Natural gas produces half the CO2 emissions of coal, so I guess that makes it half as obscene. Other advantages of natural gas are low fuel cost, low construction cost, no S02 and low NOx emissions and fast transition from idle to full power.
I was surprised that TFA stated that the Netgear WNR1000 supported IPv6 since I keep my firmware up to date and have not noticed support. Turns out that the version with IPv6 support, 1.1.2.28, does not appear in the router firmware update page but can be found in the knowledge base at: http://kb.netgear.com/app/answers/detail/a_id/18631/kw/ipv6%20wnr1000
It is a new update as of Feb 3, 2011 and its listed as being for the WNR1000v2 - no mention of the more recent v3. IPv6 compatibility is not mentioned on the product page or the spec sheet.
The photos in the linked article are small and hard to interpret. Better photos with commentary available at:
http://asiasociety.org/OnThinnerIce
Also check out the "Then and Now link". It shows several other glaciers in the region and shows measurements of the 300-400 feet (122 meters) loss of thickness of ice in several glaciers.
Its generally safe to assume that researchers and reviewers have thought of these things, too. So unless you read the article and find otherwise don't assume that the researchers have made this type of statistical gaffe.
I'm not a statistician, but they do specifically address your concern in the statistical part of the results section, where they say:
"Permutation tests were carried out on the pairwise area-normalized NMR data to statistically validate the results obtained from the O-PLS-DA analyses. Pair-wise comparison between the controls and autistic individuals showed statistical significance at a p < 0.0001 significance level (Figure 4) on all metabolites identified to be contributing to the differences between controls and autistics in the O-PLS-DA analyses (Figure 3). However, permutation tests carried out on the controls and siblings failed to find statistical significance in the urinary metabolite profiles (data not shown), which is
reflective of the weak Q2 and R2 values generated from the O-PLS-DA model."
Since this article is behind a paywall, perhaps including the abstract and the statistics sections here might be useful for people to determine whether they think the stats are valid.
Urinary Metabolic Phenotyping Differentiates Children with Autism from Their Unaffected Siblings and Age-Matched Controls
Abstract
Autism is an early onset developmental disorder with a severe life-long impact on behavior and social functioning that has associated metabolic abnormalities. The urinary metabolic phenotypes of individuals (age range=3-9 years old) diagnosed with autism using the DSM-IV-TR criteria (n = 39; male = 35; female = 4), together with their nonautistic siblings (n = 28; male = 14; female = 14) and age-matched healthy volunteers (n = 34, male = 17; female = 17) have been characterized for the first time using 1H NMR spectroscopy and pattern recognition methods. Novel findings associated with alterations in nicotinic acid metabolism within autistic individuals showing increased urinary excretion of N-methyl-2-pyridone-5-carboxamide, N-methyl nicotinic acid, and N-methyl nicotinamide indicate a perturbation in the tryptophan-nicotinic acid metabolic pathway. Multivariate statistical analysis indicated urinary patterns of the free amino acids, glutamate and taurine were significantly different between groups with the autistic children showing higher levels of urinary taurine and a lower level of urinary glutamate, indicating perturbation in sulfur and amino acid metabolism in these children. Additionally, metabolic phenotype (metabotype) differences were observed between autistic and control children, which were associated with perturbations in the relative patterns of urinary mammalian-microbial cometabolites including dimethylamine, hippurate, and phenyacetylglutamine. These biochemical changes are consistent with some of the known abnormalities of gut microbiota found in autistic individuals and the associated gastrointestinal dysfunction and may be of value in monitoring the success of therapeutic interventions.
Multivariate Statistical Analysis of the NMR Spectral Data
To further explore the metabolic differences between the three groups of participants, multivariate statistical analyses were employed on the full resolution NMR data set consisting of 34 controls, 28 siblings and 39 autistic urine samples to extract useful metabolic information. PCA was carried out on UV-scaled data to identify any inherent differences within the data set. The resulting scores plot of PC1 versus PC2 (Figure 2A) showed no clear differences between the three groups, all pairwise combinations of PCs down to PC3 were examined, which showed no discrimination indicating that the major source of variation in the data was not related to autism, but was rather dominated by interperson variability. However, by utilizing group information in PLS-DA analysis, systematic differences could be observed between the three groups (Q2 = 15%; R2
What is the threat that all these planes are supposed to defend against? The cold war is long gone and Russia's decaying military infrastructure is no match for what is already deployed by the US. They may now be a rival but certainly no longer an enemy of the West. China? Their only territorial ambition is Taiwan. Anti-aircraft and anti ship systems would seem to be the more appropriate technology if one were to think in military terms. What is making a military conflict between China and Taiwan less likely is economic interdependence between China and the rest of the world. Invading Taiwan would make many businessmen in China quite unhappy.
