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Search Results: 1 - 10 of 120366 matches for " Kristina Rydell-T?rm?nen "
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Remodeling of extra-bronchial lung vasculature following allergic airway inflammation
Kristina Rydell-Trmnen, Lena Uller, Jonas S Erjef?lt
Respiratory Research , 2008, DOI: 10.1186/1465-9921-9-18
Abstract: We used an established mouse model of allergic airway inflammation, where an allergic airway inflammation is triggered by inhalations of OVA. Remodeling of bronchial un-associated vessels was determined histologically by staining for α-smooth muscle actin, procollagen I, Ki67 and von Willebrand-factor. Myofibroblasts were defined as and visualized by double staining for α-smooth muscle actin and procollagen I. For quantification the blood vessels were divided, based on length of basement membrane, into groups; small (≤250 μm) and mid-sized (250–500 μm).We discovered marked remodeling in solitary small and mid-sized blood vessels. Smooth muscle mass increased significantly as did the number of proliferating smooth muscle and endothelial cells. The changes were similar to those previously seen in large bronchial-associated vessels. Additionally, normally poorly muscularized blood vessels changed phenotype to a more muscularized type and the number of myofibroblasts around the small and mid-sized vessels increased following allergen challenge.We demonstrate that allergic airway inflammation in mice is accompanied by remodeling of small and mid-sized pulmonary blood vessels some distance away (at least 150 μm) from the allergen-exposed bronchi. The present findings suggest the possibility that allergic airway inflammation may cause such vascular remodeling as previously associated with lung inflammatory conditions involving a risk for development of pulmonary hypertension.Allergic airway inflammation is known to be associated with persistent inflammation and tissue remodeling, such as subepithelial fibrosis, smooth muscle thickening and increased vascularity in the bronchial circulation [1-3]. Most of our knowledge of remodeling in asthma emanates from studies of bronchial biopsies involving the large airways. However, asthma is not only a large airway disease, but also affects other parts of the lung, notably the small airways and possibly the bronchial-associated bloo
Anti-Fas mAb-induced apoptosis and cytolysis of airway tissue eosinophils aggravates rather than resolves established inflammation
Lena Uller, Kristina Rydell-Trmnen, Carl GA Persson, Jonas S Erjef?lt
Respiratory Research , 2005, DOI: 10.1186/1465-9921-6-90
Abstract: Weeklong daily allergen challenges of sensitized mice were followed by airway administration of anti-Fas mAb. BAL was performed and airway-pulmonary tissues were examined using light and electron microscopy. Lung tissue analysis for CC-chemokines, apoptosis, mucus production and plasma exudation (fibrinogen) were performed.Anti-Fas mAb evoked apoptosis of 28% and cytolysis of 4% of eosinophils present in allergen-challenged airway tissues. Furthermore, a majority of the apoptotic eosinophils remained unengulfed and eventually exhibited secondary necrosis. A striking histopathology far beyond the allergic inflammation developed and included degranulated eosinophils, neutrophilia, epithelial derangement, plasma exudation, mucus-plasma plugs, and inducement of 6 CC-chemokines. In animals without eosinophilia anti-Fas evoked no inflammatory response.An efficient inducer of eosinophil apoptosis in airway tissues in vivo, anti-Fas mAb evoked unprecedented asthma-like inflammation in mouse allergic airways. This outcome may partly reflect the ability of anti-Fas to evoke direct cytolysis of non-apoptotic eosinophils in airway tissues. Additionally, since most apoptotic tissue eosinophils progressed into the pro-inflammatory cellular fate of secondary necrosis this may also explain the aggravated inflammation. Our data indicate that Fas receptor mediated eosinophil apoptosis in airway tissues in vivo may cause severe disease exacerbation due to direct cytolysis and secondary necrosis of eosinophils.Apoptosis of inflammatory cells followed by their swift removal through phagocytosis is considered a major mechanism of resolution of inflammatory conditions [1,2]. The most common chronic inflammatory disease, asthma is characterized by eosinophilia, epithelial derangement, plasma exudation, and hypersecretion [3,4]. The role of the eosinophil in this disease is currently under intense investigation [5] and much interest has been devoted to apoptosis of eosinophil granulocytes [
