3% == Citizens who *want* health insurance but are not covered. 86%==Number happy with what they've got (TIME August 10)
Admittedly off topic, but "happy with what they've got" is not a good metric for healthcare.If you are paying more for your care than you have to, getting more unnecessary or unproven (potentially harmful) procedures, getting less preventative care, and ending up with worse outcomes, then you are not getting a good deal. You may be happy with what you've got, but that does not mean that what you've got is good, especially when we have examples of countries spending less money for better outcomes while insuring everyone.
Notice I'm not arguing that we MUST do something about it, but stating that "being happy with it" is not a rational argument against trying to improve the system or even having to improve the system in order to ward off potentially disastrous consequences.
I call your metric the Bill Gates measure - paraphrased - "Everyone should be happy with 640K!"
Maybe it is in terms of global CO2 levels, but under a cap and trade system, this will turn an industry that might have to buy CO2-emission rights into one that could make money selling them!
Congrats! That's a great story - as an oncologist, I hang on to each one these I hear (my colleague likes to say that melanoma gives cancer a bad name). The treatment you went through almost certainly stimulated your immune system to fight your cancer. It is not clear if this is a specific effect, where you actually teach the immune system to attack your tumor, or simply a stimulatory effect that revs up the immune system to do a better job of attacking tumor cells that it already had some reaction to.
As you know, our only approved immune therapy for melanoma is interferon - a non-specific stimulator of immunity. There are few responders, but a small fraction (1-4%), are actually cured or disease free for years. The rest have little or no response and the side effects can be brutal or even fatal. The same goes for high dose interleukin-2 therapy for metastatic renal cell carcinoma - this treatment is usually started in an ICU setting.
The more specific cancer vaccines are always given with powerful adjuvants or co-stimulatory products. Provenge is a great example of this - some responders, but not clear what they are responding to. My Dad was in a clinical trial with a different prostate cancer vaccine and is a responder! In his case, he got the vaccine in highly immunogenic vectors - vaccinia (weak small pox, essentially) and fowlpox. This was followed by co-injection of GM-CSF - a chemotactic growth factor for a variety of antigen presenting cells. He isn't cured, but has stable disease. It's not clear if his immune system responded to the specific antigen in the vaccine or simply amplified whatever endogenous anti-tumor activity it already had brewing.
So - without bashing the achievement cited in the article - I suspect that this will not have anywhere near the impact the article claims. We certainly aren't going to be abandoning screening colonoscopy as the article suggests.
While I laud this development - we have had multiple form of immune therapy for cancer - including tumor vaccines, cancer antigen vaccines, immunostimulatory drugs, and anti-tolerance drugs for years now. There are some responders, but this field has generally been a disappointment. here's to hoping we eventually figure out how to harness this approach.
I came to agree with the toolittletoolate tag. I was seriously gearing up to buy a Kindle, but the broken-by-design and big-brother "features" that have now moved from theoretical to actual have convinced me to stay far away from this product.
I'll wait until the DRM issues have shaken out (as they have largely done with music) before considering a company-yoked product like this.
Sounds great! Seeing as how I work in an industry where we are capped at 80 hours in 6 days (we get one day off per week) averaged over a 4 week period, this seems awesome. At least we cap our maximum shift length at 30 hours, because otherwise, that would suck!
Luckily, I don't do anything critical - I just take care of you if you happen to come to my hospital.
Mod this up - this is the *KEY* argument that needs to be made in light of this work.
First - 8 of the unexpected mutations could not be found in leukemia cells from 187 other patients with AML. http://news.bbc.co.uk/2/hi/health/7706487.stm
This strongly suggests that these are "passenger" mutations that were acquired during the life of the hematopoietic stem cell that later underwent clonal expansion.
Many of the patients remaining normal stem cells probably carry a few insignificant mutations here or there, but each of these is represent at such low frequency, that they cannot be detected in the absence of clonal expansion.
Second - there is no external or functional validation. Take these genes, mutate them, and put them into in vitro or mouse models of leukemia to see if they have any effect. Heck, just start by proving that these mutations occur at a higher frequency in coding regions than in non-coding regions of the genome. Or even show that all of these genes are actually expressed in leukemic cells.