One fee structure change that I have seen proposed is a per page charge on patent applications. This would have two effects. First, it would encourage filers to consider less voluminous filings. Second, it would allow the patent office to give examiners the time needed to review longer applications since the longer applications would bring in more money.
The law you propose to limit liability has already been enacted. Its called the Price-Anderson act of 1957 (described in detail at http://www.nrc.gov/reading-rm/doc-collections/fact-sheets/funds-fs.html). It limits the liability of nuclear plant operators, but requires insurance. The current liability limit is about $10 billion. All the utilities pay into a common insurance pool that provides coverage for off site damages in case of an accident, currently up to $8.6 billion. Combined with $300 million in coverage for each reactor, the cost of any accident is insured up to $8.9 billion.
Despite this insurance being covered, it has been Wall Street that has been wary of the financial risk of nuclear plants due to massive cost overruns that occurred in nuclear plant construction in the 1970s along with demand for electricity that did not grow as projected by the utilities.
These "Long term missions" seem pretty pointless to me as well at least with current rocket technology. Where exactly would we send these astronauts? We've been to the Moon. Mars is distant making human travel there long, dangerous and expensive. And once we get people there what exactly would they do? Take samples? Machines can do that. Start a colony? That might be tough at -40C and no breathable atmosphere. The problem is that there are physics and technological limitations to what we can do. I, too, would like to catch a star freighter to hang out on the moons of a distant system for a while and explore the far reaches of space, but thats not gonna happen. Instead I'll have to spend my time getting to know this planet better. Its a pretty nice place.
I'm perfectly content to see the shuttle program end. Now that the space station is complete, the shuttle no longer has a purpose. A much smaller craft would be just fine to ferry people to the space station service the occasional space telescope. Can't say I really see much point in the manned space program at all, but as long as we have a $50 billion space station we might as well have a few folks keep the lights on. Its only justification was science and much of that was pretty thin. Mostly it was an end of the cold war political project to get countries to work together and it did OK at that. Its the rovers that have been getting the science and exploration done... for so much less money.
The 1991 NY Times article states that they achieve an 87% efficiency with compressed air, substantially better than hydro pumped storage's 70-75% efficiency.
First is the whole autism connection. First, the Slashdot headline and summary are completely misleading. The treatment is aimed at fragile X syndrome, not autism. Fragile X syndrome is NOT an autism spectrum disorder. Some people with fragile X syndrome are also diagnosed with autism, but given that people with fragile X syndrome suffer mental retardation, the diagnosis of autism in these people becomes complicated. To be fair the article isn't quite as bad as the Slashdot summary on this point, but it is definitely misleading.
Second, the article describes the role of FMRP (Fragile X Mental Retardation Protein) as "to inhibit molecular activity at the connections between nerve cells." This is so simplified as to be completely uninformative. FMRP is a regulator of mRNA. (For the non-biologists, mRNAs are essentially copies of genes that get used as templates by ribosomes to manufacture proteins.) Many mRNAs bind to FMRP. This usually reduces their ability to get transcribed into proteins by ribosomes. The result is that certain proteins, especially ones that are involved in growing synapses get over-expressed. One of the striking characteristics of the brains of people with fragile X syndrome is that they have elongated dendritic spines. (The dendritic spines are the structures that form the "receiving" end of the synapse.)
Finally, I'm skeptical of the researcher's technique of treating the syndrome by simply reducing mGLuR5 expression for two reasons. First FMRP regulates the expression of many proteins, not just mGLuR5. Second, the role of FMRP is activity-dependent. The whole point of controlling the expression levels of certain proteins in the brain is not to have them the same in every synapse, but to allow the activity of the brain to regulate the strength of the synapse. Bear's treatment may reduce seizures and even result in fewer elongated spines, but that may not relieve the mental retardation significantly if the people with fragile X still have difficulty properly regulating the strength of their synapses in response to activation. It is possible, though, that this could work and that just by getting the levels of mGluR5 into a more normal range that other mechanisms could compensate for the other mis-regulated proteins; the brain is a fairly robust system. If this works, it would be wonderful and could make meaningful improvement in the lives of many people.
Correction: Their model does modify connection strengths using a reasonable biologically-based learning rule (spike timing dependent plasticity), but just has the model simulate staring at a black square. They don't do anything with this other than comment that it changes the firing rate of the neurons.
I read the paper. They just used a giant net that did absolutely nothing. They would have done better science on a laptop. They didn't bother claiming any generalization.
TFA is bunk. (Yes, I read it.) 12 pages of bunk. Much of the article is about the computational challenges and blathers on about number of processors used and memory. Under key scientific results, they find that their model propagates waves at about the same rate as is found physiologically. So they connected a bunch of nodes in a way that produced synchronous behavior at a certain frequency. I could tune any model you give me to produce this behavior. (I have no special talent here, anyone writing models could.) Yawn. They ramble on about signals propagating between layers at reasonable rates, too. And...?
