Hormone by genotype interactions have been widely ignored by cognitive neuroscience. Yet, the dependence of cognitive performance on both baseline dopamine (DA) and current 17ß-estradiol (E2) level argues for their combined effect also in the context of reinforcement learning. Here, we assessed how the interaction between the natural rise of E2 in the late follicular phase (FP) and the 40 base-pair variable number tandem repeat polymorphism of the dopamine transporter (DAT1) affects reinforcement learning capacity. 30 women with a regular menstrual cycle performed a probabilistic feedback learning task twice during the early and late FP. In addition, 39 women, who took hormonal contraceptives (HC) to suppress natural ovulation, were tested during the “pill break” and the intake phase of HC. The present data show that DAT1-genotype may interact with transient hormonal state, but only in women with a natural menstrual cycle. We found that carriers of the 9-repeat allele (9RP) experienced a significant decrease in the ability to avoid punishment from early to late FP. Neither homozygote subjects of the 10RP allele, nor subjects from the HC group showed a change in behavior between phases. These data are consistent with neurobiological studies that found that rising E2 may reverse DA transporter function and could enhance DA efflux, which would in turn reduce punishment sensitivity particularly in subjects with a higher transporter density to begin with. Taken together, the present results, although based on a small sample, add to the growing understanding of the complex interplay between different physiological modulators of dopaminergic transmission. They may not only point out the necessity to control for hormonal state in behavioral genetic research, but may offer new starting points for studies in clinical settings.

Objective: To investigate urinary fractions of free and peptide forms of collagen crosslinks in patients with rheumatoid arthritis (n=50), osteoarthrosis (n=38), psoriatic arthritis (n=38) and in healthy volunteers (33 adults, 17 children). Methods: Pyridinoline (PYD) and deoxypyridinoline (DPD) were measured by high performance liquid chromatography. Results: In rheumatoid arthritis (RA) all fractions of PYD and DPD were significantly raised compared with osteoarthritis, psoriatic arthritis, and healthy controls. PYD and DPD correlated with disease activity in RA. In RA the collagen degradation resulted in primarily peptide bound forms. Conclusion:The correlation between total peptide bound or free collagen crosslinks in different chronic joint diseases varies; however, this variation does not allow for a reliable differentiation between inflammatory and degenerative joint diseases. P yridinoline (PYD), a trifunctional 3-hydroxypyridinium crosslink 1 and its analogue, deoxypyridinoline (DPD), 2 are two non-reducible collagen crosslinks. PYD occurs in type I and II collagen 3 and, with the exception of skin, sclerae, and cornea, in most connective tissues-that is, bone and cartilage. DPD originates mainly from bone.3 When collagen fibrils are degraded into molecular fragments as a result of osteoclastic resorption, PYD and DPD are released into the circulation. They are then cleared by the kidney and excreted through urine, where they can be detected in peptide bound and free forms. 4 It has been reported that 40% of these crosslinks are excreted into urine as free and 60% in the peptide bound form. 4 Yet it remains unclear whether the determination of free or peptide bound crosslinks can provide more information on a possibly different collagen catabolism in patients with different diseases, compared with healthy adults and children.The aim was to investigate the fractions of free and peptide bound crosslinks as well as the total excretion in patients with rheumatoid arthritis (RA), psoriatic arthritis (PsA), and osteoarthrosis (OA) compared with healthy adults and children. Inflammation markers and steroid dose were included in further correlation studies. Healthy children were investigated to discover possible differences due to growth. SUBJECTS AND METHODS Healthy controlsFifty healthy volunteers were included (33 healthy adults (HA), 12 female, 21 male, mean (SD) age 41.0 (7.8) years and 17 healthy children (HC), nine female, eight male, mean (SD) age 7.7 (3.3) years). None had a previous history of metabolic bone disease, and none were receiving drugs affecting calcium absorption, excretion, or bone metabolism. Rheumatoid arthritisThis group included 44 female and six male patients, mean age 54.9 (15.9) years with definite RA. To determine the disease activity, serum C reactive protein (CRP) and erythrocyte sedimentation rate (ESR) were measured. The daily steroid dose was also recorded. OsteoarthritisThis group included 38 patients with proven OA of the knee joints (30 female, eight male, mean age 59.0 (1...

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