Molecular characterization of human adenomyosis.

Adenomyosis is a common gynaecological disorder characterized by the abnormal growth of endometrium into the myometrium and myometrial hypertrophy/hyperplasia. Uterine fibroids are benign neoplasms of the myometrium, and they represent a diagnostic pitfall for adenomyosis. In this study, we have used the genome-wide Affymetrix U133 Plus 2.0 microarray platform to compare the gene expression patterns of adenomyosis, uterine fibroids, normal endometrium and myometrium. Unsupervised principal component analysis (PCA) revealed that these four tissue types could be segregated from one another solely based on their gene expression profiles. Analysis of variance (ANOVA), followed by Tukey means separation test, significance analysis of microarrays (SAM) and 2-fold change threshold, identified 7415 probe sets as differentially expressed among the four groups of samples. Supervised cluster analysis based on these probe sets clustered adenomyosis most closely with endometrium and uterine fibroids with myometrium, consistent with the anatomic origin of these two diseases. The Tukey means separation post hoc testing found 2073 probe sets altered between adenomyosis and normal endometrium or myometrium, and 2327 probe sets altered in expression when comparing uterine fibroids with myometrium. Using Ingenuity Pathways Analysis (IPA), we found 9 highly significant functional networks in adenomyosis and 10 in uterine fibroids. Notably, the top network in both cases was associated with functions implicated in cancer and cell death. Finally, we compared the gene expression profiles of adenomyosis and uterine fibroids and identified 471 differentially expressed probe sets that may represent potential biomarkers for the differential diagnosis of these diseases.

Risk factor analysis of intraventricular hemorrhage in low-birth-weight infants.

Sixty of 63 newborn infants weighing less than 1,250 gm, admitted consecutively to the Intensive Care Nursery during a 15-month period, were prospectively investigated for the incidence of intraventricular hemorrhage by early computerized tomography or by autopsy. Nineteen of the 60 infants had evidence of IVH. The incidence of IVH was correlated with the presence of possible neonatal, obstetrical, asphyxial, or therapeutic risk factors. There was a significant difference in only one of the risk factors: birth outside the perinatal center. Fifteen of 27 outborn infants (56%) developed IVH, whereas only four of 33 inborn infants (12%) developed IVH (P less than 0.001). There were no statistically significant differences in maternal obstetrical risk factors, infant risk factors, or indices of birth asphyxia in the inborn compared with the outborn infants. However, perinatal therapeutic risk factors differed between the two groups. Outborn infants were less likely to have received betamethasone (P less than 0.001), were less likely to have their arterial blood gases monitored and stabilized during the first 20 minutes after birth (P less than 0.001), and were given more bicarbonate (P less than 0.001) and more boluses of fluid intravenously (P less than 0.02). The risk of IVH in very low birth-weight infants may be significantly decreased by therapeutic factors at birth. Maternal transport to a perinatal center and intensive neonatal resuscitation may contribute to decreasing the incidence of intraventricular hemorrhage.

Expulsion of Nippostrongylus brasiliensis by mice deficient in mast cells.

Expulsion of the intestinal helminth, Nippostrongylus brasiliensis, occurs spontaneously about 2 weeks after a primary infection of rats and mice. Cellular changes in the small intestine coincident with the period of expulsion have suggested several mechanisms by which this 'self-cure' may be effected. Local anaphylaxis was proposed as a possible means of parasite clearance; this hypothesis has been supported by the demonstration of specific reaginic antibody production and jejunal mast cell accumulation in infected animals. In addition, increased mucus secretion and more recently, goblet cell proliferation in the jejunal mucosa of rats have been noted and considered as potentially important in mediating the self-cure reaction. The data presented below indicate that in the absence of demonstrable mast cells, the course of a primary infection with this parasite is unchanged; however, they are supportive of a role for globlet cells in the self-cure reaction.