Actually, as a tongue in cheek thing, most pilots refer to other pilots as "drivers", as in "What equipment do you drive?"
(Equipment is an informal industry term for the type of aircraft. (Type is a formal industry term for the make and model of aircraft (Type is based on certificate, not marketing make & model. (I always get lost with nested brackets.))))
(I'd rather reply to this than spend my mod points.)
Yes, long-haul commercial pilots are well paid. The problem is getting one of those jobs. There's a huge over supply of pilots. I'm a pilot myself and I'm very glad I never tried to make a living out of it.
Once you are in the company, your position is based not on skill or ability or how hard you work. It's based entirely on how senior you are. That in turn decides how much you get paid. Typically you start off in the right seat of turbo-prop commuters getting paid almost nothing. In fact, "self-sponsored" positions aren't unheard of. If you manage to stay with one company long enough that you're no longer part of the "last in, first out" cuts, then your job is safe but your salary still isn't that great. It's only when you start edging towards retirement that the pay starts to reflect the amount of training and seat-time you've put in while earning peanuts. If your company goes bankrupt or you switch companies, you may find yourself at the bottom again.
I like the way you think. I like the idea of going after the protein capsid in a catalytic manner. The problem is prions are very odd and rare things in themselves.
Technically speaking, a prion protein has to have a diseased-conformation with a lower thermodynamic energy minima than the the healthy version, otherwise it would require energy input, and thus be non-catalytic. Since most proteins are already folded to minimum energy, it's unlikely you can find a lower energy conformation that has catalytic activity for a HIV protein such as GP120 (or any other protein for that matter).
BTW, some researchers don't believe prions are really prions. They believe a small amount of genetic material may lay hidden. These researchers aren't crackpots and demonstrating the presence of DNA/RNA inside would explain a lot of weird stuff that can't be explained when it comes to prions.
(No worries about knowledge level. We're all here to learn, and I'm probably wrong about somethings.)
So, HIV goes latent, so there is effectively no virus. There is nothing for the drug to kill. When HIV goes back into the lytic cycle, you have to have the drug there to kill the virus, but you don't know when HIV goes back to lytic; it can be 2 weeks or 2 decades. You would have to keep the patient on the drug during this whole time or at least keep monitoring the patient and giving them the drug whenever it flares up.
(That's the simplified version. The more complicated version involves HIV never really going latent in the lymphoid organs, slowly infecting more and more CD4 cells, leading to AIDS. It could be that if this drug can get into the lymphoid tissues, you can reduce the viral load inside to make them long-term non-progressors, but that's more complicated.)
The RNA from HIV is retro-transcribed into DNA which is integrated into the host cell genome. It can become latent where it does not actively replicate virus. That's why HIV patients can live so long. Something then later triggers the lytic phase where the viral replication resumes, eventually leading to AIDS.
An agent that kills HIV will remove HIV from your system, but the latent virus DNA inside cells remain undetected and cannot be removed.
Even if you can kill the HIV virus, you still wouldn't have a cure.
HIV is a retrovirus. It becomes part of the infected cell's genome. Any agent that kills the virus can suppress symptoms/disease but not cure people who are already infected.
P.S. Please take off your tin-foil hat. The glare is quite annoying.
The 400x part is usually meaningless. It's just 40x objective and a 10x eye piece. What actually matters is the resolution.
Resolution can be improved by things like deconvolution as used in TFS, but that's still relatively low. You can easily start flirting with 7 digit figures when you use confocal microscopy and variations of laser excitation. See: http://en.wikipedia.org/wiki/Confocal_microscopy
As a biologist, I have no idea why they're making such a big deal of it being a $225,000 deconvolution microscope. It's cheap compared with what most institutions have. Besides which is the fact that the microscope used isn't interesting. Any high(ish) resolution fluorescent microscope would have given you the same data. The interesting part is this TRIM5a. Let's see what happens with recombinant TRIM5a in animal studies.
Instead of indicting everyone under the sun, let's do something to fix it instead of tossing people in jail. Many people contributed a little, like Murder on the Orient Express. In the end, the ultimate responsibility rested on the Pilot-in-Command who paid the price for his mistakes. Let's learn from it instead.
