Psychiatric status of sexually abused children 12 months after disclosure of abuse.

OBJECTIVE: The assessment of psychiatric status of sexually abused children 12 months after the disclosure of recent sexual abuse. METHOD: Ninety-five children, aged from 4 through 16 years, were recruited to the study from a variety of agencies other than psychiatric units. Sixty-six (69.5%) were assessed for psychiatric diagnosis on DSM-III-R using data from parents, teachers, and children 12 months after disclosure of abuse. Abuse was extra- and intrafamilial. RESULTS: Overall 63.5% of the children warranted a diagnosis on Axis I. There was a wide range of diagnoses, with particularly high rates of oppositional defiant disorder (19.6%), post-traumatic stress disorder (18.2%), anxiety disorders (30.3%), depressive disorders (12.1%), and attention-deficit hyperactivity disorder (13.6%). Boys had a higher rate of diagnosis than girls. Abuse and social variables did not predict diagnoses but mothers' mental status rated on the General Health Questionnaire did. Subjects not located at follow-up were more often male and more likely to be socioeconomically disadvantaged. Thus the estimates of psychopathology here are likely to be conservative. CONCLUSIONS: This study highlights the need of sexually abused children for skilled long-term therapy tailored to individual presentation.

Clinical features and outcome of child and adolescent schizophrenia.

Subjects admitted 12 months or more previously to two child and adolescent psychiatric units in New Zealand and the United States with a diagnosis of non-organic, nonautistic psychosis, were contacted and those who received a DSM-III-R diagnosis of schizophrenia were studied (n = 33 [New Zealand] and n = 24 [United States]). Premorbid and first-episode data were obtained from the admission record using global clinical measures of moderate reliability, outcome diagnosis and status by interviews, and professional and family reports. Mean ages at onset were 13.9 (New Zealand) and 15.6 (United States). Premorbid and clinical features resembled those in adult schizophrenia, though there were probable quantitative differences. At outcome (mean interval = 4 years) few subjects were symptom-free or independent, and mean global assessment of functioning had fallen from 55 to 40. Outcome was much worse in schizophrenia than bipolar disorder. Despite a 59 percent attrition rate and higher rates of initial misdiagnosis in the United States, and some demographic differences, New Zealand and United States samples resembled each other clinically and in outcome. Initial misdiagnosis of bipolar disorder as schizophrenia was not due to minimizing mood symptoms, which were common in both disorders. Within this age range (mostly 11-17), age at onset had only minor effects. Outcome was best predicted by premorbid personality.

Quinapril--a preclinical review of the pharmacology, pharmacokinetics, and toxicology.

Quinapril is an orally active, non-peptide, nonsulfhydryl angiotensin-converting enzyme (ACE) inhibitor that acts potently and specifically to interrupt the conversion of angiotensin I to angiotensin II in both plasma and tissue. Quinapril is enzymatically hydrolyzed to a pharmacologically active diacid form quinaprilat. Quinapril is efficacious in hypertensive models exhibiting both high (renal hypertensive rats, diuretic-treated dogs) and normal (spontaneously hypertensive rats) plasma renin activity. Quinapril does not prevent the development of hypertension when plasma renin activity (PRA) is markedly suppressed as in the deoxycorticosterone-saline treated rat. Hemodynamic studies in dogs indicate that quinapril decreases total peripheral and renal vascular resistance. Quinaprilat produces natriuresis and mild diuresis at doses that do not alter mean arterial blood pressure. Quinapril has the potential to affect plasma lipids beneficially or at least be "lipid neutral." Oral absorption of quinapril is rapid in rats, dogs, and monkeys. There is rapid and extensive distribution of radiolabel to most tissues except brain. Plasma radiolabel concentration-time profiles exhibit polyexponential decay with a prolonged terminal phase at low concentrations in all species. Metabolism to compounds other than quinaprilat is not extensive. Quinapril is excreted primarily as quinaprilat and to a lesser degree as quinapril. Quinapril is well tolerated in a variety of pharmacologic safety screens and its toxicity profile is similar to that of other ACE inhibitors. Quinapril does not adversely affect reproduction; it is not teratogenic, carcinogenic, or mutagenic.(ABSTRACT TRUNCATED AT 250 WORDS)

Structure-activity relationships in the induction of mammary gland neoplasia in male rats with substituted aminopyrazoles.

In toxicity studies with a potential antipsychotic agent, N-(4-[2-fluorobenzoyl]-1,3-dimethyl-1H-pyrazol-5-yl)-2-([3- (2-methyl-1-piperidinyl)propyl]amino)-acetamide(Z)-2-butenedioate (1:2) (FP-1), mammary gland neoplasia in male rats was induced within 13 weeks. Tumor induction by the parent compound (FP-1) and structural analogs was also explored. Rats were given 50 mg/kg/day of FP-1 or the diethyl glycine analog, FP-2. Other experimental groups received the FP nucleus, a benzoylpyrazolylacetamide, or the FP side chains alone or administered concurrently with the nucleus. Most animals survived the 13 weeks without significant clinical effects. Clinically detectable, gross subcutaneous mammary nodules developed only in rats given FP-1 or the FP nucleus coadministered with the FP-1 side chain. Additional mammary gland neoplasms were found at necropsy or on histopathologic examination of mammary glands from rats receiving FP-1, FP-2, and the FP nucleus. The neoplastic effect was not influenced by the structure of the side chains. Since these substituted aminopyrazoles are novel chemicals, the mechanism for this neoplastic effect is not yet clearly established; however, the proliferating effect resides in the nucleus of this series of compounds and is likely related to alteration of DNA in target mammary tissue.