Finally - mutations are not the only way to disrupt gene expression. Genes can be methylated, amplified, deleted, and post-transcriptionally down regulated (by miRNA for example). The genetic disaster that caused AML in this patients may have had more to do with these types of events (as is the case with a related, pre-leukemic conditon known as MDS).
So this is fascinating use of amazing technology, but also a first pass at analyzing a very complex data set. Many more cancer genomes will come in short order and we'll get a better sense of what this means.
This is the killer app for this product. I work in a hospital - the reason we don't use PDA's or iPhones to interact with our patients' electronic records is that the screen is too small to see the necessary data and the interface is too slow for entering lengthy narrative information. Laptops or tablet PC's could do this, but they are too large to carry around in your pocket.
Enter the iPhone with this projector and handwriting or voice recognition. Total game changer in my field.
Seriously - I do genomics research in cancer. We use a variety of tests that generate reams of information. Most academic institutions develop their own overly complicated and highly specialized tools to look at this data. If Google is venturing into the realm of user accessible genetic information, they must be creating simple UI tools for the masses.
I would love to get in on that aspect of things - either as a consultant or beta-tester. A Google Earth like genome browser is at the top of my wish list.
ARE YOU LISTENING MR BRIN? If so, drop me an e-mail - seriously!
This is the key issue. You are not doing a home pregnancy test when you do a genome wide scan. The answer is not yes or no.
Even if you accept that disease risk is a) not all genetic and b) is an imperfect number, there will come new associations that can not currently predict. This will include new diseases, behavioral traits such as aggression, meekness, and intelligence.
Like the associations we know about know, the degree to which the genes matter will be uncertain. But, your information will already be out there, telling others a story you may not want told and can easily be misinterpreted.
How would you like to be fired from your post office job because the NSA learns you may not be very bright, may have aggressive tendencies, and your upcoming heart attacks are going to drain the USPS healthcare pension account?
If you add a bigger screen, upgrade the processor, double the RAM and quadruple the drive space it cost a bit more. But definitely worth the extra money!
It's chess on steroids - power-ups include invisible pieces, teaching powers, recruiting enemies. It is an incredibly rich game played head-to-head against others online.
Klinger you're right on the ball. I logged in to say exactly what you did.
Type II diabetes is a failure of insulin signalling at the target tissues (liver, fat, muscle). Some people, particularly those exposed to high levels of insulin over a prolonged period (think fat or refined sugar eaters), downregulate the way their tissues respond to insulin. This means they are less effective at clearing glucose from the blood. To compensate for the elevated glucose levels, the pancreas secretes more insulin. At some point, the pancreas can no longer secrete enough insulin to lower the blood sugar and diabetes is diagnosed. In fact, the disease process had been ongoing for months to years prior to the person having high blood-sugar levels. Since islet cell shut down in the pancreas is one mechanism by which insulin levels become insufficient, an inhibitor of PKCepsilon may prevent this form happening. The diagnostic criteria of elevated blood-sugar may then not be recahed and, in that sense, a case of diabetes prevented or delayed. The underlying insulin resistance syndrome will still persist, therefore this drug does not treat the ultimate cause of Type II diabetes.
As a pill, it would be a perfect drug company product. It would replace an injectable, need to be taken lifelong, used for a disease that is rapidly rising in incidence, and the drug would be patentable ($$$).
The caveat is that PKC is a fairly important kinase. Off-target side effects could be prohibitive to drug development.
I work at the Broad Institute on the MIT campus. In the lobby of our building there is a transected cyclinder (think half a burrito cut at a 45 degree angle) made up of seventy-six ~40" LCD screens. The video on them is contiguous, with background elements floating from one screen to another and animations running accross several adjacent screens at once.
Conservatively assuming a resolution of 1366 x 768 for each screen, this is at least an 80 megapixel display.
Anyone have more details?
Slashdot Mirror
3% == Citizens who *want* health insurance but are not covered. 86%==Number happy with what they've got (TIME August 10)
Admittedly off topic, but "happy with what they've got" is not a good metric for healthcare.If you are paying more for your care than you have to, getting more unnecessary or unproven (potentially harmful) procedures, getting less preventative care, and ending up with worse outcomes, then you are not getting a good deal. You may be happy with what you've got, but that does not mean that what you've got is good, especially when we have examples of countries spending less money for better outcomes while insuring everyone.