Neutrophil cannibalism – a back up when the macrophage clearance system is insufficient
Kristina Rydell-Trmnen, Lena Uller, Jonas S Erjef?lt
Respiratory Research , 2006, DOI: 10.1186/1465-9921-7-143
Abstract: Intranasal lipopolysaccharide administration was used to induce lung inflammation in mice. The animals were sacrificed at seven time points following administration, bronchoalveolar lavage was performed and tissue samples obtained. Electron microscopy and histochemistry was used to assess neutrophil phagocytosis.Electron microscopic studies revealed that phagocytosing neutrophils was common, at 24 h after LPS administration almost 50% of the total number of neutrophils contained phagosomes, and the engulfed material was mainly derived from other neutrophils. Histochemistry on bronchoalvolar lavage cells further showed phagocytosing neutrophils to be frequently occurring.Neutrophils are previously known to phagocytose invading pathogens and harmful particles. However, this study demonstrates that neutrophils are also able to engulf apoptotic neutrophils or cell debris resulting from secondary necrosis of neutrophils. Neutrophils may thereby contribute to clearance and resolution of inflammation, thus acting as a back up system in situations when the macrophage clearance system is insufficient and/or overwhelmed.Neutrophils are short lived immune cells who invade tissues in response to a variety of stimuli, for example viral and bacterial infections [1,2]. They are professional phagocytes and contribute to resolution of inflammation by removing infectious and inflammatory stimuli [1,2]. Apart from being present during acute infections, neutrophils are also found to a variable degree during airway diseases such as COPD, asthma and ARDS/ALI [3,4]. Neutrophils have a high turnover and are normally rapidly cleared by apoptosis, followed by macrophage phagocytosis [2,5]. During infection a large number of neutrophils are present in order to efficiently clear the infection, and studies have shown that ingestion of bacteria may delay neutrophil apoptosis [2], thereby causing very large number of cells accumulating in the same area. In such cases, the normally rapid clearance
Catechol-O-Methyltransferase Gene Polymorphism Is Associated with Skeletal Muscle Properties in Older Women Alone and Together with Physical Activity
Paula H. A. Ronkainen, Eija P?ll?nen, Timo Trm?kangas, Kristina Tiainen, Markku Koskenvuo, Jaakko Kaprio, Taina Rantanen, Sarianna Sipil?, Vuokko Kovanen
PLOS ONE , 2008, DOI: 10.1371/journal.pone.0001819
Abstract: Background Muscle strength declines on average by one percent annually from midlife on. In postmenopausal women this decrement coincides with a rapid decline in estrogen production. The genetics underlying the effects of estrogen on skeletal muscle remains unclear. In the present study, we examined whether polymorphisms within COMT and ESR1 are associated with muscle properties and assessed their interaction and their combined effects with physical activity. Methodology/Principal Findings A cross-sectional data analysis was conducted with 434 63-76-year-old women from the population-based Finnish Twin Study on Aging. Body anthropometry, muscle cross-sectional area (mCSA), isometric hand grip and knee extension strengths, and leg extension power were measured. COMT Val158Met and ESR1 PvuII genotypes were determined by the RFLP method. mCSA differed by COMT genotypes (p = 0.014) being significantly larger in LL than HL individuals in unadjusted (p = 0.001) and age- and height-adjusted model (p = 0.004). When physical activity and age were entered into GEE model, COMT genotype had a significant main effect (p = 0.038) on mCSA. Furthermore, sedentary individuals with the HH genotype had lower muscle mass, strength and power, but they also appeared to benefit the most from physical activity. No association of ESR1 PvuII polymorphism with any of the muscle outcomes was observed. Conclusions/Significance The present study suggests that the COMT polymorphism, affecting the activity of the enzyme, is associated with muscle mass. Furthermore, sedentary individuals with potential high enzyme activity were the weakest group, but they may potentially benefit the most from physical activity. This observation elucidates the importance of both environmental and genetic factors in muscle properties.
