I CAN!
Saturday, June 30, 2007
Thursday, June 28, 2007
Tuesday, June 26, 2007
Monday, June 25, 2007
Dna Molecular Biology Visualizations - Wrapping And Replicat
Dna Molecular Biology Visualizations - Wrapping And Replicat
James Watson: The double helix and today's DNA mysteries
James Watson: The double helix and today's DNA mysteries
Defense against Ancient Virus Opened Door to HIV
A human protein that evolved to combat a past infection may have left us vulnerable to the virus that causes AIDS
Early humans successfully fended off a virus that infected chimpanzees by evolving a protein capable of neutralizing it, according to a new study. But what goes around comes around, evolutionarily speaking: Four million years later, the same protein seems to have left us more vulnerable than other primates to the human immunodeficiency virus (HIV).
When researchers sequenced the chimpanzee genome in 2005, the biggest difference between it and the human genome was the extinct PtERV1 retrovirus, which inserted its DNA into the cells it infected like HIV does today. Chimps had 130 copies of PtERV1, but humans had none. "The question is: Why did our sister species get infected and not humans?" says virologist Michael Emerman of the Fred Hutchinson Cancer Research Center in Seattle.
Looking for an answer, Emerman and colleagues homed in on the immune protein TRIM5α, one of several proteins involved in innate immunity, the body's first line of defense against viral infection. The TRIM5α gene varies widely among primates and has changed the most between chimps and humans, suggesting that it evolved to combat some virus humans were susceptible to, Emerman says.
Rhesus monkey TRIM5α protects against HIV-1, but the only modern virus that the human protein has any effect on is one that causes leukemia in mice—which happens to be closely related to PtERV1. TRIM5α seems to neutralize the mouse virus's inner core protein after it has entered a cell. So Emerman and colleagues resurrected the analogous protein from PtERV1, based on its remnants in chimpanzees, and inserted it into a defective version of the mouse virus, which could infect cells but not reproduce.
The altered virus was unable to infect feline cells engineered to produce human TRIM5α, the group reports online today in Science. Unexpectedly, however, the researchers found that no version of TRIM5α from any primate could neutralize both PtERV1 and HIV—it was either one or the other, Emerman says. What that implies, he says, is "humans are susceptible to HIV today because of a response to something else we had in the past."
HIV researcher Beatrice Hahn of the University of Alabama at Birmingham calls the study a "fabulous piece of molecular sleuthing" and says that understanding innate immune proteins may eventually lead to new HIV treatment strategies.
TRIM5α is not the final word on HIV susceptibility, she adds. None of the proteins protect against HIV-2, which came to us from apes like HIV-1 did, she says, but humans have apparently fended off nearly 40 other monkey retroviruses, so our innate immunity "wasn't quite as bad as you thought."
Parkinson's Gene Therapy Breakthrough May Enter Clinical Trials by Year-End
An innocuous gene-bearing virus injected into the midbrains of a dozen patients suffering from Parkinson's disease improved the subjects' motor function while causing no adverse effects, says a new study.
This is the first time gene therapy has been tested to fight Parkinson's, which affects an estimated 500,000 Americans. The promising findings, published this week in The Lancet, opens the door to a new treatment option for the neurodegenerative disease.
"The safety and effectiveness clearly indicate that this is something worth pursuing," says lead study author Michael Kaplitt, a neurological surgeon and director of movement disorders at New York-Presbyterian Hospital/Weill Cornell Medical Center. "We're not finished, clearly; we still need to do a larger, more definitive study to prove this for sure."
Parkinson's disease, a disorder that typically strikes people their 60s, is characterized by tremors, stiffness, loss of speech and difficulty with motor function. Neuroscientists have tracked its biological cause to the loss of neurons, or nerve cells, in a midbrain region called the substantia nigra, which produces the neurotransmitter dopamine (that helps maintain proper movement control). When dopamine levels are low the subthalamic nucleus, a sliver of neurons just above the substantia nigra, overproduces glutamate, which is the brain's primary excitatory chemical messenger. When hyped up it overstimulates downstream neurons, triggering a strong inhibitory response that results in disrupted movement.
Kaplitt and senior study author Matthew During, a senior research associate at Weill Cornell, focused on trying to calm down the overactive subthalamic nucleus. They used a harmless virus called an adeno-associated virus to transport a gene that codes for the enzyme glutamic acid decarboxylase (GAD) into the neurons of the subthalamic nucleus. The gene prompted these subthalamic cells to produce gamma-aminobutyric acid (GABA), the brain's primary inhibitory neurotransmitter, which made them settle down and restored normal motor function.
Because of federal regulations, the team could only inject the virus into one hemisphere of each person's brain. "This allowed us to compare the two sides of the brain," Kaplitt says, which enabled researchers to judge the effectiveness of their treatment.
Researchers monitored the 12 subjects over the next year and discovered that motor function improved from 25 percent to 65 percent. They also found that the treated sides of the brain showed normalized brain activity in key regions downstream from the subthalamic nucleus: the thalamus, also implicated in motor function, and parts of the cerebral cortex involved in movement. Most encouraging to the scientists was that the improvement persisted even when the patients were on their Parkinson's medications meaning that, as Kaplitt describes, "the therapy was causing additional improvement to the medicines."
Kaplitt and During had a number of safety concerns at the study's inception: The viral packages could damage target cells by provoking the immune system; there was a chance of overinhibition of the neurons in the subthalamic nucleus; and there were worries about unknown side effects that the researchers had not anticipated. But Kaplitt reports their fears were unfounded—there were no incidents of infection, immune response or toxicity.
In an editorial accompanying The Lancet article, Jon Stoessel, a professor of neurology at Pacific Parkinson's Research Center in Vancouver, calls the new work a "provocative approach to the treatment of neurodegenerative disease." He questions, however, whether this is a better treatment option than deep-brain stimulation, the most effective current therapy, which involves implanting a brain "pacemaker" to electrically stimulate either the thalamus or subthalamic nucleus
Kaplitt, who hopes to have a full-scale clinical trial for the gene therapy approach underway by year-end, says there are several "inherent advantages" to this new option. Most notably, there are no wires or batteries in the body that could cause infection, it avoids the risks of putting a new electrical source in the brain, and the pacemaker has to be tuned frequently, whereas the gene, according to animal studies, should remain effective for several years.
An innocuous gene-bearing virus injected into the midbrains of a dozen patients suffering from Parkinson's disease improved the subjects' motor function while causing no adverse effects, says a new study.
