Can't say I am surprised by the warning. It may be that CIPH's business has hit a plateau in terms of new system orders. This is not the first sign that that aspect of the business is slowing; the first was this summer, and is why I bailed my friends and family out. I think most major biotechs and pharmas are using these systems and are waiting for further validation before buying more. Perhaps worth a small bet that all of the "pushed out" orders will materialize. Just tough to sustain big growth rates. However, the use of multiple types of chips in individual studies is becoming more common-place, and that should drive consumables. Again, orders for the autoloader systems will also do that. Momentum should come again, but when, I don't know.
But we need news from the diagnostic front. What is happening with that canadian diagnostic company, and with Biosite? What of the company's internal program here?
Meanwhile, regarding a smaller market than AD . . .
>>Mol Biochem Parasitol. 2004 Feb;133(2):229-240.
Trypanosome apoptotic factor mediates apoptosis in human brain vascular endothelial cells.
Stiles JK, Whittaker J, Sarfo BY, Thompson WE, Powell MD, Bond VC.
Department of Microbiology, Biochemistry and Immunology, Morehouse School of Medicine, 720 Westview Dr. S.W., 30310-1495, Atlanta, GA, USA
Human African trypanosomiasis (HAT, sleeping sickness) is a devastating disease caused by infection with Trypanosoma brucei ssp. These hemoflagellates invade the central nervous system (CNS) and induce meningo-encephalitis, neuronal demyelination, blood-brain-barrier (BBB) dysfunction, peri-vascular infiltration, astrocytosis and apoptosis. The molecular basis of these manifestations is unclear. We previously reported T. brucei-induced apoptosis in cerebella and brain-stem nuclei in mice at peak parasitemia. Here, we identify and characterize a trypanosome apoptotic factor (TAF) expressed by T. brucei that mediates apoptosis in mouse-brain and human-brain vascular endothelial cells (HBVEC). Molecular, biochemical and apoptotic assays, coupled with surface enhanced laser desorption ionization (SELDI), and protein database analyses were utilized to show that TAF is a soluble, non-serum, parasite-derived, heat-labile protein that causes DNA laddering and apoptosis in HBVEC. Protein-chip assay analysis of the SELDI spectrum of infected mouse serum and procyclic culture supernatants revealed a single major peak at 8652.7Da. Further database analysis indicated that the TAF may be a procyclin or procyclin derivative. A synthetic 27 mer peptide (ProEP2-1), corresponding to a region common to EP procyclins (EP2-1), induced apoptosis in HBVEC and in cerebella of mice similar to that induced in T. brucei-infected mice. Western blot analysis utilizing an anti-procyclin monoclonal antibody (mAb) revealed that TAF is present in infected but not uninfected brain tissue lysates. Furthermore, this mAb blocked T. brucei- and ProEP2-1-induced apoptosis in HBVEC in vitro. We conclude that T. brucei TAF or its derivative(s) play a major role in the apoptosis associated with HAT pathology.<<
Cheers, Tuck |
