, ISSN 1939-4810Article in journal (Refereed) Published
Place, publisher, year, edition, pages
UroToday Inc., 2013
National Category
Natural Sciences
Research subject
Natural sciences
Identifiers
urn:nbn:se:his:diva-8578 (URN)
Available from: 2013-10-28 Created: 2013-10-28 Last updated: 2017-11-27Bibliographically approved
Larsson, D., Jonas, A., Bergsten, N., Ståhl, F. & Karlsson, S. (2012). Membrane Initiated Effects of1α,25-Dihydroxyvitamin D3 inProstate Cancer Cells: Effects on AP1 and CREB Mediated Transcription. In: Stevo Najman (Ed.), Current Frontiers and Perspectives in Cell Biology: (pp. 153-162). InTech
Open this publication in new window or tab >>Membrane Initiated Effects of1α,25-Dihydroxyvitamin D3 inProstate Cancer Cells: Effects on AP1 and CREB Mediated Transcription
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2012 (English)In: Current Frontiers and Perspectives in Cell Biology / [ed] Stevo Najman, InTech, 2012, p. 153-162Chapter in book (Refereed)
Place, publisher, year, edition, pages
InTech, 2012
National Category
Biological Sciences
Research subject
Natural sciences
Identifiers
urn:nbn:se:his:diva-6484 (URN)10.5772/32908 (DOI)978-953-51-0544-2 (ISBN)
Available from: 2012-10-09 Created: 2012-10-09 Last updated: 2017-11-27Bibliographically approved
Berggren, E., Sidenvall, B. & Larsson, D. (2011). Subarachnoid haemorrhage has long-term effects on social life. British Journal of Neuroscience Nursing, 7(1), 429-435
Open this publication in new window or tab >>Subarachnoid haemorrhage has long-term effects on social life
2011 (English)In: British Journal of Neuroscience Nursing, ISSN 1747-0307, E-ISSN 2052-2800, Vol. 7, no 1, p. 429-435Article in journal (Refereed) Published
Abstract [en]

Aim: The aim of this study was to describe memory after a subarachnoid haemorrhage (SAH) from the perspective of relatives and patients in two cohorts and also to evaluate the application of relatives' statements as a tool in nursing care and rehabilitation, in order to support the patient. Background: Cognitive sequelae due to SAH are a large disability and may influence the adjustment to daily life. Supporting patients and relatives requires knowledge concerning the patients' memory both from the perspective of patients and relatives. Method: Eleven relatives and 11 patients (Cohort 1), 11 years after the onset of an SAH and 15 relatives and 15 patients (Cohort 2) 6 years after the onset of an SAH, participated in the study. Interview questions and memory tests were used to collect data. Findings: Problems with memory, including meta-memory problems regarding relatives' statements, were common. Relatives and patients stated patients' menory in a similar manner. However, patients' statements concerning their memory corresponded in higher degree with memory test results, in comparison with relatives' statements. Conclusions: Relatives' and patients' statements are useful as tools in nursing care and rehabilitation. However, from results showing meta-memory problems and that patients' statements concerning their memory corresponded better with memory test results (in comparison with relatives' statements), it is vital to offer patients memory tests in order to prevent complications in mutual family relationships.

Place, publisher, year, edition, pages
MA Healthcare Ltd., 2011
Keywords
Subarachnoid haemorrhage, SAH, stroke, memory, memory test, interview questions
National Category
Medical and Health Sciences
Research subject
Medical sciences
Identifiers
urn:nbn:se:his:diva-4609 (URN)
Note

Preliminär publiceringinformation:

Berggren, E., Sidenvall, B., & Larsson, D. (2010). Memory ability after subarachnoid haemorrhage: relatives' and patients' statements in relation to test results. British Journal Of Neuroscience Nursing, 6(8), 383-388.

Available from: 2011-01-21 Created: 2011-01-21 Last updated: 2017-12-11Bibliographically approved
Lundh, D., Larsson, D., Nahar, N. & Mandal, A. (2010). Arsenic accumulation in plants - Outlining strategies for developing improved variety of crops for avoiding arsenic toxicity in foods. Journal of biological systems, 18(1), 223-241
Open this publication in new window or tab >>Arsenic accumulation in plants - Outlining strategies for developing improved variety of crops for avoiding arsenic toxicity in foods
2010 (English)In: Journal of biological systems, ISSN 0218-3390, Vol. 18, no 1, p. 223-241Article in journal (Refereed) Published
Abstract [en]

