Interesting to consider the total complexity of that approach though.
An iterative fibonacci solution runs in linear time. Calculating the N'th fibonacci number requires O(N) serial operations.
A fully parallel, recursive solution without memoization requires that each value in the sequence is computed more than once. Consider the example of fib(4):
You can see, that if we run this in parallel, the value of fib(1) has to be calculated twice. As the tree of operation branches out, more and more duplicate calculations are required.
A quick google suggests that the time complexity of the recursive approach is O(2^N).
> An iterative fibonacci solution runs in linear time.
Absolutely nobody is under the impression that the naive parallel implementation of fib is actually useful code or the most efficient way to do it. You're missing the point if you're suggesting a different way to do it in the first place.
It's just something to use as a running example... like on the original article this whole thread is about.
Ok, but it's a bit odd that you kept reacting with incredulity at people not knowing that fib was THE parallel example to know, and then it turns out it's a poor example because synchronous fib with memoization (which is the way many people learn it in any early CS class, and which wouldn't be possible async) is so much faster.
I think maybe if there hadn't been such a vibe of "what, you don't know X?!?" then it would have just been an interesting fact to mention that parallelization demos often use fib, because it's an easy example to grok (though a confusing one if you already understand the faster method).
You don't need any specific instructions. The hex encoded double contains the final binary representation of the floating point number. So no conversion is required to load it, except maybe for swapping around bytes on some architectures. Conceptually:
double v;
memcpy(&v, "\x00\x00\x00\x00\x00\xe4\x94\x40", sizeof(v)); // LE
I wouldn't call 55% in 7 years "only". Especially given this statistic doesn't highlight type of housing and price groups (read: housing in the far outskirts pulling averages down, though COVID is changing this dynamic). Starter wages have barely risen since then, let alone kept up. And along with the crisis, one now gets far less mortgage for the same inflation-adjusted salary than in 2013, despite the lower rates.
Unless I'm misinterpreting the tweet, she suggests that a partial vaccination campaign will somehow lead to a higher rate of mutations?
As a non-biologist, it's not immediately obvious why that would be the case. What's the mechanism that increases the chance of mutations in vaccinated hosts?
Vaccination will create pressures selecting for variants that escape vaccine-generated antibodies.
The vaccine is ~95% effective. This means you're going to have a lot of people get infected still with the vaccine's antibodies present; any mutation that happens that causes escape from these antibodies will prolong disease and increase transmission, even if that mutation renders the virus a bit less fit in a non-vaccinated host.
> The vaccine is ~95% effective. This means you're going to have a lot of people get infected still with the vaccine's antibodies present; any mutation that happens that causes escape from these antibodies will prolong disease and increase transmission, even if that mutation renders the virus a bit less fit in a non-vaccinated host.
Is that an accurate summation of those who caught it after receiving the vaccine?
Seems like if 5% of virus strains circulating aren't affected by the vaccine, we're fucked anyway. That 5% will become 100% of what's circulating in the next year and will be ubiquitous?
If it's something like "5% of people don't respond to the vaccine to build antibodies at all," on the other hand, it's much rosier...
It's more like 5% of people don't build as many or as effective of antibodies to the vaccine spike protein, and then when infected are petri dishes providing selective pressure for variants to mutate that escape these antibodies and become dominant within their bodies (and, in turn, are more readily transmitted to vaccinated people around them).
Some of the 5% may just be unlucky people who got bigger doses of the virus/higher initial infectious dose, but the same logic applies.
It may be more than 5%, even; the vaccine likely does more to prevent symptomatic illness than infection.
It's hard to estimate what the probability of this happening is. It's certainly more likely when there's more illness circulating around-- e.g. if 1 million people with the vaccine become infected it's worse than if it's 10,000.
> It's more like 5% of people don't build as many or as effective of antibodies to the vaccine spike protein, and then are petri dishes providing selective pressure for viruses that escape these antibodies.
This seems very circular to me. If they don't build very effective antibodies, they shouldn't be putting much selective pressure on the virus, because if they did, they'd be more effective in the first place.
I suppose it depends on how exactly "effective" plays out here, as well as how easy it is for the virus to mutate significantly but stay as contagious as it is, but if we get unlucky it seems like just a question of time for it to get bad. Given Jan-Mar 2019, I have little faith that the US would ever be in a position to fully eradicate even a small remaining bit, and it would instead fester and mutate in this scenario until exploding again.
