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Biomedical subjects

M Campbell

Publications and source records attributed to M Campbell.

At least 325 records · Page 18Linked to original sources

Field trial for autistic disorder in DSM-IV.

OBJECTIVE: This project focused on the development of the definition of autism for DSM-IV. METHOD: Multiple sites were involved in obtaining information regarding 977 patients with the following clinician-assigned diagnoses: autism (N = 454), other pervasive developmental disorders (N = 240), and other disorders (N = 283). A standard coding system was used, and the raters (N = 125) had a range of experience in the diagnosis of autism. Patterns of agreement among existing diagnostic systems were examined, as was the rationale for inclusion of other disorders within the class of pervasive developmental disorders. RESULTS: The DSM-III-R definition of autism was found to be overly broad. The proposed ICD-10 definition most closely approximated the clinicians' diagnoses. Inclusion of other disorders within pervasive developmental disorders appeared justified. Partly on the basis of these data, modifications in the ICD-10 definition were made; this and the DSM-IV definition are conceptually identical. CONCLUSIONS: The resulting convergence of the DSM-IV and ICD-10 systems should facilitate both research and clinical service.

Age of Onset↗

[Cytogenetic studies of Chilean children with acute lymphoblastic leukemia].

Acute lymphoblastic leukemia (ALL) is the most frequent childhood cancer. The leukemic cells of ALL patients show several well defined numeric and structural chromosomal abnormalities which are universally known for its prognostic implications. We studied a group of 44 children with ALL, to investigate the incidence of chromosome aberrations in ALL, its lymphocyte lineage and some clinical feature associations, and the finding of non previously described aberrations. A high proportion of patients (79.5%) showed chromosomal abnormalities. Most of them had a pseudodiploid karyotype (46 chromosomes), characterized mainly by a translocation. In relation to chromosome number, 27% of them were hyperdiploid with more than 50; 9% hyperdiploid between 47-50 and 7% hypodiploid (less than 46). Among structural aberrations found, were the following recurrent translocations: t (1; 19), t (4; 11), t (9; 22) in 6.8%, 9.1% and 2.3% of cases respectively, all related to an early B immunophenotype. Other translocations found, compromised regions 7q22, 9p21 - 24. Two new translocations in ALL were found: t (1; 5)(q23; q33), apparently balanced, and t (13; 21)(q14; q22), unbalanced. Other recurrent structural changes found were: deletion (6q), (7q), (9p), (11q), (12p), inversion (3q), isochromosome (7q), maker chromosomes and double minutes. The distribution of chromosome abnormalities in this group of patients was in agreement with previous reports from other investigators.

Adolescent↗

Naltrexone plasma levels, clinical response and effect on weight in autistic children.

This research measured naltrexone levels in plasma, to assess the relationship between behavioral response to naltrexone and plasma levels, and the effects of naltrexone on weight in hospitalized autistic children (n = 41). A double-blind, placebo-controlled, parallel groups design with fixed dose was used, with random assignment to naltrexone or placebo. Drug plasma levels were analyzed by gas chromatography/mass spectrometry, and weights were obtained weekly. Naltrexone levels measured in 17 children ranged from 0.12 to 5.60 ng/mL (mean = 0.71, standard error of the mean = 0.32). There was no relationship between plasma levels and age, level of intellectual functioning, scores on the 14 selected Children's Psychiatric Rating Scale (CPRS) items, Clinical Global Impressions, Global Clinical Consensus, and the CPRS hyperactivity factor. There was a trend (p = .06) for children receiving naltrexone in the highest weight percentile (> or = 90th) to lose weight (mean = -0.42 kg) but this was not the case for those in the lower weight percentiles (mean = +0.03 kg).

Autistic Disorder↗

Placebo response in aggressive children with conduct disorder.

Aggressiveness and explosiveness characterize a subgroup of children diagnosed with conduct disorder (CD). Few double-blind, placebo-controlled studies have been conducted in aggressive children with CD, and no study has differentiated placebo responders from nonresponders. This study examined factors that may differentiate placebo responders from nonresponders hospitalized in a structured setting. The sample consisted of 25 children, ages 6.25 to 11.95 years, with CD and a profile of aggressive and explosive behavior, who were assigned to placebo treatment as part of a double-blind study of lithium. Responders were compared to nonresponders with respect to a detrimental psychosocial environmental score, age, IQ, and baseline ratings on the Children's Psychiatric Rating Scale and Clinical Global Impressions. Responders had significantly higher detrimental psychosocial environmental scores than nonresponders; they were particularly more likely to come from violent homes and to have criminally charged parents. Demographic variables did not distinguish the two groups; however, even mild hyperactivity was associated with poorer response to placebo.

Aggression↗

Sibling adult T-cell leukemia/lymphoma and clustering of human T-cell lymphotropic virus type I infection in a Jamaican family.

BACKGROUND: Human T-cell lymphotropic virus type I (HTLV-I) infection is endemic in Jamaica, with an estimated crude seroprevalence of 5%. Adult T-cell lymphoma/leukemia (ATL), a disease caused by HTLV-I, has an incidence of 1-2/100,000 in the Jamaican population. Familial ATL has not previously been reported from Jamaica. METHODS: Hospital records and histologic specimens of the two cases were reviewed. HTLV-I infection was confirmed by antibody testing and by polymerase chain reaction on paraffin-embedded tissue, where serum was unavailable. Family members were identified by the patients' parents. After giving informed consent, family members were asked to complete an interviewer-administered questionnaire and to agree to phlebotomy. RESULTS: ATL developed 10 years apart in two siblings from a Jamaican family at age 16 and 24 years. A study of 19 members of their extended family, including both parents, 2 grandparents, and 3 siblings, revealed an overall HTLV-I seroprevalence of 17%. This compared with 75% among parents and siblings living in the same household as the patients. HTLV-I antibody-positive (HTLV-I-positive) and negative family members had similar mean age. Three of 3 HTLV-I-positive subjects were breast-fed, compared with 10 of 15 HTLV-I-negative subjects. Intravenous drug abuse, sex with prostitutes, homosexuality, and blood transfusion were not reported. The mean number of sexual partners were similar. Both parents, who were antibody-positive, had polylobated atypical lymphocytes in their peripheral blood. CONCLUSION: The HTLV-I antibody seroprevalence is greater in the family than in the general population, consistent with the modes of transmission. The antibody seronegativity of both grandmothers suggests sexual transmission between parents. The development of ATL at age 16 and 24 years is consistent with maternal-infant transmission and a long latent period, as reported by other authors.

Adolescent↗

Tyrosine phosphorylation of P160 BCR by P210 BCR-ABL.

It is well established that the chimeric BCR-ABL gene formed by joining parts of the BCR and ABL genes plays a key role in the pathogenesis of Philadelphia (Ph) chromosome-positive leukemias. We report that simultaneous expression of P210 BCR-ABL and P160 BCR in simian COS-1 cells yielded stable complexes of these two proteins, and induced phosphorylation of P160 BCR on tyrosine residues in vivo. Tyrosine phosphorylation of a deletion mutant encoding 553 amino acids of BCR N-terminal sequences was also detected when it was coexpressed with P210 BCR-ABL. We propose that tyrosine phosphorylation of P160 BCR by P210 BCR-ABL and their stable physical interaction may perturb normal BCR functions and that these alterations are directly involved in the pathologic processes found in Ph chromosome-associated leukemias.

Amino Acid Sequence↗