What about their simulation doing anything like what a cat might naturally do, such as detect a moving object? Nope. Instead they go on to discuss the scaling of their model, profiling and performance modeling. Perhaps one reason their model shows absolutely nothing is that they have connected their simulated neurons randomly. Yes. Randomly. Or as they put it: "The coordinates of target thalamocortical modules for each cell are determined using a Gaussian spatial density profile centered on the topographic location of the source thalamocortical module". Yep, thats random. Since their model doesn't ever change connection strengths (one form of learning) these random connections never change.
I recently heard a description of the ways you can fool someone with computational neuroscience. Here are a couple of them: "Two card monte" Write a paper that spans two fields, but has no significant results in either. The specialists in one field will feel that the work done in their field is trivial, but that exciting stuff from the other field in the paper is what makes it so special. The specialists from the other field may feel the same way. Somebody snookered the conference organizers into thinking they were doing any neuroscience at all. The other was called "Turning the prayer wheel" or burning compute cycles to gain scientific merit. Fancy hardware is cool, but it can produce absolutely trivial results as this paper confirms.
I don't mean to say that this research is entirely pointless. Indeed it has succeeded in siphoning significant funding from DARPA which might otherwise have gone into developing [killer] robot dogs.
You are right to judge this book by its cover. These claims to simulate an entire cortex are absurd. The first problem is that nobody knows how a single neuron works. We know some of the basics, but biology is complicated - very complicated - with seemingly endless feedback mechanisms operating over various time and spatial scales. To give an idea of how little we know, I'll point out that we don't know what all the receptors for the neurotransmitters are in cortex, we don't know how the cells are connected or how they make connections. We know something about these things, but are understanding is limited likely missing essential mechanisms and hardly quantitative. Neurons are not simply little adders of inputs. They are quite complex and incompletely understood.
Even if our understanding of the biology were somehow perfect, there are some serious computational challenges. Each neuron connects via synapses to on the order of 1000 other neurons. Simulating a single neuron to a reasonable degree of accuracy requires substantial computing power, so we simplify, leaving off all kinds of properties. The human brain has around 10^11 (100 billion) neurons and around 10^14 (100 trillion) synapses. A cat might save us an order of magnitude here, but we're way off the mark. The truth is that after five decades of rigorous study, we don't understand the primary cat visual cortex (V1), with plenty of reasonable arguments about how basic parts of the visual processing pathway operate. A more reasonable goal would be to simulate the visual system of a fruit fly, though this, too would require many simplifying assumptions.
This "achievement" is all about coming up with some really gross oversimplifications, like simulating "cortical columns" which contain many neurons and treating them as a single unit then throwing lots of hardware at the problem and claiming you've done something. Instead we have researchers staring at the output of a big simulation and hoping it might tell them something. If they are very clever they might learn something about their simulation. I should point out that I study computational neuroscience and believe greatly in its power, but using this type of approach, they are unlikely to learn anything about real brains.
Thanks for the post. Generally eyewitness accounts are pretty worthless in these kinds of situations because:
1.) The driver is in a state of panic when the car suddenly accelerates. Panic tends to create a state where the operator continues with a chosen course of action, despite evidence that it might be wrong, such as the car speeding up.(This was apparently one of many contributing factors to the airline crash in Buffalo, NY last year.) Panic also tends to make memories very clear, so the operator clearly remembers pressing on the [brake | gas] pedal very hard.
2.) The possibility that the driver's error has caused an accident gives a strong psychological incentive for the mind to settle on other possibilities. I do not mean that the driver intentionally chose to believe something not true, but that belief about what happened in an event was constructed out prior beliefs, such as: "I am a good driver" and "I was trying to stop". When there is a fatality involved this greatly increases the cost of believing that one was at fault.
This story is more credible since:
1.) The driver did not panic due to comfort at high speeds and as evidenced by his rational, methodical approach to working the problem.
2.) No accident was involved.
One thing which strikes me as odd about many of the accounts is that the drivers never simply turn off the car using the key, especially in the case where the passenger had time to call 911. Are people unaware that they can do this or is it related to some new electronic interface not present in my older vehicle?
The question of control in battering relationships are not that simple. Most abusers wait until they have psychological control until they start battering. I know we all like to believe in free will and everything, but its pretty scary to see the level of control batterers can establish with tactics like isolating the victim from fiends, becoming enraged at small provocations then apologizing with flowers and all, financial control (as in controlling the bank account or preventing a partner from working), monitoring phone records, and tapping into a victims doubts and fears. If the person you love and trust and used to be kind to you starts agreeing with all your self-doubts, that can be very destructive to one's self confidence and will. As far as choosing to hang around, there is often the threat of "If you ever leave, I'll kill [myself | you]". There is a reason the location of women's shelters are kept secret.
