Digilent, a partner of Xilinx, makes eval boards for Xilinx FPGAs. I bought one and plan to hack some Verilog with it. My past experiments involved a board of my own design with a FPGA and a USB-enabled microcontroller. I successfully programmed the microcontroller over the USB cable to wiggle GPIO pins, which should have allowed me to program the FPGA via JTAG. But for some reason, JTAG programming of the FPGA didn't work. This time the JTAG programming pins will be wired directly to parallel port pins and there is a Linux library for programming them, so I should have better luck this time. Fewer unknowns and variables, more easily probed.
Attention (hey, shiny!) deficit break: I stumbled across a couple of very affordable logic analyzers. Amazing stuff, just the thing for debugging errant JTAG signals.
Some nice folks have released a PCI soft core under the LGPL. I'm not ready to tackle that yet, but hope to get there before too long. Speaking of PCI,
here is a nice FPGA board for a PCI bus slot from Enterpoint in the UK. They also have a PCI soft core but the licensing is a bit pricey for a hobbyist. I wonder if the LGPLed PCI core would work on the Enterpoint board.
Tinkering with various electronics and software things, and a bit of math and science in general.
Friday, March 12, 2010
Thursday, March 11, 2010
TA-65 safety claims
Earlier I posted about TA-65, a telomerase activator, which some hope could reverse some of the effects of aging. Amiya Sarkar is a doctor in Calcutta who writes a fascinating blog on physiology and physics. He and I have emailed back and forth for a couple years now, starting with a very cool idea he had for an inexpensive open-source electrocardiogram. (One of these days we really need to get that project back on track.)
Amiya expressed the concern that any telomerase activator could be viewed as a potential cancer risk. Cancerous cells use telomerase to support the unlimited replication that characterizes cancer. The folks at Sierra Sciences openly recognize this concern, and give reasons why they believe it's a red herring, on this webpage:
Amiya expressed the concern that any telomerase activator could be viewed as a potential cancer risk. Cancerous cells use telomerase to support the unlimited replication that characterizes cancer. The folks at Sierra Sciences openly recognize this concern, and give reasons why they believe it's a red herring, on this webpage:
In most cases (85–95%), cancers accomplish this indefinite cell division by turning on telomerase. For this reason, forcing telomerase to turn off throughout the body has been suggested as a cure for cancer, and there are several telomerase inhibitor drugs presently being tested in clinical trials.In support of this, they list several papers.
So, anti-aging scientists must be out of their minds to want to turn the telomerase gene on, right?
No! Although telomerase is necessary for cancers to extend their lifespan, telomerase does not cause cancer. This has been repeatedly demonstrated: at least seven assays for cancer have been performed on telomerase-positive human cells: the soft agar assay, the contact inhibition assay, the mouse xenograft assay, the karyotype assay, the serum inhibition assay, the gene expression assay, and the checkpoint analysis assay. All reported negative results...
Paradoxically, even though cells require telomerase to become dangerous cancers, turning on telomerase may actually prevent cancer. This is not just because the risk of chromosome rearrangements is reduced, but also because telomerase can extend the lifespan of our immune cells, improving their ability to seek out and destroy cancer cells.
- Jiang, X.-R. et al. Telomerase expression in human somatic cells does not induce changes associated with a transformed phenotype. Nature Genet., 21, 111–114 (1999)
- Morales, C.P., et. al. Absence of cancer-associated changes in human fibroblasts immortalized with telomerase. Nature Genet., 21, 115–118 (1999)
- Harley, C. B. Telomerase is not an oncogene. Oncogene 21(4): 494-502 (2002).
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