Friday, June 22, 2007
LINUS PAULING
Linus Carl Pauling was born in Portland, Oregon, on 28th February, 1901, the son of a druggist, Herman Henry William Pauling, who, though born in Missouri, was of German descent, and his wife, Lucy Isabelle Darling, born in Oregon of English-Scottish ancestry.Linus attended the public elementary and high schools in the town of Condon and the city of Portland, Oregon, and entered the Oregon State College in 1917, receiving the degree of B.Sc. in chemical engineering in 1922. During the years 1919-1920 he served as a full-time teacher of quantitative analysis in the State College, after which he was appointed a Teaching Fellow in Chemistry in the California Institute of Technology and was a graduate student there from 1922 to 1925, working under Professor Roscoe G. Dickinson and Richard C. Tolman. In 1925 he was awarded the Ph.D. (summa cum laude) in chemistry, with minors in physics and mathematics.Since 1919 his interest lay in the field of molecular structure and the nature of the chemical bond, inspired by papers by Irving Langmuir on the application of the Lewis theory of the sharing of pairs of electrons between atoms to many substances. In 1921 he suggested, and attempted to carry out, an experiment on the orientation of iron atoms by a magnetic field, through the electrolytic deposition of a layer of iron in a strong magnetic field and the determination of the orientation of the iron crystallises by polishing and etching the deposit, and microscopic examination of the etch figures. With Professor Dickinson, he began in 1922 the experimental determination of the structures of some crystals, and also started theoretical work on the nature of the chemical bond.Since his appointment to the Staff of California Institute of Technology, Professor Pauling was elected Research Associate in 1925; National Research Fellow in Chemistry, 1925-1926; Fellow of the John Simon Guggenheim Memorial Foundation, 1926-1927 (through this last he worked in European Universities with Sommerfeld, Schrödinger, and Bohr); Assistant Professor of Chemistry, 1927-1929; Associate Professor, 1929-1931; Professor, 1931, when he was the first recipient of the American Chemical Society Award in Pure Chemistry - the Langmuir Prize - and Chairman of the Division of Chemistry and Chemical Engineering, and Director of the Gates and Crellin laboratories of Chemistry, 1936-1958. In 1963, he was awarded the Nobel Peace Prize.Pauling is a member of numerous professional societies in the U.S.A. as well as in many European countries, India, Japan and Chile. Awards, medals, and honorary degrees were showered upon him in America and Europe, and in addition he was elected Rationalist of the Year for 1960 and Humanist of the Year for 1961. Several books have come from his pen, ranging from his most famous one The Nature of the Chemical Bond, and the Structure of Molecules and Crystals (1939, 1949, 1960) via General Chemistry (1947, 1953), which was translated into nine languages, to No More War! (1958, 1959,1962).The subjects of the papers he published reflect his great scientific versatility: about 350 publications in the fields of experimental determination of the structure of crystals by the diffraction of X-rays and the interpretation of these structures in terms of the radii and other properties of atoms; the application of quantum mechanics to physical and chemical problems, including dielectric constants, X-ray doublets, momentum distribution of electrons in atoms, rotational motion of molecules in crystals, Van der Waals forces, etc.; the structure of metals and intermetallic compounds, the theory of ferromagnetism; the nature of the chemical bond, including the resonance phenomenon in chemistry; the experimental determination of the structure of gas molecules by the diffraction of electrons; the structure of proteins; the structure of antibodies and the nature of serological reactions; the structure and properties of hemoglobin and related substances; abnormal hemoglobin molecules in relation to the hereditary hemolytic anemias; the molecular theory of general anesthesia; an instrument for determining the partial pressure of oxygen in a gas; and other subjects.Pauling married Ava Helen Miller of Beaver Creek, Oregon, in 1923. She is of English-Scottish and German descent. They have four children, Linus (Carl) Jr. (1925), Peter Jeffress (1931), Linda Helen (1932) and Edward Crellin (1937), and thirteen grandchildren.
Spicy food can prevent cancer
Here is some spicy news for cancer patients.
In a major breakthrough, it has been revealed that tumours can be killed without any side effects though a compound called Capsaicin, an active component in chilli that makes spicy food hot and generates the heat in muscle strain remedies.
The revelation may be crucial in the development of a new generation of cancer drugs, a top scientist has said. Capsaicin is commonly used as an active ingredient in muscle rub creams and the treatments for psoriasis.
The tests, which were conducted by a research team at the Nottingham University led by Dr Timothy Bates, have shown positive results -- killing a variety of tumour cells like the pancreatic cancer, which is one of the most difficult to treat and has a five-year survival rate of less than one per cent. "We appear to have discovered a fundamental weakness with all cancer cells. Capsaicin specifically targets cancerous cells. When released onto cancer cells, capsaicin attacks the mitochondria in the cell, which is responsible for generating ATP, the major energy-producing chemical in the body. Capsaicin specifically binds to the protein within the mitochondria of tumour cells and triggers apoptosis, the process of natural cell death," Dr Bates said.
The fact that capsaicin, part of a group of food compounds called vanilloids, was a common part of the diet in many countries would dramatically reduce the number of regulatory hurdles that any anti-cancer drug would have to overcome, he added.According to Dr Bates, the findings probably explained why people in countries like India, who traditionally eat a diet which is very spicy, tend to have lower incidences of many cancers that are prevalent in the Western world.The discovery could lead to the production of drugs to cure a variety of cancers at a fraction of the �410 million cost of developing conventional medicines, as capsaicin is already consumed daily by millions of people.
In a major breakthrough, it has been revealed that tumours can be killed without any side effects though a compound called Capsaicin, an active component in chilli that makes spicy food hot and generates the heat in muscle strain remedies.
The revelation may be crucial in the development of a new generation of cancer drugs, a top scientist has said. Capsaicin is commonly used as an active ingredient in muscle rub creams and the treatments for psoriasis.
The tests, which were conducted by a research team at the Nottingham University led by Dr Timothy Bates, have shown positive results -- killing a variety of tumour cells like the pancreatic cancer, which is one of the most difficult to treat and has a five-year survival rate of less than one per cent. "We appear to have discovered a fundamental weakness with all cancer cells. Capsaicin specifically targets cancerous cells. When released onto cancer cells, capsaicin attacks the mitochondria in the cell, which is responsible for generating ATP, the major energy-producing chemical in the body. Capsaicin specifically binds to the protein within the mitochondria of tumour cells and triggers apoptosis, the process of natural cell death," Dr Bates said.
The fact that capsaicin, part of a group of food compounds called vanilloids, was a common part of the diet in many countries would dramatically reduce the number of regulatory hurdles that any anti-cancer drug would have to overcome, he added.According to Dr Bates, the findings probably explained why people in countries like India, who traditionally eat a diet which is very spicy, tend to have lower incidences of many cancers that are prevalent in the Western world.The discovery could lead to the production of drugs to cure a variety of cancers at a fraction of the �410 million cost of developing conventional medicines, as capsaicin is already consumed daily by millions of people.
Using viruses to fight cancer
Contract the common cold to fight cancer � does it sound loony?
Not really, not if cutting-edge research being done by British scientists were to see results. They are readying to launch human trials of the technique of killing tumours by infecting them viruses like that of common cold, reports The Guardian, London.
Currently, there are two weapons in the war against Big C � radiotherapy and chemotherapy. If successful, virotherapy could emerge as the third arm in the war.
Leonard Seymour, professor of gene therapy at Oxford University, will lead the trials later this year. 'In principle, you have got something that could be many times more effective than regular chemotherapy,' he said.
Those who have seen a loved one undergo chemotherapy, or went through the ordeal themselves, know how debilitating the process is. Virotherapy, on the other hand, promises none of it.
The new therapy uses cancer's own working � of suppressing the body's local immune system � as its Achilles heel. Viruses find tumours a great nesting place since there is no immune system to stop them from replicating. What's more, it's not like a great amount of the virus needs to enter the tumour. 'They replicate, you get a million copies in each cell and the cell bursts and they infect the tumour cells adjacent and repeat the process,' Prof Seymour was quoted by The Guardian as saying. He should know, for he has been working with viruses that kill cancer but don't harm healthy tissue.
It's been known for some time that viruses can kill tumour cells; in fact scientific journals have published some aspects of the work. In America viruses have been directly injected into tumours but this technique has one major flaw: it will not work if the cancer is either inaccessible or spread throughout the body.
Where Prof Seymour's solution differs is to mask the virus a la a stealth bomber, away from the radar of the body's immune system which will seek and destroy it otherwise. His technique allows the viruses to work like chemotherapy drugs � reach the tumour through the blood stream. This is done by giving the virus a polymer coat after some chemical modifications.
The virus replicates after infecting the tumour, but hearteningly the copies lack the chemical modifications. The challenge is to contain them within the tumour, otherwise they will be finished by the immune system.
Preliminary research on mice has shows the virus working on tumours that are otherwise resistant to standard cancer drugs.
Virotherapy is expected to be particularly useful in the case of secondary cancers, known as metastases.
The human clinical trials are expected to use two viruses: adenovirus, which gives you a cold-like illness if you have contracted it, and vaccinia, which causes cowpox. The viruses will be uncoated during the trials, delivering them locally to liver tumours in order to find out if the treatment works in humans. The trials, later involving polymer-coated viruses, are expected to take several years.
Researchers hope that some day viruses will become an important part of the arsenal against cancer, a disease that has dogged the human race for centuries.
Not really, not if cutting-edge research being done by British scientists were to see results. They are readying to launch human trials of the technique of killing tumours by infecting them viruses like that of common cold, reports The Guardian, London.
Currently, there are two weapons in the war against Big C � radiotherapy and chemotherapy. If successful, virotherapy could emerge as the third arm in the war.
Leonard Seymour, professor of gene therapy at Oxford University, will lead the trials later this year. 'In principle, you have got something that could be many times more effective than regular chemotherapy,' he said.
Those who have seen a loved one undergo chemotherapy, or went through the ordeal themselves, know how debilitating the process is. Virotherapy, on the other hand, promises none of it.