1. Revise procedures so that the PNF (Pilot-Not-Flying) visually confirms the flap & slats indicator instead of just reading it to the PF (Pilot Flying)
2. Design future systems such that the take-off config warning isn't on the same circuit breaker as the Total-Air-Temp sensor. (I'm a recreational pilot, not an engineer, so I don't know if there's a valid reason for them to be on the same circuit.) Also, have an EICAS warning when the take-off-config alarm is disabled.
3. Have the engineers remind the pilots / placard the cockpit to remind them that the take-off-config alarm is disabled.
4. Flapless take-off attempts leading to accidents are not a new thing to airplanes. Further training seems to be required, especially as the small aircraft we all initially learn in will take off without flaps.
1. "It is genetic mutations that in the vast majority of cases lead to twins." That's not what the article you link to says. Nor is it true. Genetic mutations do not lead to twins (at least not one that we have identified yet).
2. The genetic mutations in the article are precisely the somatic mutations that I pointed out in brackets in the original comment. Yes, there are minor differences, but they're remarkably rare given the size of the genome.
(Generally speaking. I'm sure someone can come up with something impossibly rare about somatic mutation in the early embryo stage or something, but this is generally correct.)
They used DNA because RNA is not suitable here. RNA is highly unstable, even in the lab.
Remember that HIV is a RETROvirus. It retro-transcribes itself back into DNA (and thus allowing for genomic integration). So, in a way, HIV does have DNA.
As for the "cells" thing, this was told to Xinhua news agency, which means the conversation was likely in Chinese, and somewhere things got lost in translation.
Yes, I agree. You could even do RT-PCR for virus specific sequences if you want, but the cost per test will make a lot of these tests impractical for screening purposes.
I didn't see a journal article that corresponds to this clinical trial but I'd be interested to know if the use of this vaccine precludes later HIV testing.
For the non-biologists: vaccines are often based on exposing the body to a protein from the virus (but not the entire virus). In doing so, the body produces antibodies that recognize the protein. The next time the body sees the protein (i.e. when exposed to the actual virus), the body will be able to quickly destroy the virus particles before the person becomes infected.
However, a lot of tests for viral infection is based on the presence of the antibodies in blood. So, if the person has been immunized using the vaccine, the person will have those antibodies in blood, and it becomes difficult to tell whether the antibodies came as a result of vaccination or infection.
They probably had 50. (Well, more likely 100, with 1/2 in the placebo group.) One of the non-placebo patients dropped out of the study due to some exclusion criteria not related to the vaccine (such as getting hit by a car) and you end up with the 49. It could even be as simple as the patient having moved to another city. With any clinical trial, you're bound to lose some subjects to follow up.
Drug trials go through three phases, the first of which consists of a very small number of subjects. It's essentially the first time the drug is used on humans and to see it doesn't have immediate, obvious side effects not observed in animal trials. The 2nd and 3rd phases continue to monitor safety while attempting to determine the efficacy of the drug.
Keep in mind, that a lot of the recalled drugs, such as the COX2 inhibitors like Vioxx, don't show negative side effects until your trial goes into hundreds or thousands of subjects. And even then, the drugs are continually monitored after their release to look for effects that might be present only in 0.1% even or 0.001% of the population
Oh god the horrors of orgo-chem. I nearly failed that. In fact, I still know next to nothing about it, but look at me! I'm doing my Masters in Microbiology. And no, I've never, ever had to synthesize my own organic molecules, and I don't deal with the metabolism of microbes. I do mainly molecular microbiology and pathogenesis, so lucky for me I guess. Is it too late to change your mind and talk you back into doing biology?
Slashdot Mirror
i think they are called "pilots" actually.
Actually, as a tongue in cheek thing, most pilots refer to other pilots as "drivers", as in "What equipment do you drive?"
(Equipment is an informal industry term for the type of aircraft. (Type is a formal industry term for the make and model of aircraft (Type is based on certificate, not marketing make & model. (I always get lost with nested brackets.))))
As you say citation needed, but I'd be interested to know what the median salary is, not the average.
(I'd rather reply to this than spend my mod points.)
