I don't think that having so-called "experts" contributing to Google Knol is necessarily going to make it a better overall resource that Wikipedia for several reasons.
Firstly, a lot of these early articles are seriously lacking. Let's take for example, the article on Methicillin Resistant Staphlococcus Aureus (MRSA). It's a generally well-written article, and the author looks to be fairly reputable. Nonetheless, there are arguably some significant deficiencies, that with the current format of Knol, cannot be rectified.
In the article's description, the author notes that there will be a discussion on how MRSA can be treated. Yet, when you look at that portion of the article, information on management is seriously lacking, and the description of the medications is ultimately quite useless.
At least with Wikipedia, the article would link to a corresponding article on the specific antibiotic, so you would have the opportunity to easily gain further information, whereas with Knol, this simple linking procedure is currently lacking significantly.
Now, for a simple example. Having a description that Vancomycin "is considered first line treatment" for MRSA is useless for any practicing clinician. What I would want to know are things such as dosing regimens, important things to remember such as having to measure Vancomycin trough levels every several doses (and why), what alternative medications I can use if the MRSA strain is resistant to Vancomycin, etc., all of which are extremely important in the management of MRSA. There is also a significant lack of information about what strains are prevalent, which although not necessarily important for an Internist, is important for Infectious Disease specialists, the people who are consulted on a daily basis for the management of MRSA.
I can continue to criticize the article, but the difference between it, and the Wikipedia entry are night-and-day. And my criticism isn't pointed to this article alone, there are countless very poorly written and uninformative medical articles on there thus far.
A community effort with anonymous editors will (eventually) weed out mistakes, and have the distinct advantage of constant peer review. Knol on the other hand, is unfortunately stuck with the one author knows best paradigm.
I think there have been a good number of misconceptions about Microsoft's $45 billion offer for Yahoo!, and there are a few points that we ought to make note of.
Firstly, Microsoft's valuation indicates their valuation of Yahoo! being part of Microsoft. Synergies account for the higher value!
Secondly, with the offer, Yahoo! is now "in play", and there is a consequent expectation that someone such as Google may come along and make an offer. Since it is in play, people expect an offer that comes at a premium (which of course gets priced in!). Now, this is implicitly priced into the 62% premium that Microsoft has offered, and they have set it high enough (in their estimate) so as to price out any potential offers from others.
If Google decides to get involved, they have plenty of antitrust concerns in terms of an overall takeover bid. Can they take a play out of Microsoft's playbook (e.g., 1.6% stake in Facebook) and offer a larger premium for a substantial stake of the company (e.g., $60/share for say 35% of Yahoo!)? I would not be surprised if we see such a strategy.
First of all, I am coming from a medical background, and I also have friends who are graduate students of several of the scientists cited in the article.
So, basically, here's what's going on. Clinically detectable tumors consist of heterogeneous population of cells which originate from a clonal growth of the progeny of a single cell (e.g., the monoclonal origin of neoplasms, Knudson two-hit hypothesis, etc.). Tumor stem cells (called Tumor Initiating Cells, T-ICs) not only have the capacity to initiate, but, ultimately sustain tumor growth. These cells, however, only constitute only about 0.1-2% of the total population of cells and like their normal counterparts, and have a very low rate of replication. Now do we see what the problem is?
A lot of our current drugs and therapies target the fast growing progeny of the T-ICs which constitute over 98% of the cells in the cancer, leaving the slow growing T-ICs alone! Consequently, that means that some tumors can easily recur after treatment. In other words, our drugs may have been targeting the wrong cells this entire time!
You asked a good question. The problem, however, is that HIV not only invades CD4+ cells (which are derived from lymphoid progenitor cells), but also dendritic cells and macrophages (derived from myelomonocytic progentor cells). My immunology professor back in medical school made the analogy that macrophages are like a "trojan horse" where HIV can hide out. In addition, one common misconception is that the HIV strain towards the end stages of the disease is not the same strain that the patient was infected with. It is in all likelihood a different mutated strain (which was hiding in the dendritic cells and macrophages) from the original infection. This is what leads to the sudden collapse of the CD8 T-cells and eventual collapse of the CD4 cells. Consequently, even if as you suggested, that we were able to knock-out the CD4 and CD8 cells, the "trojan horse" still remains.
The idea seems pretty insightful. I'm curious, however, as to what is the mechanism of preferential cell uptake and synthesis of the genetically engineered HIV strain if it is still using the same env gene (CD4 and CCR binding)? Did they also modify the tat and nef genes as well? Are there simply more viruses being made somehow, thus increasing its particular population?
The second thing I'm curious about is if the original HIV infection can be wiped out completely? We know that it hides out (M and T tropic strains) in the dendritic cells, lymph nodes, macrophages, etc., and can transfer from cell-to-cell without hematologic involvement, so it seems to me at least, that some latent virons of the original HIV infection will still be around.
They further suggest that the CD4 count increases, yet, how is this possible if the genetically engineered HIV strain is competing with the original strain? I'm assuming that the CD8 T-cells are possibly having an "easier" time fighting off the genetically engineered strain, and possibly giving its numbers a chance to bounce back up and stay elevated. This may lessen the burden on the CD4 cells, giving those numbers a chance to rise as well.
