The biomedical industry has one major difference when compared to the IT industry. Biology is a basic science, making microchips is not - it is engineering. The importance of both - science and engineering in generating technology and benefits to the human race (and so on), is not under debate. But fighting against fundamental issues in nature, or solving them is much harder than making smaller microchips.
There are of course, comparable scenarios when you move to the cutting-edge of the IT industry - how long have we heard of quantum computing? 10 years ? In an industry that proceeds with just darting pace, I don't have a quantum computer on my desktop yet. Is it because the researchers are incompetent ? No. It's because the problems they are trying to solve are inherently hard.
How long does it take to invent new mathematics on which useful algorithms can be built ?
Besides , biology changes with time, context, and is inherently and mathematically a complex, if not chaotic system. Anyone who has visited the E-Cell project knows how hard it is to create a standard working model of a single minimum cell, let alone create models of organisms, colonies, ecologies, epidemiologies and disease states.
Silicon, though, does not change its behaviour based on context, the complexity in creating circuits does not by far approach that of living organisms. In one way, the IT industry has been surfing the semi-conductor break-through wave for some time...and we all know what Moore's law predicts. It's hard to say what will happen in the future, but barring economic factors, the current availability of technology is only a reflection of our level of understanding and the maturity of a science. It is NOT necessarily an indicator of the competence or lethargy of the scientists pursuing a particular field.
What Mr.CEO of Intel, does not know is how much biotechnology has changed the last century. How does he think his bread, wine, beer, antibiotics, industrial chemicals like acetone, textiles, (the list goes on) are produced. What of the eradication of small pox, near total eradication of poliomyelitis, MDR for tuberculosis, 80% survival rate for breast and prostate cancer..and so on ?
These things didn't occur on their own. The community worked hard to solve these problems, even if partially.
Unfortunately, ars technica and by consequence Slashdot, have completely mis-interpreted the original paper, at least regarding the headline used. As many people have stated, there is no wonder in finding that there are genome instability hot-spots. This has been known for years. What was not obvious , is the existence of hot-spots leading to a specific kind of mutation - i.e , copy number variation (CNV). Even though CNVs are mutations in the classical sense, modern molecular biology reserves the term 'mutation' for single nucleotide or codon changes. Drastic changes at the genomic, chromosomal or transcript level are generally called by their specific names such as deletion, truncation, transposition, duplication etc. What this study seems to suggest is that certain regions of the genome (irrespective, it seems, if these regions are genes or have a known biological function) seem to have a fluctuating copy number in the genome, with the rate of fluctuation much higher than expected in a random process - suggesting the existence of a mechanism that allows for this fluctuation to occur. It implies, that evolution has caused these particular regions to become uncoupled from potential lethality or drastic abnormality that arises in organisms , when similar variations occur on other regions (for example: variation in X-chromosome number leads to Turner or Klinefelter's syndrome). The interesting question that I see, is if there is a mechanism that allows this "tolerance" to exist to variations in these particular regions, and if there is such a mechanism, can it be tailored to allow changes in other regions...leading to the possibility of creating strains of organisms specially suited for particular scientific experiments-with multiple copies of a gene etc. - animals that currently are simply impossible to create because these changes are lethal. A far shot would be therapeutics. There are certain diseases that arise simply because of a cells inability to tolerate certain changes in the genome, irrespective of whether those changes are the cause of the lethality. In other words, the cells defense system itself is the cause of the disease rather than the genetic change. This might be the case in several autoimmune diseases or developmental diseases where upon sensing a genetic change, cells undergo apoptosis - irrespective of whether the genetic change is detrimental during the natural life of the cell. So, if one reads the Nature article, there is really some news there
Unfortunately, ars technica and by consequence Slashdot, have completely mis-interpreted the original paper, at least regarding the headline used.
