The existence of child sexual abuse within the Catholic Church has shocked many. In this article, the authors review the history of child sexual abuse in the church, the recent events that brought this tragedy into societal consciousness, and the efforts by the church to conceal the abuse. Two sources of empirical literature, the general psychological writing on priest sex abuse and the psychoanalytic literature, on child sexual abuse are compared. Both sources of literature seek explanation for priests' child sexual abuse within the structure and culture of the church rather than viewing the priest as a "typical" sex predator. The authors argue that, in fact, the guilty priests are child predators who differ little from other child predators.

OBJECTIVE-22q11 deletion syndrome, a common human interstitial deletion syndrome (1:5000), is associated with a heterogeneous physical phenotype, including several factors that markedly increase the risk for olfactory disorder. Despite its potential consequences, pediatric studies of impaired olfaction are rare, and odor detection in children with 22q11 deletion syndrome has not yet been examined. METHODS-TheUniversity of Pennsylvania Smell Identification Test was administered to 62 children, including 39 with 22q11 deletion syndrome and 23 neurotypical control siblings who ranged in age from 5.3 to 14.8 years. Lowered smell detection accuracy among affected children was predicted.RESULTS-Substantially more children with 22q11 deletion syndrome (68%) as compared with neurotypical control subjects (13%) had University of Pennsylvania Smell Identification Test scores ≥2 SDs below the standardization sample mean. Frequency of impairment in younger versus older children did not differ. The score distributions of children with and without velopharyngeal insufficiency did not differ; however, markedly lower score variance among children with velopharyngeal insufficiency suggested its negative impact on olfaction. Posthoc error analyses revealed that affected children had special difficulty detecting smells that are associated with fumes and smoke.CONCLUSIONS-Odor detection failures are ubiquitous among children with 22q11 deletion syndrome and are not associated with developmental delay or performance characteristics of younger affected children. Additional studies are needed to examine further the impact on olfaction of velopharyngeal insufficiency and compromised nasal airway patency. Children with 22q11 deletion syndrome should be evaluated routinely for olfactory disorder. When deficits are identified, caregivers should be warned of potential dangers that are associated with this type of sensory impairment. 22Q11 DELETION SYNDROME (22q11DS), also referred to as DiGeorge or velocardiofacial syndrome, results from a meiotic deletion at the q11.2 site on chromosome 22. It is estimated to occur in at least 1:5000 live births 1 and may be substantially more prevalent. 2 22q11DS results in the loss of ~30 gene copies 3 and a broadly heterogeneous physical phenotype, most typically including structural velopharyngeal anomalies, craniofacial or heart anomalies, and/ or immunologic deficits secondary to thymic irregularities. 4 Interest in the early neurologic and neurocognitive development of children with 22q11DS increased dramatically after reports of higher-than-expected rates of schizophrenia among affected adults. 5Clues regarding the source of neurocognitive differences in 22q11DS may reside in its genetic profile. Among the 30 deleted gene copies are 4 that have a direct and an indirect impact on production and release of glutamate, γ-aminobutyric acid (GABA), and dopa-mine, the 3 neurotransmitters that selectively subserve pathways that link basal ganglia and frontal/ prefrontal cortex 6 and that are impli...