Don't get too excited yet. As the article states in humans the only well-established generation of new nerve cells occurs in the hippocampus, a structure which conveniently is involved in memory.
There was another study dating cells based on inclusion of radioisotopes left over from atmospheric nuclear weapons testing, apparently finding a very slow rate of new cell generation, measured in something like percent (or fraction thereof) per decade of the total. And their study only holds true if they correctly sorted their neurons from other cells that live in the brain (glia, blood vessels, etc). The study is actually pretty convincing, along with the Swedish BrdU study, but the rate of growth is less than stunning. The findings in birds of huge amounts of cortical growth are very cool and establish the principle that such massive growth can happen in an adult vertebrate.
What has not yet been established is what these new cells in humans might be doing, if anything. Even without new neurons, we can still be pretty flexible, by altering the strength of connections between neurons or forming entirely new connections.
Also even if the human brain does grow some new cells, the type of those cells is very important. for example, I heard a talk today from a guy with Parkinson's disease, which is a progressive disease of the cells of the substantia nigra, an area of the brain that is part of the system for controlling movement. He sure could use a few extra dopaminergic cells in his substantia nigra, but thats not happening for him, so the disease will kill him. So don't go on that brain cell massacre just yet.
It is an issue with the Intel drivers. Ubuntu 9.04 (Jaunty Jackalope) shipped with kernel 2.6.28, in which the Intel made some major changes in the graphics system. The Intel drivers suffered a performance regression with this kernel due to some miscommunication with xorg, most visible when viewing Flash, is also seen with other video playback, such as DVD. Intel has addressed the issue by releasing a fix to its drivers and to xorg. This issue should be fixed as of kernel 2.6.30.
OK. I'll take your angry post as sincere. As a driver and a regular cyclist who has had the experience of being rear-ended by a car (clear day, perfect straight road, inattentive driver, saw it coming and had nowhere to go), I have a couple of observations to share. First, there are idiots everywhere, some behind the wheel and some on bikes. Second, the edge of the road had many hazards that are hard for drivers to see, such as glass, sand, rocks, beer bottles, potholes, and sewer grates perfectly aligned to swallow a bike tire. Even if most of the roadway lacks these obstacles, when they do occur a cyclist may have to swerve to avoid them. Riding a bit away from the edge of the road puts the bike further from many of these obstacles and gives the option of swerving away from traffic rather than into it. A third observation I have made is that the farther I ride from the curb, the more room cars give me. It makes no sense at all, but when I try scoot over as far as I can, thats when I see mirrors whizzing by inches away from me. Finally, in situations where there are parked cars, cyclists have to ride a few feet out or risk getting "doored" and perhaps damaging the underside of passing vehicles.
Honestly, most of us cyclists are not trying to inconvenience you, but just trying to get home safely.
The article mentions the efficiency of the cell at 500x normal sunlight, so the idea here is to use inexpensive mirrors to concentrate the light onto expensive cells. The setup is bulkier, but could be cost effective, even with very expensive cells, since you buy fewer cells. With mirrors and high efficiency cells, you also can get the same power out of a much smaller installation. This setup might not be ideal for residential rooftops, but would work for large flat-roofed buildings and desert installations.
The time to recover the energy investment in the panels is much shorter than the time needed to recover your financial investment, as much of the cost of solar is labor. The energy cost of the panels is already part of the price. Suppose that the panel cost from acquiring materials, to production, delivery and installation is 50% energy and 50% labor. The energy break-even point of these panels would be 5 or 6 years, if you go by the 10-12 year financial payback and if the energy-labors costs were actually 50-50.
There has also been analysis done of the toxics that go into solar panels. It turns out that you get to break even on toxics use in a year or so, since you are displacing conventional power sources, such as coal with its heavy metals.
I'm glad that someone is finally asking the right questions about the energy recovery and toxics. I find it amazing that solar technology has progressed so far lately that people are actually looking at whether they can recover their investment, rather than installing just to be green or because they are far from the grid. (Far enough for economic parity, including batteries, for a off-the-grid system has been quoted at 0.25 miles or 0.4 km, since in the US you pay for the poles and wires the utility strings out to your place.)
I get as livid as anyone about spam, but the whole prison rape thing really bugs me. Its real and is allowed to occur by our prison system, but is not part of the sentence. Nobody, not even spammers, deserve rape. What I don't get is why it took so long to take down this known spammer.
Slashdot Mirror
Natural gas produces half the CO2 emissions of coal, so I guess that makes it half as obscene. Other advantages of natural gas are low fuel cost, low construction cost, no S02 and low NOx emissions and fast transition from idle to full power.
