Supernumerary roots in maxillary deciduous canines: A rare anomaly with a long history.

Objective: To describe two maxillary deciduous bi-rooted canines, one archeological and one modern, and examine the possible etiology of this condition.

Design: Two cases of bi-rooted canines were described and compared to published examples. Both specimens were radiographed and measured and compared to one-rooted samples.

Protective role of endogenous catalase in baseline and phenytoin-enhanced neurodevelopmental and behavioral deficits initiated in utero and in aged mice.

We used mutant catalase-deficient mice (acatalasemic, aCat) and transgenic mice expressing human catalase (hCat) to determine the neuroprotective role of catalase in utero and in aged animals treated with vehicle or the reactive oxygen species (ROS)-initiating drug phenytoin. Phenytoin-initiated postnatal death was enhanced in aCat mice and reduced in hCat mice. Catalase deficiency reduced postnatal surface righting, negative geotaxis and rotarod performances independent of drug treatment, and enhanced phenytoin-initiated negative geotaxis and rotarod deficits in aCat females.

Embryonic catalase protects against endogenous and phenytoin-enhanced DNA oxidation and embryopathies in acatalasemic and human catalase-expressing mice.

Oxidative stress and reactive oxygen species (ROS) such as hydrogen peroxide (H(2)O(2)), which is detoxified by catalase, are implicated in fetal death and birth defects. However, embryonic levels of catalase are only ∼ 5% of adult activity, and its protective role is not understood completely. Herein, we used mutant catalase-deficient mice [acatalasemic (aCat)] and transgenic mice expressing human catalase (hCat), which, respectively, exhibited 40-50% reductions and 2-fold elevations in the activities of embryonic and fetal brain catalase, to show that embryonic catalase protects the embryo from both physiological oxidative stress and the ROS-initiating antiepileptic drug phenytoin.

Embryoprotective role of endogenous catalase in acatalasemic and human catalase-expressing mouse embryos exposed in culture to developmental and phenytoin-enhanced oxidative stress.

Reactive oxygen species (ROS) are implicated in spontaneous and xenobiotic-enhanced embryopathies, and protein therapy with exogenous catalase suggests an embryoprotective role, although embryonic catalase activity is only about 5% of adult activity. Using mutant catalase-deficient (acatalasemic, aCat) mice and transgenic mice expressing human catalase (hCat, enhanced catalase activity) compared with a confirmed outbred CD-1 mouse model, we investigated the protective importance of constitutive embryonic catalase against endogenous ROS and the ROS-initiating teratogen phenytoin in embryo culture. Vehicle-exposed aCat and hCat embryos, respectively, exhibited reduced and enhanced catalase activity compared with wild-type (WT) controls, with conversely enhanced and reduced spontaneous embryopathies.