> This seems very circular to me. If they don't build very effective antibodies, they shouldn't be putting much selective pressure on the virus, because if they did, they'd be more effective in the first place.
Just to follow up / argue from another angle. It's believed to be likely that the "new" UK variant likely emerged in an immunocompromised individual. This results in A) -some- immune response, and B) prolonged infection where the virus is under evolutionary pressure to escape that immune response / original antibodies.
Someone who doesn't mount a strong response to the vaccine is a very similar case.
Not really, because they can still mount a strong response from the infection. The immune system is a lot more than just antibodies.
Even a weak response to the vaccine can activate bound antibody responses during challenge, which means the immune system is activated much faster and even though there is still infection it is much shorter, leaving less of a chance for the virus to mutate.
Even a partial response from a vaccine suppresses the virus and (usually) reduces the risk of transmission. At the same time, it creates a window where the virus is under selective pressure to escape some of the immune response from the vaccine's effects. Individuals who have smaller/partial responses to the vaccine are more likely to have this happen.
That is all I'm saying, and I don't think it's really that controversial. I'm not trying to make a robust immunological argument. I don't think it's inevitable, but it's another reason to reduce transmission. We already have the UK variant, which many have suggested is better at immune escape due to perhaps evolving during a long infection in an immunocompromised individual.
Selective responses against the vaccine are only selected for if those pressures persist during replication. It's not enough to have that pressure at the very beginning, it needs to persist all the way. This isn't really the case for a vaccine.
In other words, by the time the virus is replicating inside of you, it doesn't really have much pressure to evolve to evade those other facets of vaccine immunity, because doing so would probably hurt it.
The UK variant isn't better at evading the immune system from what we know. It's simply more infectious in general.
> Selective responses against the vaccine are only selected for if those pressures persist during replication. It's not enough to have that pressure at the very beginning, it needs to persist all the way. This isn't really the case for a vaccine.
I disagree. You have the weak vaccine response the entire duration of infection applying selective pressure. What you say seems to disagree with the consensus of the literature, e.g.
> The UK variant isn't better at evading the immune system from what we know. It's simply more infectious in general.
The mutations have been broadly described as "immune escape mutations" and are thought to have emerged from pressure to escape low numbers of existing sterilizing antibodies within the host, e.g.
"The unusually high number of spike protein mutations, other genomic properties of the variant, and the high
sequencing coverage in the UK suggest that the variant has not emerged through gradual accumulation of mutations
in the UK. It is also unlikely that the variant could have arisen through selection pressure from ongoing vaccination
programmes as the observed increase does not match the timing of such activities.
One possible explanation for the emergence of the variant is prolonged SARS-CoV-2 infection in a single patient,
potentially with reduced immunocompetence, similar to what has previously been described [17,18]. Such prolonged
infection can lead to accumulation of immune escape mutations at an elevated rate"
The article you linked first assumes only one or two antibodies.
As I said before, there is some pressure for antibodies, but the immune system is way more than that, and people can clear infections very effectively without any antibodies at all.
As for your other link, it's important to know that this a preliminary article that, on those subjects, gives ideas without data. Further research has shown that this variant does not seem to increase disease severity, and instead is just more infectious, as the spike protein evolved for higher binding affinity.
> The article you linked first assumes only one or two antibodies.
Assumes only a couple of neutralizing antibodies, which is fair for the vaccine candidates-- immune assays of Moderna's vaccine show two typical antibody binding sites against the RBD that are strongly neutralizing. I haven't seen the ELISA data for Pfizer's vaccine.
Given that we've got several papers describing how immune escape variants of other viruses have emerged in the past... I'm curious why you don't think it's much of a risk here?
> As I said before, there is some pressure for antibodies, but the immune system is way more than that, and people can clear infections very effectively without any antibodies at all.
Of course. I'm not speculating that there's going to be some nasty variant that completely eludes our immune response. I'm saying that it is likely-- and the consensus opinion-- that there is a real risk that the virus mutates to render the vaccine less effective.
> Further research has shown that this variant does not seem to increase disease severity, and instead is just more infectious, as the spike protein evolved for higher binding affinity.
Some of the mutations slightly increase binding affinity. Other deletions look like their primary fitness advantage is immune escape. A missing stop-codon also increases mutation rates for a portion of the RBD, which implies we can expect quicker emergence of subvariants.
