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Search Results: 1 - 10 of 368256 matches for " Ricardo L.B.;van den Berg "
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Molecular phylogeny, morphology and their implications for the taxonomy of Eriocaulaceae
Giulietti, Ana M.;Andrade, Maria José G.;Scatena, Vera L.;Trovó, Marcelo;Coan, Alessandra I.;Sano, Paulo T.;Santos, Francisco A.R.;Borges, Ricardo L.B.;van den Berg, Cássio;
Rodriguésia , 2012, DOI: 10.1590/S2175-78602012000100001
Abstract: the pantropical family eriocaulaceae includes ten genera and c. 1,400 species, with diversity concentrated in the new world. the last complete revision of the family was published more than 100 years ago, and until recently the generic and infrageneric relationships were poorly resolved. however, a multi-disciplinary approach over the last 30 years, using morphological and anatomical characters, has been supplemented with additional data from palynology, chemistry, embryology, population genetics, cytology and, more recently, molecular phylogenetic studies. this led to a reassessment of phylogenetic relationships within the family. in this paper we present new data for the its and trnl-f regions, analysed separately and in combination, using maximum parsimony and bayesian inference. the data confirm previous results, and show that many characters traditionally used for differentiating and circumscribing the genera within the family are homoplasious. a new generic key with characters from various sources and reflecting the current taxonomic changes is presented.
Gene therapy in animal models of rheumatoid arthritis: are we ready for the patients?
Fons AJ van de Loo, Ruben L Smeets, Wim B van den Berg
Arthritis Research & Therapy , 2004, DOI: 10.1186/ar1214
Abstract: Rheumatoid arthritis (RA) is an autoimmune disease that is characterized by chronic inflammation in the synovial joints that leads to progressive destruction of cartilage and bone. There is still dispute as to what initiates RA (e.g. autoantigens, bacteria, or viruses). There is, however, a general understanding of the inflammatory process that drives the pathological changes that are observed in arthritis. There is consensus that cytokines in particular represent the fuel of the inflammation, and that in RA cytokines (growth factors) and their inhibitors are imbalanced. A breakthrough came from work in transgenic mice [1,2], which revealed that constitutive expression of tumour necrosis factor (TNF)-α causes inflammatory arthritis in the synovial joints. Also, blocking studies with neutralizing antibodies and later using the natural IL-1 receptor antagonist (IL-1Ra) and soluble type II TNF receptor (p75) identified IL-1 and TNF as the principle inflammatory and catabolic cytokines in experimental arthritis [3-5]. Restoring cytokine balance using biologics has been successful in many experimental models of RA. This work brought the anti-TNF strategy in RA patients to the fore, and the clearly demonstrated clinical effectiveness of this strategy led to an explosion in usage of biologically based medicines (biologics) [6].This raises the question of whether gene therapy can confer additional advantages or contribute to existing therapies. To answer this we must appreciate that the current anti-TNF treatments still have three major drawbacks. First, these treatments do not cure the disease, and cessation of treatment results in a relapse of disease in RA patients. Second, repeated systemic delivery is necessary to achieve steady and efficacious levels of the agent in the inflamed joints. The treatment does not take into account the fact that the clinical course of RA is characterized by variable disease activity, with spontaneous remissions and exacerbations of chronic
Liposomal Targeting of Prednisolone Phosphate to Synovial Lining Macrophages during Experimental Arthritis Inhibits M1 Activation but Does Not Favor M2 Differentiation
Wouter Hofkens, Rik Schelbergen, Gert Storm, Wim B. van den Berg, Peter L. van Lent
PLOS ONE , 2013, DOI: 10.1371/journal.pone.0054016
Abstract: Background To determine the effects of liposomal targeting of prednisolone phosphate (Lip-PLP) to synovial lining macrophages on M1 and M2 polarization in vitro and during experimental arthritis. Material and Methods Experimental arthritis (antigen and immune complex induced) was elicited in mice and prednisolone containing liposomes were given systemically. Synovium was investigated using microarray analysis, RT-PCR and histology. Bone–marrow macrophages were stimulated towards M1 using LPS and IFNγ before treatment by PLP-liposomes. M1 and M2 markers were determined using RT-PCR. Results Microarray analysis of biopsies of inflamed synovium during antigen induced arthritis (AIA) showed an increased M1 signature characterized by upregulation of IL-1β, IL-6 and FcγRI starting from day 1 and lasting up until day 7 after arthritis induction. The M2 signature remained low throughout the 7 day course of arthritis. Treatment of AIA with intravenously delivered Lip-PLP strongly suppressed joint swelling and synovial infiltration whereas colloidal gold containing liposomes exclusively targeted the macrophages within the inflamed synovial intima layer. In vitro studies showed that Lip-PLP phagocytosed by M1 macrophages resulted in a suppression of the M1 phenotype and induction of M2 markers (IL-10, TGF-β, IL-1RII, CD163, CD206 and Ym1). In vivo, Lip-PLP treatment strongly suppressed M1 markers (TNF-α, IL-1β, IL-6, IL-12p40, iNOS, FcγRI, Ciita and CD86) after local M1 activation of lining macrophages with LPS and IFN-γ and during experimental AIA and immune complex arthritis (ICA). In contrast, M2 markers were not significantly upregulated in antigen-induced arthritis and down regulated in immune complex arthritis. Conclusion This study clearly shows that systemic treatment with PLP-liposomes selectively targets synovial lining macrophages and inhibits M1 activation. In contrast to in vitro findings, PLP-liposomes do not cause a shift of synovial lining macrophages towards M2.