Yes, long-haul commercial pilots are well paid. The problem is getting one of those jobs. There's a huge over supply of pilots. I'm a pilot myself and I'm very glad I never tried to make a living out of it.
Once you are in the company, your position is based not on skill or ability or how hard you work. It's based entirely on how senior you are. That in turn decides how much you get paid. Typically you start off in the right seat of turbo-prop commuters getting paid almost nothing. In fact, "self-sponsored" positions aren't unheard of. If you manage to stay with one company long enough that you're no longer part of the "last in, first out" cuts, then your job is safe but your salary still isn't that great. It's only when you start edging towards retirement that the pay starts to reflect the amount of training and seat-time you've put in while earning peanuts. If your company goes bankrupt or you switch companies, you may find yourself at the bottom again.
I like the way you think. I like the idea of going after the protein capsid in a catalytic manner. The problem is prions are very odd and rare things in themselves.
Technically speaking, a prion protein has to have a diseased-conformation with a lower thermodynamic energy minima than the the healthy version, otherwise it would require energy input, and thus be non-catalytic. Since most proteins are already folded to minimum energy, it's unlikely you can find a lower energy conformation that has catalytic activity for a HIV protein such as GP120 (or any other protein for that matter).
BTW, some researchers don't believe prions are really prions. They believe a small amount of genetic material may lay hidden. These researchers aren't crackpots and demonstrating the presence of DNA/RNA inside would explain a lot of weird stuff that can't be explained when it comes to prions.
(No worries about knowledge level. We're all here to learn, and I'm probably wrong about somethings.)
So, HIV goes latent, so there is effectively no virus. There is nothing for the drug to kill. When HIV goes back into the lytic cycle, you have to have the drug there to kill the virus, but you don't know when HIV goes back to lytic; it can be 2 weeks or 2 decades. You would have to keep the patient on the drug during this whole time or at least keep monitoring the patient and giving them the drug whenever it flares up.
(That's the simplified version. The more complicated version involves HIV never really going latent in the lymphoid organs, slowly infecting more and more CD4 cells, leading to AIDS. It could be that if this drug can get into the lymphoid tissues, you can reduce the viral load inside to make them long-term non-progressors, but that's more complicated.)
The RNA from HIV is retro-transcribed into DNA which is integrated into the host cell genome. It can become latent where it does not actively replicate virus. That's why HIV patients can live so long. Something then later triggers the lytic phase where the viral replication resumes, eventually leading to AIDS.
An agent that kills HIV will remove HIV from your system, but the latent virus DNA inside cells remain undetected and cannot be removed.
Even if you can kill the HIV virus, you still wouldn't have a cure.
HIV is a retrovirus. It becomes part of the infected cell's genome. Any agent that kills the virus can suppress symptoms/disease but not cure people who are already infected.
P.S. Please take off your tin-foil hat. The glare is quite annoying.
The 400x part is usually meaningless. It's just 40x objective and a 10x eye piece. What actually matters is the resolution.
Resolution can be improved by things like deconvolution as used in TFS, but that's still relatively low. You can easily start flirting with 7 digit figures when you use confocal microscopy and variations of laser excitation. See: http://en.wikipedia.org/wiki/Confocal_microscopy
As a biologist, I have no idea why they're making such a big deal of it being a $225,000 deconvolution microscope. It's cheap compared with what most institutions have. Besides which is the fact that the microscope used isn't interesting. Any high(ish) resolution fluorescent microscope would have given you the same data. The interesting part is this TRIM5a. Let's see what happens with recombinant TRIM5a in animal studies.
Life is kind of a crap game. The graphics are great but the gameplay sucks!
What kind of lawyer takes on a case like this?
Are they alive? Maybe he can sue them too!
Instead of indicting everyone under the sun, let's do something to fix it instead of tossing people in jail. Many people contributed a little, like Murder on the Orient Express. In the end, the ultimate responsibility rested on the Pilot-in-Command who paid the price for his mistakes. Let's learn from it instead.
1. Revise procedures so that the PNF (Pilot-Not-Flying) visually confirms the flap & slats indicator instead of just reading it to the PF (Pilot Flying)
2. Design future systems such that the take-off config warning isn't on the same circuit breaker as the Total-Air-Temp sensor. (I'm a recreational pilot, not an engineer, so I don't know if there's a valid reason for them to be on the same circuit.) Also, have an EICAS warning when the take-off-config alarm is disabled.
