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Transmissible spongiform encephalopathies are initiated by extracerebral exposure to the causative agent, and early prion replication occurs in lymphoid organs. In this issue Mabbott et al. (485) and Klein et al. (488) identify mechanisms of peripheral prion pathogenesis. In mice, depletion or deficiency of specific complement components or receptors protected against disease following peripheral infection. The cover shows vacuolation damage in the cerebral cortex of mice infected with scrapie (right), with a superimposed anatomical drawing of the brain (left).
Stem cells have traditionally been characterized as either embryonic (pluripotent) or organ-specific. Recent work suggests that the latter can "transdifferentiate" into other cell types, carrying significant implications for possible clinical use of these cells. Here the authors critically examine the existing data, and suggest standards for the evaluation of these and future studies.
At the start of 2001, the UK became the first to approve the creation and use of embryos for stem cell research. In response to a report by the country's Chief Medical Officer, Parliament condoned the decision last December. Because of the nature of this legislation, approval was also needed by the House of Lords which was granted in January. Although onlookers may assume that scientists in Britain are fully behind the decision, the subject elicits as much controversy within the UK biomedical research community as elsewhere. The following two Commentary articles, written by experts working in the field of reproductive research in London, illustrate this disunity.
Although angiogenic factors provide hope for patients with ischemic diseases, a whirlwind of controversy surrounds their purported involvement in development of atherosclerosis (pages 425–429).
The persistence of latently infected T cells is a major hurdle to eradication of HIV by antiviral therapy. It now seems that HIV latency can occur during normal T-cell differentiation in the thymus, and is regulated by the overall state of cellular gene transcription (pages 459–464).
The genetic basis of Fanconi anemia (FA) is mysterious and complex, as none of the five genes previously associated with the disorder have homology to genes encoding proteins of known function. The product of a sixth, newly-cloned FA-associated gene has been linked to BRCA1, and may finally offer some insight into the mechanism by which FA increases cancer susceptibility.
Acute myelogenous leukemias are caused by point mutations as well as several different types of chromosomal translocations, but little is known about how these genetic defects lead to disruptions in hematopoiesis and eventual leukemogenesis. Two recent studies suggest that the resulting mutant gene products can alter function of the transcription factor C/EBPα and tip the balance from differentiation toward cancer (pages 444–451).
Microarray analysis can be used to differentiate gene expression patterns between various types of tumors, including breast tumors caused by BRCA1 and BRCA2 mutations. But what must be done before this technology can be used in the clinic?
Two recent studies implicate the complement system in prion disease pathogenesis, suggesting that there are multiple, non-exclusive pathways of neuroinvasion (pages 485–487 & 488–492).
COX-2 is involved in prostaglandin synthesis and expressed throughout the nervous system, where it participates in pain sensitivity and in synaptic plasticity. Microsomal prostaglandin E synthase, expressed throughout the nervous system microvasculature, may be another important player in neural aspects of the inflammatory response.
Drug addiction is a major therapeutic challenge, as little is known about the changes in neural function that occur during its development. DNA microarray analysis has revealed a new component in the dopamine-receptor–signaling cascade that may contribute to the neural and behavioral plasticity associated with addiction.