Quantitative 7T phase imaging in premanifest Huntington disease.

BACKGROUND AND PURPOSE: In vivo MR imaging and postmortem neuropathologic studies have demonstrated elevated iron concentration and atrophy within the striatum of patients with Huntington disease, implicating neuronal loss and iron accumulation in the pathogenesis of this neurodegenerative disorder. We used 7T MR imaging to determine whether quantitative phase, a measurement that reflects both iron content and tissue microstructure, is altered in subjects with premanifest Huntington disease. MATERIALS AND METHODS: Local field shift, calculated from 7T MR phase images, was quantified in 13 subjects with premanifest Huntington disease and 13 age- and sex-matched controls. All participants underwent 3T and 7T MR imaging, including volumetric T1 and 7T gradient recalled-echo sequences. Local field shift maps were created from 7T phase data and registered to caudate ROIs automatically parcellated from the 3T T1 images. Huntington disease-specific disease burden and neurocognitive and motor evaluations were also performed and compared with local field shift. RESULTS: Subjects with premanifest Huntington disease had smaller caudate volume and higher local field shift than controls. A significant correlation between these measurements was not detected, and prediction accuracy for disease state improved with inclusion of both variables. A positive correlation between local field shift and genetic disease burden was also found, and there was a trend toward significant correlations between local field shift and neurocognitive tests of working memory and executive function. CONCLUSIONS: Subjects with premanifest Huntington disease exhibit differences in 7T MR imaging phase within the caudate nuclei that correlate with genetic disease burden and trend with neurocognitive assessments. Ultra-high-field MR imaging of quantitative phase may be a useful approach for monitoring neurodegeneration in premanifest Huntington disease.

Oligohydramnios and the appropriately grown fetus.

The perinatal implications of oligohydramnios prior to 37 weeks of gestation, in the absence of intrauterine growth restriction (IUGR), rupture of membranes or fetal anomalies, are unknown. We compared the outcomes of 65 women with oligohydramnios (amniotic fluid index ([AFI] < or = 8 cm) by sonography to those of a control group matched by sonogram indication. Study patients were between 17 and 37 weeks of gestation, with appropriately grown fetuses on index sonogram and no other detected explanation for amniotic fluid abnormalities. Patients were managed expectantly with fetal testing and follow-up sonograms for fetal growth. Delivery was not recommended solely for oligohydramnios until 37 weeks of gestation. Patients with isolated oligohydramnios prior to 37 weeks of gestation, when compared to a control group with normal amniotic fluid volume, had a significantly higher incidence of premature delivery (odds ratio [OR] 3.23, 95% confidence interval [CI] 1.4-7.3) but did not appear to be at increased risk of IUGR, intrauterine death, or birth asphyxia.

Estrogen regulation of an eosinophil chemotactic factor in the immature rat uterus.

Associated with the generalized uterine growth stimulated by estradiol in the rat are specific responses including messenger RNA (mRNA) synthesis, protein synthesis, and peroxidase activity. The increase in peroxidase activity, although sensitive to inhibitors of RNA and protein synthesis, results from an estradiol-stimulated influx of eosinophils into the uterus. We postulated the existence of an estradiol-regulated uterine chemotactic factor, testing this by an in vitro chemotactic assay with eosinophils isolated from mature rats. Treatment of immature rats with 1 microgram estradiol for 24 h resulted in a significant increase in eosinophil chemotaxis compared to uterine extracts of vehicle-treated rats. This increase was seen as early as 3 h after estradiol administration and was maximal at 24 h. The magnitude of the chemotactic response was dependent on the dose of estradiol administered (1-100 micrograms). Estrone or estriol treatment resulted in chemotactic activity greater than control but less than estradiol. Direct addition of estradiol to extracts of control animals did not increase chemotaxis. The estradiol-stimulated chemotaxis was blocked by in vivo treatment with the antiestrogen tamoxifen and by inhibitors of RNA and protein synthesis. Analysis of extracts from estradiol-treated uteri shows that the chemotactic factor is heat labile, pronase sensitive, and has a mass of approximately 20 kilodaltons (kDa). These data suggest that the estradiol-stimulated influx of eosinophils into the rat uterus is mediated by the synthesis, modification, or release of a protein whose synthesis is estradiol receptor mediated.