As many people have stated, there is no wonder in finding that there are genome instability hot-spots. This has been known for years. What was not obvious , is the existence of hot-spots leading to a specific kind of mutation - i.e , copy number variation (CNV). Even though CNVs are mutations in the classical sense, modern molecular biology reserves the term 'mutation' for single nucleotide or codon changes. Drastic changes at the genomic, chromosomal or transcript level are generally called by their specific names such as deletion, truncation, transposition, duplication etc.
What this study seems to suggest is that certain regions of the genome (irrespective, it seems, if these regions are genes or have a known biological function) seem to have a fluctuating copy number in the genome, with the rate of fluctuation much higher than expected in a random process - suggesting the existence of a mechanism that allows for this fluctuation to occur. It implies, that evolution has caused these particular regions to become uncoupled from potential lethality or drastic abnormality that arises in organisms , when similar variations occur on other regions (for example: variation in X-chromosome number leads to Turner or Klinefelter's syndrome).
The interesting question that I see, is if there is a mechanism that allows this "tolerance" to exist to variations in these particular regions, and if there is such a mechanism, can it be tailored to allow changes in other regions...leading to the possibility of creating strains of organisms specially suited for particular scientific experiments-with multiple copies of a gene etc. - animals that currently are simply impossible to create because these changes are lethal.
A far shot would be therapeutics. There are certain diseases that arise simply because of a cells inability to tolerate certain changes in the genome, irrespective of whether those changes are the cause of the lethality. In other words, the cells defense system itself is the cause of the disease rather than the genetic change. This might be the case in several autoimmune diseases or developmental diseases where upon sensing a genetic change, cells undergo apoptosis - irrespective of whether the genetic change is detrimental during the natural life of the cell.
So, if one reads the Nature article, there is really some news there.
"The work in our laboratory was initiated after the last world war by calculations of maximal efficiencies for some field crops, taking high annual yields in Holland, from agricultural data, making allowance for roots, stubbles, etc., and comparing them with the average energy on the cultivated surface during the growth period (27). Considering only wave lengths available for photosynthesis, the efficiencies were between 0.5 and 2 %, and the large deviation from photosynthetic efficiency in laboratory experiments of short duration-viz., 20 to 30 %-was the starting point of our work. Earlier computations of efficiency of higher plant growth are discussed in detail in (11). The possible reasons for the relatively low long term efficiency are as follows (27): 1) too high incident light intensities under field conditions; 2) too low C02 content of the air; 3) too low temperatures; 4) other limiting factors, e.g., too little water; 5)loss of light between the plants; and 6) factors, provisionally difficult for analysis, e.g., fluctuating rate of photosynthesis, possible "afternoon depression," respiratory losses."
learning to use a mathematics package like Mathematica or MATLAB. I'd go with the former to begin with. I just got a book that solved some basic scientific questions regarding making models of physiological processes and tried to replicate those in Mathematica. In the process of learning the syntax for Mathematica, you're forced to learn calculus, which I used Google search for in order to understand the problem completely.
The result was very satisfactory because the computer did the number crunching, I could concentrate on the conceptual understanding in calculus rather than spending time doing calculations by hand.
Well, since Platensimycin inhibits FabF, which is 3-oxo-[acyl carrier protein] synthase II, and vancomycin prevents incorporation of N-acetylmuramic acid and N-acetylglucosamine - peptide subunits from being incorporated into the peptidoglycan matrix;
their mechanisms are exclusive. Theoretically, Platensimycin will therefore work on both MRSA and VRSA strains. Practically, strain sensitivities vary , but with the current level of information, one would expect the new drug to be just as effective on VRSA strains.
There is a catch to this. A lot of mutations[I use the term loosely as it is used on Slashdot] occur due to the individuals tendency to acquire them, ie, genetic predisposition.
If somatic cell mutations occur and confer an advantage to the organism, it will presumably manifest as a greater chance for the organism to pass on its genes, and thus pass on the genetic predisposition to acquire that mutation.
