348 patients reached the primary endpoint (A-002 n=278, placebo n=70). Mean sPLA,-IIA concentration fell by 86.7%, from 15 . 7 pmol/L to 2 . 1 pmol/L, in the overall active treatment group, and by 4.8%, from 15.7 pmol/L to 14.3 pmol/L, in the placebo group (p<0.0001 treatment vs placebo). The reductions in sPLA(2)-IIA concentration in the A-002 groups
were dose dependent (ranging from 69.2% in the 50 mg group to 95.8% in the 500 mg group) and differed significantly from placebo (p<0 . 0001 for all doses). In the 500 mg A-002 treatment group, there was one serious adverse event (exacerbation of underlying chronic obstructive pulmonary disease), but the proportion of patients reporting treatment-emergent adverse events
did not differ from placebo. The main side-effects of the drug included headache (n=20), nausea (n=17), and buy Givinostat diarrhoea (n=12).
Interpretation The reductions in sPLA(2)-IIA concentration suggest that A-002 might be an effective anti-atherosclerotic agent.
Funding Anthera Pharmaceuticals.”
“Rheumatoid arthritis is a systemic, inflammatory, autoimmune disorder. Enhanced understanding of molecular pathogenesis has enabled development of innovative biological agents that target specific parts of VE 822 the immune system. These treatments have changed the course and face of rheumatoid arthritis and outcomes for patients and society New knowledge has emerged of how environmental factors interact with susceptibility genes and the immune system in the pathogenesis of a major subset of rheumatoid arthritis. Research
undertaken on the longitudinal disease process and molecular pathology of joint inflammation has led to new therapeutic strategies that promote early use of disease-modifying drugs with tight disease control and distinct and quantifiable treatment goals. Today, such approaches can halt most cases of joint destruction but not all instances of joint inflammation and comorbidity Understanding the cause and pathogenesis of different rheumatoid arthritis subsets will selleck chemicals llc lead not only to individualised treatments during early phases of the illness but also, possibly, to disease prevention.”
“The stimulation of a tumour-specific T-cell response has several theoretical advantages over other forms of cancer treatment. First, T cells can home in to antigen-expressing tumour deposits no matter where they are located in the body-even in deep tissue beds. Additionally, T cells can continue to proliferate in response to immunogenic proteins expressed in cancer until all the tumour cells are eradicated. Finally, immunological memory can be generated, allowing for eradication of antigen-bearing tumours if they reoccur. We will highlight two direct methods of stimulating tumour-specific T-cell immunity: active immunisation with cancer vaccines and infusion of competent T cells via adoptive T-cell treatment.