Contamination of food with arsenics is a potential health risk for both humans and animals in many regions of the world, especially in Asia. Arsenics can be accumulated in humans, animals and plants for a longer period and a long-term exposure of humans to arsenics results in severe damage of kidney, lever, heart etc. and many other vascular diseases. Arsenic contamination in human may also lead to development of cancer. In this paper we report our results on data mining approach (an in silico analysis based on searching of the existing genomic databases) for identification and characterization of genes that might be responsible for uptake, accumulation or metabolism of arsenics. For these in silico analyses we have involved the model plant Arabidopsis thaliana in our investigation. By employing a system biology model (a kinetic model) we have studied the molecular mechanisms of these processes in this plant. This model contains equations for uptake, metabolism and sequestration of different types of arsenic; As(V), As(III), MMAA and DMAA. The model was then implemented in the software XPP. The model was also validated against the data existing in the literatures. Based on the results of these in silico studies we have developed some strategies that can be used for reducing arsenic contents in different parts of the plant. Data mining experiments resulted in identification of two candidate genes (ACR2, arsenate reductase 2 and PCS1, phytochelatin synthase 1) that are involved either in uptake, transport or cellular localization of arsenic in A. thaliana. However, our system biology model revealed that by increasing the level of arsenate reductase together with an increased rate of arsenite sequestration in the vacuoles (by involving an arsenite efflux pump MRP1/2), it is possible to reduce the amount of arsenics in the shoots of A. thaliana to 11–12%.

Place, publisher, year, edition, pages
World Scientific Publishing Co., 2010
Keywords
Arsenic Toxicity; Arsenic Accumulation; Kinetic Model; Strategy for Arsenics
National Category
Natural Sciences
Research subject
Natural sciences
Identifiers
urn:nbn:se:his:diva-4325 (URN)10.1142/S0218339010003214 (DOI)000275713700011 ()2-s2.0-77951694527 (Scopus ID)
Available from: 2010-08-25 Created: 2010-08-25 Last updated: 2017-12-21Bibliographically approved
Sogaard, P., Szekeres, F., Garcia-Roves, P. M., Larsson, D., Chibalin, A. V. & Zierath, J. R. (2010). Spatial Insulin Signalling in Isolated Skeletal Muscle Preparations. Journal of Cellular Biochemistry, 109(5), 943-949
Open this publication in new window or tab >>Spatial Insulin Signalling in Isolated Skeletal Muscle Preparations
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2010 (English)In: Journal of Cellular Biochemistry, ISSN 0730-2312, E-ISSN 1097-4644, Vol. 109, no 5, p. 943-949Article in journal (Refereed) Published
Abstract [en]

During in vitro incubation in the absence or presence of insulin, glycogen depletion occurs in the inner core of the muscle specimen, concomitant with increased staining of hypoxia-induced-factor-1-alpha and caspase-3, markers of hypoxia and apoptosis, respectively. The aim of this study was to determine whether insulin is able to diffuse across the entire muscle specimen in sufficient amounts to activate signalling cascades to promote glucose uptake and glycogenesis within isolated mouse skeletal muscle. Phosphoprotein multiplex assay on lysates from muscle preparation was performed to detect phosphorylation of insulin-receptor on Tyr1146, Akt on Ser473 and glycogen-synthases-kinase-3 on Ser21/Ser9. To address the spatial resolution of insulin signalling, immunohistochemistry studies on cryosections were performed. Our results provide evidence to suggest that during the in vitro incubation, insulin sufficiently diffuses into the centre of tubular mouse muscles to promote phosphorylation of these signalling events. Interestingly, increased insulin signalling was observed in the core of the incubated muscle specimens, correlating with the location of oxidative fibres. In conclusion, insulin action was not restricted due to insufficient diffusion of the hormone during in vitro incubation in either extensor digitorum longus or soleus muscles from mouse under the specific experimental settings employed in this study. Hence, we suggest that the glycogen depleted core as earlier observed is not due to insufficient insulin action.

