Pemphigus autoimmunity: Hypotheses and realities

The goal of contemporary research in pemphigus vulgaris and pemphigus foliaceus is to achieve and maintain clinical remission without corticosteroids. Recent advances of knowledge on pemphigus autoimmunity scrutinize old dogmas, resolve controversies, and open novel perspectives for treatment. Elucidation of intimate mechanisms of keratinocyte detachment and death in pemphigus has challenged the monopathogenic explanation of disease immunopathology. Over 50 organ-specific and non-organ-specific antigens can be targeted by pemphigus autoimmunity, including desmosomal cadherins and other adhesion molecules, PERP cholinergic and other cell membrane (CM) receptors, and mitochondrial proteins. The initial insult is sustained by the autoantibodies to the cell membrane receptor antigens triggering the intracellular signaling by Src, epidermal growth factor receptor kinase, protein kinases A and C, phospholipase C, mTOR, p38 MAPK, JNK, other tyrosine kinases, and calmodulin that cause basal cell shrinkage and ripping desmosomes off the CM. Autoantibodies synergize with effectors of apoptotic and oncotic pathways, serine proteases, and inflammatory cytokines to overcome the natural resistance and activate the cell death program in keratinocytes. The process of keratinocyte shrinkage/detachment and death via apoptosis/oncosis has been termed apoptolysis to emphasize that it is triggered by the same signal effectors and mediated by the same cell death enzymes. The natural course of pemphigus has improved due to a substantial progress in developing of the steroid-sparing therapies combining the immunosuppressive and direct anti-acantholytic effects. Further elucidation of the molecular mechanisms mediating immune dysregulation and apoptolysis in pemphigus should improve our understanding of disease pathogenesis and facilitate development of steroid-free treatment of patients

Thermal decomposition kinetics of the antiparkinson drug “entacapone” under isothermal and non-isothermal conditions

© 2017 Akadémiai Kiadó, Budapest, Hungary The thermal decomposition kinetics of entacapone (ENT) have been investigated via thermogravimetric analysis under non-isothermal and isothermal conditions which provide useful stability information for their processing in the pharmaceutical industry and also for predicting shelf life and suitable storage conditions. The determination of the kinetic parameters for the decomposition process under non-isothermal conditions in a nitrogen atmosphere at four heating rates (5, 10, 15, and 20 °C min −1 ) was performed. Kinetic parameters of the decomposition process for ENT were calculated through Friedman, Flynn–Wall–Ozawa, Kissinger–Akahira–Sunose, and Li–Tang methods. This work demonstrates that the activation energies calculated from the decomposition reactions by different methods are consistent with each other. Moreover, the thermodynamic functions of the decomposition reaction were also calculated

Is a checkup required for general itching? [Faut-il faire un bilan de prurit systématique ?]

International audienc

DRESS syndrome and agranulocytosis, a rare combination [Syndrome d'hypersensibilité médicamenteuse et agranulocytose, une association rare]

International audienc

Itch and systemic sclerosis: frequency, clinical characteristics and consequences

International audienc