One problem, however, is that it's only a matter of time before the original HIV (T tropic) strain mutates. Normally, this would knock-off the humoral system, e.g., CD8 and CD4 counts plummet, just as the new strains begin their assault. With the genetically engineered strain, I'm not so sure what sequence this will occur.
Just an idea, if they can actually use this method, along with tweaking the surface antigen genes to actually mutate (and yes, there are millions of possibilities, and I'm assuming that natural selection doesn't require every possibility), we may actually be able to get the humoral system to recognize a sufficient number of antigenic sites and possibilities to be able to mount a full response, and eventually cure the person of HIV!
No predictions? How about super-symmetry? How about the graviton? If we develop the technology to visualize or measure a string at the Planck length, I'm sure that we can argue that string theory is testable. The notion that it is impossible to do such a measurement is nonsensical.
The argument basically comes down to while scientists have yet to come up with a stringent test of a string theory prediction, it does not mean that it will never be possible. Falsafiability does not take that into consideration, and hence one of the many criticisms of Popper.
How can string theory not even be wrong when even that statement doesn't have all the information?
The flaw once again is the assumption that it will never be testable. We are assuming that the only test is one that requires the scale of a galaxy or universe for that matter. We do not know enough about string theory yet to perhaps look for a simpler scale or experiment that can be carried out with current technology. Furthermore, as I mentioned before, these critics are relying on a notion of science that has set assumptions which themselves are subject to criticism and change. Flasification and testable hypotheses fit quite in line with Popper, but there are enough criticisms of his works which indicate that these are not absolutes nor logical necessities in all cases.
String theory may not fit in with those definitions, but that does not mean that it is a science that is ought not to be explored further. Once again, for general relativity to emerge naturally from string theory including the parameters for the graviton, we have at least an idea of what to look for if we could ever measure one. No theory can claim to have that.
How do we know that we will never be able to measure a single graviton (which is predicted to be close to the Planck length)? The history of science clearly demonstrates that when the experts said things were impossible, they were proven wrong.
String theory is too profound of a discovery to be simply something of mathematical elegance and pure chance.
Fundamentally, I have to disagree with the argument that string theory is not testable. It may currently not be testable, but that doesn't say that it will never be testable. Secondly, the author is the article is himself making the assumption that Kuhn or Popper's notions of scientific paradigms are entirely correct. In fact, an example from history is the marginal revolution (economic theory) which occured from 1871-1915 which does not conform to Kuhn's model of scientific change. The marginal revolution was not a response to important problems or anomalies that existed in the classical literature.
The author's reliance on these notions of Kuhn and Popper is the weakness in his argument.
String theorists may in fact argue that the elegance in their theory is unmatched by anything we currently have, and the fact that general relativity emerges naturally is profound even if we have yet to fully understand the implications.
These author's ought to therefore take their own advice and attempt to reconcile general relativity and quantum mechanics instead of bashing a theory which doesn't conform to their notions of what a theory ought to be.
I really find it hard to imagine that after over 30 years of work that string theory is wrong. Correct me if I'm mistaken, but as far as I know, string theory is the only generalization of quantum field theory that makes sense! For those who don't remember, general relativity and quantum field theory are not exactly compatible. Whereas quantum field theory makes it impossible to incorporate general relativity, string theory demands it! No other mathematical framework can claim to have that.
String theorists have yet to provide any empirical proof of their theory. This is not, however, sufficient reason to dismiss their theory outright. Testing some of the fundamental predictions of string theory may not currently be possible, but that does not mean that it will never be possible. What demands a plausible explanation, however, is why general relativity and quantum mechanics are not compatible with one another despite the failure to demonstrate an experiment which shows either theory to be wrong.
Yet, both theories cannot be entirely correct as general relativity "breaks-down" at the quantum scale, and quantum mechanics at larger scales. There must therefore be an underlying theory which combines the two, and the best we have today is string theory (or M-Theory for that matter).
I don't think Google could pull this off, at least at the scale that this article discusses. I doubt that there is enough dark fiber remaining in an amount comparable to even Akamai, one of the largest networks in the world.
Moreover, I doubt something like GoogleNet could even overtake the Internet as we know it. What I can see, however, is a GoogleNet in terms of a web service combining Google's all over the place software approach into a single unified framework.
Finally, as usual, I hope Google isn't discounting the presence of Microsoft. Microsoft, has in-fact, the world's largest VoIP and gaming network with Xbox Live, a fact that many people often seem to forget. And to think, it only took them a fairly short while to get it up and running.
I had the opportunity to actually take several courses with Dr. Reisz several years ago at UTM, including my first introduction to human anatomy and physiology course. At the time, I was certainly surprised to learn about the homology that musculoskeletal systems had across species, even those separated by millions of years of evolution.
I was also farily surprised to learn about some of the more optimal "solutions" that evolution came up with, including things such as the development of the cardiovascular systems ranging from say two-chambered hearts, to four-chambered hearts.
