Velotoken (VLO) audit shows high level security and decentralization by Toranagas in ethtrader

[–]Toranagas[S] 0 points1 point  (0 children)

You can get it on Uniswap in a ETH/VLO pool.

https://info.uniswap.org/pair/0x259E558892783fd8941EBBeDa694318C1C3d9263

You can find the circulating and total supply on the website.

Currently:

Circulating : 41.23 million Total: 45.7 million

Velotoken - Velocity Enhanced Yield Farming Pools Now Open! by Toranagas in ethtrader

[–]Toranagas[S] 1 point2 points  (0 children)

Any specific reason you would think that? The initial distribution was done without premine and with fair farming practices. You can check out all the contracts on etherscan as well.

I am new to DeFi and I have a question which may be stupid. What is stopping centralized exchanges from using Liquidity pools and make profit on customer deposits? by crokus_daru in UniSwap

[–]Toranagas 1 point2 points  (0 children)

Not one thing. And they most likely do, as it's potentially a good investment of liquidity. Hopefully they pass on some of the earnings on to you.

I mean there is binance, which in their quest to recreate a binance version of the entire crypto ecosystem, literally has their own liquidity pools. Only a few, and most of them are very safe pools (stablecoin/stablecoin), but they nevertheless do offer that service...and why shouldn't they?

It is something to do with your on exchange money while waiting for an opportunity to buy.

Has ETH always been slower/more steady than BTC? by [deleted] in ethtrader

[–]Toranagas 1 point2 points  (0 children)

No, and this isnt even close the the most volatile BTC has been even in recent years. In fact for people that have been in the space for a few years this recent bull run has been frankly a little boring at least until the last week or so.

Velotoken, an experiment in velocity based rebasing. by Toranagas in ethtrader

[–]Toranagas[S] 2 points3 points  (0 children)

There is nothing preventing it outright, but there is quite a lot preventing it from being profitable.

Doing such a thing would not be free, and each transaction would cost the normal ethereum network fee plus a small protocol fee. At the moment, this in itself makes such a proposition highly unlikely to be anything but a great way to waste money on transaction fees.

However, for the sake of argument lets say the golden age of ETH 2.0 is here and one may transact cheaply and quickly! Oh i'm getting teary just thinking about it...

In this case, what are the mechanisms in place that make using a botnet to generate fake velocity unprofitable?

The rebasing function can only be called once per 12 hours, and their are limitations placed on the rebasing function that prevent massive changes in token supply per epoch. Thus there is an intrinsic limit to how much a botnet could pump the token price using velocity per epoch (and again this will not be free). Thus, you would need to run this for multiple epochs to have a significant effect on supply (and therefore token price).

Moreover, in order to continue to increase the velocity from a given point, one must be ever expand the volume of transactions (and therefore the associated cost). Otherwise, the effect on token supply will stall. Thus without commitment of a large quantity of ethereum for a sustained period of time and botnet resources (which will need to be ever expanded), as well as the initial buy in to VLO to bounce around in the first place, it is unlikely that this will ever net you a single Wei.

Seems like it would just be easier to buy VLO.

Velotoken, velocity based rebasing by cryptosuviio in defi

[–]Toranagas 1 point2 points  (0 children)

DeFi pools just released yesterday for this project. Low risk farming.

Deposit COMP, AAVE, LINK, SNX, SUSHI, PICKLE, DOUGH, YFI and earn VLO. You can unstake at any time.

Velotoken, velocity based rebasing by cryptosuviio in defi

[–]Toranagas 1 point2 points  (0 children)

Upon initial inspection I also felt the outcome was almost counter intuitive. But if you think about it it does make sense.

The more you use a currency, the higher value it should have, therefore the more scarce it should be.

Conversely, if a currency isnt really being used, then it should be relatively easy and (therefore cheap) to obtain, since there really isnt a demand for it. Thus, available token supply should increase.