The new therapy uses cancer's own working � of suppressing the body's local immune system � as its Achilles heel. Viruses find tumours a great nesting place since there is no immune system to stop them from replicating. What's more, it's not like a great amount of the virus needs to enter the tumour. 'They replicate, you get a million copies in each cell and the cell bursts and they infect the tumour cells adjacent and repeat the process,' Prof Seymour was quoted by The Guardian as saying. He should know, for he has been working with viruses that kill cancer but don't harm healthy tissue.
It's been known for some time that viruses can kill tumour cells; in fact scientific journals have published some aspects of the work. In America viruses have been directly injected into tumours but this technique has one major flaw: it will not work if the cancer is either inaccessible or spread throughout the body.
Where Prof Seymour's solution differs is to mask the virus a la a stealth bomber, away from the radar of the body's immune system which will seek and destroy it otherwise. His technique allows the viruses to work like chemotherapy drugs � reach the tumour through the blood stream. This is done by giving the virus a polymer coat after some chemical modifications.
The virus replicates after infecting the tumour, but hearteningly the copies lack the chemical modifications. The challenge is to contain them within the tumour, otherwise they will be finished by the immune system.
Preliminary research on mice has shows the virus working on tumours that are otherwise resistant to standard cancer drugs.
Virotherapy is expected to be particularly useful in the case of secondary cancers, known as metastases.
The human clinical trials are expected to use two viruses: adenovirus, which gives you a cold-like illness if you have contracted it, and vaccinia, which causes cowpox. The viruses will be uncoated during the trials, delivering them locally to liver tumours in order to find out if the treatment works in humans. The trials, later involving polymer-coated viruses, are expected to take several years.
Researchers hope that some day viruses will become an important part of the arsenal against cancer, a disease that has dogged the human race for centuries.
Biotech boom -- but where are the jobs?
Everyone wants to enter a field which is 'hot'. One such field is biotech. You would have read innumerable articles on the scope of bitechnology. The jobs opening up in the sector. And, of course, the poster pin-up company, Biocon.
As a report in The Hindu notes: Career counsellors and those engaged in educational guidance... are flooded with inquiries about biotechnology courses and their scope. Biotechnology today looks like what information technology was in the 1990s.
But are prospects really that bright? Today, an engineer from an average college can easily land an IT job. What about the biotech graduate?
First of all, there is this huge debate over whether biotech should be offered at all the undergrad level. M Radhakrishna Pillai, director of Rajiv Gandhi Centre for Biotechnology, Thiruvananthapuram, told The Hindu: 'Biotechnology cannot exist at the BSc level, where one should learn the basic science. BSc Biotechnology courses have created a confused lot in Kerala, defeating the very purpose of the subject.'
The same holds true of other states. A number of colleges and universities, especially the private and deemed variety, are offering 'BSc Biotech'. Students who were trying for a medical course but failed to get through would rather opt for a biotech course than a regular BSc. At least kisi ko kehne mein tho better lagta hai.
For the colleges also, it's a happy thing. Fees for an undergraduate biotech course are far higher than a BSc. One assumes this is because the college will provide better facilities, more qualified teachers, etc. Sadly, this is generally not the case. In most cases, biotech students actually use the same labs as the students doing microbiology/ life science!
What about PG?
At the post graduate level, the Jawaharlal Nehru University, Delhi, is the most reputed college and the toughest to get into. The combined entrance exam held by JNU can also get you into 32 other colleges offering biotech at MSc/ MTech level. Benaras Hindu University, Goa University, Anna University (Chennai) and Pune University are some of the next best choices.
Now, this is the case in every profession. Everyone can't get into the best college. However, in biotech, there are certain unique problems.
JNU has a tie-up with DBT (department of biotechnology) which makes it easy for their students to work on live projects during the course of their MSc. Others do not have it so easy. When it comes to industrial training, you may actually have to pay for it.
For example, students of PTU (Punjab Technical University), Indore, who went to IIT Delhi last year for two months training, paid Rs 15,000 (boarding and lodging extra). This money goes towards facilities (eg, kits, labs, equipment, etc) and the students get to work on a live experiment.
There is the option of doing a project with a company also -- some give you a stipend while others don't pay but don't charge you either. However, it is believed that having an IIT Delhi project on your resume will help when you go out for a job, so students don't mind paying. For IIT, this is a way to get some additional funding for projects.
A win-win for both but still, it's a little strange...
And what about the job?
Okay, so now you graduate and start looking for a job. If there is such a 'boom' happening, it must be pretty easy, right?
Unfortunately, that's not the case.
Shweta Agrawal, an MSc Biotech, has been looking out for a job for last six months. "I have given 15-20 interviews. The problem is there are very few real 'biotech' jobs," she says. The company may be 'biotech', but the job expected of an MSc is database management -- not experimental.
Rajat Gurutaj, a final year student at BIT Bangalore, adds, "My sister is an MSc Biotech and she did not have a job after graduation for six months. Finally, she went to the UK. According to her, there are absolutely no jobs here in India. My friend is doing BE Biotech from a reputed college in Bangalore -- their course is not much different from BE Chemical and, again, no jobs. He is joining an IT firm after graduation".
Students say it's very hard for a fresher to get a job in QC (quality control) or R & D because most companies have small teams and there isn't much job hopping. What's more, pharmacy graduates are preferred because they can do formulation as well as QC.
A quick look at various job sites would tell you that openings for fresh MSc Biotech are few and far between. BSc Biotech ki to baat hi chhodiye. Actually from the job point of view, even MSc Chemistry may be better for you!
An exception to all the above would be the handful who complete a BTech from IIT (KGP, Delhi, Madras and Bombay) or a Masters in biology from IISc.
"If I don't get a job of my choice soon I will start preparing for MBA," says Shweta. "The fact is, by now, an MBA from even the most unknown university would have got a job for Rs 10,000-15,000 pm," she sighs.
The alternate option of course is to do a Phd -- either in India or abroad. However, even after a PhD, prospects in India remain limited. You would most likely join a government laboratory (that's where much of the challenging work is being done). At age 28, armed with a Phd, you would earn Rs 8,000-10,000 as starting salary.
So if you are planning to do biotech, keep all this in mind before making your decision. Don't be lured by the idea of a boom and the fact that it sounds cool.
Take up biotech only if you have a deep love for the subject and wish to get into research. In order to do this, however, you must be open to doing a PhD.
Otherwise, MBA aapke liye theek rahega. And oh, there is an MBA (biotech) being offered as well...
One last bit of advice. Don't fall for it, go for a more general degree!
As a report in The Hindu notes: Career counsellors and those engaged in educational guidance... are flooded with inquiries about biotechnology courses and their scope. Biotechnology today looks like what information technology was in the 1990s.
But are prospects really that bright? Today, an engineer from an average college can easily land an IT job. What about the biotech graduate?
First of all, there is this huge debate over whether biotech should be offered at all the undergrad level. M Radhakrishna Pillai, director of Rajiv Gandhi Centre for Biotechnology, Thiruvananthapuram, told The Hindu: 'Biotechnology cannot exist at the BSc level, where one should learn the basic science. BSc Biotechnology courses have created a confused lot in Kerala, defeating the very purpose of the subject.'
The same holds true of other states. A number of colleges and universities, especially the private and deemed variety, are offering 'BSc Biotech'. Students who were trying for a medical course but failed to get through would rather opt for a biotech course than a regular BSc. At least kisi ko kehne mein tho better lagta hai.
For the colleges also, it's a happy thing. Fees for an undergraduate biotech course are far higher than a BSc. One assumes this is because the college will provide better facilities, more qualified teachers, etc. Sadly, this is generally not the case. In most cases, biotech students actually use the same labs as the students doing microbiology/ life science!
What about PG?
At the post graduate level, the Jawaharlal Nehru University, Delhi, is the most reputed college and the toughest to get into. The combined entrance exam held by JNU can also get you into 32 other colleges offering biotech at MSc/ MTech level. Benaras Hindu University, Goa University, Anna University (Chennai) and Pune University are some of the next best choices.
Now, this is the case in every profession. Everyone can't get into the best college. However, in biotech, there are certain unique problems.
JNU has a tie-up with DBT (department of biotechnology) which makes it easy for their students to work on live projects during the course of their MSc. Others do not have it so easy. When it comes to industrial training, you may actually have to pay for it.
For example, students of PTU (Punjab Technical University), Indore, who went to IIT Delhi last year for two months training, paid Rs 15,000 (boarding and lodging extra). This money goes towards facilities (eg, kits, labs, equipment, etc) and the students get to work on a live experiment.