One on-field implication of this, is that many types of cancers tend to develop resistance to drugs through identical (!) molecular mchanisms, even though resistance is obviously developed de novo in different individuals with the same type of cancer. This is because the administration of a same drug applies identical selection pressure and thus causes the identical, (apparently) most probable and stable phenotype to appear in the cells.
I do not understand what the fuss is about here. I am not talking about the ID-Evo debate.
What the good Dr.Thornton seems to have discovered, is only a case of moonlighting, which is well known in biology. Moonlighting is the phenomenon when a single protein fulfills several, often unrelated and even more often unexpected functions in a cell. Biologists are aware of this fact, and hence understand this to be one of the basic ways in which molecular evolution occurs. The fact that an aldosterone receptor can exist before aldosterone is not really surprising. Drug designers are designing molecules all the time for which receptors already exist.
Basically, I do not think that it is a novel as the NYtimes would have us beleive.
Here is an interesting paper describing several such moonlighting occurences.[Warning: PDF]. Further a presentation for non-biologists on moonlighting is here
One of the leading researchers in the field of moonlighting proteins is Dr.Joel Sussman. He works on how the AChE enzyme may be affecting a variety of other aspects in neural cell biology.
They did a similar thing with the iPod screens getting sctratched.
So let me get this, rolling out defective a product and then doing excellent service to fix it, is a good business strategy ?
No wonder Apple could never make gross profits.
I use Openoffice 2.0 on my computer and be advised that I faced serious compatibility issues when editing certain Microsoft Word (Office XP) files in Openoffice writer. These files were edited using the "Track changes" option in MS Office, that allows you to automatically mark changes that you have made to the file. Openoffice simply does not understand such a file and loads it without the accompanying change tracking information.
Admiteddly, I liked OpenOffice at first and thought that MS Office could finally be replaced. However, several experiences (problems with huge loading time, slowing down the PC, OpenDocument format not popular etc.), including the above mentioned one, have forced me back to MS Office, and my personal conclusion is that MS Office has a lot more features and is much better as a regular word processing app. I hate paying Microsoft, but in this case, they take the cake. I'll have to wait for Oo3.
PS : The only OO features that I noticed MS does not have, are the ability to render equations and make PDFs. However, MS Office + MathType + Adobe Acrobat Prof./any free PDF renderer can take care of that.
Well, I think that may be an accent issue. To tell you the truth, I never heard an Indian speak English the way Apu does.
The French have an accent, the Dutch have an accent. Hell, even the English have their own accent. But so far, honestly, I have only heard Americans claim that their's is the "correct" way to pronounce/speak English.
English is generally spoken well in India because of the reason that very early on, in about the 1850s, the British colonists discovered that there are too many sub-cultures and corresponding number of languages here (75 major languages and 1430 dialects, +/- 20 depending how one defines a language or a dialect). So English has always been the official language here. Its too cumbersome to make bureacracy etc work in multiple languages.
The confusion that forms the basis of that joke (I saw that Simpsons episode too), is exactly the reason I would like people to use correct terminology.:)
Changing to plurals, is different from naming cultures/people wrongly, because in the latter case, people who read such articles are misled to beleive something that is not true.
"Americans", by the way, is the correct term for people from the U.S.A because they live in America, named after Amerigo Vespucci, who discovered the land.
I think this has been done enough. I live in India and don't know of any "in bred Indian tribes". The Indian tribes that I know of are so intermingled with the population that they are not in bred at all.
I think what the author wants to talk about is "Native Americans". They are not Indians, and they only reason they were called so is because poor Columbus thought he had reached India when he reached North America. So why do some people keep calling them Indians? Celebrating Columbus' mistake?
Slashdot Mirror
There are of course, comparable scenarios when you move to the cutting-edge of the IT industry - how long have we heard of quantum computing? 10 years ? In an industry that proceeds with just darting pace, I don't have a quantum computer on my desktop yet. Is it because the researchers are incompetent ? No. It's because the problems they are trying to solve are inherently hard.