Place, publisher, year, edition, pages
Wiley-Liss, Inc., 2010
Keywords
In Vitro Incubation, Immunohistochemistry, Extensor Digitorum Longus, Soleus, Spatial
National Category
Natural Sciences
Research subject
Natural sciences
Identifiers
urn:nbn:se:his:diva-4330 (URN)10.1002/jcb.22470 (DOI)000276418900013 ()20069552 (PubMedID)2-s2.0-77950407958 (Scopus ID)
Available from: 2010-08-26 Created: 2010-08-26 Last updated: 2017-12-12Bibliographically approved
Karlsson, S., Olausson, J., Lundh, D., Sögård, P., Mandal, A., Holmström, K.-O., . . . Larsson, D. (2010). Vitamin D and prostate cancer: The role of membrane initiated signaling pathways in prostate cancer progression. Journal of Steroid Biochemistry and Molecular Biology, 121(1-2), 413-416
Open this publication in new window or tab >>Vitamin D and prostate cancer: The role of membrane initiated signaling pathways in prostate cancer progression
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2010 (English)In: Journal of Steroid Biochemistry and Molecular Biology, ISSN 0960-0760, E-ISSN 1879-1220, Vol. 121, no 1-2, p. 413-416Article in journal (Refereed) Published
Abstract [en]

1,25-Dihydroxyvitamin D3 (1,25(OH)2D3) has been demonstrated to mediate both genomic and non-genomic responses in prostate cancer (CaP) cells. Here, we give an overview of membrane initiated 1,25(OH)2D3 signaling in prostate cancer cell progression. The presence of PDIA3 was investigated and homologous modeling of the putative PDIA3 receptor complex was conducted. Furthermore, the cellular distribution of nVDR was analyzed. We could show that both nVDR and PDIA3 are expressed in the prostate cancer cell lines investigated. The homologous modeling of PDIA3 showed that the receptor complex exists in a trimer formation, which suggests for allosteric activity. Our findings support previous reports and suggest that 1,25(OH)2D3 is an important therapeutic agent in inhibiting prostate cancer progression. Furthermore, our data show that 1,25(OH)2D3 regulate prostate cell biology via multiple pathways and targeting specific pathways for 1,25(OH)2D3 might provide more effective therapies compared to the vitamin D therapies currently clinically tested.

Place, publisher, year, edition, pages
Elsevier, 2010
Keywords
1, 25(OH)2D3, Prostate cancer, Membrane receptors, PDIA3, nVDR, Receptor modeling
National Category
Natural Sciences
Research subject
Natural sciences
Identifiers
urn:nbn:se:his:diva-4528 (URN)10.1016/j.jsbmb.2010.03.083 (DOI)000280600200091 ()20398754 (PubMedID)2-s2.0-77954760891 (Scopus ID)
Available from: 2011-01-03 Created: 2011-01-03 Last updated: 2017-12-20Bibliographically approved
Holmén, J., Jansson, A. & Larsson, D. (2009). A Kinetic Overview of the Receptors Involved in 1,25-Dihydroxyvitamin D3 and 24,25-Dihydroxyvitamin D3 Signaling: A Systems Biology Approach. Critical Reviews in Eukaryotic Gene Expression, 19(3), 181-196
Open this publication in new window or tab >>A Kinetic Overview of the Receptors Involved in 1,25-Dihydroxyvitamin D3 and 24,25-Dihydroxyvitamin D3 Signaling: A Systems Biology Approach
2009 (English)In: Critical Reviews in Eukaryotic Gene Expression, ISSN 1045-4403, E-ISSN 2162-6502, Vol. 19, no 3, p. 181-196Article, review/survey (Refereed) Published
Abstract [en]

The vitamin D endocrine system modulates an arsenal of important biological functions in more than 30 different tissues in short- and long-term perspectives. Two membrane receptors and one nuclear receptor are suggested to be involved in the vitamin D signaling system, but the function and physiological relevance of the receptors are debated. The complexity of the vitamin D endocrine system makes it necessary to combine experimental data with in silico simulations to get a holistic view of vitamin D-dependent regulation of tissue and cell physiology. This review focus on binding characteristics for the three putative vitamin D receptors and proposes a future systems biology approach including mathematical modeling that will be helpful together with experimental methods in depicting antitumoral and other biological effects promoted by the vitamin D endocrine system.

Place, publisher, year, edition, pages
Begell House, 2009
Keywords
vitamin D, mathematical modeling, nVDR, PDIA3, catalase, receptor kinetics
National Category
Natural Sciences
Research subject
Natural sciences
Identifiers
urn:nbn:se:his:diva-3510 (URN)10.1615/CritRevEukarGeneExpr.v19.i3.20 (DOI)000270313600003 ()19883364 (PubMedID)2-s2.0-67650314922 (Scopus ID)
Available from: 2009-12-01 Created: 2009-12-01 Last updated: 2017-12-12Bibliographically approved
Sögaard, P., Szekeres, F., Holmström, M., Larsson, D., Harlén, M., Garcia-Roves, P. & Chibalin, A. V. (2009). Effects of fibre type and diffusion distance on mouse skeletal muscle glycogen content in vitro. Journal of Cellular Biochemistry, 107(6), 1189-1197
Open this publication in new window or tab >>Effects of fibre type and diffusion distance on mouse skeletal muscle glycogen content in vitro
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2009 (English)In: Journal of Cellular Biochemistry, ISSN 0730-2312, E-ISSN 1097-4644, Vol. 107, no 6, p. 1189-1197Article in journal (Refereed) Published
Abstract [en]