It's like you're having an argument I never was having: I have never said that this is likely to cause more severe disease. I am just saying that the virus will be under selective pressure to evade the vaccine-induced immune responses-- which is something I think everyone agrees. This is less likely to happen if there's less infection around and people get vaccinated quicker.
Even in the worst case, where such a variant evolves quickly-- I don't think we're that bad off. As you mention, there's other immune responses. Strong T cell mediated immunity will almost certainly be cross-reactive and strongly reduce the risk of severe illness. We'll have more time to adjust vaccines without mortality accruing as quickly. It is still something we'd prefer to avoid at all costs.
The point of the argument here, from my point of view, is this. In the one to three months between full vaccination of vulnerable individuals and drastically reduced R due to general vaccination, is a variant of the virus going to appear that will be able to effectively infect vaccinated people and spread enough for the pandemic to continue?
The answer to this is very probably no. There is a huge difference between the virus making the vaccine less effective eventually, the virus making the vaccine less effective within one to three months, and the virus making the vaccine sufficiently less effective that it can sustain an epidemic among vaccinated individuals. The second is not very likely at all, because for it to happen a variant of the virus would have to mutate, and outcompete the dominant variant, that has a spike protein sufficiently different that it can keep R>1 among vaccinated individuals.
For this, the virus would not only have to evade antibody response sufficiently for there to not be sterilizing immunity, but it would have to do evade the much swifter and effective non-serological immune response enough to stay infectious.
All of this would have to happen in a subset of the population that has a 20x lower chance of being infected and even when that happens, the infection would be much shorter with most of it with completely different evolutionary pressures.
In one to three months.
It would also have to compete effectively against other variants in the non-vaccinated population while it is doing so, because non-vaccinated people are by very far the dominant infection vector. So it would have to evolve this not only in vaccinated, but also non-vaccinated patients, unless you believe that these extensive mutations will happen in one, vaccinated, patient, which is pretty much impossible.
> The point of the argument here, from my point of view, is this. In the one to three months between full vaccination of vulnerable individuals and drastically reduced R due to general vaccination,
Not a given. It's very likely, but we don't know how effective the vaccines will be in preventing transmission. Certainly there is past precedent for the opposite.
Also, there's likely to be pockets of population with poor vaccine penetration, so even if it confers sterilizing protection, we're likely to see endemic spread in these subpopulations continually challenging the vaccinated population.
> is a variant of the virus going to appear that will be able to effectively infect vaccinated people and spread enough for the pandemic to continue?
We see a hepatitis B vaccine escape variant every year or two, despite a much lower community disease burden. I don't think anyone can know how likely this is.
> All of this would have to happen in a subset of the population that has a 20x lower chance of being infected and even when that happens,
It's not very likely that the population has a 20x lower chance of being infected; the vaccine almost certainly does more to prevent symptomatic illness than any infection. They've shown a 20x lower chance of symptomatic illness. You're also leaving out the critical window before the first dose where protection (against symptomatic illness) slowly climbs over weeks to 70-80%.
> It would also have to compete effectively against other variants in the non-vaccinated population while it is doing so
Already the currently circulating variants are not equally neutralized by the vaccine. There's going to be immediate pressure making the variants that are least impeded more prevalent.
> unless you believe that these extensive mutations will happen in one, vaccinated, patient, which is pretty much impossible.
Again, the most likely scenario for the emergence for the UK variant is prolonged infection in one person with a low immune response. People like this are well represented in the groups we're immunizing first, too.
These things aren't mutually exclusive, though: you start off by favoring the current variants that the vaccine is least effective against. Then, you have ongoing evolution in vaccinated individuals with lower responses. Then the favored variants become endemic, circulating mostly in subpopulations with lower vaccine coverage and occasionally finding vaccinated people who are more susceptible.
How quickly it all happens depends upon total disease burden. I agree we will probably not get a worst-case escape variant in the first few months of the vaccination campaign, but I think we'll probably see some adaptation towards escape and lowered efficacy. Indeed, you don't even need mutation for that: just preferential selection for existing variants with lower vaccine efficacy.
No one's done the assays on the UK variant yet, but I will not be surprised if the current vaccines are somewhat less effective against it.
If the disease remains endemic with relatively high levels of circulation, variants that escape the current vaccines will be all but certain in the long term.