I was surprised that TFA stated that the Netgear WNR1000 supported IPv6 since I keep my firmware up to date and have not noticed support. Turns out that the version with IPv6 support, 1.1.2.28, does not appear in the router firmware update page but can be found in the knowledge base at: http://kb.netgear.com/app/answers/detail/a_id/18631/kw/ipv6%20wnr1000
It is a new update as of Feb 3, 2011 and its listed as being for the WNR1000v2 - no mention of the more recent v3. IPv6 compatibility is not mentioned on the product page or the spec sheet.
The photos in the linked article are small and hard to interpret. Better photos with commentary available at: http://asiasociety.org/OnThinnerIce Also check out the "Then and Now link". It shows several other glaciers in the region and shows measurements of the 300-400 feet (122 meters) loss of thickness of ice in several glaciers.
Its generally safe to assume that researchers and reviewers have thought of these things, too. So unless you read the article and find otherwise don't assume that the researchers have made this type of statistical gaffe.
I'm not a statistician, but they do specifically address your concern in the statistical part of the results section, where they say:
"Permutation tests were carried out on the pairwise area-normalized NMR data to statistically validate the results obtained from the O-PLS-DA analyses. Pair-wise comparison between the controls and autistic individuals showed statistical significance at a p < 0.0001 significance level (Figure 4) on all metabolites identified to be contributing to the differences between controls and autistics in the O-PLS-DA analyses (Figure 3). However, permutation tests carried out on the controls and siblings failed to find statistical significance in the urinary metabolite profiles (data not shown), which is reflective of the weak Q2 and R2 values generated from the O-PLS-DA model."
Since this article is behind a paywall, perhaps including the abstract and the statistics sections here might be useful for people to determine whether they think the stats are valid.
Urinary Metabolic Phenotyping Differentiates Children with Autism from Their Unaffected Siblings and Age-Matched Controls
Abstract
Autism is an early onset developmental disorder with a severe life-long impact on behavior and social functioning that has associated metabolic abnormalities. The urinary metabolic phenotypes of individuals (age range=3-9 years old) diagnosed with autism using the DSM-IV-TR criteria (n = 39; male = 35; female = 4), together with their nonautistic siblings (n = 28; male = 14; female = 14) and age-matched healthy volunteers (n = 34, male = 17; female = 17) have been characterized for the first time using 1H NMR spectroscopy and pattern recognition methods. Novel findings associated with alterations in nicotinic acid metabolism within autistic individuals showing increased urinary excretion of N-methyl-2-pyridone-5-carboxamide, N-methyl nicotinic acid, and N-methyl nicotinamide indicate a perturbation in the tryptophan-nicotinic acid metabolic pathway. Multivariate statistical analysis indicated urinary patterns of the free amino acids, glutamate and taurine were significantly different between groups with the autistic children showing higher levels of urinary taurine and a lower level of urinary glutamate, indicating perturbation in sulfur and amino acid metabolism in these children. Additionally, metabolic phenotype (metabotype) differences were observed between autistic and control children, which were associated with perturbations in the relative patterns of urinary mammalian-microbial cometabolites including dimethylamine, hippurate, and phenyacetylglutamine. These biochemical changes are consistent with some of the known abnormalities of gut microbiota found in autistic individuals and the associated gastrointestinal dysfunction and may be of value in monitoring the success of therapeutic interventions.
Multivariate Statistical Analysis of the NMR Spectral Data
To further explore the metabolic differences between the three groups of participants, multivariate statistical analyses were employed on the full resolution NMR data set consisting of 34 controls, 28 siblings and 39 autistic urine samples to extract useful metabolic information. PCA was carried out on UV-scaled data to identify any inherent differences within the data set. The resulting scores plot of PC1 versus PC2 (Figure 2A) showed no clear differences between the three groups, all pairwise combinations of PCs down to PC3 were examined, which showed no discrimination indicating that the major source of variation in the data was not related to autism, but was rather dominated by interperson variability. However, by utilizing group information in PLS-DA analysis, systematic differences could be observed between the three groups (Q2 = 15%; R2
What is the threat that all these planes are supposed to defend against? The cold war is long gone and Russia's decaying military infrastructure is no match for what is already deployed by the US. They may now be a rival but certainly no longer an enemy of the West. China? Their only territorial ambition is Taiwan. Anti-aircraft and anti ship systems would seem to be the more appropriate technology if one were to think in military terms. What is making a military conflict between China and Taiwan less likely is economic interdependence between China and the rest of the world. Invading Taiwan would make many businessmen in China quite unhappy.
One fee structure change that I have seen proposed is a per page charge on patent applications. This would have two effects. First, it would encourage filers to consider less voluminous filings. Second, it would allow the patent office to give examiners the time needed to review longer applications since the longer applications would bring in more money.
