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    Citrullination and autoimmunity.

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    Autoimmune diseases are characterized by the body's own immune system attack to the self-tissues, a condition enabled, in predisposed subjects, by the reduction of self-tolerance. A central role has been recently recognized to post-translational modifications, since they can promote generation of neo-(auto)antigens and in turn an autoimmune response. During the last years great attention has been paid to citrullination, because of its role in inducing anti-citrullinated proteins/peptide antibodies (ACPA), a class of autoantibodies with diagnostic, predictive and prognostic value for Rheumatoid Arthritis (RA). Nonetheless, citrullination has been reported to be a process present in a wide range of inflammatory tissues. Indeed, citrullinated proteins have been detected also in other inflammatory arthritides and in inflammatory conditions other than arthritides (polymyositis, inflammatory bowel disease and chronic tonsillitis). Moreover, environmental exposure to cigarette smoke and nanomaterials of air pollution may be able to induce citrullination in lung cells prior to any detectable onset of inflammatory responses, suggesting that protein citrullination could be considered as a sign of early cellular damage. Accordingly, citrullination seems to be implicated in all those para-physiological processes, such as cells death pathways, in which intracellular calcium concentration raises to higher levels than in physiologic conditions: hence, peptidylarginine deiminases enzymes are activated during apoptosis, autophagy and NETosis, processes which are well-known to be implicated in autoimmunity. Taken together, these data support the hypothesis that rather than being a disease-dependent process, citrullination is an inflammatory-dependent condition that plays a central role in autoimmune diseases

    Impedance vector distribution by body mass index and conventional bioelectrical impedance analysis in obese women

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    BACKGROUND AND AIM: To compare the body fluid status assessments provided by conventional bioelectrical impedance analysis (BIA) and vector BIA in moderate and severe obesity. METHODS AND RESULTS: We studied 516 normotensive Caucasian women (mean age: 48 +/- 9.2 years), who were age-matched and divided into four groups on the basis of their body mass index (BMI): 99 normal weight women with a BMI of 19-25 Kg/m2; 228 preobese overweight women with a BMI of 25-30 Kg/m2; 132 women with class I-II obesity (BMI: 30-35 Kg/m2), and 57 women with class III obesity (BMI: 40-64 Kg/m2). Single-frequency (50 kHz) tetrapolar (hand-foot) bioelectrical impedance measurements were made, and total body water (TBW) and extracellular water (ECW) were estimated using conventional BIA regression equations. The RXc graph method was used for vector BIA, with the set of 327 women with a BMI of 19-30 Kg/m2 being adopted as the reference population. Mean vector displacement followed a definite pattern, with progressive vector shortening as the BMI increased, and along a fixed phase angle. This pattern indicates more TBW due to a greater soft tissue mass with average normal hydration. Short and downsloping vectors indicating fluid overload were more frequent in the group with class III obesity than in the group with class I obesity (19 vs 5%). The absolute values of TBW and ECW were significantly higher in the obese and overweight subjects than in those with normal weight subjects. TBW as a percentage of body weight was significantly lower in the obese subjects. CONCLUSIONS: BMI influenced the impedance vector distribution pattern, which proved to be consistent up to a BMI of 64 Kg/m2. Obese women with an altered body composition can be identified and monitored using vector BIA
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