Bacterial infection stimulates nitric oxide (NO) production in chondrocytes. However, the role of NO in chondrocyte apoptosis after infection remains unclear. The purpose of the study was to test if inhibition of NO could ameliorate apoptosis and modulate matrix protein gene expression in bacteria-infected chondrocytes. It was shown that pre-treating chondrocytes with L-NAME (1 mM) significantly decreased the release of NO (from 72 to 14 pM) and the extent of apoptosis (from 52.9% to 18.9%). Pre-treatment with L-NAME also counteracted the bacteria-induced downregulation of Type I1 collagen (from 26% to 79%) and aggrecan (from 63% to 105%) mRNA levels. Inhibition of NO after the induction of infection could not decrease the extent of apoptosis and modulate matrix protein gene expression. The results of this study support the hypothesis that NO has an important role in bacteriainduced chondrocyte apoptosis. Pre-treatment but not post-treatment could ameliorate the extent of apoptosis and reestablish the cartilage matrix protein gene expression. This study suggests that in addition to NO, other mechanisms may be responsible for the sustained destruction of articular cartilage in the post-infectious arthropathy.

Tolterodine is a drug substance contammg (+)-N,Ndiisopropyl-3-(2-hydroxy-5-methylphenyl)-3-phenylprolylamine hydrogen L(+)-tartrate CC26H37N07).The drug is used for the treatment of minary frequency, urgency and/or urge incontinence. The synthesis of tolterodin L(+)-tartrate is a well established procedure. The crystal structure of tolterodine L(+)-tartrate was determined from single crystal x-ray data at room temperature and 30 K. The structure is monoclinic with two formula units in.the unit cell and all the atoms in the general position of the space-group P2J. The unit cell dimensions at 30 K are a= 9.1759, b = 16.3965c =l2.9196A. = 93.427". In the final stage of the refinement the 3568 reflections recorded at 30 K were refined to an R-value of 4.0%.