There is the option of doing a project with a company also -- some give you a stipend while others don't pay but don't charge you either. However, it is believed that having an IIT Delhi project on your resume will help when you go out for a job, so students don't mind paying. For IIT, this is a way to get some additional funding for projects.
A win-win for both but still, it's a little strange...
And what about the job?
Okay, so now you graduate and start looking for a job. If there is such a 'boom' happening, it must be pretty easy, right?
Unfortunately, that's not the case.
Shweta Agrawal, an MSc Biotech, has been looking out for a job for last six months. "I have given 15-20 interviews. The problem is there are very few real 'biotech' jobs," she says. The company may be 'biotech', but the job expected of an MSc is database management -- not experimental.
Rajat Gurutaj, a final year student at BIT Bangalore, adds, "My sister is an MSc Biotech and she did not have a job after graduation for six months. Finally, she went to the UK. According to her, there are absolutely no jobs here in India. My friend is doing BE Biotech from a reputed college in Bangalore -- their course is not much different from BE Chemical and, again, no jobs. He is joining an IT firm after graduation".
Students say it's very hard for a fresher to get a job in QC (quality control) or R & D because most companies have small teams and there isn't much job hopping. What's more, pharmacy graduates are preferred because they can do formulation as well as QC.
A quick look at various job sites would tell you that openings for fresh MSc Biotech are few and far between. BSc Biotech ki to baat hi chhodiye. Actually from the job point of view, even MSc Chemistry may be better for you!
An exception to all the above would be the handful who complete a BTech from IIT (KGP, Delhi, Madras and Bombay) or a Masters in biology from IISc.
"If I don't get a job of my choice soon I will start preparing for MBA," says Shweta. "The fact is, by now, an MBA from even the most unknown university would have got a job for Rs 10,000-15,000 pm," she sighs.
The alternate option of course is to do a Phd -- either in India or abroad. However, even after a PhD, prospects in India remain limited. You would most likely join a government laboratory (that's where much of the challenging work is being done). At age 28, armed with a Phd, you would earn Rs 8,000-10,000 as starting salary.
So if you are planning to do biotech, keep all this in mind before making your decision. Don't be lured by the idea of a boom and the fact that it sounds cool.
Take up biotech only if you have a deep love for the subject and wish to get into research. In order to do this, however, you must be open to doing a PhD.
Otherwise, MBA aapke liye theek rahega. And oh, there is an MBA (biotech) being offered as well...
One last bit of advice. Don't fall for it, go for a more general degree!
Tuesday, June 19, 2007
Newton predicted the world will end in...
Jerusalem - Renowned British scientist Sir Isaac Newton, the father of modern physics and astronomy, predicted the world would end in 2060 in a 1704 letter that went on show in Jerusalem on Sunday.A famed rationalist, who secured a royal exemption from the ordination in the Church of England that was normally expected of academics of his day so he would not have to follow its teachings, Newton nonetheless based his prediction on a Biblical text.Working from verses in the Book of Daniel, the elaborator of the classical laws of gravity, motion and optics argued that the world would end 1 260 years after the foundation of the Holy Roman Empire in western Europe in 800 AD.The letter, on show at Jerusalem's Hebrew University as part of an exhibition entitled "Newton's Secrets", is part of an array of papers of the British scientist bequeathed to the institution by a wealthy collector of scientific manuscripts.The university said it was the first time the letter had been put on public show since 1969.Newton's late 17th century work at Cambridge University was the foundation stone of modern science until the discovery of relativity and quantum mechanics in the last century.But it has long been known that the ground-breaking physicist from Grantham, England, also took a keen interest in superstitions of his day that have long since fallen foul of modern science.Newton spent four years in the 1670s preparing a work on alchemy, the notion that base metals can be turned into gold.
Cancer stem cells similar to normal stem cells thwart anti-cancer agents
Current cancer therapies often succeed at initially eliminating the bulk of the disease, including all rapidly proliferating cells, but are eventually thwarted because they cannot eliminate a small reservoir of multiple-drug-resistant tumor cells, called cancer stem cells, which ultimately become the source of disease recurrence and eventual metastasis.
Now, research by scientists at the University of Pittsburgh School of Medicine suggests that for chemotherapy to be truly effective in treating lung cancers, for example, it must be able to target a small subset of cancer stem cells, which they have shown share the same protective mechanisms as normal lung stem cells. They presented this ground-breaking research at the Tissue Engineering and Regenerative Medicine International Society (TERMIS) North American Chapter meeting in Toronto.
The University of Pittsburgh researchers, led by Vera Donnenberg, Ph.D., assistant professor of surgery and pharmaceutical sciences, University of Pittsburgh Schools of Medicine and Pharmacy, used cell surface markers and dyes to identify cancer stem cells as well as normal adult stem cells and their progeny in samples obtained from normal lung and lung cancer tissue samples. The researchers identified a very small, rare set of resting cancer stem cells in the lung cancer samples that looked and behaved much like normal adult lung tissue stem cells. Both the cancer and normal stem cells were protected equally by multiple drug resistance transporters, even if the bulk of the tumor responded to chemotherapy.
According to Dr. Donnenberg, the very fact that cancers can and do relapse after apparently successful therapy indicates the survival of a drug-resistant, tumor-initiating population of cells in many types of refractory cancers. "Because of the similarities between the way that normal stem cells and cancer stem cells protect themselves, cancer therapies have to be designed specifically to target cancer stem cells while sparing normal stem cells," she explained.
Now, research by scientists at the University of Pittsburgh School of Medicine suggests that for chemotherapy to be truly effective in treating lung cancers, for example, it must be able to target a small subset of cancer stem cells, which they have shown share the same protective mechanisms as normal lung stem cells. They presented this ground-breaking research at the Tissue Engineering and Regenerative Medicine International Society (TERMIS) North American Chapter meeting in Toronto.
The University of Pittsburgh researchers, led by Vera Donnenberg, Ph.D., assistant professor of surgery and pharmaceutical sciences, University of Pittsburgh Schools of Medicine and Pharmacy, used cell surface markers and dyes to identify cancer stem cells as well as normal adult stem cells and their progeny in samples obtained from normal lung and lung cancer tissue samples. The researchers identified a very small, rare set of resting cancer stem cells in the lung cancer samples that looked and behaved much like normal adult lung tissue stem cells. Both the cancer and normal stem cells were protected equally by multiple drug resistance transporters, even if the bulk of the tumor responded to chemotherapy.
According to Dr. Donnenberg, the very fact that cancers can and do relapse after apparently successful therapy indicates the survival of a drug-resistant, tumor-initiating population of cells in many types of refractory cancers. "Because of the similarities between the way that normal stem cells and cancer stem cells protect themselves, cancer therapies have to be designed specifically to target cancer stem cells while sparing normal stem cells," she explained.
Russian men dying from booze
New research has revealed that an alarming number of Russian men are drinking themselves to death.
A new study has found that the over consumption of alcohol is a factor in almost half of the deaths of Russia's working-aged men.
The researchers say heavy alcohol use, including the ingestion of alcohol-based liquids not meant to be ingested, attributed to the deaths of nearly half of all working-aged men living in Izhevsk, Russia.
Hazardous drinking includes both excessive consumption of regular beverage-alcohol such as beer, wine, and spirits and the drinking of non-beverage alcohol such as colognes, medical tinctures and cleaning agents.
According to lead author Dr. David A. Leon, the life expectancy for men in Russia is already low at 59 years, and for reasons unknown there have been wide fluctuations in death rates over the last 20 years but it could be related to hazardous drinking.
The researchers had access to information on markers of problem drinking, frequency of alcohol consumption, education, and smoking for 1,468 cases and 1,496 controls.
Of the participants 751 cases were classed as problem drinkers or drank non-beverage alcohol, compared with 192 controls.
Even after adjustments were made for smoking and education over a 2-year time period the mortality odds ratio for these men, compared with those who either abstained or were non-problematic beverage drinkers, was much higher and 43% of deaths were attributable to hazardous drinking.
The deaths were all in men aged 25-54 years and occurred between October 20th, 2003, and October 3rd, 2005.
The staple of many a Russian's diet, Vodka, is expensive and as a result many men to turn to cologne, medicinal tinctures, and cleaning agents as a way to get a quick buzz.