Two Cellular Protein Kinases, DNA-PK and PKA, Phosphorylate the Adenoviral L4-33K Protein and Have Opposite Effects on L1 Alternative RNA Splicing
Heidi Trmnen Persson, Anne Kristin Aksaas, Anne Katrine Kvissel, Tanel Punga, ?ke Engstr?m, Bj?rn Steen Sk?lhegg, G?ran Akusj?rvi
PLOS ONE , 2012, DOI: 10.1371/journal.pone.0031871
Abstract: Accumulation of the complex set of alternatively processed mRNA from the adenovirus major late transcription unit (MLTU) is subjected to a temporal regulation involving both changes in poly (A) site choice and alternative 3′ splice site usage. We have previously shown that the adenovirus L4-33K protein functions as an alternative splicing factor involved in activating the shift from L1-52,55K to L1-IIIa mRNA. Here we show that L4-33K specifically associates with the catalytic subunit of the DNA-dependent protein kinase (DNA-PK) in uninfected and adenovirus-infected nuclear extracts. Further, we show that L4-33K is highly phosphorylated by DNA-PK in vitro in a double stranded DNA-independent manner. Importantly, DNA-PK deficient cells show an enhanced production of the L1-IIIa mRNA suggesting an inhibitory role of DNA-PK on the temporal switch in L1 alternative RNA splicing. Moreover, we show that L4-33K also is phosphorylated by protein kinase A (PKA), and that PKA has an enhancer effect on L4-33K-stimulated L1-IIIa splicing. Hence, we demonstrate that these kinases have opposite effects on L4-33K function; DNA-PK as an inhibitor and PKA as an activator of L1-IIIa mRNA splicing. Taken together, this is the first report identifying protein kinases that phosphorylate L4-33K and to suggest novel regulatory roles for DNA-PK and PKA in adenovirus alternative RNA splicing.
Application of Paper-Supported Printed Gold Electrodes for Impedimetric Immunosensor Development
Petri Ihalainen,Himadri Majumdar,Tapani Viitala,Bj?rn T?rngren,Tuomas N?rjeoja,Anni M??tt?nen,Jawad Sarfraz,Harri H?rm,Marjo Yliperttula,Ronald ?sterbacka,Jouko Peltonen
Biosensors , 2013, DOI: 10.3390/bios3010001
Abstract: In this article, we report on the formation and mode-of-operation of an affinity biosensor, where alternate layers of biotin/streptavidin/biotinylated-CRP-antigen/anti-CRP antibody are grown on printed gold electrodes on disposable paper-substrates. We have successfully demonstrated and detected the formation of consecutive layers of supra-molecular protein assembly using an electrical (impedimetric) technique. The formation process is also supplemented and verified using conventional surface plasmon resonance (SPR) measurements and surface sensitive characterization techniques, such as X-ray photoelectron spectroscopy (XPS) and atomic force microscopy (AFM). The article provides a possible biosensor development scheme, where—(1) fabrication of paper substrate (2) synthesis of gold nanoparticle inks (3) inkjet printing of gold electrodes on paper (4) formation of the biorecognition layers on the gold electrodes and (5) electrical (impedimetric) analysis of growth—all are coupled together to form a test-structure for a recyclable and inexpensive point-of-care diagnostic platform.