In vitro incubation of isolated rodent skeletal muscle is a widely used procedure in metabolic research. One concern with this method is the development of an anoxic state during the incubation period that can cause muscle glycogen depletion. Our aim was to investigate whether in vitro incubation conditions influence glycogen concentration in glycolytic extensor digitorum longus (EDL) and oxidative soleus mouse muscle. Quantitative immunohistochemistry was applied to assess glycogen content in incubated skeletal muscle. Glycogen concentration was depleted, independent of insulin-stimulation in the incubated skeletal muscle. The extent of glycogen depletion was correlated with the oxidative fibre distribution and with the induction of hypoxia-induced-factor-1-alpha. Insulin exposure partially prevented glycogen depletion in soleus, but not in EDL muscle, providing evidence that glucose diffusion is not a limiting step to maintain glycogen content. Our results provide evidence to suggest that the anoxic milieu and the intrinsic characteristics of the skeletal muscle fibre type play a major role in inducing glycogen depletion in during in vitro incubations.

Place, publisher, year, edition, pages
John Wiley & Sons, 2009
Keywords
immunohistochemistry, muscle glycogen, fibre type, insulin action, anoxia
National Category
Natural Sciences
Research subject
Natural sciences
Identifiers
urn:nbn:se:his:diva-3291 (URN)10.1002/jcb.22223 (DOI)000268826900016 ()19507232 (PubMedID)2-s2.0-68049113343 (Scopus ID)
Available from: 2009-07-09 Created: 2009-07-09 Last updated: 2017-12-13Bibliographically approved
Larsson, D., Hagberg, M., Nahren, M., Kjellberg, C., Senneberg, E., Tahmasebifar, N. & Johansson, V. (2008). Membrane Initiated Signaling by 1,25α-dihydroxyvitamin D3 in LNCaP Prostate Cancer Cells. Springer
Open this publication in new window or tab >>Membrane Initiated Signaling by 1,25α-dihydroxyvitamin D3 in LNCaP Prostate Cancer Cells
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2008 (English)Conference paper, Published paper (Other academic)
Abstract [en]

Prostate cancer (PC) is one of the most common cancers among men, and vitamin D and its metabolites are candidates for prevention and therapy of this disease. The vitamin D metabolites, 1, 25-dihydroxyvitamin D3 (1,25D) and 25-hydroxyvitamin D3, decreases cellular proliferation and invasiveness, and stimulates differentiation of PC cells. However, the underlying mechanisms are not fully clarified, and there is evidence that some of these effects of the vitamin D system are mediated by specific membrane-associated receptors/binding proteins in addition to its nuclear receptor, suggesting multiple regulatory pathways. The aim of the present study was to examine the role of membrane initiated pathways mediating effects of 1,25D on cell invasiveness in LNCaP cells. Treatment with 1,25D evoked a dose-dependent activation of the JNK/SAPK MAPK signaling pathways within 10 min, demonstrating membrane initiated signaling of 1,25D in LNCaP cells. Furthermore, treatment with 1,25D decreased LNCaP cell invasiveness by approximately 20% after 48h. Using an inhibitor (SP600125) for the JNK/SAPK MAPK signaling pathway in combination with 1,25D on LNCaP cells, the inhibitory action of 1,25D on invasiveness was eliminated. In conclusion, 1,25D decrease invasiveness of LNCaP cells by interaction with a putative membrane associated receptor, which activate membrane, initiated signaling via the JNK/SAPK MAPK signaling pathway.

Place, publisher, year, edition, pages
Springer, 2008
Series
Advances in Experimental Medicine and Biology, ISSN 0065-2598 ; 617
National Category
Medical and Health Sciences
Research subject
Medical sciences
Identifiers
urn:nbn:se:his:diva-2731 (URN)10.1007/978-0-387-69080-3 (DOI)000253701800059 ()2-s2.0-46749094667 (Scopus ID)978-0-387-69078-0 (ISBN)
Available from: 2009-02-11 Created: 2009-02-11 Last updated: 2017-11-27Bibliographically approved
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ORCID iD: ORCID iD iconorcid.org/0000-0002-4724-0269

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