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The ability to isolate and culture liver progenitor cells could lead to new therapies for a variety of hepatic diseases. On page 1229, Lagasse et al. report that hematopoietic stem cells can differentiate into hepatocytes in vivo, and can be used to correct an animal model of severe liver disease, hereditary tyrosinemia type I. These findings contradict the conventional assumption that stem cells are restricted in development to a specific tissue type. The artwork on the cover shows hematopoietic stem cells (lower half of image) morphing into liver cells (top half of image).
The development of clinical investigators remains a thorny national problem. The National Institutes of Health has instituted new granting programs to support clinical research that have already stimulated 450 new applications for support; private foundations have also joined the effort.
Current therapies for Parkinson disease focus mainly on symptomatic relief, but gene therapy approaches may offer the prospect of halting or reversing the progress of the disease process itself. A recent study provides evidence that sustained delivery of glial cell line-derived neurotrophic factor to the nigrostriatal system provides neuroprotection and functional recovery in a primate model of Parkinson disease.
Proteins carrying (CAG)n repeat expansions are believed to cause neurological diseases such as Huntington Disease through their toxic gain-of-function. It may be, however, that loss of normal protein function can also contribute to pathogenesis.
Constitutive activation of Notch signaling in hematopoietic cells establishes an immortalized hematopoietic stem cell population capable of developing into both myeloid and lymphoid lineages. This system will be useful in determining Notch-mediated mechanisms of hematopoietic differentiation (pages 1278–1281).
The extraordinary plasticity of tissue stem cells, such as the ability of blood stem cells to differentiate into liver, would intrigue even the ancient alchemists. Recent discoveries also force us to rethink cell lineage relationships and expand the potential for cell-based therapies (pages 1229–1234).
The exact mechanism by which exfoliative toxin A (ETA), producedby Staphylococcal aureus, causes epidermal blistering has been elusive.A combined knowledge of the pathogenesis of pemphigus, cell adhesion mechanisms,and the amino acid sequence of ETA led to a simple answer (pages 1275–1277).
Signature tagged mutagenesis of N. meningitidis has identified genes that are required for septicemic infection. However, these high-tech studies also raise questions about how to choose the isolates of pathogens that will yield the most useful information (pages 1269–1274).
We are finally beginning to unlock the mechanisms underlying Ca2+-stimulated muscle differentiation and cytokine-mediated muscle wasting. Gaining a better understanding of the signaling pathways that regulate muscle development and decay improves the prospects for repairing aged, injured and diseased muscle.
Developing a modern vaccine that is able to duplicate the protective immunity observered after immunization with irradiated P. falciparum (Pf) sporozoites requires identification of antigenic Pf proteins. The identification of Pf Liver Stage Antigen-3 and its ability to protect chimpanzees against sporozoite challenge suggests we are headed in the right direction (pages 1258–1263).