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Intravenous immunoglobulin treatment of the post-polio syndrome: sustained effects on quality of life variables and cytokine expression after one year follow up
Henrik Gonzalez, Mohsen Khademi, Kristian Borg, Tomas Olsson
Journal of Neuroinflammation , 2012, DOI: 10.1186/1742-2094-9-167
Abstract: From a previous study with 135 PPS patients included, 41 patients were further evaluated before un-blinding for one year (21 placebo and 20 treated with IVIG, Xepol? 50?mg/ml), and were assessed for clinical variables by performing the Short Form-36 survey (SF-36) questionnaire assessment, the 6 minute walk distance test (6MWT) and registering pain level by Visual Analogue Scale (VAS) after IVIG treatment. A separate cohort of 37 PPS patients went through lumbar puncture (LP) at baseline and 20 patients, treated with IVIG, repeated the LP one year later. Thirty patients affected with other neurological diseases (OND) were used as control group. Inflammatory cytokines TNF, TGFβ, IFNγ, IL-23, IL-13 and IL-10 were measured in blood cells and CSF cells with RT-PCR.Scores of the physical components of SF-36 were significantly higher at the one year follow up time-point in the IVIG-treated patients when compared to baseline as well as to the control subjects. Pain VAS score and 6MWT improved significantly in the IVIG-treated patients when compared with baseline Relative expression of TNF and IFN-γ in both PBMCs and CSF from PPS patients were increased compared to OND subjects at baseline (p?<?0.05). One year after IVIG-treatment a decreased expression of IFN-γ and IL23 was found in CSF of PPS patients, while anti-inflammatory IL-13 was increased (p?<?0.05).IVIG has effects on relevant QoL variables and inflammatory cytokines up to one year in patients with PPS. This gives a basis for scheduling IVIG in upcoming trials with this therapy.
Flexible Mild Heaters in Structural Conservation of Paintings: State of the Art and Conceptual Design of a New Carbon Nanotubes-based Heater
Tomas Markevicius,Nina Olsson,Rocco Furferi,Helmut Meyer
Journal of Applied Sciences , 2012,
Abstract: Thermal treatments constitute the core in the success for most structural treatments, such as consolidation, treating planar deformations, reinforcing degraded support and others. Among the wide range of devices for thermal treatments of paintings proposed in scientific and technical literature, flexible heaters appear to be the most promising technology, especially for working with large painting or in situ. The present study provides a comprehensive review of flexible mild heater systems devised for structural conservation of paintings in the last decades, bringing forward the issues related to the instrumentation used for thermal treatments, stressing the importance of accurate control and the inadequateness of available devices. By highlighting the actual limitations of existing devices, a different approach, which employs Carbon Nanotubes-based flexible heaters is then proposed in its conceptual form. The design of such device, called IMAT (Intelligent Mobile Accurate Thermo-electrical device) is supported by the European Community in the context of the EC-FP7 Environment Theme (ENV-NMP.2011.2.2-5) into a three-year project started on November 2011.
Differences in the Defense Mechanism Technique modified (DMTm) between Depressive and Somatoform Disorder Patients  [PDF]
Lars Olsson
Open Journal of Depression (OJD) , 2015, DOI: 10.4236/ojd.2015.41001
Abstract: Differences in the Defense Mechanism Technique modified (DMTm), a percept-genetic tachistoscopic technique, between 56 patients with a main diagnosis of mild, moderate or severe unipolar depression and 42 with a main diagnosis of somatoform disorder were studied. As expected, the affect defenses of inhibition, introaggression and barrier isolation—all through their specified motive related to the depressive position of the affect positions model of the Andersson developmental and psychodynamic model of the mind—appeared more often with the depressive than the somatoform patients. Repression scored at the place of the threatening person in the DMTm pictures (Pp-repression) was more often found with the depressive patients, projected introaggression and no Pp-repression but repression scored at the place of the non-threatening person (H-repression) with the somatoform. In total less than four scorings of affect anxiety and affect defense, seen to indicate alexithymia, characterized the somatoform patients and those with mild depression. Denial through reversal II 3 and denial through reversal IV were common with the somatoform patients and those with severe depression. Denial was uncommon with mild depression. Denial, denial through reversal II 3 and denial through reversal IV increased the more severe the depression. The findings were interpreted according to the Andersson model.
