and to add to my own post:

There are 17 diseases that the breath analyser detects, if each has a false positive rate of 10%, we have the following:
9999 * 17 = 169,983 false positives per 100,000 people per year.
It'd be like one of those kids' athletic competitions, everyone gets a prize.

I'm sorry, but a 10% false positive rate is terrible, especially for screening purposes.


For example:
Lets assume that a true diagnosis for disease X is at a rate of 10 in 100,000 people per year (fairly reasonable incidence rate for a lot of diseases).

Assuming there are no false negatives, the number of diagnoses that are made using the test will be:
Number of true positives + 10% of the true negatives

Number of true positives = 10
Number of true negatives = 99,990

# of diagnoses made = 10 + 0.10*99,990
= 10,009
The 9999 false positives would have to have further follow up tests and possibly erroneous treatment. This then of course puts a significant financial burden on the heathcare system.

They've tried it over: https://linux.slashdot.org/sto...
and over: https://linux.slashdot.org/sto...
and over again: https://linux.slashdot.org/sto...

and failed: https://linux.slashdot.org/sto...
and failed again: https://tech.slashdot.org/stor...

What's different about this time around?

I work in health informatics/epidemiology putting together and analysing large datasets for various eHealth projects (government, academia and private industry). The entire system of standardised data formats etc... that makes doctors' lives painful is, in many ways, supposed to make mine easier. Unfortunately nothing could be further from the truth.

Somewhere along the way the message has been lost, and from where I sit it's due to a lack of communication between clinicians, bean counters and IT people. Clinicians often have a rather arrogant view of the world. They tend to assume technology is easy and the only reason they can't do it is that they haven't been bothered yet. The don't treat IT professionals as being specialists in their own right. Rather, they treat them as service people, in much the same way as you would pay someone to mow your lawns (it's menial and I don't have the time blah blah...).

On the other hand IT professionals (the ones that do the UI stuff) rarely seem to understand or care why the data is being collected, just that it is. This of course leads them to make all sorts of assumptions that often turn out to be completely incorrect. One such system that I've seen had 2 options for gender, male and female. This system was supposed to be used in a urology department that often dealt with intersex people.

Finally we come to the bean counters, for some reason healthcare and healthcare IT seem to attract the worst of the worst PHBs which just compounds the entire problem.

Over half of long term non progressors go on to lose their non-progressing status. The median time to losing LTNP status is 11 years.

For further information see: Madec Y et al. Early control of HIV-1 infection in long-term nonprogressors followed since diagnosis in the ANRS SEROCO/HEMOCO cohort. J AIDS 50: 19-26, 2009.

There, I fixed that for you. It's rather unlikely that the subject wouldn't need some kind of treatment later on.

This is not true, vaccinated people would not test HIV positive. first line HIV screens look for certain kinds of antibodies, the particular antibody the article is referring is not one of those antibodies.

The initial HIV screen is a combined antibody/antigen assay, if that is positive a follow up screen, called a Western Blot, is done. The western blot looks for additional antibodies, such as: p24, gag, pol etc... If enough of these bands are positive then the person is considered HIV positive. There are cases where a western blot can return as indeterminate, in some cases (like a grp IV) the person is most likely positive but may not be. Interestingly, with the introduction of post exposure prophylaxis many people are now returning indeterminate western blots and never fully sero-convert despite being HIV positive. In these cases pro-viral DNA is used as a diagnosis.

I'm not sure if you're trolling or not, but I'll reply on the off chance you are just misinformed.

Plasomdium spp., the causal agent of malaria, lives in mosquitos and humans. It does not live anywhere else, not in the water or ground or air. It reproduces in humans and is spread to a mosquito when a person is bitten. The parasite is the re-transmitted back to a human when that mosquito bites again. The parasite does not require a certain temperature to grow to be infectious within the mosquito. The ONLY way the malaria parasite can be transmitted to a mosquito is via a human host. If no humans within a region have malaria, then there is no way for malaria transmission to occur, and thus no malaria.

Following on from this, if there is no malaria in humans, the only disease reservoir will be the mosquito. If there is 0 prevalence of malaria within a region for longer than the lifespan of a mosquito (typically ~50 days) the malaria parasite will be eliminated.

No, there is not a large pool of the malaria parasite in the thames valley. This is a stupid statement. Malaria doesn't lie dormant in the environment, waiting for the right conditions to appear. It can only survive in the host or vector. The only place it can lie 'dormant' is within the human host. Given there have been no cases of malaria transmission in England for a very long time we can safely say that there is no 'large pool of the malaria microbe'. Your statement that winters being too cold to allow mosquito and parasite to mix together clearly indicates you've got no clue what you're talking about. The reason that cold weather prevents malaria is that the adult mosquitos are dead, only the eggs are present (and malaria doesn't live in mosquito eggs). If the adults are dead there are no transmission events because there are no mosquitos around to bite.

He does spend his own money: http://www.gatesfoundation.org...

I wonder if this would be able to help musicians with focal dystonia (http://en.wikipedia.org/wiki/Focal_dystonia)

Wrong. The striatum (which governs procedural memory) is only indirectly affected in parkinson's. Parkinson's is caused by the death of dopamine producing cells in the substantia nigra which is the region that communicates with the striatum. The memory of these movements (such as playing a piano) is still there, but the ability to access them is not. One of the things that is noticeable about parkinson's patients is that many of the jerky movements and tics caused by the medication are often movements that would otherwise be normal in a different setting (some of the ones I've seen include: moving pieces on a chess board, dancing and writing on a blackboard).

The link in the article is short on details, however the recordings were played louder and the birds did not respond. (the full paper is available as a pre-print from proceedings B)

would you care to give a reference for p70 being used to create iPS (induced pluripotency)? As far as I am aware the genes typically used are oct-4, sox2, c-myc, nanog, lin28, klf4 and p53 (both p53 and c-myc are oncogenes, the rest are not) Interestingly a paper was published a few months ago which describes a method for transient expression of these genes. This eliminates (or at least greatly reduces) the risk of cancer arising from stem cell treatment as the expression of any oncogenes is only long enough to revert the cell back to a pluripotent state.