It's also very sensible to presume that quadrapeds eventually evolved into bipeds in some dinosaur species. Of course, all we needed was proof for that assumption, and that's what this discovery was all about.
Is it possible that the species found in the egg had congenital defects or was simply too small for its developmental age? Highly unlikely in my opinion. Too many other morphological factors involved.
On that end, I completely agree. I guess the differences come down to the PowerBook arguably looking aesthetically nicer, and also weighing a bit less. The PowerBook is also somewhat of a status symbol I'd suppose.
If Apple upgraded the video card to a 9600 or 9700 on the 12" PowerBook, I guess the price differential would be slightly more worth it.
Let's see. The PowerBook G4's offer: a larger screen, significantly better video cards, faster CPUs, backlight keyboard, Gigabit Ethernet, PC Card slots, and in my opinion, a much nicer build.
Personally, I'm surrounded by PC's all day, and whenever I bring in my PowerBook G4, I can't help but get stares and comments.
I know at least three people who say they're going to get an iBook in the next month to see what the Mac experience is all about. I've told them, however, that they're all going to end up buying a PowerBook anyhow. They've asked me why, and I've simply replied, "You'll see!", and smiled.
Finally, some of the features may sound useless, but the Gigabit ethernet actually comes in quite handy when having to looking DICOM and PACS images.
Making it Windows XP is in my opinion, a very wise move. Windows XP is already approaching 5 years of age, and it wouldn't really be sensible to have retroactive support for any of their older operating systems. Moreover, it would probably be in Microsoft's best interests to keep the browser tied to SP2 and beyond.
Just think of the reasons why the average computer user will use IE. Is it because it is a better browser? Or is it convenience? Or do they not know any better? Probably the latter two reasons.
Why do I use Firefox as opposed to IE? Tabbed browsing and plugins, namely AdBlock. Even on my PowerBook G4, I still tend to use Firefox over Safari only simply because of AdBlock. Other than that reason, I'd primarily be using Safari (and no, I don't use PithHelmet). Heck, most Mac users I know use Safari because that's what came with their computer. Hence, the same reasoning for Windows users using IE applies to Mac users using Safari.
Ultimately, I think IE use will actually increase after IE7 is released.
ECT is horrible, I agree. I cannot even imagine how it was before the days of having muscle relaxants! Remember though, it is only suggested refractory to other treatments. I personally believe that NSRIs (eg: Effexor) along with cognitive therapy are the best course of treatment at the moment.
About the sleep apnea. Makes sense. They did, however, encounter patients who have horseness of breath which suggests that the recurrent laryngeals (branches of the vagus which supply the intrinsic muslces of the larynx except the cricothyroid) are getting too much stimulation. You're right though, perhaps with some tweaking, it could be made to work.
I'm sure that's definitely a posibility, and in many cases, maybe the etiology of the disease.
One of the questions I have to raise, however, is why there is a sudden decrease in NE and 5-HT activity? Because major depressive disorder also tends to run in families, that would suggest that there is some underlying genetic problem where behavioural modification may not always treat the root of the problem.
Ultimately, drugs along with therapy have tended to show the best results. That may of course change the more we learn:)
Sorry that you feel that way. First of all, I didn't mention that SSRIs are the be-all, end-all treatment options. Far from it in fact.
I believe that I mentioned Venalfaxine (Effexor), which isn't really a SSRI. Heck, we can also give MAOIs; Nardil, Parnate, Eldepryl, etc. Don't forget suicide related to tyramine with those though;)
Hrm, off the top of my head, we can also use sibutramine which is typically used for obesity treatments, off-label for depression. It blocks the reuptake of our typical three: NE, 5-HT, and DA.
With regards to depakote, those effects are well known for bipolar. We can also give tegretol for that (both drugs usually for the manic phase though). SSRIs are typical for the depressive state.
Anyhow, I already admited my ignorance of the vagus nerve stimulation and of treatments related to it. Perhaps the vagus nerve has some effect in the locus coeruleus? We can sit and argue here all day about what we can use to treat these people and how much we think we know. At the end of the day, although we think we know a lot, we "know" very little and we ought to humble ourselves with that.
Sorry to hear about your disease. Nevertheless, you cannot deny the objective evidence with regards to NE and 5-HT (in the locus coeruleus, etc.). With that in mind, we have seen clear objective evidence that drugs such as SSRIs have significantly improved the lives of (and "cured") many people.
I assume that you know some of the drug treatments available; Effexor, Wellbutrin, Zyban, Celexa, Prozac, etc. I also assume that you know that ECT is another treatment option for major depressive disorder refractory to other treatment.
You simply cannot take your single example and suggest that your self-medicating is a solution that will work for everyone. It may (appear to) work for you, but suggesting that you do not have a neurochemical imbalance isn't necessarily objective.
Do you what one of the major causes of death is with people who have major depressive disorder? Suicide. Not a good thing.