Notice I'm not arguing that we MUST do something about it, but stating that "being happy with it" is not a rational argument against trying to improve the system or even having to improve the system in order to ward off potentially disastrous consequences.
I call your metric the Bill Gates measure - paraphrased - "Everyone should be happy with 640K!"
I see one of the early tags is 'negligible.'
Maybe it is in terms of global CO2 levels, but under a cap and trade system, this will turn an industry that might have to buy CO2-emission rights into one that could make money selling them!
Congrats! That's a great story - as an oncologist, I hang on to each one these I hear (my colleague likes to say that melanoma gives cancer a bad name). The treatment you went through almost certainly stimulated your immune system to fight your cancer. It is not clear if this is a specific effect, where you actually teach the immune system to attack your tumor, or simply a stimulatory effect that revs up the immune system to do a better job of attacking tumor cells that it already had some reaction to.
As you know, our only approved immune therapy for melanoma is interferon - a non-specific stimulator of immunity. There are few responders, but a small fraction (1-4%), are actually cured or disease free for years. The rest have little or no response and the side effects can be brutal or even fatal. The same goes for high dose interleukin-2 therapy for metastatic renal cell carcinoma - this treatment is usually started in an ICU setting.
The more specific cancer vaccines are always given with powerful adjuvants or co-stimulatory products. Provenge is a great example of this - some responders, but not clear what they are responding to. My Dad was in a clinical trial with a different prostate cancer vaccine and is a responder! In his case, he got the vaccine in highly immunogenic vectors - vaccinia (weak small pox, essentially) and fowlpox. This was followed by co-injection of GM-CSF - a chemotactic growth factor for a variety of antigen presenting cells. He isn't cured, but has stable disease. It's not clear if his immune system responded to the specific antigen in the vaccine or simply amplified whatever endogenous anti-tumor activity it already had brewing.
So - without bashing the achievement cited in the article - I suspect that this will not have anywhere near the impact the article claims. We certainly aren't going to be abandoning screening colonoscopy as the article suggests.
While I laud this development - we have had multiple form of immune therapy for cancer - including tumor vaccines, cancer antigen vaccines, immunostimulatory drugs, and anti-tolerance drugs for years now. There are some responders, but this field has generally been a disappointment. here's to hoping we eventually figure out how to harness this approach.
I came to agree with the toolittletoolate tag. I was seriously gearing up to buy a Kindle, but the broken-by-design and big-brother "features" that have now moved from theoretical to actual have convinced me to stay far away from this product.
I'll wait until the DRM issues have shaken out (as they have largely done with music) before considering a company-yoked product like this.
The pinhole camera on an iPhone has an aperture smaller than the human pupil.
This works easily, on regular microscopes, without any special attachment.
A regular microscope is going to be much more versatile.
I'll have to read the PLoS Online article to see what I'm missing.
And you would have to lift the plates back up or use a conveyor belt which would erode the energy gains.
Sounds great! Seeing as how I work in an industry where we are capped at 80 hours in 6 days (we get one day off per week) averaged over a 4 week period, this seems awesome. At least we cap our maximum shift length at 30 hours, because otherwise, that would suck!
Luckily, I don't do anything critical - I just take care of you if you happen to come to my hospital.
Mod this up - this is the *KEY* argument that needs to be made in light of this work. First - 8 of the unexpected mutations could not be found in leukemia cells from 187 other patients with AML. http://news.bbc.co.uk/2/hi/health/7706487.stm
This strongly suggests that these are "passenger" mutations that were acquired during the life of the hematopoietic stem cell that later underwent clonal expansion.
Many of the patients remaining normal stem cells probably carry a few insignificant mutations here or there, but each of these is represent at such low frequency, that they cannot be detected in the absence of clonal expansion.
Second - there is no external or functional validation. Take these genes, mutate them, and put them into in vitro or mouse models of leukemia to see if they have any effect. Heck, just start by proving that these mutations occur at a higher frequency in coding regions than in non-coding regions of the genome. Or even show that all of these genes are actually expressed in leukemic cells.
Finally - mutations are not the only way to disrupt gene expression. Genes can be methylated, amplified, deleted, and post-transcriptionally down regulated (by miRNA for example). The genetic disaster that caused AML in this patients may have had more to do with these types of events (as is the case with a related, pre-leukemic conditon known as MDS).
