Effects of medication, behavioral, and combined treatments on parents' and children's attributions for the behavior of children with attention-deficit hyperactivity disorder

Seventy-four mothers and 41 fathers and their 6 to 13 year old sons with attention-deficit hyperactivity disorder (ADHD) watched videos of child ADHD symptoms, compliance, and noncompliance. Participants were told either that the child was receiving medication, behavioral treatment, a combination of the two, or was not receiving treatment and were asked to rate the cause of the behavior. Parents attributed less control but greater stability to positive child behaviors when the child was receiving medication. However, for negative behaviors, medication increased attributions of control but diminished stability. With behavior management. compliance was seen as more external and stable and noncompliance as more controllable but less stable. For all treatments, boys reported increased control over ADHD symptoms and noncompliance. The implications of these treatment-related attributions for parenting and children's self-perceptions are discussed.     

Human Leucocyte Differentiation Antigen nomenclature: update on CD nomenclature. Report of IUIS/WHO Subcommittee

The 7th International Workshop on Human Leucocyte Differentiation Antigens (HLDA7) studied a number of newly characterised molecules relevant to human leucocyte differentiation and function. The HLDA organisation, which devised and continues to maintain the CD nomenclature, is responsible, under the auspices of IUIS and WHO, for the nomenclature of all leucocyte differentiation markers. The 7th Workshop redefined a number of (principally carbohydrate) molecules, and assigned CD names to approximately 80 new molecules. This update lists, in tabular form, the redefined and newly assigned names, together with antibodies, which have been confirmed under Workshop conditions as specific for the new and redefined molecules. The major features of the cellular expression patterns are summarised, and a LocusLink accession number provided to enable the reader to access more detailed information through http://www.ncbi.nlm.nih.gov/LocusLink.     

Tumours of histiocytes and accessory dendritic cells: an immunohistochemical approach to classification from the International Lymphoma Study Group based on 61 cases

Neoplasms of histiocytes and dendritic cells are rare, and their phenotypic and biological definition is incomplete. Seeking to identify antigens detectable in paraffin-embedded sections that might allow a more complete, rational immunophenotypic classification of histiocytic/dendritic cell neoplasms, the International Lymphoma Study Group (ILSG) stained 61 tumours of suspected histiocytic/dendritic cell type with a panel of 15 antibodies including those reactive with histiocytes (CD68, lysozyme (LYS)), Langerhans cells (CD1a), follicular dendritic cells (FDC: CD21, CD35) and S100 protein. This analysis revealed that 57 cases (93%) fit into four major immunophenotypic groups (one histiocytic and three dendritic cell types) utilizing six markers: CD68, LYS, CD1a, S100, CD21, and CD35. The four (7%) unclassified cases were further classifiable into the above four groups using additional morphological and ultrastructural features. The four groups then included: (i) histiocytic sarcoma (n=18) with the following phenotype: CD68 (100%), LYS (94%), CD1a (0%), S100 (33%), CD21/35 (0%). The median age was 46 years. Presentation was predominantly extranodal (72%) with high mortality (58% dead of disease (DOD)). Three had systemic involvement consistent with 'malignant histiocytosis'; (ii) Langerhans cell tumour (LCT) (n=26) which expressed: CD68 (96%), LYS (42%), CD1a (100%), S100 (100%), CD21/35 (0%). There were two morphological variants: cytologically typical (n=17) designated LCT; and cytologically malignant (n=9) designated Langerhans cell sarcoma (LCS). The LCS were often not easily recognized morphologically as LC-derived, but were diagnosed based on CD1a staining. LCT and LCS differed in median age (33 versus 41 years), male:female ratio (3.7:1 versus 1:2), and death rate (31% versus 50% DOD). Four LCT patients had systemic involvement typical of Letterer-Siwe disease; (iii) follicular dendritic cell tumour/sarcoma (FDCT) (n=13) which expressed: CD68 (54%), LYS (8%), CD1a (0%), S100 (16%), FDC markers CD21/35 (100%), EMA (40%). These patients were adults (median age 65 years) with predominantly localized nodal disease (75%) and low mortality (9% DOD); (iv) interdigitating dendritic cell tumour/sarcoma (IDCT) (n=4) which expressed: CD68 (50%), LYS (25%), CD1a (0%), S100 (100%), CD21/35 (0%). The patients were adults (median 71 years) with localized nodal disease (75%) without mortality (0% DOD). In conclusion, definitive immunophenotypic classification of histiocytic and accessory cell neoplasms into four categories was possible in 93% of the cases using six antigens detected in paraffin-embedded sections. Exceptional cases (7%) were resolvable when added morphological and ultrastructural features were considered. We propose a classification combining immunophenotype and morphology with five categories, including Langerhans cell sarcoma. This simplified scheme is practical for everyday diagnostic use and should provide a framework for additional investigation of these unusual neoplasms.     