Pylstertmotte (Lepidoptera: Sphingidae) van die Nasionale Krugerwildtuin
M. A. van den Berg,J. B. Vermeulen,H. H. Braack,Antoinette L. Braack
Koedoe : African Protected Area Conservation and Science , 1975, DOI: 10.4102/koedoe.v18i1.912
Abstract: 'n Totaal van 42 spesies van pylstertmotte is in die Nasionale Krugerwildtuin versamel. Die bekendste hiervan is die patatrusper (Herse convolvuli (L)) en die dood-skedelmot (Acherontia atropos (L)). Die volgende spesies wat versamel is, se voorkoms is nog nie voorheen vir die Republiek van Suid-Afrika aangemeld nie nl. Pemba flavillacea (Walk.), Praedora plagiata (R. &J.), Leptoclanis basalis (Walk.), Polyptychus calcareus (R. &J.), Polyptychus compar (R. &J.), Nephele aequivalens (Walk.), Nephele peneus (Cram.), Hippotion roseipennis (Butler) en Xenosphingia jansei (Jord.). Die verspreiding van Oligographa juniperi (Bsd.) wat langs die kusgebiede van Natal en die Oos-Kaap aangetrefword, is op verskeie plekke in die Krugerwildtuin versamel.
Innovation in currency inspection: direct and multiplicative effects of controlling application
L.B. Krivoruchko
Marketing ì Mened?ment Innovacìj , 2011,
Abstract: The article highlights the components of the economic effect of controlling systems application to the process of currency inspection as an innovation of this process. The methodological approach for estimation of mentioned effect is proposed.
Effect of naturally occurring napthoquinones on root-knot nematode Meioidogyne javanica
L.B. DAMA
Indian Phytopathology , 2012,
Abstract: The effect of naturally occurring napthoquinones were studied in vitro on root-knot nematode, Meloidogyne javanica, at concentration 200 J,Jg110 ml waterlflask containing 100 nematodes exposed for 6 h, 12 hand 24 h. The plumbagin showed 100% mortality, juglone 97.94% and lawsone 58.31% at 24 h exposure. The effect of these napthoquinones were found to be nematicidal on root-knot nematodes.
G.D. Collin's Fauna Surinamensis
L.B. Holthuis
Nieuwe West-Indische Gids , 1958,
Abstract:
Nadere gegevens betreffende H. E. van Rijgersma
Holthuis L.B.
Nieuwe West-Indische Gids , 1961,
Abstract:
链柔性与相互作用对高分子溶液的介电性质和热力学性质的影响
L.Bè
高分子学报 , 1965,
Abstract:
TGF β-induced cartilage repair is maintained but fibrosis is blocked in the presence of Smad7
Esmeralda N Blaney Davidson, Elly L Vitters, Wim B van den Berg, Peter M van der Kraan
Arthritis Research & Therapy , 2006, DOI: 10.1186/ar1931
Abstract: Osteoarthritis (OA) is a degenerative joint disease characterized by cartilage breakdown, synovial fibrosis, and bone spurs. An imbalance between catabolic and anabolic factors favoring the catabolic side is very likely involved in the pathological features of OA.Currently, many attempts are being made to repair the cartilage that has been damaged in OA. One approach focuses on shifting the metabolic imbalance back by stimulating the anabolic side. Transforming growth factor-β (TGF-β) is one of the anabolic factors involved in cartilage maintenance and appears to be a good candidate for cartilage repair. TGF-β is a stimulator of extracellular matrix production, like collagen type II and proteoglycan (PG), in chondrocytes and it downregulates matrix-degrading enzymes [1]. High amounts of TGF-β are stored in healthy cartilage [2-6], whereas in OA cartilage the expression of TGF-β is reduced [7]. Injection of TGF-β into naive murine knee joints results in an increase in PG content of the articular cartilage [8]. Moreover, in murine experimental rheumatoid arthritis, injection of TGF-β protected cartilage from PG loss [9]. In addition, TGF-β counteracts the anabolic factor interleukin-1 (IL-1), which is a very potent inducer of cartilage degradation [10,11] both in vivo and in vitro [1,12-16]. These data indicate that TGF-β has great potential as a tool for stimulating cartilage repair.To obtain sufficient amounts of TGF-β in the joint for a prolonged period of time, an adenovirus can be used as a vehicle. In vitro, chondrocytes that are transfected with an adenovirus encoding TGF-β responded by elevation of PG and collagen production [17]. We wanted to assess whether adenoviral overexpression of TGF-β in the synovial lining could stimulate repair of damaged cartilage in vivo.Unfortunately, introducing high amounts of TGF-β into a knee joint has adverse effects. Administration of 20 ng TGF-β is already sufficient to result in an increased cellularity of the synovial lin
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