Sorry, be depression (chronic or acute) is characterized by decreased levels of norepinephrine (NE) and serotonin (5-HT) in the brain. This causes depressed mood since serotonin is one of the primary neurotransmitters involved in the regulation of mood. How is it when 5-HT imbalances are corrected that the patient's mood's are enhanced? If that's not a disease, then what is?
Coming from a medical perspective, I'm finding it a little difficult to understand what exactly vagus nerve stimulation has to do with depression.
Firstly, depression is characterized by decreased levels of norepinephrine (NE) and serotonin (5-HT). They also have a depressed mood or anhendonia, along with 5 other specifiers (according to the DSM-IV) including sleep disturbances, loss of interest, guilt, etc.
Nearly every current line of treatment that I know of has nothing to do with vagus nerve stimulation. And although the vagus nerve has several branches for structures in the proximity of the brain, it hasn't really been shown (as far as I know) to have anything to do with depression.
In fact, drugs which attack the neurotransmitter complications are used. These may include, Venalfaxine (Effexor) is a reuptake inhibitor of 5-HT and NE(?), and SSRIs including Prozac and Celexa, which block the reuptake of 5-HT can also be perscribed. This means that these neurotransmitters remain in their respective synaptic clefts longer, hence resulting in mood enhancement.
The vagus nerve stimulators enhances vagus nerve activity (which is parasympathetic) resulting in heart rate decrease, GI motility and secretion, etc. In other words, things that the body does when it is in a relaxed state. Perhaps their relaxed states result in enhanced mood?
Ultimately, if a patient has severe chronic depression that does not respond to any of these treatments, they have a choice of undergoing electroconvulsive therapy which somehow "resets" the brains, and somehow "resets" the neurochemical imbalance.
It's no wonder that Steve Jobs et. al. decided not to pursue the Cell microprocessor for Apple's future! Most likely, Apple compared it to the G5 and Intel CPUs and found its real-world performance to be significantly lacking.
Indirectly at least, this article basically demonstrates why Apple decided to go Intel.
I didn't say that it is not feasible, I said that it was not really feasible. I completely agree that it is possible to use all these Office "clones" and most of the time, not have any document incompatibilities. However, the main issue is that MS Office is the de facto standard.
An earlier claim arguing that MS Office is constrained because it cannot import native Keynote files is problematic because Keynote is not a de facto standard whatsoever. Unfortunately, that semantical argument doesn't work in this context.
People are constrained by their employers choice of software, and the fact that most organizations and academic institutions have standardized on MS Office isn't a coincidence either.
Moreover, the first thing that most people unfamiliar to the Macintosh platform usually worry about is if MS Office works. Just something to think about.
Although it's great to have a number of office applications, Microsoft Office is still the de facto standard whether some of us like it or not.
A lot of these Office clones seem to be fairly limited in function as compared to MS Office. For example, Apple Keynote still tends to loose a lot of formatting when importing PowerPoint documents. From Office 2004 to 2003 (on PC), however, I have yet to encounter any such problems. In the professional world, this is a fact of life everyday, and taking the risk of possible document incompatibilities is one often not taken.
At the end of the day, it is great to have alternatives. Moving away from MS Office, however, is not really feasible in the real world (well, not yet at least!)
Plus, students can get a huge discount on Office 2004 anyhow. Is free better than $100 or so? That's for you to decide.
I certainly would not perscribe oxytocin for these purposes. Oxytocin is typically used to induce labor and reduce postpartum bleeding.
In terms of mechanism of action, during pregnancy, oxytocin receptors in the uterus are up-regulated and the release of oxytocin from the posterior pituitary results in one of the few positive feedback mechanisms in the human body.
Despite this, the role of oxytocin in normal labor is uncertain.
We certainly do not want to be using it for "trust" if we do not even know how it fully functions during normal labor.
In a traditional bookbuilding IPO, the discretion employed by the underwriters ought to eliminate problems associated with information asymmetry, and ought to decrease average levels of underpricing. This should consequently result in the underwriter maximizing the issuer's initial capital gains. Nonetheless, this lies on the assumption that there are minimal conflicts of interest, and that these interests are controlled. Loughran and Ritter (2004), however, found that underwriters quite often will allocate shares on the basis of previous business with certain institutional investors. The "dot con" was a perfect example of this.
At times, these investors would also have to give commissions back to the underwriter in return for share allocations in some favorable IPOs. It can therefore be argued that the underwriter also has incentives to not act in the best interest of the issuer, and we can clearly see this when the average underpricing of a stock is significant.
One of the risks of using the auction is that those who bid very high can potentially corrupt the process, and cause inaccurate pricing. What may occur is that an institutional investor could bid at a (significantly) elevated level to ensure a share allocation. Their bid may not be representative of what they consider the value of the company to be. Nonetheless, if bidders are considered rational economic agents, high bidding will not only occur with a few investors, since people would expect a large degree of high bidding. This would therefore be incorporated in their valuation of the issuing company. Hence, the argument that if everyone overbids that the IPO will be overpriced may not necessarily be true in all circumstances. And Wall Street hates this theoretical implication, and the fact that they lose their leverage.