Adrenocortical adenoma and carcinoma: histopathological and molecular comparative analysis.

We compared histomorphological features and molecular expression profiles of adrenocortical adenomas (ACAd) and carcinomas (ACCa). A critical histopathological review (mean, 11 slides per patient) was conducted of 37 ACAd and 67 ACCa. Paraffin-embedded tissue cores of ACAd (n = 33) and ACCa (n = 38) were arrayed in triplicate on tissue microarrays. Expression profiles of p53, mdm-2, p21, Bcl-2, cyclin D1, p27, and Ki-67 were investigated by immunohistochemistry and correlated with histopathology and patient outcome using standard statistical methodology. Median follow-up period was 5 years. Tumor necrosis, atypical mitoses, and >1 mitosis per 50 high-power fields were factors that were highly specific for ACCa (P <.001). Number (0 to 4) of unfavorable markers [Ki-67 (+), p21 (+), p27 (+), mdm-2(-)] expressed was significantly associated with mitotic activity and morphologic index (i.e., number of adverse morphologic features) and highly predictive of malignancy (P <.001). Ki-67 overexpression occurred in 0 ACAd and 36% ACCa (P <.001) and was significantly associated with mitotic rate and unfavorable morphologic index (P <.001). Tumor necrosis, atypical mitoses, >5 mitoses per 50 high-power fields, sinusoidal invasion, histologic index of >5, and presence of more than two unfavorable molecular markers were associated significantly with metastasis in ACCa. Well-established histopathologic criteria and Ki-67 can specifically distinguish ACCAd from ACCa. Tumor cell proliferation (Ki-67) correlates with mitotic activity and morphologic index. Tumor morphology is a better predictor of metastatic risk in ACCa than current immunohistochemistry-detected cell cycle regulatory and proliferation-associated proteins.     

Additional evidence that "plasmacytoid T-cell lymphoma" associated with chronic myeloproliferative disorders is of macrophage/monocyte origin

Plasmacytoid T-cell lymphoma (PTL) is a rare lymphoma with unique morphologic, immunologic, and clinical features. Thus far, only three cases have been reported, each terminating in myeloid leukemia. The macrophage/monocyte rather than T-cell origin of "plasmacytoid T-cells" in reactive lymph nodes has been suggested in the past, but there has been no extensive investigation to demonstrate whether the PTLs are also of this lineage. The authors now report on a patient with PTL who had a long history of clinically stable idiopathic myelofibrosis. Immunocytochemical staining of the neoplastic plasmacytoid cells, with a large panel of monoclonal antibodies used on fresh-frozen and paraffin-embedded tissue sections, showed that the neoplastic cells expressed several macrophage/monocyte-associated markers, i.e., CD31, CD36 (thrombospondin receptor), and CD68 (KP1). Other markers of the macrophage/monocyte lineage (e.g., CD11b, CD11c, CD16) were absent. The neoplastic cells lacked B-cell-associated antigens and lacked most T-cell-associated markers, with the exception of CD2 and CD4. These findings are in close agreement with those of previous studies on normal plasmacytoid T-cells and support the macrophage/monocytic origin of PTL. Molecular hybridization studies provided additional support for the nonlymphoid origin of the plasmacytoid cells by demonstrating the absence of T-cell-receptor beta-chain and immunoglobulin heavy-chain gene rearrangements in the neoplastic cells. The results of the authors' studies indicate that "plasmacytoid T-cell lymphoma" associated with a chronic myeloproliferative disorder is of macrophage/monocyte lineage.     

Structure of the corpus luteum in the ovulatory polycystic ovary.

BACKGROUND: Women with polycystic ovaries (PCO) have a wide spectrum of presentation from anovulation and amenorrhoea to apparently regular, ovulatory menstrual cycles. We have recently reported a subtle defect in steroidogenic function in the luteal phase in the latter and an increase in the number of degenerating corpora lutea (CL) were observed in ovulatory PCO (ovPCO) during dissection. The possibility was therefore investigated of differences in structure or degeneration in CL formed during ovulatory cycles in women with PCO. METHODS: This study compared the histology of the CL in ovPCO with that in the normal ovary. Corpora lutea were collected from nine normal ovaries (days 1-27 of the cycle) and from 13 women with ovPCO (days 5-38). RESULTS: Variations in the degree of regression, both in relation to onset of menses and between different areas within individual CL, were recorded in both groups. During development and regression no obvious differences were observed between either group apart from an apparent increase in luteal haemorrhage, which was more common and more extensive in CL from PCO. CONCLUSIONS: The findings suggest that possible luteal phase abnormalities of steroid secretion in women with ovulatory PCO are not associated with obvious morphological defects in the CL, however it is possible that the persistence of luteal structures seen in PCO was a consequence of increased luteal haemorrhage.