17 research outputs found

    Infrared spectroscopic study of micronised geothite

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    Infrared spectra of micronised goethite between 4000 cm-1 and 20 cm-1 were studied. Stretching and bending vibrations of structural hydroxy-groups were assigned using data on deuterated samples and comparison with α-Fe2O3 obtained by thermal decomposition. The existence of two different kinds of surface hydroxyls was also confirmed and an interpretation of their nature proposed. Various measured low-frequency bands were assigned to vibrations of the structural FeO6 blocks. © 1978

    Anti-tumour necrosis factor-alpha therapy increases body weight in patients with chronic plaque psoriasis: a retrospective cohort study.

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    Background Chronic plaque psoriasis is associated with overweight or obesity. Anti–tumour necrosis factor- α (anti-TNF- α ) treatments are now frequently used in psoriasis management. TNF- α is deeply involved in body weight homeostasis, which may be affected by TNF- α –targeted therapy. Objective To investigate whether anti-TNF- α treatments is associated with changes in body weight in patients with chronic plaque psoriasis. Methods We performed a retrospective controlled analysis comparing the variations in body weight and body mass index (BMI) in three closed cohorts of psoriatic patients during a 6-month treatment with etanercept ( N = 58), infliximab ( N = 40) or methotrexate ( N = 43). Results We observed a body weight increment of 1.5 ± 2.7 kg (mean ± SD; P = 0.0002) and 2.5 ± 3.3 kg ( P = 0.004) in patients treated with etanercept and infliximab, respectively. In contrast, a non-significant change (0.6 ± 1.4 kg; P = 0.4) was measured in patients treated with methotrexate. The BMI increased with 0.5 ± 0.5 ( P = 0.01) and 0.8 ± 1 ( P = 0.003) points in patients treated with etanercept and infliximab, respectively, whereas it did not change (< 0.2 ± 0.5; P = 0.06) in patients treated with methotrexate. About one fourth of patients experienced a 4- to 10-kg weight gain. Differences in body weight variations among patients treated with anti-TNF- α therapies and methotrexate were statistically significant ( P = 0.0005). We could not identify clinical parameters predicting this phenomenon. Conclusions Patients with psoriasis treated with long-term anti-TNF- α therapies may manifest a body weight gain. This effect should be taken into account in the global approach to patients with psoriasis

    Expression of the class A macrophage scavenger receptor on specific subpopulations of murine dendritic cells limits their endotoxin response

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    Dendritic cells (DC) function at the interface of innate and acquired immunity and are uniquely sensitive to specific stimuli. Pattern recognition receptors (PRR) on these cells are critically important because of their ability to recognise and initiate responses to conserved microbial-associated molecular signatures. With the exception of Toll-like receptors (TLR), we know relatively little about the specific distribution of other PRR amongst populations of DC. Here, we describe the expression of the murine class A macrophage scavenger receptor (SR-A) and show that it is restricted to specific subpopulations of bone marrow-derived and splenic DC. Importantly, we demonstrate that the receptor significantly alters the response of DC to endotoxin. In contrast to the activities of other PRR that have so far been examined, uniquely SR-A limits the maturation response; SR-A-/- cells display enhanced CD40 expression and TNF-alpha production. We discuss the potential contributions of SR-A to DC biology in the context of the known multiple activities of this receptor

    Complement dependent amplification of the innate response to a cognate microbial ligand by the long pentraxin PTX3

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    The long pentraxin PTX3 is a fluid-phase pattern recognition receptor, which plays a nonredundant role in resistance against selected pathogens. PTX3 has properties similar to Abs; its production is induced by pathogen recognition, it recognizes microbial moieties, activates complement, and facilitates cellular recognition by phagocytes. The mechanisms responsible for the effector function of PTX3 in vivo have not been elucidated. OmpA, a major outer membrane protein of Gram-negative Enterobacteriaceae, is a microbial moiety recognized by PTX3. In the air pouch model, KpOmpA induces an inflammatory response, which is amplified by coadministration of PTX3 in terms of leukocyte recruitment and proinflammatory cytokine production. PTX3 did not affect the inflammatory response to LPS, a microbial moiety not recognized by PTX3. As PTX3 binds to C1q and modulates the activation of the complement cascade, we assessed the involvement of complement in the amplification of the response elicited by KpOmpA and PTX3. Experiments performed using cobra venom factor, C1-esterase inhibitor, and soluble complement receptor 1 indicate that PTX3 amplifies the inflammatory response to KpOmpA through complement activation. The results reported here demonstrate that PTX3 activates a complement-dependent humoral amplification loop of the innate response to a microbial ligan
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