A new study has found that the over consumption of alcohol is a factor in almost half of the deaths of Russia's working-aged men.
The researchers say heavy alcohol use, including the ingestion of alcohol-based liquids not meant to be ingested, attributed to the deaths of nearly half of all working-aged men living in Izhevsk, Russia.
Hazardous drinking includes both excessive consumption of regular beverage-alcohol such as beer, wine, and spirits and the drinking of non-beverage alcohol such as colognes, medical tinctures and cleaning agents.
According to lead author Dr. David A. Leon, the life expectancy for men in Russia is already low at 59 years, and for reasons unknown there have been wide fluctuations in death rates over the last 20 years but it could be related to hazardous drinking.
The researchers had access to information on markers of problem drinking, frequency of alcohol consumption, education, and smoking for 1,468 cases and 1,496 controls.
Of the participants 751 cases were classed as problem drinkers or drank non-beverage alcohol, compared with 192 controls.
Even after adjustments were made for smoking and education over a 2-year time period the mortality odds ratio for these men, compared with those who either abstained or were non-problematic beverage drinkers, was much higher and 43% of deaths were attributable to hazardous drinking.
The deaths were all in men aged 25-54 years and occurred between October 20th, 2003, and October 3rd, 2005.
The staple of many a Russian's diet, Vodka, is expensive and as a result many men to turn to cologne, medicinal tinctures, and cleaning agents as a way to get a quick buzz.
Alzheimer's-associated enzyme beta-secretase can disrupt neural activity in the brain
An enzyme involved in the formation of the amyloid-beta protein associated with Alzheimer's disease can also alter the mechanism by which signals are transmitted between brain cells, the disruption of which can cause seizures.
These findings from researchers at the MassGeneral Institute for Neurodegenerative Disorders (MGH-MIND) may explain the increased incidence of seizures in Alzheimer's patients and suggest that potential treatments that block this enzyme - called beta-secretase or BACE - may alleviate their occurrence. The report will appear in the journal Nature Cell Biology and is receiving early online release.
"We have found a molecular pathway by which BACE can modulate the activity of sodium channels on neuronal cell membranes," says study leader Dora Kovacs, PhD, director of the Neurobiology of Disease Laboratory in the Genetics and Aging Research Unit at MGH-MIND. "That implies that elevated BACE activity may be responsible for the seizures frequently observed in Alzheimer's patients."
Alzheimer's disease is characterized by plaques within the brain of the toxic amyloid-beta protein. Amyloid-beta is formed when the larger amyloid precursor protein (APP) is clipped by two enzymes , BACE and gamma-secretase , which releases the amyloid-beta fragment.
Signaling impulses in nerve cells are transmitted via voltage-gated sodium channels, structures on the cell membrane that transmit electrochemical signal by admitting charged sodium particles into the cell's interior. Sodium channels consist of an alpha subunit, which makes up the body of the channel, and one or two beta subunits that help to regulate the channels, activity.
Previous studies from Kovacs, team and others showed that the BACE and gamma-secretase enzymes that release amyloid-beta from APP also act on the beta2 subunit of neuronal sodium channels. The current study was designed to examine how this processing of the beta2 subunit may alter neuronal function.
Lead author Doo Yeon Kim, PhD, and colleagues first confirmed that the beta2 subunit, similar to APP, can be acted on by BACE and gamma-secretase, releasing a portion of the beta2 molecule from the cell membrane. A series of experiments using brain tissue from animal models and from Alzheimer's patients revealed the following series of cellular events: Elevated levels of the free beta2 segment within the cell appear to increase production of the alpha subunits, but those molecules are not incorporated into new sodium channels on the cell surface. The resulting deficit of membrane sodium channels inhibits the passage of neuronal signals into and through the cells.
Neuronal sodium-channel dysfunction is known to cause seizures in both mice and humans. In a supplement to the current paper the investigators present evidence that sodium channel metabolism is altered in the brains of Alzheimer's patients compared with non-demented individuals of similar age.
"Our study suggests that the BACE inhibitors currently being developed to reduce amyloid-beta generation in Alzheimer's disease patients may also help prevent seizures by alleviating disrupted neural activity," Kovacs explains. "However, complete inhibition of BACE activity could interfere with the enzyme's normal regulation of sodium channels, so therapeutic strategies using those inhibitors will need to be carefully designed." Kovacs is an associate professor of Neurology at Harvard Medical School.
These findings from researchers at the MassGeneral Institute for Neurodegenerative Disorders (MGH-MIND) may explain the increased incidence of seizures in Alzheimer's patients and suggest that potential treatments that block this enzyme - called beta-secretase or BACE - may alleviate their occurrence. The report will appear in the journal Nature Cell Biology and is receiving early online release.
"We have found a molecular pathway by which BACE can modulate the activity of sodium channels on neuronal cell membranes," says study leader Dora Kovacs, PhD, director of the Neurobiology of Disease Laboratory in the Genetics and Aging Research Unit at MGH-MIND. "That implies that elevated BACE activity may be responsible for the seizures frequently observed in Alzheimer's patients."
Alzheimer's disease is characterized by plaques within the brain of the toxic amyloid-beta protein. Amyloid-beta is formed when the larger amyloid precursor protein (APP) is clipped by two enzymes , BACE and gamma-secretase , which releases the amyloid-beta fragment.
Signaling impulses in nerve cells are transmitted via voltage-gated sodium channels, structures on the cell membrane that transmit electrochemical signal by admitting charged sodium particles into the cell's interior. Sodium channels consist of an alpha subunit, which makes up the body of the channel, and one or two beta subunits that help to regulate the channels, activity.
Previous studies from Kovacs, team and others showed that the BACE and gamma-secretase enzymes that release amyloid-beta from APP also act on the beta2 subunit of neuronal sodium channels. The current study was designed to examine how this processing of the beta2 subunit may alter neuronal function.
Lead author Doo Yeon Kim, PhD, and colleagues first confirmed that the beta2 subunit, similar to APP, can be acted on by BACE and gamma-secretase, releasing a portion of the beta2 molecule from the cell membrane. A series of experiments using brain tissue from animal models and from Alzheimer's patients revealed the following series of cellular events: Elevated levels of the free beta2 segment within the cell appear to increase production of the alpha subunits, but those molecules are not incorporated into new sodium channels on the cell surface. The resulting deficit of membrane sodium channels inhibits the passage of neuronal signals into and through the cells.
Neuronal sodium-channel dysfunction is known to cause seizures in both mice and humans. In a supplement to the current paper the investigators present evidence that sodium channel metabolism is altered in the brains of Alzheimer's patients compared with non-demented individuals of similar age.
"Our study suggests that the BACE inhibitors currently being developed to reduce amyloid-beta generation in Alzheimer's disease patients may also help prevent seizures by alleviating disrupted neural activity," Kovacs explains. "However, complete inhibition of BACE activity could interfere with the enzyme's normal regulation of sodium channels, so therapeutic strategies using those inhibitors will need to be carefully designed." Kovacs is an associate professor of Neurology at Harvard Medical School.
Monday, June 11, 2007
Swami Vivekanda
Truth, purity, and unselfishness—wherever these are present, there is no power below or above the sun to crush the possessor thereof. Equipped with these, one individual is able to face the whole universe in opposition
No one should be judged by their defects. The virtues a person has are his especially; his errors are the common weaknesses of humanity and should never be counted in estimating his character
We get caught. How? Not by what we give but by what we expect. We get misery in return for our love: not from the fact that we love but from the fact that we want love in return. There is no misery where there is no want. Desire, want, is the father of all misery. Desires are bound by the laws of success and failure. Desires must bring misery.
The great secret of true success, of true happiness, then, is this: the man or woman who asks for no return, the perfectly unselfish person, is the most successful
There are hundreds of thousands of microbes surrounding us, but they cannot harm us unless we become weak, until the body is ready and predisposed to receive them. There may be a million microbes of misery floating about us. Never mind! They dare not approach us, they have no power to get a hold on us, until the mind is weakened. This is the great fact: strength is life. Weakness is death. Strength is felicity, life eternal, immortal. Weakness is constant strain and misery: weakness is death
Learn to feel yourself in other bodies, to know that we are all one. Throw all other nonsense to the winds. Spit out your actions, good or bad, and never think of them again. What is done is done. Throw off superstition. Have no weakness even in the face of death. Do not repent, do not brood over past deeds. Be âzâd (“free”).