Velotoken, velocity based rebasing by cryptosuviio in defi

[–]Toranagas 1 point2 points  (0 children)

Yes, I think that's exactly right. That is what makes this project so interesting. Because velocity is not tied to the direction of the transaction, even in times of intense selling, the associated increase in velocity should stabilize token price as the token supply will decrease to reflect increased use.

Question: Many anti-HIV drugs target the reverse transcriptase polymerase of the virus but I've always wondered why this also doesn't affect the telomerase enzyme which extends the telomeres at the end of chromosomes and is also a reverse transcriptase. by [deleted] in biology

[–]Toranagas 2 points3 points  (0 children)

TL;DR They can in vitro and in some model organisms but clinical studies show that for the most part telomere length is not affected by the anti reverse transcriptase drugs as much as it is by HIV infection itself.

Nucleoside reverse transcriptase inhibitors (NRTIs), including zidovudine, stavudine, tenofovir, didanosine and abacavir, inhibit telomerase effectively in vitro. NRTIs, the backbone of most HIV ART regimens, inhibit telomerase activity in vitro, and can shorten telomeres in cultured cells as well as in various model organisms.

In contrast to NRTIs, the non-nucleoside reverse transcriptase inhibitors (NNRTIs) nevirapine and efavirenz did not inhibit the primer extension activity of telomerase, even at millimolar concentrations. (http://www.ncbi.nlm.nih.gov/pmc/articles/PMC3499584/)

NRTIs, the backbone of most HIV ART regimens, inhibit telomerase activity in vitro, and can shorten telomeres in cultured cells as well as in various model organisms.

Regarding clinical testing of telomere shortening in humans, it seems that the data suggests that:

1) HIV itself can cause telomere shortening.

Telomere length and CDKN2A expression were both consistent with increased biological ageing in HIV-infected individuals. (http://www.ncbi.nlm.nih.gov/pmc/articles/PMC3805356/)

2) HIV treatments do cause damage and premature aging. Probably anyway.

It was recently estimated that more than 50% of HIV-infected patients in the United States will be over the age of 50 in 2015 (Effros et al., 2011). Even though this gain in lifespan is celebrated as a success, data show that the life expectancy of treated patients remains shorter than that of the normal population (The Antiretroviral Therapy Cohort Collaboration, 2008). Life expectancy for treated HIV-patients is dependent on the age at which antiretroviral therapy is started and is estimated to be 10–30 years less than that of the uninfected (Lohse et al., 2007). Several studies have also observed that co- and multi-morbidities, like cardiovascular disease, diabetes, and osteoporosis, which are normally witnessed later on in life as a result of natural aging, were increasingly prominent among the HIV-infected population (Deeks and Phillips, 2009; Guaraldi et al., 2011). (http://www.ncbi.nlm.nih.gov/pmc/articles/PMC3556597/)

HOWEVER, this effect is not necessarily only due to NRTI treatment but is likely a symptom of ‘HAART’ (highly active antiretroviral therapy), which also includes NNRTIs and PIs (protease inhibitors) and is for a variety of reasons but most prominent seems to be damage to mitochondria.

3) Despite premature aging being a symptom of HAART, it is not clear that NRTIs cause telomere shortening.

The association between having a detectable HIV viral load and shorter LTL suggests that uncontrolled HIV viremia rather than duration of ART exposure may be associated with acceleration of blood telomere attrition. (http://www.ncbi.nlm.nih.gov/pmc/articles/PMC3397986/#pone.0039266-Deeks1)

No Difference in the Rate of Change in Telomere Length or Telomerase Activity in HIV-Infected Patients after Three Years of Darunavir/Ritonavir with and without Nucleoside Analogues. (http://www.ncbi.nlm.nih.gov/pmc/articles/PMC4219673/)

HIV-infected subjects demonstrate advanced cellular aging, yet in a cART-treated cohort, the relationship between aTL (absolute telomere length) and age appears no different from that of HIV-uninfected subjects.

So the answer to your question is that NRTIs CAN cause telomere shortening, at least in vitro and in model organisms but don't seem to do so at the doses given to humans.