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I don't think that having so-called "experts" contributing to Google Knol is necessarily going to make it a better overall resource that Wikipedia for several reasons.
Firstly, a lot of these early articles are seriously lacking. Let's take for example, the article on Methicillin Resistant Staphlococcus Aureus (MRSA). It's a generally well-written article, and the author looks to be fairly reputable. Nonetheless, there are arguably some significant deficiencies, that with the current format of Knol, cannot be rectified.
In the article's description, the author notes that there will be a discussion on how MRSA can be treated. Yet, when you look at that portion of the article, information on management is seriously lacking, and the description of the medications is ultimately quite useless.
At least with Wikipedia, the article would link to a corresponding article on the specific antibiotic, so you would have the opportunity to easily gain further information, whereas with Knol, this simple linking procedure is currently lacking significantly.
Now, for a simple example. Having a description that Vancomycin "is considered first line treatment" for MRSA is useless for any practicing clinician. What I would want to know are things such as dosing regimens, important things to remember such as having to measure Vancomycin trough levels every several doses (and why), what alternative medications I can use if the MRSA strain is resistant to Vancomycin, etc., all of which are extremely important in the management of MRSA. There is also a significant lack of information about what strains are prevalent, which although not necessarily important for an Internist, is important for Infectious Disease specialists, the people who are consulted on a daily basis for the management of MRSA.
I can continue to criticize the article, but the difference between it, and the Wikipedia entry are night-and-day. And my criticism isn't pointed to this article alone, there are countless very poorly written and uninformative medical articles on there thus far.
A community effort with anonymous editors will (eventually) weed out mistakes, and have the distinct advantage of constant peer review. Knol on the other hand, is unfortunately stuck with the one author knows best paradigm.
I think there have been a good number of misconceptions about Microsoft's $45 billion offer for Yahoo!, and there are a few points that we ought to make note of.
Firstly, Microsoft's valuation indicates their valuation of Yahoo! being part of Microsoft. Synergies account for the higher value!
Secondly, with the offer, Yahoo! is now "in play", and there is a consequent expectation that someone such as Google may come along and make an offer. Since it is in play, people expect an offer that comes at a premium (which of course gets priced in!). Now, this is implicitly priced into the 62% premium that Microsoft has offered, and they have set it high enough (in their estimate) so as to price out any potential offers from others.
If Google decides to get involved, they have plenty of antitrust concerns in terms of an overall takeover bid. Can they take a play out of Microsoft's playbook (e.g., 1.6% stake in Facebook) and offer a larger premium for a substantial stake of the company (e.g., $60/share for say 35% of Yahoo!)? I would not be surprised if we see such a strategy.
First of all, I am coming from a medical background, and I also have friends who are graduate students of several of the scientists cited in the article.
So, basically, here's what's going on. Clinically detectable tumors consist of heterogeneous population of cells which originate from a clonal growth of the progeny of a single cell (e.g., the monoclonal origin of neoplasms, Knudson two-hit hypothesis, etc.). Tumor stem cells (called Tumor Initiating Cells, T-ICs) not only have the capacity to initiate, but, ultimately sustain tumor growth. These cells, however, only constitute only about 0.1-2% of the total population of cells and like their normal counterparts, and have a very low rate of replication. Now do we see what the problem is?
A lot of our current drugs and therapies target the fast growing progeny of the T-ICs which constitute over 98% of the cells in the cancer, leaving the slow growing T-ICs alone! Consequently, that means that some tumors can easily recur after treatment. In other words, our drugs may have been targeting the wrong cells this entire time!
You asked a good question. The problem, however, is that HIV not only invades CD4+ cells (which are derived from lymphoid progenitor cells), but also dendritic cells and macrophages (derived from myelomonocytic progentor cells). My immunology professor back in medical school made the analogy that macrophages are like a "trojan horse" where HIV can hide out. In addition, one common misconception is that the HIV strain towards the end stages of the disease is not the same strain that the patient was infected with. It is in all likelihood a different mutated strain (which was hiding in the dendritic cells and macrophages) from the original infection. This is what leads to the sudden collapse of the CD8 T-cells and eventual collapse of the CD4 cells. Consequently, even if as you suggested, that we were able to knock-out the CD4 and CD8 cells, the "trojan horse" still remains.
The idea seems pretty insightful. I'm curious, however, as to what is the mechanism of preferential cell uptake and synthesis of the genetically engineered HIV strain if it is still using the same env gene (CD4 and CCR binding)? Did they also modify the tat and nef genes as well? Are there simply more viruses being made somehow, thus increasing its particular population?
The second thing I'm curious about is if the original HIV infection can be wiped out completely? We know that it hides out (M and T tropic strains) in the dendritic cells, lymph nodes, macrophages, etc., and can transfer from cell-to-cell without hematologic involvement, so it seems to me at least, that some latent virons of the original HIV infection will still be around.
They further suggest that the CD4 count increases, yet, how is this possible if the genetically engineered HIV strain is competing with the original strain? I'm assuming that the CD8 T-cells are possibly having an "easier" time fighting off the genetically engineered strain, and possibly giving its numbers a chance to bounce back up and stay elevated. This may lessen the burden on the CD4 cells, giving those numbers a chance to rise as well.