Think always: “I am ever-pure, ever-knowing, and ever-free. How can I do anything evil? Can I ever be befooled like ordinary people with the insignificant charms of lust and wealth?” Strengthen the mind with such thoughts. This will surely bring real good
Think day and night, “I am of the essence of that Supreme Existence, Knowledge, Bliss—what fear and anxiety have I? This body, mind, and intellect are all transient, and That which is beyond these is myself
The highest manifestation of strength is to keep ourselves calm and on our own feet.Look here—we shall die! Bear this in mind always, and then the spirit within will wake up. Only then will meanness vanish from you, practicality in work will come, you will get new vigor in mind and body, and those who come in contact with you will also feel that they have really got something uplifting from you
My child, what I want is muscles of iron and nerves of steel, inside which dwells a mind of the same material as that of which the thunderbolt is made.
Work unto death—I am with you, and when I am gone, my spirit will work with you. This life comes and goes—wealth, fame, enjoyments are only of a few days. It is better, far better, to die on the field of duty, preaching the truth, than to die like a worldly worm. Advance
Stand up, be bold, and take the blame on your own shoulders. Do not go about throwing mud at others; for all the faults you suffer from, you are the sole and only cause
The less the thought of the body, the better it is for us. For it is the body that drags us down. It is attachment, identification, which makes us miserable
Brave, bold people, these are what we want. What we want is vigor in the blood, strength in the nerves, iron muscles and nerves of steel, not softening namby-pamby ideas. Avoid all these. Avoid all mystery. There is no mystery in religion
Do not hate anybody, because that hatred which comes out from you must, in the long run, come back to you. If you love, that love will come back to you, completing the circle
Be brave! Be strong! Be fearless! Once you have taken up the spiritual life, fight as long as there is any life in you. Even though you know you are going to be killed, fight till you “are killed.” Don’t die of fright. Die fighting. Don’t go down till you are knocked down.
To succeed you must have tremendous perseverance, tremendous will. “I will drink the ocean,” says the persevering soul, “at my will mountains will crumble.” Have that sort of energy, that sort of will, work hard, and you will reach the goal.
If you really want the good of others, the whole universe may stand against you and cannot hurt you. It must crumble before your power of the Lord Himself in you if you are sincere and really unselfish
Look here—we shall die! Bear this in mind always, and then the spirit within will wake up. Then meanness will vanish from you, practicality in work will come, you will get new vigor in mind and body, and those who come in contact with you will also feel that they have really got something uplifting from you.
Fear is death, fear is sin, fear is hell, fear is unrighteousness. All the negative thoughts and ideas that are in this world have proceeded from this evil spirit of fear.
Molecular differences between early and advanced melanomas could provide new drug targets
The cell-signaling molecule Akt is a primary trigger that leads malignant melanomas on the skin's surface to begin growing vertically beneath the skin and turn into deadly invasive cancers, scientists have found. Understanding this key molecular difference between radial melanomas that spread on the surface of the skin and melanomas that grow vertically and invasively could provide new targets for the development of drugs to treat individuals with advanced stage melanomas.
Radial melanomas that have not spread below the skin can be treated surgically and have a survival rate of 98 percent beyond five years, according to the American Cancer Society. But when melanomas grow downward, the tumors become highly resistant to chemotherapy and radiation and the five-year survival rate falls rapidly, to 64 percent if the disease has reached the lymph nodes and 16 percent if it has spread to other organs.
The discovery of Akt's significant role in the progression of melanomas was made by scientists in the Department of Dermatology at Emory University School of Medicine and published in the March issue of the Journal of Clinical Investigation. Senior author is Jack L. Arbiser, MD, PhD, and lead author is Baskaran Govindarajan, PhD.
When the scientists introduced the gene for Akt into radial growth melanoma cells, the cells expressed nearly eight times as much of the growth factor protein VEGF. VEGF is known to be a powerful stimulator of angiogenesis Ð the growth of microscopic blood vessels that nourish cancerous tumors and lead to unregulated cell growth. When melanoma cells overexpressing Akt were introduced into immunocompromised (nude) mice, the mice developed aggressive tumors that expressed high levels of VEGF, whereas a control group of mice developed no tumors.
Another result of Akt overexpression was the increased production of reactive oxygen (ROS). Reactive oxygen is created during cellular metabolism and has long been associated with triggering angiogenesis and the resulting growth of tumors. The scientists also found that the Akt-induced melanoma cells produced more of the enzyme NOX4, one of the NOX family of genes known to increase generation of ROS and to trigger angiogenesis.
The scientists also found that in cells with greater Akt expression, there was an increase in impaired mitochondria-- the energy factories of cells. Their research showed, however, that these mutations in mitochondria were likely the result of the prolonged exposure to increased oxidative stress caused by Akt overexpression, but that the mitochondrial mutations were not essential for the aggressive growth of melanomas induced by Akt.
"Our research shows that Akt overexpression on its own is sufficient to transform radial growth melanoma cells into highly invasive tumors via reactive oxygen pathways," says Dr. Arbiser. "This could provide us with promising targets for anti-cancer drug therapy. We will continue to work on refining the exact mechanisms of how Akt influences the aggressive growth of melanomas."
Radial melanomas that have not spread below the skin can be treated surgically and have a survival rate of 98 percent beyond five years, according to the American Cancer Society. But when melanomas grow downward, the tumors become highly resistant to chemotherapy and radiation and the five-year survival rate falls rapidly, to 64 percent if the disease has reached the lymph nodes and 16 percent if it has spread to other organs.
The discovery of Akt's significant role in the progression of melanomas was made by scientists in the Department of Dermatology at Emory University School of Medicine and published in the March issue of the Journal of Clinical Investigation. Senior author is Jack L. Arbiser, MD, PhD, and lead author is Baskaran Govindarajan, PhD.
When the scientists introduced the gene for Akt into radial growth melanoma cells, the cells expressed nearly eight times as much of the growth factor protein VEGF. VEGF is known to be a powerful stimulator of angiogenesis Ð the growth of microscopic blood vessels that nourish cancerous tumors and lead to unregulated cell growth. When melanoma cells overexpressing Akt were introduced into immunocompromised (nude) mice, the mice developed aggressive tumors that expressed high levels of VEGF, whereas a control group of mice developed no tumors.
Another result of Akt overexpression was the increased production of reactive oxygen (ROS). Reactive oxygen is created during cellular metabolism and has long been associated with triggering angiogenesis and the resulting growth of tumors. The scientists also found that the Akt-induced melanoma cells produced more of the enzyme NOX4, one of the NOX family of genes known to increase generation of ROS and to trigger angiogenesis.
The scientists also found that in cells with greater Akt expression, there was an increase in impaired mitochondria-- the energy factories of cells. Their research showed, however, that these mutations in mitochondria were likely the result of the prolonged exposure to increased oxidative stress caused by Akt overexpression, but that the mitochondrial mutations were not essential for the aggressive growth of melanomas induced by Akt.
"Our research shows that Akt overexpression on its own is sufficient to transform radial growth melanoma cells into highly invasive tumors via reactive oxygen pathways," says Dr. Arbiser. "This could provide us with promising targets for anti-cancer drug therapy. We will continue to work on refining the exact mechanisms of how Akt influences the aggressive growth of melanomas."
Drug screen for cancer patients found
PHILADEPHIA, Pa., March 9 (UPI) -- Researchers at the University of Pennsylvania have found a way to screen cancer patients to see if they're suitable for a promising class of anti-cancer drugs.
The researchers propose screening cancer patients for proteasome inhibitors by testing for p53, a tumor-suppressor protein.
The anti-cancer proteasome inhibitors might be ineffective in patients whose tumors do not produce p53, said the researchers at the university's schools of medicine and veterinary medicine.
However, proteasome inhibitors are highly effective against lymphomas that do produce p53, the researchers said.
"Proteasomes resemble paper shredders - they break down proteins such as p53 into smaller pieces," said associate pathology professor Andrei Thomas-Tikhonenko. "A proteosome inhibitor effectively jams the shredder so that p53 is not immediately broken down."
The study appears online in the journal Blood , in advance of print publication in Ju
ne 2007
The researchers propose screening cancer patients for proteasome inhibitors by testing for p53, a tumor-suppressor protein.
