Utility of sonographic transcerebellar diameter in the assessment of gestational age in normal and intrauterine growth-retarded fetuses.

BACKGROUND: The fetal cerebellum has been shown to be least affected by external pressures and molding during pregnancy and therefore might provide more accurate estimation of GA. AIMS: To study the utility of transcerebellar diameter (TCD) measured by ultrasound for the detection of GA in normal and intrauterine growth-retarded (IUGR) fetuses. SUBJECTS AND METHODS: This cross-sectional study comprised 500 antenatal patients with a GA between 14 and 39 weeks and who were certain of their last menstrual periods. The TCD was measured ultrasonographically and the corresponding GA was determined. The GA was also determined with other customarily used sonographic parameters such as biparietal diameter (BPD), head circumference (HC), abdominal circumference (AC), and femur length (FL) and compared with TCD. Data of normal pregnancy patients was used to formulate nomograms by taking the 5th, 50th, and 95th percentile measurements. TCD to AC ratio was also calculated in both normal (n = 424) and IUGR pregnancies (n = 76). RESULTS: TCD showed significant correlation with gestational age (GA) measured by last menstrual period (LMP) as well as with GA calculated with other biometric fetal parameters. TCD also showed significant correlation with GA in normal (R2 = 0.979) as well as with IUGR pregnancies (R2 = 0.942). TCD to AC ratio remained fairly constant in normal pregnancies while it was increased in IUGR pregnancies. CONCLUSIONS: TCD and TCD/AC ratio can be employed as an objective parameter to establish the GA in normal as well as IUGR pregnancy cases.

Chronic treatment of C6 glioma cells with antidepressant drugs results in a redistribution of Gsalpha.

Previous studies have demonstrated that chronic treatment of C6 glioma cells with the antidepressants desipramine and fluoxetine increases the Triton X-100 solubility of the G protein Gsalpha (Toki et al., 1999). The antidepressants also caused a 50% decrease in the amount of Gsalpha localized to caveolae-enriched membrane domains. In this study, laser scanning confocal microscopy reveals that Gsalpha is localized to the plasma membrane as well as the cytosol in both treated and control cells. However, striking differences are seen in the distribution of Gsalpha in the long cellular processes after chronic treatment with these antidepressant drugs. Control cells display Gsalpha along the entire process with an especially high concentration of that G protein at the distal ends. Desipramine- or fluoxetine-treated cells show a more centralized clustering of Gsalpha in the Golgi region of the cell and a drastic reduction of Gsalpha in the cellular processes. There is no change in the distribution of Goalpha after desipramine treatment and the antipsychotic drug chlorpromazine does not alter Gsalpha. These results suggest that antidepressant-induced changes in the association of Gsalpha with the plasma membrane may translate into altered cellular localization of this signal transducing protein. Thus, modification of the coupling between Gs-coupled receptors and adenylyl cyclase may underlie both antidepressant therapy and depressive illnesses. This report also suggests that modification of the membrane domain occupied by Gsalpha might represent a mechanism for chronic antidepressant effects.