1 ax-Adrenoceptor densities were studied in cardiac membrane preparations from several mammalian species including human failing hearts under identical experiment conditions; the al-adrenoceptor antagonist, [3H]-prazosin, was used as radioligand. End-stage heart failure (NYHA IV) in human hearts was due to idiopathic dilated cardiomyopathy. 2 The ventricular a1-adrenoceptor densities were not significantly different in guinea-pig, mouse, pig, calf, and man (11 to 18 fmol mg-' protein) but about 5 to 8 fold smaller than in rat (about 90 fmol mg-' protein). Right and left ventricular receptor densities were similar in these species. 3 A sufficient amount of right and left atrial tissue was obtained from rabbit, pig, calf, and man only. The a,-adrenoceptor densities in both atria of these species were found to be at the detection limit of the method used (less than 8 fmol mg-protein). 4 The equilibrium dissociation constant (KD) was similar in all species studied ranging from 0.047 + 0.006 to 0.063 ± 0.007 nmol 1'.5 It is concluded that differences in z1-adrenoceptor density between atria and ventricles may exist in mammalian species. The exceptionally high density of these receptors in rat ventricles seem to be a particular feature in these animals.

Objective: Cyclin D1 was an important molecular involved in the pathological process of osteoarthritis (OA). The purpose of this study was to identify the effect and potential mechanism of Cyclin D1 for the proliferation and apoptosis of OA chondrocytes. Methods: We used polymerase chain reaction (PCR) method to identify the expression levels of Cyclin D1 and downstream Wnt/b-catenin pathway-related genes in OA chondrocytes according to the grade of OA. Small interfering RNA (siRNA) or overexpression of Cyclin D1 were used to identify the role of Cyclin D1 in cell proliferation and apoptosis. Next, we used XAV-939 to inhibit the Wnt/b-catenin pathway and explore the relevant mechanism. Results: Cyclin D1 was significantly decreased with OA grade (p < .05). After siCyclin D1 transfection, the expression level of WNT3 and nuclear b-catenin were significantly increased, while Wnt10a and total b-catenin were not obviously changed. Co-cultured with XAV-939 and siCyclin D1 abolished the effects of siCyclin D1 on proliferation and apoptosis of OA chondrocytes (p < .05). Conclusions: Cyclin D1 regulated chondrocyte proliferation and apoptosis through Wnt3/b-catenin instead of Wnt10a/b-catenin signalling pathway.