The anti-cancer proteasome inhibitors might be ineffective in patients whose tumors do not produce p53, said the researchers at the university's schools of medicine and veterinary medicine.
However, proteasome inhibitors are highly effective against lymphomas that do produce p53, the researchers said.
"Proteasomes resemble paper shredders - they break down proteins such as p53 into smaller pieces," said associate pathology professor Andrei Thomas-Tikhonenko. "A proteosome inhibitor effectively jams the shredder so that p53 is not immediately broken down."
The study appears online in the journal Blood , in advance of print publication in Ju
ne 2007
Drug screen for cancer patients found
PHILADEPHIA, Pa., March 9 (UPI) -- Researchers at the University of Pennsylvania have found a way to screen cancer patients to see if they're suitable for a promising class of anti-cancer drugs.
The researchers propose screening cancer patients for proteasome inhibitors by testing for p53, a tumor-suppressor protein.
The anti-cancer proteasome inhibitors might be ineffective in patients whose tumors do not produce p53, said the researchers at the university's schools of medicine and veterinary medicine.
However, proteasome inhibitors are highly effective against lymphomas that do produce p53, the researchers said.
"Proteasomes resemble paper shredders - they break down proteins such as p53 into smaller pieces," said associate pathology professor Andrei Thomas-Tikhonenko. "A proteosome inhibitor effectively jams the shredder so that p53 is not immediately broken down."
The study appears online in the journal Blood , in advance of print publication in Ju
ne 2007
The researchers propose screening cancer patients for proteasome inhibitors by testing for p53, a tumor-suppressor protein.
The anti-cancer proteasome inhibitors might be ineffective in patients whose tumors do not produce p53, said the researchers at the university's schools of medicine and veterinary medicine.
However, proteasome inhibitors are highly effective against lymphomas that do produce p53, the researchers said.
"Proteasomes resemble paper shredders - they break down proteins such as p53 into smaller pieces," said associate pathology professor Andrei Thomas-Tikhonenko. "A proteosome inhibitor effectively jams the shredder so that p53 is not immediately broken down."
The study appears online in the journal Blood , in advance of print publication in Ju
ne 2007
Natural killer cells : Tumour Cells tout trogocytosis
A new report in The EMBO Journal describes the transfer of HLA-G molecules by trogocytosis from tumour cells to activated natural killer (NK) cells, which might be a mechanism of protection for HLA-G-negative tumour cells that are in the vicinity of HLA-G-positive tumour cells.
Trogocytosis is the rapid transfer of intact cell-surface proteins between cells in contact with each other, and has been observed between NK cells and tumour cells. But why this process occurs between these two cell types has been unclear. In this study, Caumartin et al. examined HLA-G, a non-classical MHC class I molecule that is expressed by various tumour cells in vivo and for which engagement with inhibitory receptors on NK cells is known to block NK-cell-mediated cytolysis. They asked whether HLA-G could be transferred from tumour cells to NK cells and, if so, what the functional consequences might be.
Cell-culture experiments showed that activated but not resting NK cells display HLA-G1 on their cell surfaces following contact with HLA-G1-expressing tumour cells. But did the NK cells become HLA-G1-positive by trogocytosis? The authors first ruled out the possibilities of endogenous expression of HLA-G1 by the NK cells and binding of shed soluble HLA-G1 to receptors on NK cells, and then showed that cell–cell contact was necessary for NK-cell surface display of HLA-G1. They confirmed that trogocytosis was indeed the mechanism involved by demonstrating the fast kinetics of the transfer of HLA-G1 molecules from the tumour cells to the NK cells, and the limited lifetime of the transferred molecules, both of which, along with the dependence on cell–cell contact, are the main parameters of trogocytosis.
Caumartin et al. next investigated whether trogocytosis of HLA-G1 had functional consequences for NK cells and, in particular, whether it could constitute an immune-escape mechanism for tumour cells, given that HLA-G1 engages inhibitory receptors on NK cells resulting in immunosuppression. The authors showed that the acquisition of HLA-G1 by activated, cytotoxic NK effector cells blocked their proliferation and temporarily inhibited their cytolytic function. Further investigation revealed that the transfer of HLA-G1 molecules from tumour cells to NK cells in fact induced a temporary immunosuppressive state in the NK-cell population (that is, NK cells could cross-inhibit the cytotoxic functions of other NK cells), and that this was due to the interaction of trogocytosed HLA-G1 with the inhibitory receptor immunoglobulin-like transcript 2 (ILT2) on other NK cells.
So, once the activated NK cells acquire HLA-G1 from tumour cells by trogocytosis they stop proliferating, are no longer cytolytic and behave as suppressor cells, and so can potentially protect tumour cells from NK-cell-mediated cytolysis. The unique qualities of this process are that it effects a switch from effector to suppressor cell through the transfer of a molecule that the recipient cell does not endogenously express, and that it is temporary and does not alter the true nature of the cell. These data highlight the key role of the cellular microenvironment in the immune response
Trogocytosis is the rapid transfer of intact cell-surface proteins between cells in contact with each other, and has been observed between NK cells and tumour cells. But why this process occurs between these two cell types has been unclear. In this study, Caumartin et al. examined HLA-G, a non-classical MHC class I molecule that is expressed by various tumour cells in vivo and for which engagement with inhibitory receptors on NK cells is known to block NK-cell-mediated cytolysis. They asked whether HLA-G could be transferred from tumour cells to NK cells and, if so, what the functional consequences might be.
Cell-culture experiments showed that activated but not resting NK cells display HLA-G1 on their cell surfaces following contact with HLA-G1-expressing tumour cells. But did the NK cells become HLA-G1-positive by trogocytosis? The authors first ruled out the possibilities of endogenous expression of HLA-G1 by the NK cells and binding of shed soluble HLA-G1 to receptors on NK cells, and then showed that cell–cell contact was necessary for NK-cell surface display of HLA-G1. They confirmed that trogocytosis was indeed the mechanism involved by demonstrating the fast kinetics of the transfer of HLA-G1 molecules from the tumour cells to the NK cells, and the limited lifetime of the transferred molecules, both of which, along with the dependence on cell–cell contact, are the main parameters of trogocytosis.
Caumartin et al. next investigated whether trogocytosis of HLA-G1 had functional consequences for NK cells and, in particular, whether it could constitute an immune-escape mechanism for tumour cells, given that HLA-G1 engages inhibitory receptors on NK cells resulting in immunosuppression. The authors showed that the acquisition of HLA-G1 by activated, cytotoxic NK effector cells blocked their proliferation and temporarily inhibited their cytolytic function. Further investigation revealed that the transfer of HLA-G1 molecules from tumour cells to NK cells in fact induced a temporary immunosuppressive state in the NK-cell population (that is, NK cells could cross-inhibit the cytotoxic functions of other NK cells), and that this was due to the interaction of trogocytosed HLA-G1 with the inhibitory receptor immunoglobulin-like transcript 2 (ILT2) on other NK cells.
So, once the activated NK cells acquire HLA-G1 from tumour cells by trogocytosis they stop proliferating, are no longer cytolytic and behave as suppressor cells, and so can potentially protect tumour cells from NK-cell-mediated cytolysis. The unique qualities of this process are that it effects a switch from effector to suppressor cell through the transfer of a molecule that the recipient cell does not endogenously express, and that it is temporary and does not alter the true nature of the cell. These data highlight the key role of the cellular microenvironment in the immune response
Signalling : DNA damage is Stressful
DNA damage activates a complex signalling network that functions to mediate DNA repair and activate cell-cycle checkpoints. Michael Yaffe and colleagues now show that p53-deficient tumour cells rely on an alternative, parallel signalling pathway to activate cell-cycle checkpoints after treatment with DNA-damaging anticancer drugs.
DNA-damage checkpoints are primarily activated by ataxia-telangiectasia mutated (ATM) and ataxia-telangiectasia mutated and Rad3-related (ATR) kinases, predominantly through the activation of the mediator kinases CHK2 and CHK1, respectively. Previous data indicated that another mediator kinase, mitogen-activated protein kinase-activated protein kinase 2 (MAPKAPK2), which is a downstream kinase of the p38 MAPK, also functions in checkpoint activation in response to cellular stress, such as heat shock and UV irradiation. Therefore, Yaffe and colleagues investigated whether p38 and MAPKAPK2 are part of the DNA-damage signalling network.
