8/24/2007 - Factor CITED in Wilms tumor
Wilms' tumor, a childhood kidney cancer, is thought to result from the abnormal retention and failed maturation of embryonic kidney cells. Harold Lovvorn III, M.D., Mark de Caestecker, M.D., Ph.D., and colleagues have now added to the evidence that Wilms' tumors have an embryonic origin.
The investigators report in the July Neoplasia that a transcriptional regulator called CITED1 known from their previous studies to be expressed in the developing but not the mature kidney persists in both primary human and experimental rat Wilms' tumors. They also demonstrate that CITED1's cellular location changes to the nucleus in the tumors and that the level of CITED1 expression in primary human Wilms' tumors correlates with the stage of the disease. The findings establish CITED1 as a new marker of malignant Wilms' tumors and suggest that the factor may have a role in tumor initiation and progression.
Fish oil makes fatter, healthier mice
Fish oils, the source of cardioprotective omega-3 fatty acids, can lower plasma lipids and reduce the risk of heart disease. Scientists have speculated that white adipose tissue (WAT) the body's predominant type of fat might mediate fish oil's beneficial effects by regulating lipid storage and inflammation.
To investigate, Saraswathi Viswanathan, Ph.D., Alyssa Hasty, Ph.D., and colleagues fed LDL receptor-deficient mice a widely used animal model of atherosclerosis a diet supplemented with fish oil. They found that fish oil supplementation significantly increased lipid storage in WAT, as evidenced by increased total body fat and fat cell hypertrophy. Despite having more body fat than controls fed olive oil, fish oil-fed mice had reduced plasma lipids, improved WAT-specific inflammation and insulin sensitivity, and decreased atherosclerotic lesion area. The results, reported in the July Journal of Nutrition, suggest that although obesity is a risk factor for metabolic syndrome, proper storage of lipids within white fat may offer protection against elevation of plasma lipids and atherosclerosis.
Protecting patient privacy
Understanding the genetics of human disease will require the sharing of patient clinical and genetic information, often through large-scale DNA databanks. However, the potential for re-identification of anonymized patient biomedical data raises privacy concerns that often limit the amount of data that hospitals disclose.
In the July issue of Artificial Intelligence in Medicine, Bradley Malin, Ph.D., demonstrates a method by which patient anonymity can be protected in large shared databases. Malin describes several algorithms, using a novel patient protection model called k-unlinkability, that can be used to prevent the re-identification of seemingly anonymous DNA from the patients' patterns of hospital visits/discharges, or trails. He then evaluated the algorithms with patient data derived from publicly available hospital discharge databases. The findings demonstrate that, using these algorithms, significant quantities (around 95 percent) of sensitive patient DNA records can be disclosed without risking re-identification.
How about another round?
The rush from that first glass of booze often prompts a second. To get at the molecular mechanisms underlying alcohol's acute reinforcing actions, Danny Winder, Ph.D., and colleagues are examining how ethanol affects neurons in the ventral bed nucleus of the stria terminalis (vBNST), a brain area implicated in behavioral responses to ethanol.
The investigators, led by postdoctoral fellow Thomas Kash, Ph.D., report in Neuropsychopharmacology that ethanol reduces NMDA receptor-evoked excitatory currents in vBNST neurons, through a postsynaptic mechanism. They further demonstrate that the NR2B subunit of the NMDA receptor is required for ethanol inhibition and that this effect occurs in vBNST neurons that project to neurons in the ventral tegmental area, part of the brain's motivation and reward centers.
The findings provide both a potential mechanism and molecular target for the acute actions of alcohol in the vBNST and suggest that alcohol alters signaling in an important reward-regulating feedback loop.
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