Naess H.,University of Bergen |
Glad S.,University of Bergen |
Storstein A.,University of Bergen |
Rinaldo C.H.,University of Tromso |
And 3 more authors.
Background: To report the clinical course of PML in an apparently immunocompetent patient treated with cidofovir.Case Presentation: A 35-year-old immunocompetent man who developed progressive hemianopsia, aphasia, and limb weakness underwent repeated MRI scans of the brain, spinal fluid analyses, and brain biopsy. Before diagnosis was established based on brain biopsy, he was consecutively treated with methylprednisolone, acyclovir, ceftriaxone and plasmapheresis, but he deteriorated rapidly suggestive of the immune reconstitution inflammatory syndrome (IRIS). He started to recover two weeks after the initiation of treatment with cidofovir and has had no relapse at 3 1/2 years of follow-up. MRI has shown marked improvement.Conclusions: PML should be considered in immunocompetent patients with a typical clinical course and MRI findings compatible with PML. Treatment with cidofovir should be considered as early as possible in the disease course. © 2010 Naess et al; licensee BioMed Central Ltd. Source
Shimizu T.,Max Planck Institute for Extraterrestrial Physics |
Nosenko T.,Max Planck Institute for Extraterrestrial Physics |
Morfill G.E.,Max Planck Institute for Extraterrestrial Physics |
Sato T.,Tohoku University |
And 2 more authors.
Plasma Processes and Polymers
Chemical characteristics and bactericidal properties of two low-temperature atmospheric-pressure Ar plasma devices are investigated: one of them with UV and the other with almost no UV on treated samples. The control of the UV radiation is achieved by two nozzles. One has a straight shape, and the other has a 90°-bent. The bent nozzle blocks the light produced inside the torch, whilst allowing the plasma gas to reach the samples. The use of the straight nozzle allows the treatment by both the plasma gas and UV. We demonstrate that even an almost UV-free plasma treatment has bactericidal properties. Our measurements suggest that reactive species represent the main bactericidal factor of our low-temperature plasma. © 2010 WlLEY-VCH Verlag GmbH & Co. KGaA. Source
Rynes J.,University of Cologne |
Rynes J.,University of South Bohemia |
Donohoe C.D.,University of Cologne |
Frommolt P.,Cologne Center for Genomics |
And 3 more authors.
Molecular and Cellular Biology
Integration of metabolic and immune responses during animal development ensures energy balance, permitting both growth and defense. Disturbed homeostasis causes organ failure, growth retardation, and metabolic disorders. Here, we show that the Drosophila melanogaster activating transcription factor 3 (Atf3) safeguards metabolic and immune system homeostasis. Loss of Atf3 results in chronic inflammation and starvation responses mounted primarily by the larval gut epithelium, while the fat body suffers lipid overload, causing energy imbalance and death. Hyperactive proinflammatory and stress signaling through NF-κB/Relish, Jun N-terminal kinase, and FOXO in atf3 mutants deregulates genes important for immune defense, digestion, and lipid metabolism. Reducing the dose of either FOXO or Relish normalizes both lipid metabolism and gene expression in atf3 mutants. The function of Atf3 is conserved, as human ATF3 averts some of the Drosophila mutant phenotypes, improving their survival. The single Drosophila Atf3 may incorporate the diversified roles of two related mammalian proteins. © 2012, American Society for Microbiology. Source
Lauscher J.C.,Charite - Medical University of Berlin |
Grone J.,Charite - Medical University of Berlin |
Dullat S.,Charite - Medical University of Berlin |
Hotz B.,Charite - Medical University of Berlin |
And 4 more authors.
Recent studies have demonstrated that increased expression of coding region determinant-binding protein (CRD-BP) in response to β-catenin signaling leads to the stabilization of β-TrCP1, a substrate-specific component of SCF E3 ubiquitin ligase complex, resulting in an accelerated degradation of IκBα and activation of canonical nuclear factor-κB (NF-κB) pathway. Here, we show that the noncanonical NF-κB1 p105 pathway is constitutively activated in colorectal carcinoma specimens, being particularly associated with β-catenin-mediated increased expression of CRD-BP and β-TrCP1. In the carcinoma tissues exhibiting high levels of nuclear β-catenin the phospho-p105 levels were increased and total p105 amounts were decreased in comparison to that of normal tissue indicating an activation of this NF-κB pathway. Knockdown of CRD-BP in colorectal cancer cell line SW620 resulted in significantly higher basal levels of both NF-κB inhibitory proteins, p105 and IκBβ. Furthermore decreased NF-κB binding activity was observed in CRD-BP siRNA-transfected SW620 cells as compared with those transfected with control siRNA. Altogether, our findings suggest that activation of NF-κB1 p105 signaling in colorectal carcinoma might be attributed to β-catenin-mediated induction of CRD-BP and β-TrCP1. © 2009 Wiley-Liss, Inc. Source
Huber S.,Ludwig Maximilians University of Munich |
Hoffmann R.,Institute for Medical Microbiology |
Muskens F.,Erasmus Medical Center |
Voehringer D.,Ludwig Maximilians University of Munich
Alternatively activated macrophages (AAM) accumulate in tissues during Th2-associated immune responses like helminth infections and allergic disorders. These cells differentiate in response to interleukin 4 (IL-4)/IL-13-mediated activation of Stat6 and possess potent inhibitory activity against T cells. The molecular mechanism that leads to T-cell suppression remains unclear and could involve soluble factors or inhibitory ligands. Microarray analysis revealed that the inhibitory ligand, programmed death ligand 2 (PD-L2) was strongly induced by IL-4 in macrophages from wild-type but not Stat6-deficient mice. PD-L2 expression correlated with other established markers for AAM-like Relm-α/Fizz1, arginase1, or Ym1 and thereby serves as useful surface marker to identify and isolate AAM from tissues. Antibodies against PD-L2 blocked the inhibitory activity of AAM and retroviral expression of PD-L2 in macrophages from Stat6 -/- mice was sufficient to inhibit T-cell proliferation, which demonstrates that PD-L2 mediates potent and nonredundant inhibition of T cells independently of other Stat6-regulated genes. Infection of conditional IL-4/IL-13-deficient mice with the helminth Nippostrongylus brasiliensis further showed that PD-L2 expression was dependent on IL-4/IL-13 from Th2 cells. In vivo blockade of PD-L2 during N brasiliensis infection caused an enhanced Th2 response in the lung, indicating that AAM inhibit Th2 cells by expression of PD-L2. © 2010 by The American Society of Hematology. Source