Sclerosing epithelioid fiberosarcoma: short T2 on MR imaging

A case of sclerosing epithelioid fibrosarcoma and its appearance on MRI is presented. The tumor showed a zonal architecture on MRI with a large central core of very low signal intensity and a peripheral rim of intermediate to high signal intensity on T1- and T2-weighted spin echo pulse sequences. The core showed decreased cellularity with dense collagen deposition on histologic examination, and the peripheral zone increased cellularity with increased nuclear atypia. The presence of a prominent region of very low signal intensity on T1- and T2-weighted images can be seen with neural tumors, giant cell tumor of the tendon sheath, aggressive fibromatosis, and, in rare instances, with soft tissue sarcomas rich in collagen.     

Pulmonary oxidative stress response in young children with cystic fibrosis

BACKGROUND: It has been suggested that oxidative stress contributes to lung injury in cystic fibrosis. There is, however, no direct evidence of increased pulmonary oxidative stress in cystic fibrosis nor of the effects of inflammation on the major pulmonary antioxidant, glutathione. A study was undertaken to measure these parameters in infants and young children in the presence or absence of pulmonary inflammation. METHODS: Thirty two infants and young children with cystic fibrosis of mean (SD) age 21.4 (15.3) months (range 2-54) and seven non-cystic fibrosis control subjects of mean (SD) age 21.0 (21.2) months (range 2-54) were studied using bronchoalveolar lavage (BAL). On the basis of the BAL findings the cystic fibrosis group was divided into those with (CF-I) and those without pulmonary inflammation (CF- NI). Levels of lipid hydroperoxide, total glutathione, and gamma- glutamyl transpeptidase (gamma-GT) were then measured in the BAL fluid. RESULTS: The concentrations of lipid hydroperoxide and gamma-GT in the epithelial lining fluid were significantly increased in the CF-I group compared with the control and CF-NI groups, each of which had similar values for these parameters (ratio of geometric means for CF-I group versus control for lipid hydroperoxide 5.4 (95% confidence interval (CI) 1.8 to 15.8) and for gamma-GT 5.2 (95% CI 1.4 to 19.4)). The glutathione concentration tended to be lower in the CF-I subjects but the difference did not reach statistical significance. CONCLUSIONS: These results demonstrate that the airways in patients with cystic fibrosis are exposed to increased oxidative stress which appears to be a consequence of pulmonary inflammation rather than part of the primary cystic fibrosis defect. The increase in gamma-GT in the CF-I group suggests a mechanism by which extracellular glutathione could be utilised by airway epithelial cells.


     

Education modifies the effect of apolipoprotein epsilon 4 on cognitive decline

OBJECTIVES: To assess the influence of education on the association between apolipoprotein E and cognitive change. DESIGN: Prospective cohort. PARTICIPANTS: HMO-based sample of 2168 non-demented community-dwelling elderly followed over 6 years. MEASUREMENTS: Generalized estimating equations were used with the difference between baseline and follow-up cognitive abilities screening instrument (CASI) as the outcome variable. RESULTS: At follow-up, 6% of the sample had a decline of 1.5 S.D. or greater on the CASI. Compared to individuals without an APOE4 allele, individuals with a single APOE4 allele did not have greater CASI decline. By contrast, individuals with two APOE4 alleles experienced greater decline in cognitive performance and the magnitude of that decline decreased as years of educational attainment increased. These relationships held after adjusting for age, gender, ethnicity, depression, diabetes, and history of vascular disease. CONCLUSION: Lower education was associated with steep 4-year cognitive decline for APOE4 homozygotes but not for APOE4 heterozygotes. Potentially modifiable host factors such as education could influence the association of high-risk genotypes and cognitive decline.     

Medical students' attitudes in a PBL curriculum: trust, altruism, and cynicism.

PURPOSE: Studies have shown that medical students become more cynical and less altruistic as they advance in training. However, these studies were conducted in traditional medical schools, and many used unvalidated tools. This study examined students' attitudes in a problem-based learning (PBL) curriculum using reliable and valid measures. METHOD: Medical students and PGY-1 residents at Mercer University School of Medicine in Macon, Georgia, completed Wrightsman's Philosophies of Human Natures Scale (PHNS) in 1999 and 2000. Chronbach's alpha assessed internal reliability among subscales, and test-retest reliability coefficients confirmed acceptable reliability. For 114 students who completed both surveys, changes in PHNS scores were analyzed, with particular attention to the subscales of trustworthiness, altruism, and cynicism. RESULTS: Students assessed at the beginning of their second year increased the extent to which they believed people are trustworthy and increased their beliefs in how altruistic people are. They also showed a significant decrease in cynicism. There was not a significant change in trustworthiness, altruism, or cynicism among the participants beyond first year. In general, female students held less cynical views about others and believed people to be more trustworthy. CONCLUSIONS: Contrary to prior reports, this study found that more advanced trainees were not more cynical or less altruistic than their more junior counterparts. Indeed, a significant and positive change of attitudes among the participants during their first year of medical school refuted earlier reports. Thus, results of earlier studies and the effect of a PBL curriculum on attitudes of medical students need to be re-examined.     

Projection neurons in the rat dorsolateral septal nucleus possess recurrent axon collaterals

Projection neurons in the rat dorsolateral septal nucleus (DLSN) were labeled intracellularly with horseradish peroxidase (HRP) in an in vitro slice preparation. The labeled neurons exhibited widespread 'isodendritic' type dendritic fields. Each of the neurons was identified as a projection neuron by the tracing of its main axon out of DLSN. The axons of these neurons gave rise to intrinsic collaterals which branched to form an extensive axon plexus which was confined to DLSN. These axon collaterals exhibited numerous en passant swellings suggestive of boutons. It is proposed that the recurrent axon collaterals of DLSN projection neurons may form an anatomical substrate for local inhibition within DLSN.     

AOP2 (antioxidant protein 2): structure and function of a unique thiol-specific antioxidant

The accumulation of reactive oxygen species (ROS) in response to extracellular signals or intracellular biochemical processes can be regulated by the coordinate action of many antioxidant proteins. Because moderate levels of ROS can act as intracellular messengers in many of these processes, this modulation is critical for the transduction of specific signals. The thiol-specific antioxidant (TSA) family is a highly conserved group of enzymes that can reduce hydroperoxides in the presence of a thiol-containing electron donor. AOP2 (antioxidant protein 2) is a newly described member that shows significant evolutionary conservation between many different organisms. The protein contains three motifs that are highly conserved within the TSA family, including a cysteine residue that is the active site of oxidation for this class of proteins. Although AOP2 possesses TSA activity, it has several unique characteristics, including the absence of a second cysteine residue that is conserved in all other TSA proteins, the presence of a unique carboxy-terminal domain, and a demonstrated phospholipase activity. Furthermore, AOP2 shows conservation of several amino acids important in dimer formation and active site configuration that are not found in the other family members. Together, these data strongly suggest that AOP2 is a novel thiol-dependent antioxidant that functions to scavenge particular hydroperoxides in the cell and mediate specific signals. There is also evidence supporting a role for AOP2 in certain disease processes including atherosclerosis. Further evaluation of this protein and its substrate specificity will likely shed light on its precise role in cellular oxidant defense, signal transduction and pathogenesis.