One problem, however, is that it's only a matter of time before the original HIV (T tropic) strain mutates. Normally, this would knock-off the humoral system, e.g., CD8 and CD4 counts plummet, just as the new strains begin their assault. With the genetically engineered strain, I'm not so sure what sequence this will occur.
Just an idea, if they can actually use this method, along with tweaking the surface antigen genes to actually mutate (and yes, there are millions of possibilities, and I'm assuming that natural selection doesn't require every possibility), we may actually be able to get the humoral system to recognize a sufficient number of antigenic sites and possibilities to be able to mount a full response, and eventually cure the person of HIV!
No predictions? How about super-symmetry? How about the graviton? If we develop the technology to visualize or measure a string at the Planck length, I'm sure that we can argue that string theory is testable. The notion that it is impossible to do such a measurement is nonsensical.
The argument basically comes down to while scientists have yet to come up with a stringent test of a string theory prediction, it does not mean that it will never be possible. Falsafiability does not take that into consideration, and hence one of the many criticisms of Popper.
How can string theory not even be wrong when even that statement doesn't have all the information?
The flaw once again is the assumption that it will never be testable. We are assuming that the only test is one that requires the scale of a galaxy or universe for that matter. We do not know enough about string theory yet to perhaps look for a simpler scale or experiment that can be carried out with current technology. Furthermore, as I mentioned before, these critics are relying on a notion of science that has set assumptions which themselves are subject to criticism and change. Flasification and testable hypotheses fit quite in line with Popper, but there are enough criticisms of his works which indicate that these are not absolutes nor logical necessities in all cases.
String theory may not fit in with those definitions, but that does not mean that it is a science that is ought not to be explored further. Once again, for general relativity to emerge naturally from string theory including the parameters for the graviton, we have at least an idea of what to look for if we could ever measure one. No theory can claim to have that.
How do we know that we will never be able to measure a single graviton (which is predicted to be close to the Planck length)? The history of science clearly demonstrates that when the experts said things were impossible, they were proven wrong.
String theory is too profound of a discovery to be simply something of mathematical elegance and pure chance.
Fundamentally, I have to disagree with the argument that string theory is not testable. It may currently not be testable, but that doesn't say that it will never be testable. Secondly, the author is the article is himself making the assumption that Kuhn or Popper's notions of scientific paradigms are entirely correct. In fact, an example from history is the marginal revolution (economic theory) which occured from 1871-1915 which does not conform to Kuhn's model of scientific change. The marginal revolution was not a response to important problems or anomalies that existed in the classical literature.
The author's reliance on these notions of Kuhn and Popper is the weakness in his argument.
String theorists may in fact argue that the elegance in their theory is unmatched by anything we currently have, and the fact that general relativity emerges naturally is profound even if we have yet to fully understand the implications.
These author's ought to therefore take their own advice and attempt to reconcile general relativity and quantum mechanics instead of bashing a theory which doesn't conform to their notions of what a theory ought to be.
I really find it hard to imagine that after over 30 years of work that string theory is wrong. Correct me if I'm mistaken, but as far as I know, string theory is the only generalization of quantum field theory that makes sense! For those who don't remember, general relativity and quantum field theory are not exactly compatible. Whereas quantum field theory makes it impossible to incorporate general relativity, string theory demands it! No other mathematical framework can claim to have that.
String theorists have yet to provide any empirical proof of their theory. This is not, however, sufficient reason to dismiss their theory outright. Testing some of the fundamental predictions of string theory may not currently be possible, but that does not mean that it will never be possible. What demands a plausible explanation, however, is why general relativity and quantum mechanics are not compatible with one another despite the failure to demonstrate an experiment which shows either theory to be wrong.
Yet, both theories cannot be entirely correct as general relativity "breaks-down" at the quantum scale, and quantum mechanics at larger scales. There must therefore be an underlying theory which combines the two, and the best we have today is string theory (or M-Theory for that matter).
I don't think Google could pull this off, at least at the scale that this article discusses. I doubt that there is enough dark fiber remaining in an amount comparable to even Akamai, one of the largest networks in the world.
Moreover, I doubt something like GoogleNet could even overtake the Internet as we know it. What I can see, however, is a GoogleNet in terms of a web service combining Google's all over the place software approach into a single unified framework.
Finally, as usual, I hope Google isn't discounting the presence of Microsoft. Microsoft, has in-fact, the world's largest VoIP and gaming network with Xbox Live, a fact that many people often seem to forget. And to think, it only took them a fairly short while to get it up and running.
I had the opportunity to actually take several courses with Dr. Reisz several years ago at UTM, including my first introduction to human anatomy and physiology course. At the time, I was certainly surprised to learn about the homology that musculoskeletal systems had across species, even those separated by millions of years of evolution.
I was also farily surprised to learn about some of the more optimal "solutions" that evolution came up with, including things such as the development of the cardiovascular systems ranging from say two-chambered hearts, to four-chambered hearts.