Influence of Perineurial Cells and Toll-Like Receptors 2 and 9 on Herpes simplex Type 1 Entry to the Central Nervous System in Rat Encephalitis
Biborka Bereczky-Veress,Nada Abdelmagid,Fredrik Piehl,Tomas Bergstr?m,Tomas Olsson,Birgit Sk?ldenberg,Margarita Diez
PLOS ONE , 2012, DOI: 10.1371/journal.pone.0012350
Abstract: Herpes simplex encephalitis (HSE) is a rare disease with high mortality and significant morbidity among survivors. We have previously shown that susceptibility to HSE was host-strain dependent, as severe, lethal HSE developed after injection of human Herpes simplex type 1 virus (HSV-1) into the whiskers area of DA rats, whereas PVG rats remained completely asymptomatic. In the present study we investigated the early immunokinetics in these strains to address the underlying molecular mechanisms for the observed difference. The virus distribution and the immunological responses were compared in the whiskers area, trigeminal ganglia and brain stem after 12 hours and the first four days following infection using immunohistochemistry and qRT-PCR. A conspicuous immunopathological finding was a strain-dependent difference in the spread of the HSV-1 virus to the trigeminal ganglia, only seen in DA rats already from 12 hpi. In the whiskers area infected perineurial cells were abundant in the susceptible DA strain after 2 dpi, whereas in the resistant PVG rats HSV-1 spread was confined only to the epineurium. In both strains activation of Iba1+/ED1+ phagocytic cells followed the distribution pattern of HSV-1 staining, which was visible already at 12 hours after infection. Notably, in PVG rats higher mRNA expression of Toll-like receptors (Tlr) -2 and -9, together with increased staining for Iba1/ED1 was detected in the whiskers area. In contrast, all other Tlr-pathway markers were expressed at higher levels in the susceptible DA rats. Our data demonstrate the novel observation that genetically encoded properties of the host nerve and perineurial cells, recruitment of phagocyting cells together with the low expression of Tlr2 and -9 in the periphery define the susceptibility to HSV-1 entry into the nervous system.
Alternative Splicing and Transcriptome Profiling of Experimental Autoimmune Encephalomyelitis Using Genome-Wide Exon Arrays
Alan Gillett,Klio Maratou,Chris Fewings,Robert A. Harris,Maja Jagodic,Tim Aitman,Tomas Olsson
PLOS ONE , 2012, DOI: 10.1371/journal.pone.0007773
Abstract: Multiple Sclerosis (MS) is a chronic inflammatory disease causing demyelination and nerve loss in the central nervous system. Experimental autoimmune encephalomyelitis (EAE) is an animal model of MS that is widely used to investigate complex pathogenic mechanisms. Transcriptional control through isoform selection and mRNA levels determines pathway activation and ultimately susceptibility to disease.
Cytokine responses during chronic denervation
Saku Ruohonen, Mohsen Khademi, Maja Jagodic, Hanna-Stiina Taskinen, Tomas Olsson, Matias R?ytt?