>We see a hepatitis B vaccine escape variant every year or two, despite a much lower community disease burden. I don't think anyone can know how likely this is.
Hepatitis B is a disease that lasts much, much longer than COVID-19, which exponentially increases the likelihood of such an event. Moreso, Hepatitis B immunity from vaccines is often very weak due to a lot of people not getting booster shots in adulthood.
>It's not very likely that the population has a 20x lower chance of being infected; the vaccine almost certainly does more to prevent symptomatic illness than any infection. They've shown a 20x lower chance of symptomatic illness. You're also leaving out the critical window before the first dose where protection (against symptomatic illness) slowly climbs over weeks to 70-80%.
Vaccines have been trialled using not symptomatic illness, but actually PCR tests for immunity, and found over 90% immunity with symptoms||viralRNA as a standard. So no, it's actually around 10-20x less likely to have infection, too. For things like severe ilness, it's more like 99-100%.
>It's not very likely that the population has a 20x lower chance of being infected; the vaccine almost certainly does more to prevent symptomatic illness than any infection. They've shown a 20x lower chance of symptomatic illness. You're also leaving out the critical window before the first dose where protection (against symptomatic illness) slowly climbs over weeks to 70-80%.
During this window if the individual is vaccinated before antibodies show up there is very little pressure to evolve resistance against them.
>Again, the most likely scenario for the emergence for the UK variant is prolonged infection in one person with a low immune response. People like this are well represented in the groups we're immunizing first, too.
Given the fact that we have seen zero severe illness in even very old people with many vaccines, this is even less likely than for a non-vaccinated but immunocompromised person, for which this scale of mutation didn't even happen yet, 1 year in. And by the way, the hypothesis - which is as of yet unconfirmed and whose certainty became lower after similar mutations were found in South Africa - is that this process happened in an unvaccinated immunocompromised individual during a month+ infection period. If the same individual was vaccinated, this would have been impossible, and we haven't seen this kind of illness in any vaccinated individuals.
>These things aren't mutually exclusive, though: you start off by favoring the current variants that the vaccine is least effective against. Then, you have ongoing evolution in vaccinated individuals with lower responses. Then the favored variants become endemic, circulating mostly in subpopulations with lower vaccine coverage and occasionally finding vaccinated people who are more susceptible.
Even for those, the vaccine is still incredibly efficacious. The differences IIRC are barely statistically significant. If you have a source for more significant variations I'd love to see it.
Crucially though, in the scenario you are suggesting where the virus is spreading in non-vaccinated populations, that the actual strain to acquire enough changes to become effective against vaccinated individuals absolutely needs to outcompete other strains, which isn't likely. This is because even if the virus were to infect one of the few vaccinated but less protected individuals, which would in this case probably be under 1% of infections, those mutations need not be a hindrance in the 99% of infections which won't be of less protected individuals that have more than benign infections in populations with low vaccination rates.
It's possible that this happens, eventually - think years. Not in the 1-3 months period we're talking about. The result is that it doesn't make sense to vaccinate 20-40 year olds in priority or to sell the vaccine on the free market, at all.
> Vaccines have been trialled using not symptomatic illness, but actually PCR tests for immunity, and found over 90% immunity with symptoms||viralRNA as a standard. So no, it's actually around 10-20x less likely to have infection, too. For things like severe ilness, it's more like 99-100%.
The only vaccine I'm aware of that had weekly PCR surveillance was the Oxford/AstraZeneca vaccine, which showed an efficacy of 57% against a positive swab (95% CI -- 41% to 66%; 95% CI efficacy against asymptomatic illness -17.2% to 54.9%). If you know another one that showed 90%+, please cite! Both the Moderna and Pfizer trials relied upon symptomatic illness (symptoms + PCR confirmation) as an outcome measure.
> During this window if the individual is vaccinated before antibodies show up there is very little pressure to evolve resistance against them.
No, but you can get a infection that shows up as antibody response is ramping. Neither infection and vaccine response are nice clean instantaneous, atomic events.
> Given the fact that we have seen zero severe illness in even very old people with many vaccines
You have to consider the statistical power of the study. In the very old people (75+), you're talking about 0 vs. 5 cases (symptomatic) in the Moderna study, for instance, with unknown impact on any symptomatic infections. You seem to be concluding an awful lot based on 0 vs 5 symptomatic cases in a short study period for what the outcome will be across a population of 18 million people in the US.