It's also very sensible to presume that quadrapeds eventually evolved into bipeds in some dinosaur species. Of course, all we needed was proof for that assumption, and that's what this discovery was all about.
Is it possible that the species found in the egg had congenital defects or was simply too small for its developmental age? Highly unlikely in my opinion. Too many other morphological factors involved.
On that end, I completely agree. I guess the differences come down to the PowerBook arguably looking aesthetically nicer, and also weighing a bit less. The PowerBook is also somewhat of a status symbol I'd suppose.
If Apple upgraded the video card to a 9600 or 9700 on the 12" PowerBook, I guess the price differential would be slightly more worth it.
Let's see. The PowerBook G4's offer: a larger screen, significantly better video cards, faster CPUs, backlight keyboard, Gigabit Ethernet, PC Card slots, and in my opinion, a much nicer build.
Personally, I'm surrounded by PC's all day, and whenever I bring in my PowerBook G4, I can't help but get stares and comments.
I know at least three people who say they're going to get an iBook in the next month to see what the Mac experience is all about. I've told them, however, that they're all going to end up buying a PowerBook anyhow. They've asked me why, and I've simply replied, "You'll see!", and smiled.
Finally, some of the features may sound useless, but the Gigabit ethernet actually comes in quite handy when having to looking DICOM and PACS images.
Making it Windows XP is in my opinion, a very wise move. Windows XP is already approaching 5 years of age, and it wouldn't really be sensible to have retroactive support for any of their older operating systems. Moreover, it would probably be in Microsoft's best interests to keep the browser tied to SP2 and beyond.
Just think of the reasons why the average computer user will use IE. Is it because it is a better browser? Or is it convenience? Or do they not know any better? Probably the latter two reasons.
Why do I use Firefox as opposed to IE? Tabbed browsing and plugins, namely AdBlock. Even on my PowerBook G4, I still tend to use Firefox over Safari only simply because of AdBlock. Other than that reason, I'd primarily be using Safari (and no, I don't use PithHelmet). Heck, most Mac users I know use Safari because that's what came with their computer. Hence, the same reasoning for Windows users using IE applies to Mac users using Safari.
Ultimately, I think IE use will actually increase after IE7 is released.
ECT is horrible, I agree. I cannot even imagine how it was before the days of having muscle relaxants! Remember though, it is only suggested refractory to other treatments. I personally believe that NSRIs (eg: Effexor) along with cognitive therapy are the best course of treatment at the moment.
About the sleep apnea. Makes sense. They did, however, encounter patients who have horseness of breath which suggests that the recurrent laryngeals (branches of the vagus which supply the intrinsic muslces of the larynx except the cricothyroid) are getting too much stimulation. You're right though, perhaps with some tweaking, it could be made to work.
I'm sure that's definitely a posibility, and in many cases, maybe the etiology of the disease.
:)
One of the questions I have to raise, however, is why there is a sudden decrease in NE and 5-HT activity? Because major depressive disorder also tends to run in families, that would suggest that there is some underlying genetic problem where behavioural modification may not always treat the root of the problem.
Ultimately, drugs along with therapy have tended to show the best results. That may of course change the more we learn
Sorry that you feel that way. First of all, I didn't mention that SSRIs are the be-all, end-all treatment options. Far from it in fact.
;)
I believe that I mentioned Venalfaxine (Effexor), which isn't really a SSRI. Heck, we can also give MAOIs; Nardil, Parnate, Eldepryl, etc. Don't forget suicide related to tyramine with those though
Hrm, off the top of my head, we can also use sibutramine which is typically used for obesity treatments, off-label for depression. It blocks the reuptake of our typical three: NE, 5-HT, and DA.
With regards to depakote, those effects are well known for bipolar. We can also give tegretol for that (both drugs usually for the manic phase though). SSRIs are typical for the depressive state.
Anyhow, I already admited my ignorance of the vagus nerve stimulation and of treatments related to it. Perhaps the vagus nerve has some effect in the locus coeruleus? We can sit and argue here all day about what we can use to treat these people and how much we think we know. At the end of the day, although we think we know a lot, we "know" very little and we ought to humble ourselves with that.
Sorry to hear about your disease. Nevertheless, you cannot deny the objective evidence with regards to NE and 5-HT (in the locus coeruleus, etc.). With that in mind, we have seen clear objective evidence that drugs such as SSRIs have significantly improved the lives of (and "cured") many people.
I assume that you know some of the drug treatments available; Effexor, Wellbutrin, Zyban, Celexa, Prozac, etc. I also assume that you know that ECT is another treatment option for major depressive disorder refractory to other treatment.
You simply cannot take your single example and suggest that your self-medicating is a solution that will work for everyone. It may (appear to) work for you, but suggesting that you do not have a neurochemical imbalance isn't necessarily objective.
Do you what one of the major causes of death is with people who have major depressive disorder? Suicide. Not a good thing.
