Novel males can disrupt early pregnancy in female house mice (Mus musculus). In Experiment 1, exposure to novel males disrupted pregnancy, but exposure to male urine did not. In Experiment 2, urine from male or female mice or rats painted on females' noses did not influence pregnancy. In Experiment 3, the conjunction of urine painted on female's noses and vulval stimulation did not affect pregnancy more than water with similar stimulation. In Experiment 4, males housed above females were separated from them by a wire mesh grid; intact males disrupted pregnancy, but castrated ones did not. In Experiment 5, such housing of castrated males or ovariectomized females produced a strong disruption of pregnancy if the stimulus animal was given testosterone but not if it was given oil injections. In Experiment 6, transfers of odorous emissions failed to disrupt pregnancy. Contact and androgen activity are necessary for strange males to disrupt pregnancy.

Two experiments were undertaken to investigate the cause of the observed tendency of Mongolian gerbil dams to gestate more male than female fetuses in their right uterine horns and more female than male fetuses in their left uterine horns. It was found in Expt 1 that female gerbils that had both ovaries removed and portions of their right ovary placed in both ovarian capsules gestated significantly more male fetuses than did females that had both ovaries removed and portions of their left ovaries placed in both ovarian capsules. Expt 2 showed that female gerbils that had both their ovaries removed and then returned to their original locations gestated more males in their right uterine horns than in their left, while females that had the positions of their ovaries exchanged gestated more male fetuses in their left uterine horns than in their right. The data were consistent with the hypothesis that lateral asymmetries in gerbil ovaries rather than in gerbil uterine horns cause partial uterine segregation of gerbil fetuses by sex.

Although pacemaker recalls are common, the optimal mechanism for risk assessment and triage of patients at risk for sudden loss of device system function is unknown. A retrospective chart review of 120 patients with factory proven failed devices was performed. Logistic regression analysis was used to determine clinical correlates of emergency room versus outpatient clinic presentation at time of device failure. Twenty-two patients (18%) presented to emergency and 98 (82%) to clinic. Sixty-three devices had no device output at the time of presentation. Multivariate logistic regression analysis revealed that antiarrhythmic drug use (odds ratio: 7.4, 95% CI: 2.0-28.0), atrioventricular nodal disease as an indication for pacing (odds ratio: 2.8, 95% CI: 1.2-3.0), and female gender (odds ratio: 2.2, 95% CI: 1.0-4.5) were the only significant correlates of emergency room presentations. Pacemaker dependency (escape heart rate < 40 beats/min) did not correlate with location of presentation even though no device output at the time of presentation was associated with emergency room presentation (odds ratio: 2.5, 95% CI: 1.1-5.8). Neither the presence of structural heart disease nor symptoms at the time of device implantation (syncope or presyncope) were correlated with location of presentation upon unexpected device failure. Although there were no deaths in the 120 failed devices studied, there were 26 deaths in the total group of 227 patients with recalled devices that could not be studied. Antiarrhythmic drug use, electrocardiographic pacing indication, and female gender may be more sensitive predictors of emergency room presentation and significant symptoms in the event of unanticipated pacemaker failure. The inability of any retrospective analysis to accurately assess mortality in the setting of pacemaker system failure underscores the need for prospective databases in recall situations.

The combination of low dose sotalol and a class Ia agent greatly prolongs refractoriness. The magnitude of the effect increases at shorter coupling intervals.