> If the same individual was vaccinated, this would have been impossible
Why? We've seen it happen in the wild with COVID (long illness times and failed immune clearance), and we've seen it with existing vaccines in other illnesses. "Impossible" is a very stronk word.
> Even for those, the vaccine is still incredibly efficacious. The differences IIRC are barely statistically significant. If you have a source for more significant variations I'd love to see it.
We don't know the efficacy for subvariants. We have nowhere near enough n. We do know that even during the phase 2 trial, there are serum neutralization titers for variants that the error bars do not overlap for, and the MLEs are an order of magnitude apart.
> It's possible that this happens, eventually - think years. Not in the 1-3 months period we're talking about.
First, it's more like a 6 month period, and longer when we consider the entire world.
> The result is that it doesn't make sense to vaccinate 20-40 year olds in priority or to sell the vaccine on the free market, at all.
Which, I understand, are things the original article advocated for, but I never did-- indeed I mocked it in other comments e.g. here https://news.ycombinator.com/item?id=25609607https://news.ycombinator.com/item?id=25609600 and in a comment on the original article. So really, come on. Argue with what I'm saying, not the make-believe argument you'd like to have.
The epidemiological and immunological communities consider it a risk, and I've shared papers. Here's what widely-followed Derek Lowe has to say:
"The good news continues to be that none of the mutations studied so far in the general population seem to be able to evade the antibodies raised by the current vaccines. That doesn’t mean that it can’t happen – and as we start putting selection pressure on the virus by vaccinating people we’ll have to keep a close eye out for anything like that developing. But then we have to consider transmission. If an antibody-evading form of the virus also becomes harder to catch, well, it’s going to be less of a worry. But if we were to start doing a better job at not spreading the virus in general, that would be sort of nice, because that would reduce the chance that any nasty mutated forms get any kind of traction in general. If some sort of supervirus mutation occurs in a single patient who doesn’t then get close enough to other people for it to spread, then it’s a tree falling in a forest that doesn’t make much of a sound."
"It’s all a race between several different factors. But here in the US we have so many people infected (and so much transmission going on) that frankly we’re making ourselves vulnerable to any more dangerous mutations that might crop up. In fact, if something like that were to emerge, the odds are better that it would do so here, from what I can see. We’re giving the virus every opportunity to reproduce and for the subsequent viral variations to then go out and try their luck infecting lots of other people. Vaccinating enough people quickly enough would interrupt these processes, and so would doing the sorts of public health measures that we’ve all been hearing about for months. But the first is going to depend on vaccine supplies, logistics, and public acceptance, and the second, well, look around you, si monumentum requiris."
> This seems very circular to me. If they don't build very effective antibodies, they shouldn't be putting much selective pressure on the virus, because if they did, they'd be more effective in the first place.
If a normal person generates a dozen types of antibodies to the vaccine's spike protein, and a couple types are strongly sterilizing...
And you happen to have an immune response where you generate 8/12 of these, and only one of the strongly sterilizing variant, and you are more prone to become infected as a result...
Then, once infected, the virus will be under selective pressure during your illness to escape some of those 8 antibodies. In turn, whomever you spread it to will have a harder time.
> Maybe multiple vaccines mitigates this a bit...
Maybe. But the portion of the spike protein they're expressing and the resulting antibody profiles look very similar.
> Given Jan-Mar 2019, I have little faith that the US would ever be in a position to fully eradicate even a small remaining bit, and it would instead fester and mutate in this scenario until exploding again.
Yes, but one silver lining is that there would still be some immunity / cross-reactivity / t cell mediated immunity, etc. People would still be less likely to have severe illness, I believe.
It's a lot more complex than that. Immune responses are a lot more complex than antibodies. People can actually get rid of an infection before they have a lot of antibodies.
The virus in this case would have to evolve in your body to escape not just 4-6 of the 12 antibodies, but most of them, otherwise it still won't be able to cause productive infections before it starts getting neutralized and the immune system detecting neutralized viruses mounts a stronger response.
Yes. I know immunology is way more complicated than I understand, and that I'm oversimplifying even from my level of understanding. There's all kinds of immune responses we're interested in here.
However, sterilizing antibodies are most interesting because they are the strongest factor in preventing transmission.
