Polycystic ovaries: MR imaging

To determine the characteristic appearance of polycystic ovaries on magnetic resonance (MR) images, seven women with polycystic ovarian disease (PCOD) underwent MR examination of the pelvis. These MR images were compared with sonograms. Histologic material was available in two patients. Six of the seven women had characteristic, small peripheral cysts, best seen on T2-weighted MR images; these cysts were seen sonographically in only one case. The centers of nine of 14 ovaries were of low intensity with all MR pulse sequences; this low intensity corresponded with low echogenicity in six cases. Histologically, these areas correlated with hypertrophic cellular stroma. Coexisting central teratomas were seen in three ovaries. The ability of MR to display the findings of PCOD better than ultrasound and its ability to demonstrate coexisting pathologic conditions are valuable in imaging the female pelvis.     

The Genetic Correlation Between Impulsivity and Sensation Seeking Traits

A number of studies have demonstrated associations between sensation seeking traits and measures of impulsivity. This study examined genetic contributions to the observed correlations between imupulsivity and sensation seeking traits. Fifty-seven pairs of identical and 49 pairs of fraternal twins who were reared apart and 90 individuals who also participated in the Minnesota Study of Twins Reared Apart completed the Control scale of the Multidimensional Personality Questionnaire (MPQ; Tellegen, 1982) and the four subscales of the Sensation Seeking Scale (SSS; Zuckerman, 1979), Consistent with previous studies, the Control scale was significantly correlated with the SSS. A Cholesky decomposition of the data indicated that the phenotypic correlations between the Control scale and the four subscales of the SSS were mediated almost entirely by genetic factors. In the final reduced model the proportion of the genetic variance of the Control scale in common with the SSS was estimated as 55%, and the rest of the genetic variance (45%) was attributed to the genetic variance specific to the Control scale. The results emphasize the importance of common biological mechanisms underlying associations between impulsivity and sensation seeking traits.     

Human thrombopoietin levels are high when thrombocytopenia is due to megakaryocyte deficiency and low when due to increased platelet destruction

Thrombopoietin (TPO), the ligand for c-mpl, stimulates proliferation of committed megakaryocytic progenitors and induces maturation of megakaryocytes. To better understand factors regulating TPO levels, we measured blood levels of TPO in patients with impaired platelet production due to aplastic anemia (AA) and with platelet destructive disorders, including idiopathic thrombocytopenic purpura (ITP), posttransfusion purpura (PTP), drug purpura (DP), and X-linked thrombocytopenia (XLTP). The TPO receptor capture enzyme immunoassay (EIA) used had a detection limit of integral of approximately-150 to 200 pg/mL. TPO was undetectable in 88 of 89 normal individuals. Eighteen of 19 patients with AA and a mean platelet count (MPC) of 18,000/microliters (2,000 to 61,000/microliters) had markedly elevated TPO levels (mean, 1,467 pg/mL; range, 597 to 3,834 pg/mL). Eight AA patients who responded to immunosuppressive therapy with their MPC increasing to 140,000/microliters (92,000 to 175,000/microliters) had substantial decreases in TPO (mean, 440 pg/mL; range, 193 to 771 pg/mL). Initial TPO levels did not differ significantly between responders and nonresponders. In contrast, all 21 patients with ITP and an MPC of 16,000/microliters (1,000 to 51,000 /microliters) had undetectable TPO levels, as did 6 patients with acute PTP or DP and 2 patients with XLTP. Megakaryocyte mass, reflected in the rate of platelet production, appears to be the major determinant of TPO levels in thrombocytopenic patients rather than circulating platelet levels per se. Measurement of serum TPO may be useful in differentiating thrombocytopenias due to peripheral destruction from those due to thrombopoietic failure.     

Tourette's disorder in a set of reared-apart triplets: genetic and environmental influences

Tourette's disorder was diagnosed in triplets reared apart from early infancy and reunited as adults. These data, combined with data on other family members, support the findings of research studies that have demonstrated genetic influences on Tourette's disorder.     

Lean-body-mass composition and resting energy expenditure before and after long-term overfeeding.

This report deals with the association between the constituents of lean body mass (LBM) and resting metabolic rate (RMR) before and after a 100-d overfeeding period. Computed-tomography (CT) scan of 22 young adult males at nine different body levels were used to estimate adipose tissue mass (ATMCT), LBMCT, skeletal-muscle mass (SMMCT), and non-muscular LBMCT (NM-LBMCT). Before overfeeding, all body constituents, except ATMCT, were significantly correlated with RMR. Only body mass changes were significantly correlated with RMR changes. Comparison of these results with those of several studies in the literature reveals that the relationship between RMR and fat-free mass is highly influenced by the size of the SD for the latter variable. In stepwise-multiple-regression analysis, only SMMCT could be used to predict RMR. It was concluded that SMMCT and ATMCT, but not NM-LBMCT, increased during overfeeding and that the best correlates of RMR remain LBMCT, SMMCT, and body mass.     

Genetic effect in resting and exercise metabolic rates

Two studies dealing with the contribution of the genotype in individual differences for resting metabolic rate (RMR), thermic effect of a 4.2 MJ carbohydrate meal (TEM), and energy cost of submaximal exercise are reported. The genetic effect for RMR and TEM was studied in 31 pairs of parent-child, 21 pairs of dizygotic (DZ) twins, and 37 pairs of monozygotic (MZ) twins, whereas the heritability of the energy cost of submaximal exercise was determined from data on 22 pairs of DZ twins and 31 pairs of MZ twins. The heritability of RMR reached approximately 40% of the variance remaining after adjustment for age, gender, and fat-free mass, (FFM). The genetic effect for TEM was equivalent to at least 40% to 50% of the variation in the energy expended during four hours after the meal test. A highly significant genetic effect was found for fasting plasma glucose (greater than .72), but the results for fasting plasma insulin are unclear. No significant genetic variance was seen for the glucose and insulin response to the carbohydrate meal. Finally, heritability for the metabolic rate during cycle exercise was high (greater than or equal to .46) at low power output, but it became nonsignificant when the energy cost reached about 6 times the RMR.