Journal of Neuroinflammation , 2005, DOI: 10.1186/1742-2094-2-26
Abstract: Transected rat sciatic nerve was sutured and ligated to prevent reinnervation. The samples were collected from the left sciatic nerve distally and proximally from the point of transection. The endoneurium was separated from the surrounding epi- and perineurium to examine the expression of cytokines in both of these compartments. Macrophage invasion into endoneurium was investigated and Schwann cell proliferation was followed as well as the expression of cytokines IL-1β, IL-10, IFN-γ and TNF-α mRNA. The samples were collected from 1 day up to 5 weeks after the primary operation.At days 1 to 3 after injury in the epi-/perineurium of the proximal and distal stump, a marked expression of the pro-inflammatory cytokines TNF-α and IL-1β and of the anti-inflammatory cytokine IL-10 was observed. Concurrently, numerous macrophages started to gather into the epineurium of both proximal and distal stumps. At day 7 the number of macrophages decreased in the perineurium and increased markedly in the endoneurium of both stumps. At this time point marked expression of TNF-α and IFN-γ mRNA was observed in the endo- and epi-/perineurium of the proximal stump. At day 14 a marked increase in the expression of IL-1β could be noted in the proximal stump epi-/perineurium and in the distal stump endoneurium. At that time point many macrophages were observed in the longitudinally sectioned epineurium of the proximal 2 area as well as in the cross-section slides from the distal stump. At day 35 TNF-α, IL-1β and IL-10 mRNA appeared abundantly in the proximal epi-/perineurium together with macrophages.The present studies show that even during chronic denervation there is a cyclic expression pattern for the studied cytokines. Contrary to the previous findings on reinnervating nerves the studied cytokines show increased expression up to 35 days. The high expressions of pro-inflammatory and anti-inflammatory cytokines in the proximal epi-/perineurial area at day 35 may be involved in the formatio
Tasquinimod (ABR-215050), a quinoline-3-carboxamide anti-angiogenic agent, modulates the expression of thrombospondin-1 in human prostate tumors
Anders Olsson, Anders Bj?rk, Johan Vallon-Christersson, John T Isaacs, Tomas Leanderson
Molecular Cancer , 2010, DOI: 10.1186/1476-4598-9-107
Abstract: One of the most significant differentially expressed genes both in vitro and in vivo after exposure to tasquinimod, was thrombospondin-1 (TSP1). The up-regulation of TSP1 mRNA in LNCaP tumor cells both in vitro and in vivo correlated with an increased expression and extra cellular secretion of TSP1 protein. When nude mice bearing CWR-22RH human prostate tumors were treated with oral tasquinimod, there was a profound growth inhibition, associated with an up-regulation of TSP1 and a down- regulation of HIF-1 alpha protein, androgen receptor protein (AR) and glucose transporter-1 protein within the tumor tissue. Changes in TSP1 expression were paralleled by an anti-angiogenic response, as documented by decreased or unchanged tumor tissue levels of VEGF (a HIF-1 alpha down stream target) in the tumors from tasquinimod treated mice.We conclude that tasquinimod-induced up-regulation of TSP1 is part of a mechanism involving down-regulation of HIF1α and VEGF, which in turn leads to reduced angiogenesis via inhibition of the "angiogenic switch", that could explain tasquinimods therapeutic potential.During the last decades, development of new cancer treatments that are capable of inhibiting tumor growth by inhibition of the blood supply has received great attention [1,2]. The quinoline compound tasquinimod [ABR-215050; CAS number 254964-60-8; 4-hydroxy-5-methoxy-N,1-dimethyl-2-oxo-N-[(4-trifluoromethyl) phenyl]-1,2-dihydroquinoline-3-carboxamide] has emerged as a candidate [3], by virtue of its pharmacological profile with anti-angiogenic and anti-tumor potency in experimental human prostate cancer models [4,5]. Thrombospondin-1 (TSP1) is a 450 kDa glycoprotein initially found in platelets, but also synthesized and secreted by many normal and transformed cells. TSP1 has been shown to be a potent natural inhibitor of tumor progression and metastases via inhibition of angiogenesis and migration or by activation of TGFβ (for review see [6-8]). Several mechanisms have been propos
Altered expression of T cell Immunoglobulin-Mucin (TIM) molecules in bronchoalveolar lavage CD4+ T cells in sarcoidosis
Farah Idali, Jan Wahlstr?m, Benita Dahlberg, Mohsen Khademi, Tomas Olsson, Anders Eklund, Johan Grunewald
Respiratory Research , 2009, DOI: 10.1186/1465-9921-10-42