How long does it take to invent new mathematics on which useful algorithms can be built ?
Besides , biology changes with time, context, and is inherently and mathematically a complex, if not chaotic system. Anyone who has visited the E-Cell project knows how hard it is to create a standard working model of a single minimum cell, let alone create models of organisms, colonies, ecologies, epidemiologies and disease states.
Silicon, though, does not change its behaviour based on context, the complexity in creating circuits does not by far approach that of living organisms. In one way, the IT industry has been surfing the semi-conductor break-through wave for some time...and we all know what Moore's law predicts. It's hard to say what will happen in the future, but barring economic factors, the current availability of technology is only a reflection of our level of understanding and the maturity of a science. It is NOT necessarily an indicator of the competence or lethargy of the scientists pursuing a particular field.
What Mr.CEO of Intel, does not know is how much biotechnology has changed the last century. How does he think his bread, wine, beer, antibiotics, industrial chemicals like acetone, textiles, (the list goes on) are produced. What of the eradication of small pox, near total eradication of poliomyelitis, MDR for tuberculosis, 80% survival rate for breast and prostate cancer ..and so on ?
These things didn't occur on their own. The community worked hard to solve these problems, even if partially.
Unfortunately, ars technica and by consequence Slashdot, have completely mis-interpreted the original paper, at least regarding the headline used. As many people have stated, there is no wonder in finding that there are genome instability hot-spots. This has been known for years. What was not obvious , is the existence of hot-spots leading to a specific kind of mutation - i.e , copy number variation (CNV). Even though CNVs are mutations in the classical sense, modern molecular biology reserves the term 'mutation' for single nucleotide or codon changes. Drastic changes at the genomic, chromosomal or transcript level are generally called by their specific names such as deletion, truncation, transposition, duplication etc. What this study seems to suggest is that certain regions of the genome (irrespective, it seems, if these regions are genes or have a known biological function) seem to have a fluctuating copy number in the genome, with the rate of fluctuation much higher than expected in a random process - suggesting the existence of a mechanism that allows for this fluctuation to occur. It implies, that evolution has caused these particular regions to become uncoupled from potential lethality or drastic abnormality that arises in organisms , when similar variations occur on other regions (for example: variation in X-chromosome number leads to Turner or Klinefelter's syndrome). The interesting question that I see, is if there is a mechanism that allows this "tolerance" to exist to variations in these particular regions, and if there is such a mechanism, can it be tailored to allow changes in other regions...leading to the possibility of creating strains of organisms specially suited for particular scientific experiments-with multiple copies of a gene etc. - animals that currently are simply impossible to create because these changes are lethal. A far shot would be therapeutics. There are certain diseases that arise simply because of a cells inability to tolerate certain changes in the genome, irrespective of whether those changes are the cause of the lethality. In other words, the cells defense system itself is the cause of the disease rather than the genetic change. This might be the case in several autoimmune diseases or developmental diseases where upon sensing a genetic change, cells undergo apoptosis - irrespective of whether the genetic change is detrimental during the natural life of the cell. So, if one reads the Nature article, there is really some news there
Unfortunately, ars technica and by consequence Slashdot, have completely mis-interpreted the original paper, at least regarding the headline used. As many people have stated, there is no wonder in finding that there are genome instability hot-spots. This has been known for years. What was not obvious , is the existence of hot-spots leading to a specific kind of mutation - i.e , copy number variation (CNV). Even though CNVs are mutations in the classical sense, modern molecular biology reserves the term 'mutation' for single nucleotide or codon changes. Drastic changes at the genomic, chromosomal or transcript level are generally called by their specific names such as deletion, truncation, transposition, duplication etc. What this study seems to suggest is that certain regions of the genome (irrespective, it seems, if these regions are genes or have a known biological function) seem to have a fluctuating copy number in the genome, with the rate of fluctuation much higher than expected in a random process - suggesting the existence of a mechanism that allows for this fluctuation to occur. It implies, that evolution has caused these particular regions to become uncoupled from potential lethality or drastic abnormality that arises in organisms , when similar variations occur on other regions (for example: variation in X-chromosome number leads to Turner or Klinefelter's syndrome). The interesting question that I see, is if there is a mechanism that allows this "tolerance" to exist to variations in these particular regions, and if there is such a mechanism, can it be tailored to allow changes in other regions...leading to the possibility of creating strains of organisms specially suited for particular scientific experiments-with multiple copies of a gene etc. - animals that currently are simply impossible to create because these changes are lethal. A far shot would be therapeutics. There are certain diseases that arise simply because of a cells inability to tolerate certain changes in the genome, irrespective of whether those changes are the cause of the lethality. In other words, the cells defense system itself is the cause of the disease rather than the genetic change. This might be the case in several autoimmune diseases or developmental diseases where upon sensing a genetic change, cells undergo apoptosis - irrespective of whether the genetic change is detrimental during the natural life of the cell. So, if one reads the Nature article, there is really some news there.
