Role of child and maternal processes in the psychological adjustment of children with sickle cell disease.

In this study, 64% of children aged 7–12 yrs with sickle cell disease were found to have a parent-reported behavior problem, and 50% met the criteria for a Diagnostic and Statistical Manual of Mental Disorders-III-Revised (DSM-III-R) diagnosis based on a structured clinical interview of the child. Internalizing types of behavior problems and diagnoses were the most frequent. Support was provided for a transactional stress and coping model in delineating the processes associated with child adjustment. In particular, maternal anxiety accounted for 16–33% of the variance in mother-reported internalizing and externalizing behavior problems, respectively, and child pain-coping strategies accounted for 21% of the variance in child-reported adjustment problems. (PsycINFO Database Record (c) 2010 APA, all rights reserved)     

Identification and characterization of the murine homologue of CD22, a B lymphocyte-restricted adhesion molecule

The human B lymphocyte-specific Ag, CD22, is a cell adhesion molecule expressed on the surface during a narrow window of B cell development, coincident with surface IgD. A ligand for CD22 has recently been identified on human T cells as the low molecular mass isoform of the leukocyte common Ag, CD45RO. CD22 has been reported to function in the regulation of both T and B cell activation in vitro. In this study, we report the isolation and expression of a molecular cDNA clone encoding the murine homologue of CD22, mCD22. Within their predicted protein sequences, murine and human sequences overall have 62% identity, which includes 18 of 20 extracellular cysteines and six of six cytoplasmic tyrosines. BHK cells transfected with mCD22 cDNA specifically adhere to resting and activated T lymphocytes and in addition bound activated, but not resting, B cells. Five Th clones were analyzed for their ability to adhere to mCD22; two Th0 clones and one Th1 clone bound CD22+ BHK transfectants, but not all T cell clones bound CD22+ cells: another Th1 clone and a Th2 clone did not. mCD22+ BHK transfectants were also specifically bound by the B cell-specific mAb, NIM-R6, demonstrating that this mAb is specific for murine CD22. Human cell lines expressing the counter-receptors for human CD22 were also examined for adhesion to the murine CD22 homologue; the epitope responsible for B cell adhesion to CD22 is conserved, whereas the T cell epitope binding to CD22 is not. The cDNA and mAb to murine CD22 will be useful for defining the in vivo function of CD22.     

What influences patients' reports of three aspects of hospital services?

OBJECTIVES: Market forces make it essential to know what policies and actions influence patients' reports of hospital services. No studies have examined the role of patient characteristics, labor quality and staff characteristics, nonlabor resources, managerial practices, and employee attitudes within a single investigation. METHODS: The authors collected, simultaneously, data about labor, management and service processes, nonlabor resources, and employee attitudes on 117 nonintensive medical-surgical inpatient units in 17 hospitals selected from a pool of 69 institutions within a metropolitan area by a stratified random sample. Of the 2,595 patients who agreed to participate, 2,051 (79%) completed telephone interviews regarding their experiences with physical care, education, and pain management services within 26 days of hospital discharge. RESULTS: A significant amount of variation in patients' service reports was explained (adjusted R2 = 0.41 physical care, 0.35 pain management, 0.44 education). Although the predictors varied for each service report, patient characteristics, especially those related to personal resources, had a large explanatory role. A labor assignment pattern that could explain why earlier studies found labor quality and staff characteristics to have only a weak role in the prediction of patients' service reports was noted. CONCLUSIONS: The results related to patient characteristics may indicate opportunities to improve care by confronting service design strategies that erroneously rely on a homogeneous patient population. Measurement challenges identified by this study must be addressed to determine the role of labor quantity and staff characteristics.     

Prostanoid biosynthesis by blood monocytes of children with hyperprostaglandin E syndrome

Hyperprostaglandin E syndrome (HPS), the prenatal variant of Bartter's syndrome, is characterized by a marked and selective stimulation of prostaglandin E (PGE2) synthesis. In the study group HPS patients showed increased urinary levels of PGE2, an index of renal, and of 11 alpha-hydroxy-9,15-dioxo-2,3,4,5,20-pentanor-19-carboxyprostano ic acid (PGE-M), an index of systemic PGE2 synthesis of 470% and of 570%, respectively. In addition, plasma concentration of PGE-M was also elevated 6.3-fold when compared with a control group. The urinary levels of other prostanoids were unaltered. During indomethacin treatment in both groups prostanoid excretion rates were suppressed to similar levels. To investigate the origin of stimulated prostanoid biosynthesis in HPS patients CD14+ monocytes were isolated from plasma samples, and the prostanoid synthesis was analyzed. The pattern and amounts of metabolites synthesized from endogenous arachidonic acid pools did not vary significantly between monocytes of the HPS and the control group. Thromboxane A2 (TXA2) was formed as the major prostanoid product. Using PGH2 as an exogenous substrate, again no difference in PGE2 biosynthesis was observed, indicating no difference in PGE-synthetic activity between both groups. Additionally, mRNA expression analysis of CD14+ monocytes via RT-PCR delineated the constitutive expression of cyclooxygenase-1, cyclooxygenase-2, and thromboxane synthase mRNA in cells from HPS patients and controls without statistical differences between these two groups. In conclusion, our data show that monocytes are not the source for the increased PGE2 biosynthesis in children with HPS, and a genetic defect in PGE synthesis can be excluded as the primary event in the pathogenesis in HPS.