The law you propose to limit liability has already been enacted. Its called the Price-Anderson act of 1957 (described in detail at http://www.nrc.gov/reading-rm/doc-collections/fact-sheets/funds-fs.html). It limits the liability of nuclear plant operators, but requires insurance. The current liability limit is about $10 billion. All the utilities pay into a common insurance pool that provides coverage for off site damages in case of an accident, currently up to $8.6 billion. Combined with $300 million in coverage for each reactor, the cost of any accident is insured up to $8.9 billion.
Despite this insurance being covered, it has been Wall Street that has been wary of the financial risk of nuclear plants due to massive cost overruns that occurred in nuclear plant construction in the 1970s along with demand for electricity that did not grow as projected by the utilities.
These "Long term missions" seem pretty pointless to me as well at least with current rocket technology. Where exactly would we send these astronauts? We've been to the Moon. Mars is distant making human travel there long, dangerous and expensive. And once we get people there what exactly would they do? Take samples? Machines can do that. Start a colony? That might be tough at -40C and no breathable atmosphere. The problem is that there are physics and technological limitations to what we can do. I, too, would like to catch a star freighter to hang out on the moons of a distant system for a while and explore the far reaches of space, but thats not gonna happen. Instead I'll have to spend my time getting to know this planet better. Its a pretty nice place.
I'm perfectly content to see the shuttle program end. Now that the space station is complete, the shuttle no longer has a purpose. A much smaller craft would be just fine to ferry people to the space station service the occasional space telescope. Can't say I really see much point in the manned space program at all, but as long as we have a $50 billion space station we might as well have a few folks keep the lights on. Its only justification was science and much of that was pretty thin. Mostly it was an end of the cold war political project to get countries to work together and it did OK at that. Its the rovers that have been getting the science and exploration done ... for so much less money.
The 1991 NY Times article states that they achieve an 87% efficiency with compressed air, substantially better than hydro pumped storage's 70-75% efficiency.
... and a few other comments.
First is the whole autism connection. First, the Slashdot headline and summary are completely misleading. The treatment is aimed at fragile X syndrome, not autism. Fragile X syndrome is NOT an autism spectrum disorder. Some people with fragile X syndrome are also diagnosed with autism, but given that people with fragile X syndrome suffer mental retardation, the diagnosis of autism in these people becomes complicated. To be fair the article isn't quite as bad as the Slashdot summary on this point, but it is definitely misleading.
Second, the article describes the role of FMRP (Fragile X Mental Retardation Protein) as "to inhibit molecular activity at the connections between nerve cells." This is so simplified as to be completely uninformative. FMRP is a regulator of mRNA. (For the non-biologists, mRNAs are essentially copies of genes that get used as templates by ribosomes to manufacture proteins.) Many mRNAs bind to FMRP. This usually reduces their ability to get transcribed into proteins by ribosomes. The result is that certain proteins, especially ones that are involved in growing synapses get over-expressed. One of the striking characteristics of the brains of people with fragile X syndrome is that they have elongated dendritic spines. (The dendritic spines are the structures that form the "receiving" end of the synapse.)
Finally, I'm skeptical of the researcher's technique of treating the syndrome by simply reducing mGLuR5 expression for two reasons. First FMRP regulates the expression of many proteins, not just mGLuR5. Second, the role of FMRP is activity-dependent. The whole point of controlling the expression levels of certain proteins in the brain is not to have them the same in every synapse, but to allow the activity of the brain to regulate the strength of the synapse. Bear's treatment may reduce seizures and even result in fewer elongated spines, but that may not relieve the mental retardation significantly if the people with fragile X still have difficulty properly regulating the strength of their synapses in response to activation. It is possible, though, that this could work and that just by getting the levels of mGluR5 into a more normal range that other mechanisms could compensate for the other mis-regulated proteins; the brain is a fairly robust system. If this works, it would be wonderful and could make meaningful improvement in the lives of many people.
Correction: Their model does modify connection strengths using a reasonable biologically-based learning rule (spike timing dependent plasticity), but just has the model simulate staring at a black square. They don't do anything with this other than comment that it changes the firing rate of the neurons.
I read the paper. They just used a giant net that did absolutely nothing. They would have done better science on a laptop. They didn't bother claiming any generalization.
TFA is bunk. (Yes, I read it.) 12 pages of bunk. Much of the article is about the computational challenges and blathers on about number of processors used and memory. Under key scientific results, they find that their model propagates waves at about the same rate as is found physiologically. So they connected a bunch of nodes in a way that produced synchronous behavior at a certain frequency. I could tune any model you give me to produce this behavior. (I have no special talent here, anyone writing models could.) Yawn. They ramble on about signals propagating between layers at reasonable rates, too. And ...?