People with weak immune responses of various kinds can be expected to have more infections and to be infected for longer times, and they provide selective pressure to evade the remaining mechanisms.
Does the chance of seeing a vaccine-defeating mutation increase after injecting parts of the population with a less-effective vaccine (compared to the baseline scenario of no vaccinations at all)? What mechanism is responsible for that?
The answer is only obvious to me if both the original virus variant and the mutation compete for some kind of shared resource. But that shouldn't be the case here, right?
The original virus and the mutation compete for survival in a host body with a partially effective vaccination.
If you generate only a subset of the typical complement of antibodies that a vaccinated individual does, and are less protected and become infected as a result... then any virus variants that emerge within your body that escape any of your antibodies will have a fitness advantage. In turn, that virus will have an advantage spreading to other vaccinated individuals, too.
It is a low probability event in each individual, but if you generate enough individuals like this and infect them all, it's sure to happen eventually. We can't really estimate what the probability of this happening is, but it's certainly less likely if the efficacy is high and there's less disease circulating.
They aren’t. Also, it doesn’t seem to make sense to use only French examples in midst of English written text. I don’t think its a major problem of course and main project page contains English examples, I just found that funny.
Most CSV files do not follow this standard of course. But you could normalize all CSV files to RFC4180 (or any other consistent format) as the first step of your processing pipeline.
The issue with encountering CSV in the wild is that everybody who appreciates standards and interoperability ditched it a long time ago. If you are consuming CSV files in the wild, you can be sure that whoever is supplying them to you is using horrible tools to create them and will be unwilling or unable to address issues you find in them.
> The issue with encountering CSV in the wild is that everybody who appreciates standards and interoperability ditched it a long time ago.
I worked on a team that used CSV somewhat extensively. For the data we generated, it was RFC complaint. It's pretty trivial to get RFC-compliant CSVs, too; most languages have a library — ours was in the standard library, too.
We also had a ("terrible", as we joked) idea to create a subset of CSV that would contain typing information in a required header row. (We never did it, and it is a bad idea.)
> If you are consuming CSV files in the wild, you can be sure that whoever is supplying them to you is using horrible tools to create them and will be unwilling or unable to address issues you find in them.
…but this is absolutely true. We also consumed CSVs from external sources and contractors, and this was an absolute drain on our productivity. I've also worked with engineers of this caliber, and changing CSV wouldn't change the terrible output. I've seen folks approach eMail, HTTP with a cavalier "oh, it's a trivial text format, I don't need a library!" attitude, and inevitably get it wrong. Pointing out the flaws in their implementation and that a library would fulfill their use-case just fine is just met with more hacks (not fixes) to try to further munge the output into shape. It is decidedly not software engineering. I've seen this even with JSON.
But yeah, even with RFC standard CSV, you shouldn't be parsing it with awk. It is the wrong tool.
I generally went for turning them into either tab-separated files or used the ASCII codes for record separator and its brethren depending on the job. I never wanted to touch CSV again after parsing it once.
But if you’re writing code to normalize before sending to awk, why not just process in the normalization program instead of using awk’s bizarre syntax?
Depends on what you're using to normalize I suppose. Maybe that's Awk too! Maybe Awk is easier for exploration when the data is already clean but you have to write some parsing layer in Java or something and that's not conducive to one-liner exploration.
Some (maybe only slightly related or relevant) background:
In Germany, there is a pretty serious problem with dangerous driving and street racing: In the last ten or so years, there has been long string of downtown races that have killed numerous innocent bystanders in all major German cities.
This went so far that recently the German law has been changed and killing somebody while participating in a street race is now treated as "first degree murder". This year, the first conviction under this law was upheld by the German "supreme court". Still, street racing is on the rise.
Now, the uncomfortable truth is that the demographics of the offenders skew towards young German men that do not consider themselves to be culturally German or even European.
I am not trying to enter a debate on the how much value different cultures place on life.
What I am trying to do is to point out that when you consider how the human mind works, it is almost inevitable that these issues are starting to appear to be interlinked. What you have here is a very hot debate on road safety, which is already a topic that is very emotionally charged for a lot of people. Considering that there does actually seem to be a cultural correlation, it is somewhat predictable, if sad, that the public debate around here is now slowly starting to turn into an cultural/ethnic argument.
