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The past decade has brought increasing evidence to support aggressive therapeutic intervention in early rheumatoid arthritis (RA). Treat-to-target strategies that focus on frequent monitoring and treatment adjustments to achieve states of low disease activity or clinical remission have shown superior long-term results. Both oral disease-modifying antirheumatic drugs and biologic agents are effective in treating early RA. It remains unclear if initial combination therapy or biologic use is more effective in early active disease as compared with the traditional approach. The authors review various studies on the treatment of early RA with a focus on studies with a treat-to-target approach., (Copyright © 2012 Elsevier Inc. All rights reserved.)

1) Investigation and evaluation of antifibrinolytic activity of some new compounds has been carried out using two technics based, one on the "standard clots" method and the other one on labelled clots methods. 2) Among the first four members of the linear amino diacids 2-aminopimelic acid possesses a slight antifibrinolytic activity, the others are non active. 3) The two dipeptides having the same chain length as EACA behave differently ; beta alanyl-glycine is practically inactive whilst glycyl-beta alanine possesses a significant inhibiting power. The question is raised as to whether this active dipeptide might play an antifibrinolytic role in the organism. 4) Among the cyclic epsilon-amino acids tested, alpha aminocampholic acid and dl cis (2,2 dimethyl-3-alpha-aminoethyl) cyclobutaneacetic acid possess and activity slightly superior to that of EACA.

Temporary B-cell tolerance to the trinitrophenyl (TNP) hapten can be produced in BDF1 mice by intraperitoneal injection of trinitrobenzene sulfonic acid (TNBS). Antigen-binding cells (ABC) specific to TNP, measured as TNP donkey erythrocyte rosettes, are found in tolerant mice as well as in immune mice. We have studied the surface immunoglobulin isotype profile of these TNP-binding lymphocytes (TNP-ABC) in four groups of animals: nonimmune, immune, tolerant, and tolerant-challenged. Immune mice received intravenous TNP sheep erythrocytes (TNP-SRC), whereas tolerant-challenged mice received TNP-SRC and TNBS on Day 0. TNP-ABC from mice immunized with TNP-SRC exhibit increased expression of surface IgG and decreased expression of surface IgD, compared to the ABC from nonimmune mice. Tolerant mice have a higher proportion of ABC with surface IgG, and a lower proportion with surface IgD, than nonimmune mice. Tolerant-challenged mice have a lower proportion of ABC with surface IgG, and a higher proportion with surface IgD, than immune mice. Thus, B-cell tolerance in this model entails an attenuation of the surface immunoglobulin isotype switch (loss of IgD and gain of IgG) on ABC seen in the normal immune response. For most TNP-ABC, tolerogen exposure prevents the switch in surface isotypes normally induced by exposure to TNP antigen; i.e., the tolerance lesion precedes the surface isotype switch. However, a minority of the TNP-ABC appear to switch surface isotypes in response to the tolerogen itself.