What about their simulation doing anything like what a cat might naturally do, such as detect a moving object? Nope. Instead they go on to discuss the scaling of their model, profiling and performance modeling. Perhaps one reason their model shows absolutely nothing is that they have connected their simulated neurons randomly. Yes. Randomly. Or as they put it: "The coordinates of target thalamocortical modules for each cell are determined using a Gaussian spatial density profile centered on the topographic location of the source thalamocortical module". Yep, thats random. Since their model doesn't ever change connection strengths (one form of learning) these random connections never change.
I recently heard a description of the ways you can fool someone with computational neuroscience. Here are a couple of them: "Two card monte" Write a paper that spans two fields, but has no significant results in either. The specialists in one field will feel that the work done in their field is trivial, but that exciting stuff from the other field in the paper is what makes it so special. The specialists from the other field may feel the same way. Somebody snookered the conference organizers into thinking they were doing any neuroscience at all. The other was called "Turning the prayer wheel" or burning compute cycles to gain scientific merit. Fancy hardware is cool, but it can produce absolutely trivial results as this paper confirms.
I don't mean to say that this research is entirely pointless. Indeed it has succeeded in siphoning significant funding from DARPA which might otherwise have gone into developing [killer] robot dogs.
You are right to judge this book by its cover. These claims to simulate an entire cortex are absurd. The first problem is that nobody knows how a single neuron works. We know some of the basics, but biology is complicated - very complicated - with seemingly endless feedback mechanisms operating over various time and spatial scales. To give an idea of how little we know, I'll point out that we don't know what all the receptors for the neurotransmitters are in cortex, we don't know how the cells are connected or how they make connections. We know something about these things, but are understanding is limited likely missing essential mechanisms and hardly quantitative. Neurons are not simply little adders of inputs. They are quite complex and incompletely understood.
Even if our understanding of the biology were somehow perfect, there are some serious computational challenges. Each neuron connects via synapses to on the order of 1000 other neurons. Simulating a single neuron to a reasonable degree of accuracy requires substantial computing power, so we simplify, leaving off all kinds of properties. The human brain has around 10^11 (100 billion) neurons and around 10^14 (100 trillion) synapses. A cat might save us an order of magnitude here, but we're way off the mark. The truth is that after five decades of rigorous study, we don't understand the primary cat visual cortex (V1), with plenty of reasonable arguments about how basic parts of the visual processing pathway operate. A more reasonable goal would be to simulate the visual system of a fruit fly, though this, too would require many simplifying assumptions.
This "achievement" is all about coming up with some really gross oversimplifications, like simulating "cortical columns" which contain many neurons and treating them as a single unit then throwing lots of hardware at the problem and claiming you've done something. Instead we have researchers staring at the output of a big simulation and hoping it might tell them something. If they are very clever they might learn something about their simulation. I should point out that I study computational neuroscience and believe greatly in its power, but using this type of approach, they are unlikely to learn anything about real brains.
Thanks for the post. Generally eyewitness accounts are pretty worthless in these kinds of situations because:
1.) The driver is in a state of panic when the car suddenly accelerates. Panic tends to create a state where the operator continues with a chosen course of action, despite evidence that it might be wrong, such as the car speeding up.(This was apparently one of many contributing factors to the airline crash in Buffalo, NY last year.) Panic also tends to make memories very clear, so the operator clearly remembers pressing on the [brake | gas] pedal very hard.
2.) The possibility that the driver's error has caused an accident gives a strong psychological incentive for the mind to settle on other possibilities. I do not mean that the driver intentionally chose to believe something not true, but that belief about what happened in an event was constructed out prior beliefs, such as: "I am a good driver" and "I was trying to stop". When there is a fatality involved this greatly increases the cost of believing that one was at fault.
This story is more credible since:
1.) The driver did not panic due to comfort at high speeds and as evidenced by his rational, methodical approach to working the problem.
2.) No accident was involved.
One thing which strikes me as odd about many of the accounts is that the drivers never simply turn off the car using the key, especially in the case where the passenger had time to call 911. Are people unaware that they can do this or is it related to some new electronic interface not present in my older vehicle?
The question of control in battering relationships are not that simple. Most abusers wait until they have psychological control until they start battering. I know we all like to believe in free will and everything, but its pretty scary to see the level of control batterers can establish with tactics like isolating the victim from fiends, becoming enraged at small provocations then apologizing with flowers and all, financial control (as in controlling the bank account or preventing a partner from working), monitoring phone records, and tapping into a victims doubts and fears. If the person you love and trust and used to be kind to you starts agreeing with all your self-doubts, that can be very destructive to one's self confidence and will. As far as choosing to hang around, there is often the threat of "If you ever leave, I'll kill [myself | you]". There is a reason the location of women's shelters are kept secret.