Calcium Carbonate versus Sevelamer Hydrochloride as Phosphate Binders after Long-Term Disease Progression in 5/6 Nephrectomized Rats
Suvi Trmnen,Arttu Er?ranta,Asko Riutta,Peeter K??bi,Teemu Honkanen,Emmanouil Karavalakis,Onni Niemel?,Heikki Tokola,Heikki Ruskoaho,Jukka Mustonen,Ilkka P?rsti
Advances in Nephrology , 2014, DOI: 10.1155/2014/538392
Abstract: Our aim was to compare the effects of calcium carbonate and sevelamer-HCl treatments on calcium-phosphate metabolism and renal function in 5/6 nephrectomized (NX) rats so that long-term disease progression preceded the treatment. After 15-week progression, calcium carbonate (3.0%), sevelamer-HCl (3.0%), or control diets (0.3% calcium) were given for 9 weeks. Subtotal nephrectomy reduced creatinine clearance (?40%), plasma calcidiol (?25%), and calcitriol (?70%) and increased phosphate (+37%), parathyroid hormone (PTH) (11-fold), and fibroblast growth factor-23 (FGF-23) (4-fold). In NX rats, calcium carbonate diet increased plasma (+20%) and urinary calcium (6-fold), reduced plasma phosphate (?50%) and calcidiol (?30%), decreased creatinine clearance (?35%) and FGF 23 (?85%), and suppressed PTH without influencing blood pH. In NX rats, sevelamer-HCl increased urinary calcium (4-fold) and decreased creatinine clearance (?45%), PTH (?75%), blood pH (by 0.20 units), plasma calcidiol (?40%), and calcitriol (?65%). Plasma phosphate and FGF-23 were unchanged. In conclusion, when initiated after long-term progression of experimental renal insufficiency, calcium carbonate diet reduced plasma phosphate and FGF-23 while sevelamer-HCl did not. The former induced hypercalcemia, the latter induced acidosis, while both treatments reduced vitamin D metabolites and deteriorated renal function. Thus, delayed initiation influences the effects of these phosphate binders in remnant kidney rats. 1. Introduction Cardiovascular disease is a major cause of mortality in chronic renal insufficiency (CRI) with a 20-fold increase in the risk of cardiovascular death compared with normal population [1]. Hyperphosphatemia and secondary hyperparathyroidism (SHPT) [2] significantly contribute to the cardiovascular pathology and mineral-bone disorders in CRI. In order to halt these changes, oral phosphate binders such as calcium carbonate and sevelamer are widely used. High intake of calcium carbonate may predispose to vascular calcifications in CRI, especially if the phosphate levels remain inappropriately high [2]. Consequently, treatment with sevelamer, a calcium- and aluminium-free and nonabsorbable polyallylamine anion exchange resin, may result in less vascular calcifications and reduced mortality in dialysis patients. However, according to recent Cochrane review, the superiority of sevelamer over calcium carbonate remains unclear [3]. In experimental animal models, increased calcium intake has resulted in beneficial effects on blood pressure (BP), endothelial function,
Subshifts, MSO Logic, and Collapsing Hierarchies
Ilkka Trm
Computer Science , 2014,
Abstract: We use monadic second-order logic to define two-dimensional subshifts, or sets of colorings of the infinite plane. We present a natural family of quantifier alternation hierarchies, and show that they all collapse to the third level. In particular, this solves an open problem of [Jeandel & Theyssier 2013]. The results are in stark contrast with picture languages, where such hierarchies are usually infinite.
A Uniquely Ergodic Cellular Automaton
Ilkka Trm
Computer Science , 2013,
Abstract: We construct a one-dimensional uniquely ergodic cellular automaton which is not nilpotent. This automaton can perform asymptotically infinitely sparse computation, which nevertheless never disappears completely. The construction builds on the self-simulating automaton of G\'acs. We also prove related results of dynamical and computational nature, including the undecidability of unique ergodicity, and the undecidability of nilpotency in uniquely ergodic cellular automata.
Quantifier Extensions of Multidimensional Sofic Shifts
Ilkka Trm
Computer Science , 2014,
Abstract: We define a pair of simple combinatorial operations on subshifts, called existential and universal extensions, and study their basic properties. We prove that the existential extension of a sofic shift by another sofic shift is always sofic, and the same holds for the universal extension in one dimension. However, we also show by a construction that universal extensions of two-dimensional sofic shifts may not be sofic, even if the subshift we extend by is very simple.
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