Abstract: We used real-time polymerase chain reaction to investigate the differential gene expression of TIM-1 and TIM-3 as well as a few Th1 and Th2 cytokines (IL-2, IFN-γ, IL-4, IL-5 and IL-13) in CD4+ T cells isolated from bronchoalveolar lavage fluid (BALF) of patients (n = 28) and healthy controls (n = 8). Using flow cytometry, we were also able to analyse TIM-3 protein expression in 10 patients and 6 healthy controls.A decreased TIM-3 mRNA (p < 0.05) and protein (p < 0.05) expression was observed in patients, and the level of TIM-3 mRNA correlated negatively with the CD4/CD8 T cell ratio in BALF cells of patients. Compared to a distinct subgroup of patients i.e. those with L?fgren's syndrome, BALF CD4+ T cells from non- L?fgren's patients expressed decreased mRNA levels of TIM-1 (p < 0.05). mRNA expression of IL-2 was increased in patients (p < 0.01) and non-L?fgren's patients expressed significantly higher levels of IFN-γ mRNA (p < 0.05) versus patients with L?fgren's syndrome.These findings are the first data on the expression of TIM-1 and TIM-3 molecules in sarcoidosis. The reduced TIM-3 expression in the lungs of patients may result in a defective T cell ability to control the Th1 immune response and could thus contribute to the pathogenesis of sarcoidosis. The down-regulated TIM-1 expression in non-L?fgren'spatients is in agreement with an exaggerated Th1 response in these patients.Sarcoidosis is a T helper (Th) 1-mediated inflammatory disease with unknown aetiology, characterized by the formation of noncaseating granulomas, and involving accumulations of macrophages and T cells, primarily affecting the lungs [1]. In pulmonary sarcoidosis, an acute onset usually indicates a self-limiting disease course, whereas an insidious onset may be followed by persistent disease with a risk for fibrosis [1]. An imbalance in the expression of Th1/Th2 cytokines by alveolar cells has been suggested to be of importance for the outcome of a pulmonary immune response in sarcoidosis
Imatinib Ameliorates Neuroinflammation in a Rat Model of Multiple Sclerosis by Enhancing Blood-Brain Barrier Integrity and by Modulating the Peripheral Immune Response
Milena Z. Adzemovic, Manuel Zeitelhofer, Ulf Eriksson, Tomas Olsson, Ingrid Nilsson
PLOS ONE , 2013, DOI: 10.1371/journal.pone.0056586
Abstract: Central nervous system (CNS) disorders such as ischemic stroke, multiple sclerosis (MS) or Alzheime?s disease are characterized by the loss of blood-brain barrier (BBB) integrity. Here we demonstrate that the small tyrosine kinase inhibitor imatinib enhances BBB integrity in experimental autoimmune encephalomyelitis, an animal model of multiple sclerosis (MS). Treatment was accompanied by decreased CNS inflammation and demyelination and especially reduced T-cell recruitment. This was supported by downregulation of the chemokine receptor (CCR) 2 in CNS and lymph nodes, and by modulation of the peripheral immune response towards an anti-inflammatory phenotype. Interestingly, imatinib ameliorated neuroinflammation, even when the treatment was initiated after the clinical manifestation of the disease. We have previously shown that imatinib reduces BBB disruption and stroke volume after experimentally induced ischemic stroke by targeting platelet-derived growth factor receptor -α (PDGFR-α) signaling. Here we demonstrate that PDGFR-α signaling is a central regulator of BBB integrity during neuroinflammation and therefore imatinib should be considered as a potentially effective treatment for MS.
Mice Lacking NCF1 Exhibit Reduced Growth of Implanted Melanoma and Carcinoma Tumors
Tiina Kelkka, Angela Pizzolla, Juha Petteri Laurila, Tomas Friman, Renata Gustafsson, Eva K?llberg, Olof Olsson, Tomas Leanderson, Kristofer Rubin, Marko Salmi, Sirpa Jalkanen, Rikard Holmdahl
PLOS ONE , 2013, DOI: 10.1371/journal.pone.0084148
Abstract: The NADPH oxidase 2 (NOX2) complex is a professional producer of reactive oxygen species (ROS) and is mainly expressed in phagocytes. While the activity of the NOX2 complex is essential for immunity against pathogens and protection against autoimmunity, its role in the development of malignant tumors remains unclear. We compared wild type and Ncf1m1J mutated mice, which lack functional NOX2 complex, in four different tumor models. Ncf1m1J mutated mice developed significantly smaller tumors in two melanoma models in which B16 melanoma cells expressing a hematopoietic growth factor FLT3L or luciferase reporter were used. Ncf1m1J mutated mice developed significantly fewer Lewis Lung Carcinoma (LLC) tumors, but the tumors that did develop, grew at a pace that was similar to the wild type mice. In the spontaneously arising prostate carcinoma model (TRAMP), tumor growth was not affected. The lack of ROS-mediated protection against tumor growth was associated with increased production of immunity-associated cytokines. A significant increase in Th2 associated cytokines was observed in the LLC model. Our present data show that ROS regulate rejection of the antigenic B16-luc and LLC tumors, whereas the data do not support a role for ROS in growth of intrinsically generated tumors.
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