3. Have the engineers remind the pilots / placard the cockpit to remind them that the take-off-config alarm is disabled.
4. Flapless take-off attempts leading to accidents are not a new thing to airplanes. Further training seems to be required, especially as the small aircraft we all initially learn in will take off without flaps.
1. "It is genetic mutations that in the vast majority of cases lead to twins." That's not what the article you link to says. Nor is it true. Genetic mutations do not lead to twins (at least not one that we have identified yet).
2. The genetic mutations in the article are precisely the somatic mutations that I pointed out in brackets in the original comment. Yes, there are minor differences, but they're remarkably rare given the size of the genome.
Yes, an identical twin would have identical DNA.
(Generally speaking. I'm sure someone can come up with something impossibly rare about somatic mutation in the early embryo stage or something, but this is generally correct.)
You can prove anything with statistics.
No. You can prove anything with BAD statistics. Unfortunately, most statistics are bad.
-Scientist Statistician (enough to know that I don't know statistics)
They used DNA because RNA is not suitable here. RNA is highly unstable, even in the lab.
Remember that HIV is a RETROvirus. It retro-transcribes itself back into DNA (and thus allowing for genomic integration). So, in a way, HIV does have DNA.
As for the "cells" thing, this was told to Xinhua news agency, which means the conversation was likely in Chinese, and somewhere things got lost in translation.
Yes, I agree. You could even do RT-PCR for virus specific sequences if you want, but the cost per test will make a lot of these tests impractical for screening purposes.
Anybody who has taken an English course should have laughed at the (wording of the) claim that what I said:
"to see it doesn't have immediate, obvious side effects not observed in animal trials"
to be equal to what he said:
"to prove that a drug is safe"
Thanks for stuffing those words in my mouth.
PS. I've taken both statistic and epidemiology and I'm a microbiologist.
I didn't see a journal article that corresponds to this clinical trial but I'd be interested to know if the use of this vaccine precludes later HIV testing.
For the non-biologists: vaccines are often based on exposing the body to a protein from the virus (but not the entire virus). In doing so, the body produces antibodies that recognize the protein. The next time the body sees the protein (i.e. when exposed to the actual virus), the body will be able to quickly destroy the virus particles before the person becomes infected.
However, a lot of tests for viral infection is based on the presence of the antibodies in blood. So, if the person has been immunized using the vaccine, the person will have those antibodies in blood, and it becomes difficult to tell whether the antibodies came as a result of vaccination or infection.
Since you're so sure, do you mind if I jab you this needle?
No? Thought so.
They probably had 50. (Well, more likely 100, with 1/2 in the placebo group.) One of the non-placebo patients dropped out of the study due to some exclusion criteria not related to the vaccine (such as getting hit by a car) and you end up with the 49. It could even be as simple as the patient having moved to another city. With any clinical trial, you're bound to lose some subjects to follow up.
That's why this is a Phase I trial.
Drug trials go through three phases, the first of which consists of a very small number of subjects. It's essentially the first time the drug is used on humans and to see it doesn't have immediate, obvious side effects not observed in animal trials. The 2nd and 3rd phases continue to monitor safety while attempting to determine the efficacy of the drug.
Keep in mind, that a lot of the recalled drugs, such as the COX2 inhibitors like Vioxx, don't show negative side effects until your trial goes into hundreds or thousands of subjects. And even then, the drugs are continually monitored after their release to look for effects that might be present only in 0.1% even or 0.001% of the population
Oh god the horrors of orgo-chem. I nearly failed that. In fact, I still know next to nothing about it, but look at me! I'm doing my Masters in Microbiology. And no, I've never, ever had to synthesize my own organic molecules, and I don't deal with the metabolism of microbes. I do mainly molecular microbiology and pathogenesis, so lucky for me I guess. Is it too late to change your mind and talk you back into doing biology?
Yes, we are. We're omnivores. http://www.beyondveg.com/billings-t/comp-anat/comp -anat-1a.shtml