"The work in our laboratory was initiated after the last world war by calculations of maximal efficiencies for some field crops, taking high annual yields in Holland, from agricultural data, making allowance for roots, stubbles, etc., and comparing them with the average energy on the cultivated surface during the growth period (27). Considering only wave lengths available for photosynthesis, the efficiencies were between 0.5 and 2 %, and the large deviation from photosynthetic efficiency in laboratory experiments of short duration-viz., 20 to 30 %-was the starting point of our work. Earlier computations of efficiency of higher plant growth are discussed in detail in (11). The possible reasons for the relatively low long term efficiency are as follows (27): 1) too high incident light intensities under field conditions; 2) too low C02 content of the air; 3) too low temperatures; 4) other limiting factors, e.g., too little water; 5)loss of light between the plants; and 6) factors, provisionally difficult for analysis, e.g., fluctuating rate of photosynthesis, possible "afternoon depression," respiratory losses."
Not to mention the inherently low efficiency of light-harvesting in photosynthesis in general which hovers around 1% of total insolation recieved.
learning to use a mathematics package like Mathematica or MATLAB. I'd go with the former to begin with. I just got a book that solved some basic scientific questions regarding making models of physiological processes and tried to replicate those in Mathematica. In the process of learning the syntax for Mathematica, you're forced to learn calculus, which I used Google search for in order to understand the problem completely. The result was very satisfactory because the computer did the number crunching, I could concentrate on the conceptual understanding in calculus rather than spending time doing calculations by hand.
Window Live CD
Police departments suddenly faced gangs are looking for help on the gangs' own easy-to-find Web sites.
What the hell does that mean?
Well, since Platensimycin inhibits FabF, which is 3-oxo-[acyl carrier protein] synthase II, and vancomycin prevents incorporation of N-acetylmuramic acid and N-acetylglucosamine - peptide subunits from being incorporated into the peptidoglycan matrix; their mechanisms are exclusive. Theoretically, Platensimycin will therefore work on both MRSA and VRSA strains. Practically, strain sensitivities vary , but with the current level of information, one would expect the new drug to be just as effective on VRSA strains.
There is a catch to this. A lot of mutations[I use the term loosely as it is used on Slashdot] occur due to the individuals tendency to acquire them, ie, genetic predisposition.
If somatic cell mutations occur and confer an advantage to the organism, it will presumably manifest as a greater chance for the organism to pass on its genes, and thus pass on the genetic predisposition to acquire that mutation.
One on-field implication of this, is that many types of cancers tend to develop resistance to drugs through identical (!) molecular mchanisms, even though resistance is obviously developed de novo in different individuals with the same type of cancer. This is because the administration of a same drug applies identical selection pressure and thus causes the identical, (apparently) most probable and stable phenotype to appear in the cells.