Sorry, be depression (chronic or acute) is characterized by decreased levels of norepinephrine (NE) and serotonin (5-HT) in the brain. This causes depressed mood since serotonin is one of the primary neurotransmitters involved in the regulation of mood. How is it when 5-HT imbalances are corrected that the patient's mood's are enhanced? If that's not a disease, then what is?
Coming from a medical perspective, I'm finding it a little difficult to understand what exactly vagus nerve stimulation has to do with depression.
Firstly, depression is characterized by decreased levels of norepinephrine (NE) and serotonin (5-HT). They also have a depressed mood or anhendonia, along with 5 other specifiers (according to the DSM-IV) including sleep disturbances, loss of interest, guilt, etc.
Nearly every current line of treatment that I know of has nothing to do with vagus nerve stimulation. And although the vagus nerve has several branches for structures in the proximity of the brain, it hasn't really been shown (as far as I know) to have anything to do with depression.
In fact, drugs which attack the neurotransmitter complications are used. These may include, Venalfaxine (Effexor) is a reuptake inhibitor of 5-HT and NE(?), and SSRIs including Prozac and Celexa, which block the reuptake of 5-HT can also be perscribed. This means that these neurotransmitters remain in their respective synaptic clefts longer, hence resulting in mood enhancement.
The vagus nerve stimulators enhances vagus nerve activity (which is parasympathetic) resulting in heart rate decrease, GI motility and secretion, etc. In other words, things that the body does when it is in a relaxed state. Perhaps their relaxed states result in enhanced mood?
Ultimately, if a patient has severe chronic depression that does not respond to any of these treatments, they have a choice of undergoing electroconvulsive therapy which somehow "resets" the brains, and somehow "resets" the neurochemical imbalance.
It's no wonder that Steve Jobs et. al. decided not to pursue the Cell microprocessor for Apple's future! Most likely, Apple compared it to the G5 and Intel CPUs and found its real-world performance to be significantly lacking.
Indirectly at least, this article basically demonstrates why Apple decided to go Intel.
I didn't say that it is not feasible, I said that it was not really feasible. I completely agree that it is possible to use all these Office "clones" and most of the time, not have any document incompatibilities. However, the main issue is that MS Office is the de facto standard.
An earlier claim arguing that MS Office is constrained because it cannot import native Keynote files is problematic because Keynote is not a de facto standard whatsoever. Unfortunately, that semantical argument doesn't work in this context.
People are constrained by their employers choice of software, and the fact that most organizations and academic institutions have standardized on MS Office isn't a coincidence either.
Moreover, the first thing that most people unfamiliar to the Macintosh platform usually worry about is if MS Office works. Just something to think about.
Although it's great to have a number of office applications, Microsoft Office is still the de facto standard whether some of us like it or not.
A lot of these Office clones seem to be fairly limited in function as compared to MS Office. For example, Apple Keynote still tends to loose a lot of formatting when importing PowerPoint documents. From Office 2004 to 2003 (on PC), however, I have yet to encounter any such problems. In the professional world, this is a fact of life everyday, and taking the risk of possible document incompatibilities is one often not taken.
At the end of the day, it is great to have alternatives. Moving away from MS Office, however, is not really feasible in the real world (well, not yet at least!)
Plus, students can get a huge discount on Office 2004 anyhow. Is free better than $100 or so? That's for you to decide.
I certainly would not perscribe oxytocin for these purposes. Oxytocin is typically used to induce labor and reduce postpartum bleeding.
In terms of mechanism of action, during pregnancy, oxytocin receptors in the uterus are up-regulated and the release of oxytocin from the posterior pituitary results in one of the few positive feedback mechanisms in the human body.
Despite this, the role of oxytocin in normal labor is uncertain.
We certainly do not want to be using it for "trust" if we do not even know how it fully functions during normal labor.
In a traditional bookbuilding IPO, the discretion employed by the underwriters ought to eliminate problems associated with information asymmetry, and ought to decrease average levels of underpricing. This should consequently result in the underwriter maximizing the issuer's initial capital gains. Nonetheless, this lies on the assumption that there are minimal conflicts of interest, and that these interests are controlled. Loughran and Ritter (2004), however, found that underwriters quite often will allocate shares on the basis of previous business with certain institutional investors. The "dot con" was a perfect example of this.
At times, these investors would also have to give commissions back to the underwriter in return for share allocations in some favorable IPOs. It can therefore be argued that the underwriter also has incentives to not act in the best interest of the issuer, and we can clearly see this when the average underpricing of a stock is significant.
One of the risks of using the auction is that those who bid very high can potentially corrupt the process, and cause inaccurate pricing. What may occur is that an institutional investor could bid at a (significantly) elevated level to ensure a share allocation. Their bid may not be representative of what they consider the value of the company to be. Nonetheless, if bidders are considered rational economic agents, high bidding will not only occur with a few investors, since people would expect a large degree of high bidding. This would therefore be incorporated in their valuation of the issuing company. Hence, the argument that if everyone overbids that the IPO will be overpriced may not necessarily be true in all circumstances. And Wall Street hates this theoretical implication, and the fact that they lose their leverage.