My personal opinion is that we need a massive crackdown on street racing and dangerous driving to prevent this topic from turning into yet another ethnic fault line in Germany.
I'm with you... Once in Thailand I was shocked that nobody on mopeds wears a helmet. My conclusion was that the people doesn't value their lives high enough. Sadly, I don't know how to put it differently. I don't know if this is culture, education, or what.
Yeah this thing is quite luxurious I’m not sure the authors realized this. Either that or this sponsored content. I know you’re not supposed to say that here, but it really felt like that. Seemed to be totally lacking any critical perspective. Couldn’t figure it out.
I also don’t get how these are supposed to be safe for 14 year olds and pedestrians.
...not to mention they focus on 14 year olds (like they're marketing to parents?). The idea that children should be driving around in vehicles that are the result of millions of man-hours of engineering and thousands of man-hours of labor (adults and likely other children in other countries in the supply chain)... well, that's intensely luxurious. End-of-days luxurious, in my opinion.
Wow. I'm a very grown adult, and I've never been on a vacation that cost $5k.
I've owned several cars, but the most expensive, shiny, sexy one cost $2.4k.
The idea of being a child having $10k spent on me just for summer fun is mind-blowing.
That feels luxurious to me.
I am under the impression that most parents who send their children to university in the US have to scrimp and save to pay for it. Like it's a really big deal. Sometimes only one child of two can go, because there isn't enough to pay for both. So it's not likely there's a lot of cash readily available for summer fun for each child in the years leading up to it.
Round that up to 10k€ and you can get a real car like a Hyundai i10. Meanwhile the Ami is filled with compromises everywhere. Strange windows and doors. Only two seats. Limited max speed.
In fairness, it had to be said that in Italy (fiat Punto, I guess you're Italian?) in the time where no license was required to drive 50cc and no helmet was mandatory it was pretty much a anarchy on streets.
I had to get a license at 16 to drive a 125cc (both theoretical and actual driving test) and many of my peers had taken a smaller test (theoretical only) at 14 to drive their 50cc.
I am satisfied that such exams are now mandatory and helmets are mandatory too.
Well you're right, I misremembered. Also I just looked it up and I think it was actually a Panda and not a Punto (only owned it for a short time around 2009 and it was already close to worthless when I bought it). Still, I think it doesn't change the point much: at 500kg you're closer to a small car than to the lightweight moped for which these exceptions were made...
In the same way, a Panda is a ton. Generally speaking, the lightest you're every going to find in cars is 800kg. I drove a Clio 1 Phase 1, that was 820kg. And let's be honest, it wasn't much more than an engine, seats, and a body. Even a Twizy, which is absolutely nothing is in the 475kg range. Engines are heavy.
But yes, you are closer to a car. if it's truly 500kg.
If these are like most electric cars, the batteries are in a flat compartment at the bottom of the chassis in a box design, giving incredible torsional rigidity and a very low centre of mass, so great cornering. They could be pretty safe for the occupants, even fanging it down a narrow European street. However, not so safe for pedestrians. I'm guessing these won't come with ABS or mm wave collision detection emergency brakes; it's one of those items that is cheap to manufacture and install, but the IP and testing is expensive.
Well you do need to pass a theoretical and practical exam to get the Age 14 moped license. And since automatic mopeds are around 200kg it's much less dangerous.
Unemployment in Germany didn't go up much because they reclassified the "unemployed" as "furloughed". The end result is the same though, recipients are living entirely off government assistance.
7.3 million germans are currently fourloughed. That is 21% of the workforce!
A major difference is between losing your job and keeping it, and businesses keeping their trained workforce. A lot of people work less instead of not at all. Come better days, it will be much easier to get back on track, hopefully.
I also feel like the project recommendations on Github have become really... stale.
At some point, the sidebar would display a new set of projects almost every time you hit refresh. Now, there hardly seems to be any rotation at all; I've been seeing the same projects for weeks. Somebody should check if the cron job for updating the list has crashed :)
An iterative fibonacci solution runs in linear time. Calculating the N'th fibonacci number requires O(N) serial operations.
A fully parallel, recursive solution without memoization requires that each value in the sequence is computed more than once. Consider the example of fib(4):
You can see, that if we run this in parallel, the value of fib(1) has to be calculated twice. As the tree of operation branches out, more and more duplicate calculations are required.A quick google suggests that the time complexity of the recursive approach is O(2^N).