I do not understand what the fuss is about here. I am not talking about the ID-Evo debate. What the good Dr.Thornton seems to have discovered, is only a case of moonlighting, which is well known in biology. Moonlighting is the phenomenon when a single protein fulfills several, often unrelated and even more often unexpected functions in a cell. Biologists are aware of this fact, and hence understand this to be one of the basic ways in which molecular evolution occurs. The fact that an aldosterone receptor can exist before aldosterone is not really surprising. Drug designers are designing molecules all the time for which receptors already exist. Basically, I do not think that it is a novel as the NYtimes would have us beleive. Here is an interesting paper describing several such moonlighting occurences.[Warning: PDF]. Further a presentation for non-biologists on moonlighting is here One of the leading researchers in the field of moonlighting proteins is Dr.Joel Sussman. He works on how the AChE enzyme may be affecting a variety of other aspects in neural cell biology.
They did a similar thing with the iPod screens getting sctratched. So let me get this, rolling out defective a product and then doing excellent service to fix it, is a good business strategy ? No wonder Apple could never make gross profits.
PS : I didnt say "memory hog" . I said huge loading time. MS Office starts in about 4 seconds the first time.
Read my post. There is no "Track Changes" option in Oo that is compatible with Word files made with that option on.
I use Openoffice 2.0 on my computer and be advised that I faced serious compatibility issues when editing certain Microsoft Word (Office XP) files in Openoffice writer.
These files were edited using the "Track changes" option in MS Office, that allows you to automatically mark changes that you have made to the file. Openoffice simply does not understand such a file and loads it without the accompanying change tracking information.
Admiteddly, I liked OpenOffice at first and thought that MS Office could finally be replaced. However, several experiences (problems with huge loading time, slowing down the PC, OpenDocument format not popular etc.), including the above mentioned one, have forced me back to MS Office, and my personal conclusion is that MS Office has a lot more features and is much better as a regular word processing app. I hate paying Microsoft, but in this case, they take the cake. I'll have to wait for Oo3.
PS : The only OO features that I noticed MS does not have, are the ability to render equations and make PDFs. However, MS Office + MathType + Adobe Acrobat Prof./any free PDF renderer can take care of that.
When cultures of the immigrant and native peoples amalgamate , then the new / modified culture formed could then be called indiginous.
Well, I think that may be an accent issue. To tell you the truth, I never heard an Indian speak English the way Apu does. The French have an accent, the Dutch have an accent. Hell, even the English have their own accent. But so far, honestly, I have only heard Americans claim that their's is the "correct" way to pronounce/speak English. English is generally spoken well in India because of the reason that very early on, in about the 1850s, the British colonists discovered that there are too many sub-cultures and corresponding number of languages here (75 major languages and 1430 dialects, +/- 20 depending how one defines a language or a dialect). So English has always been the official language here. Its too cumbersome to make bureacracy etc work in multiple languages.
The confusion that forms the basis of that joke (I saw that Simpsons episode too), is exactly the reason I would like people to use correct terminology. :)
Hmm, I never thought of Whites and Indians having any issues, except with the displeasure with outsourcing.
hmm...Dan, could you tell me that means more explicity please ? Just curiosity...Slashdot got something against Indians?
Then you are part of the immigrant population to America...as defined from the time Amerigo christened the land.
Changing to plurals, is different from naming cultures/people wrongly, because in the latter case, people who read such articles are misled to beleive something that is not true. "Americans", by the way, is the correct term for people from the U.S.A because they live in America, named after Amerigo Vespucci, who discovered the land.
I think this has been done enough. I live in India and don't know of any "in bred Indian tribes". The Indian tribes that I know of are so intermingled with the population that they are not in bred at all. I think what the author wants to talk about is "Native Americans". They are not Indians, and they only reason they were called so is because poor Columbus thought he had reached India when he reached North America. So why do some people keep calling them Indians? Celebrating Columbus' mistake?