Don't get too excited yet. As the article states in humans the only well-established generation of new nerve cells occurs in the hippocampus, a structure which conveniently is involved in memory.
There was another study dating cells based on inclusion of radioisotopes left over from atmospheric nuclear weapons testing, apparently finding a very slow rate of new cell generation, measured in something like percent (or fraction thereof) per decade of the total. And their study only holds true if they correctly sorted their neurons from other cells that live in the brain (glia, blood vessels, etc). The study is actually pretty convincing, along with the Swedish BrdU study, but the rate of growth is less than stunning. The findings in birds of huge amounts of cortical growth are very cool and establish the principle that such massive growth can happen in an adult vertebrate.
What has not yet been established is what these new cells in humans might be doing, if anything. Even without new neurons, we can still be pretty flexible, by altering the strength of connections between neurons or forming entirely new connections.
Also even if the human brain does grow some new cells, the type of those cells is very important. for example, I heard a talk today from a guy with Parkinson's disease, which is a progressive disease of the cells of the substantia nigra, an area of the brain that is part of the system for controlling movement. He sure could use a few extra dopaminergic cells in his substantia nigra, but thats not happening for him, so the disease will kill him. So don't go on that brain cell massacre just yet.
It is an issue with the Intel drivers. Ubuntu 9.04 (Jaunty Jackalope) shipped with kernel 2.6.28, in which the Intel made some major changes in the graphics system. The Intel drivers suffered a performance regression with this kernel due to some miscommunication with xorg, most visible when viewing Flash, is also seen with other video playback, such as DVD. Intel has addressed the issue by releasing a fix to its drivers and to xorg. This issue should be fixed as of kernel 2.6.30.
Here is a description the issue and some workarounds:
http://ubuntuforums.org/showthread.php?t=1130582
Here is the Ubuntu Launchpad bug report:
https://bugs.launchpad.net/ubuntu/+source/xserver-xorg-video-intel/+bug/314928
No. When flash fails it becomes unwritable, not unreadable. Your data is safe, your capacity declines.
Just mistook sarcastic response to troll as a troll. That will teach me never to mod while browsing above -1.
OK. I'll take your angry post as sincere. As a driver and a regular cyclist who has had the experience of being rear-ended by a car (clear day, perfect straight road, inattentive driver, saw it coming and had nowhere to go), I have a couple of observations to share. First, there are idiots everywhere, some behind the wheel and some on bikes. Second, the edge of the road had many hazards that are hard for drivers to see, such as glass, sand, rocks, beer bottles, potholes, and sewer grates perfectly aligned to swallow a bike tire. Even if most of the roadway lacks these obstacles, when they do occur a cyclist may have to swerve to avoid them. Riding a bit away from the edge of the road puts the bike further from many of these obstacles and gives the option of swerving away from traffic rather than into it. A third observation I have made is that the farther I ride from the curb, the more room cars give me. It makes no sense at all, but when I try scoot over as far as I can, thats when I see mirrors whizzing by inches away from me. Finally, in situations where there are parked cars, cyclists have to ride a few feet out or risk getting "doored" and perhaps damaging the underside of passing vehicles.
Honestly, most of us cyclists are not trying to inconvenience you, but just trying to get home safely.
The article mentions the efficiency of the cell at 500x normal sunlight, so the idea here is to use inexpensive mirrors to concentrate the light onto expensive cells. The setup is bulkier, but could be cost effective, even with very expensive cells, since you buy fewer cells. With mirrors and high efficiency cells, you also can get the same power out of a much smaller installation. This setup might not be ideal for residential rooftops, but would work for large flat-roofed buildings and desert installations.
The time to recover the energy investment in the panels is much shorter than the time needed to recover your financial investment, as much of the cost of solar is labor. The energy cost of the panels is already part of the price. Suppose that the panel cost from acquiring materials, to production, delivery and installation is 50% energy and 50% labor. The energy break-even point of these panels would be 5 or 6 years, if you go by the 10-12 year financial payback and if the energy-labors costs were actually 50-50.
There has also been analysis done of the toxics that go into solar panels. It turns out that you get to break even on toxics use in a year or so, since you are displacing conventional power sources, such as coal with its heavy metals.
I'm glad that someone is finally asking the right questions about the energy recovery and toxics. I find it amazing that solar technology has progressed so far lately that people are actually looking at whether they can recover their investment, rather than installing just to be green or because they are far from the grid. (Far enough for economic parity, including batteries, for a off-the-grid system has been quoted at 0.25 miles or 0.4 km, since in the US you pay for the poles and wires the utility strings out to your place.)
I get as livid as anyone about spam, but the whole prison rape thing really bugs me. Its real and is allowed to occur by our prison system, but is not part of the sentence. Nobody, not even spammers, deserve rape. What I don't get is why it took so long to take down this known spammer.