Influence on binding of third-order torque to second-order angulation

Using an earlier model, which described the critical contact angle for binding from second-order angulation alone, a more generalized model is derived that combines the effects of angulation and torque. From this vantage point, the onset of binding is evaluated for 3 scenarios: second-order angulation alone, third-order torque only, and a combination of second-order angulation and third-order torque. These scenarios are detailed by plotting the critical contact angle for binding against the torque angle as a function of 10 wire dimensions (16 x 16, 16 x 22, 17 x 17, 17 x 22, 17 x 25, 18 x 18, 18 x 22, 18 x 25, 19 x 25, and 21 x 25 mil), 4 bracket widths (70, 100, 130, and 160 mil), and 4 bracket slots (18, 20.5, 22, and 24.5 mil). From these plots, we learn that each wire base dimension (eg, an 18-mil base as found in 18 x 18-mil, 18 x 22-mil and 18 x 25-mil archwires) has a common maximum critical contact angle for binding. Moreover, each wire-slot combination has a common maximum torque angle, which is independent of bracket width. Finally, we learn that archwire-bracket combinations that use a metric 0.5-mm slot might have some advantages with regard to torquing--given the current philosophy that light, continuous forces are more favorable.     

Reversal of startle gating deficits in transgenic mice overexpressing corticotropin-releasing factor by antipsychotic drugs.

Chronically elevated levels of corticotropin-releasing factor (CRF) in transgenic mice overexpressing CRF in the brain (CRF-OE) appear to be associated with alterations commonly associated with major depressive disorder, as well as with sensorimotor gating deficits commonly associated with schizophrenia. In the present study, we tested the hypothesis that antipsychotics may be effective in normalizing prepulse inhibition (PPI) of acoustic startle in CRF-OE mice, which display impaired sensorimotor gating compared to wild-type (WT) mice. The typical antipsychotic haloperidol and atypical antipsychotic risperidone improved PPI in the CRF-OE mice, but were ineffective in WT mice. The atypical antipsychotic clozapine did not influence PPI in CRF-OE mice, but reduced gating in WT mice. This effect of clozapine in the CRF-OE mice may thus be regarded as a relative improvement, consistent with the observed effect of haloperidol and risperidone. As expected, the anxiolytic, nonantipsychotic chlordiazepoxide was devoid of any effect. All four compounds dose-dependently reduced the acoustic startle response irrespective of genotype. These results indicate that antipsychotic drugs are effective in improving startle gating deficits in the CRF-OE mice. Hence, the CRF-OE mouse model may represent an animal model for certain aspects of psychotic depression, and could be a valuable tool for research addressing the impact of chronically elevated levels of CRF on information processing.