So this is fascinating use of amazing technology, but also a first pass at analyzing a very complex data set. Many more cancer genomes will come in short order and we'll get a better sense of what this means.
Excellent point. Add to that the fact that superfluid helium is not a uniform Bose-Einstein Condensate and you have full debunking.
This is the killer app for this product. I work in a hospital - the reason we don't use PDA's or iPhones to interact with our patients' electronic records is that the screen is too small to see the necessary data and the interface is too slow for entering lengthy narrative information. Laptops or tablet PC's could do this, but they are too large to carry around in your pocket. Enter the iPhone with this projector and handwriting or voice recognition. Total game changer in my field.
At least it seems like you could use some of the latter.
Seriously - I do genomics research in cancer. We use a variety of tests that generate reams of information. Most academic institutions develop their own overly complicated and highly specialized tools to look at this data. If Google is venturing into the realm of user accessible genetic information, they must be creating simple UI tools for the masses.
I would love to get in on that aspect of things - either as a consultant or beta-tester. A Google Earth like genome browser is at the top of my wish list.
ARE YOU LISTENING MR BRIN? If so, drop me an e-mail - seriously!
This is the key issue. You are not doing a home pregnancy test when you do a genome wide scan. The answer is not yes or no. Even if you accept that disease risk is a) not all genetic and b) is an imperfect number, there will come new associations that can not currently predict. This will include new diseases, behavioral traits such as aggression, meekness, and intelligence. Like the associations we know about know, the degree to which the genes matter will be uncertain. But, your information will already be out there, telling others a story you may not want told and can easily be misinterpreted. How would you like to be fired from your post office job because the NSA learns you may not be very bright, may have aggressive tendencies, and your upcoming heart attacks are going to drain the USPS healthcare pension account?
If you add a bigger screen, upgrade the processor, double the RAM and quadruple the drive space it cost a bit more. But definitely worth the extra money!
PLA is poly-lactic acid (C3H6O3), not lactose (C12H22O11 a disaccharide made up of galactose and glucose). I think poly-lactose eventually = cheese.
In any case, the ants would probably get to it before long.
Check it out at http://www.quadradius.com/.
It's chess on steroids - power-ups include invisible pieces, teaching powers, recruiting enemies. It is an incredibly rich game played head-to-head against others online.
Here's what others think about the game: http://forums.footballguys.com/forum/lofiversion/index.php/t324856.html
I have no affiliation with the site, but I'm about eight months into my addiction....
Klinger you're right on the ball. I logged in to say exactly what you did. Type II diabetes is a failure of insulin signalling at the target tissues (liver, fat, muscle). Some people, particularly those exposed to high levels of insulin over a prolonged period (think fat or refined sugar eaters), downregulate the way their tissues respond to insulin. This means they are less effective at clearing glucose from the blood. To compensate for the elevated glucose levels, the pancreas secretes more insulin. At some point, the pancreas can no longer secrete enough insulin to lower the blood sugar and diabetes is diagnosed. In fact, the disease process had been ongoing for months to years prior to the person having high blood-sugar levels. Since islet cell shut down in the pancreas is one mechanism by which insulin levels become insufficient, an inhibitor of PKCepsilon may prevent this form happening. The diagnostic criteria of elevated blood-sugar may then not be recahed and, in that sense, a case of diabetes prevented or delayed. The underlying insulin resistance syndrome will still persist, therefore this drug does not treat the ultimate cause of Type II diabetes. As a pill, it would be a perfect drug company product. It would replace an injectable, need to be taken lifelong, used for a disease that is rapidly rising in incidence, and the drug would be patentable ($$$). The caveat is that PKC is a fairly important kinase. Off-target side effects could be prohibitive to drug development.
Here's picture of the Broad display: http://www.justinmanor.com/Broad/crx.jpg
I work at the Broad Institute on the MIT campus. In the lobby of our building there is a transected cyclinder (think half a burrito cut at a 45 degree angle) made up of seventy-six ~40" LCD screens. The video on them is contiguous, with background elements floating from one screen to another and animations running accross several adjacent screens at once. Conservatively assuming a resolution of 1366 x 768 for each screen, this is at least an 80 megapixel display. Anyone have more details?