The authors showed that the treatment of cells with the anticancer agents cisplatin, camptothecin and doxorubicin increased the activating phosphorylation of p38 and MAPKAPK2. Furthermore, the p38-dependent phosphorylation of MAPKAPK2 occurred downstream of ATR in response to cisplatin and camptothecin, and downstream of ATR and ATM in response to doxorubicin. A major effector of DNA-damage checkpoint activation is p53. The authors showed that the p38–MAPKAPK2 arm of the DNA-damage response pathway was required for the survival of mouse embryonic fibroblasts (MEFs) after treatment with doxorubicin or cisplatin only when p53 was not present. Moreover, they showed that MAPKAPK2 is required for the activation of the G2/M and intra-S phase checkpoints in Trp53-/- MEFs after treatment with doxorubicin and cisplatin. In this context, MAPKAPK2 was required for checkpoint activation upstream of cell division cycle 25A and B (CDC25A and CDC25, despite the ATR-dependent activation of CHK1 in a parallel pathway.
So, given that most tumour cells are p53-deficient, could MAPKAPK2 be a clinically relevant anticancer target? The authors injected HRASV12-transformed Trp53-/- MEFs in which MAPKAPK2 was downregulated by short hairpin RNA into nude mice. The MAPKAPK2-deficient tumours that developed were slightly larger than controls but showed a dramatic decrease in size and weight when doxorubicin or cisplatin was administered, indicating that MAPKAPK2 inhibition might sensitize tumours to DNA-damaging agents. In addition, they showed that UCN01, a CHK1 and CHK2 small-molecule inhibitor that is currently in clinical trials, also inhibits MAPKAPK2 at a similar concentration to CHK1 (CHK2 inhibition requires higher concentrations of the drug).
Therefore, the simultaneous inhibition of CHK1 and MAPKAPK2 might account for the tumour sensitization effects of UCN01 that prompted the clinical trials. It remains unclear how and why ATR- and ATM-dependent checkpoint activation operates through p38–MAPKAPK2, CHK1 and CHK2. Because the MAPKAPK2-dependency is only apparent when p53 is not present and, unlike CHK1, MAPKAPK2 is not essential, the development of specific MAPKAPK2 inhibitors could be a viable approach to sensitizing cancer cells to DNA-damaging agents.
DNA-damage checkpoints are primarily activated by ataxia-telangiectasia mutated (ATM) and ataxia-telangiectasia mutated and Rad3-related (ATR) kinases, predominantly through the activation of the mediator kinases CHK2 and CHK1, respectively. Previous data indicated that another mediator kinase, mitogen-activated protein kinase-activated protein kinase 2 (MAPKAPK2), which is a downstream kinase of the p38 MAPK, also functions in checkpoint activation in response to cellular stress, such as heat shock and UV irradiation. Therefore, Yaffe and colleagues investigated whether p38 and MAPKAPK2 are part of the DNA-damage signalling network.
The authors showed that the treatment of cells with the anticancer agents cisplatin, camptothecin and doxorubicin increased the activating phosphorylation of p38 and MAPKAPK2. Furthermore, the p38-dependent phosphorylation of MAPKAPK2 occurred downstream of ATR in response to cisplatin and camptothecin, and downstream of ATR and ATM in response to doxorubicin. A major effector of DNA-damage checkpoint activation is p53. The authors showed that the p38–MAPKAPK2 arm of the DNA-damage response pathway was required for the survival of mouse embryonic fibroblasts (MEFs) after treatment with doxorubicin or cisplatin only when p53 was not present. Moreover, they showed that MAPKAPK2 is required for the activation of the G2/M and intra-S phase checkpoints in Trp53-/- MEFs after treatment with doxorubicin and cisplatin. In this context, MAPKAPK2 was required for checkpoint activation upstream of cell division cycle 25A and B (CDC25A and CDC25, despite the ATR-dependent activation of CHK1 in a parallel pathway.
So, given that most tumour cells are p53-deficient, could MAPKAPK2 be a clinically relevant anticancer target? The authors injected HRASV12-transformed Trp53-/- MEFs in which MAPKAPK2 was downregulated by short hairpin RNA into nude mice. The MAPKAPK2-deficient tumours that developed were slightly larger than controls but showed a dramatic decrease in size and weight when doxorubicin or cisplatin was administered, indicating that MAPKAPK2 inhibition might sensitize tumours to DNA-damaging agents. In addition, they showed that UCN01, a CHK1 and CHK2 small-molecule inhibitor that is currently in clinical trials, also inhibits MAPKAPK2 at a similar concentration to CHK1 (CHK2 inhibition requires higher concentrations of the drug).
Therefore, the simultaneous inhibition of CHK1 and MAPKAPK2 might account for the tumour sensitization effects of UCN01 that prompted the clinical trials. It remains unclear how and why ATR- and ATM-dependent checkpoint activation operates through p38–MAPKAPK2, CHK1 and CHK2. Because the MAPKAPK2-dependency is only apparent when p53 is not present and, unlike CHK1, MAPKAPK2 is not essential, the development of specific MAPKAPK2 inhibitors could be a viable approach to sensitizing cancer cells to DNA-damaging agents.
A Weak spot in HIV spotted
Scientists have discovered a place on the outside part of AIDS virus that might be vulnerable to antibodies blocking the virus from infecting human cells. This could mean that an anti-HIV vaccine is possible in the future.
According to Peter Kwong, researcher at U.S National Institute of Health (NIH), this study is likely to contribute to finding HIV's "site of vulnerability" which could then be targeted with a vaccine that prevents the initial infection.
Schematic diagram of the human immunodeficiency virus (HIV).
The team of researchers have made atomic-level images of HIV and revealed the structure of a protein on the surface of the virus. This protein, called gp120, binds to an infection-fighting antibody and seems to be susceptible to attacks by this antibody called 'b12'. B12 can broadly neutralize the virus.
Researchers detailed the precise interaction as the virus tries to hook on to and infect cells sent to protect the body. They have captured an image of how the virus of human immunodeficiency attacks the human cells. Dr. Gary Nabel, an NIH vaccine expert and a co-author of the research, describes this first contact between the virus and the cells as a 'cautious handshake' which then becomes a 'hearty bear hug'. The virus grabs and infects the cells that are aimed at protecting the body.
Then the virus mutates quickly to fight the immune system's attacks as well as to counter the effect of antibodies that block the proteins with help of which HIV binds to a cell to infect it.
Scientists agree that a vaccine against AIDS would be an ideal way to stop the pandemic of this disease, but, with all importance of these findings, much work and studies are still needed. This implies that any vaccine against AIDS is probably still many years away.
The AIDS virus has killed more than 25 million people since it was first detected in 1981. Sub-Saharan Africa is the most severely affected by the epidemic. Approximately 40 million people live with HIV.
About a dozen potential vaccines are currently under development. Two products, one by Merck and one by Sanofi-Aventis, are now in advanced human trials
AIDS "super bug" diagnosed in New York
A drug-resistant and quick-acting form of HIV, the virus that causes AIDS, has been detected in New York City, according to officials.
Although diagnosed in only one man so far, this mutated version of the virus progresses to AIDS faster than other forms of HIV, officials said. Diagnosed with HIV in mid-October, the unnamed New York City man developed the full-blown form AIDS by mid-January. Normally HIV infection can take up to 10 years to develop into AIDS.
Dr. Ronald O. Valdiserri, the director of HIV/AIDS prevention at the Centers for Disease Control & Prevention (CDC), told the New York Times this new strain of virus is unique because of the rapid progression of the disease and its resistance to multiple AIDS drug regimens. Although the New York case appears to be isolated at this time, the CDC has sent a nation-wide alert to health departments in every state.
"It appears this individual has contracted a new, particularly virulent strain of HIV that swiftly advanced to AIDS in just a few short months," Charles Farthing, MD, AIDS Healthcare Foundation's Chief of Medicine said in a press release. "Unfortunately, it also seems that few of the AIDS treatments currently available today can be used in his case, as this particular strain of infection appears to be resistant to most known AIDS drugs."
Dr. Thomas R. Frieden, commissioner of the New York City Department of Health and Mental Hygiene, urged all newly-diagnosed HIV patients to get tested to see if they have this new form of the virus. He also said all sexually active people should be tested for the HI virus.
New York health officials said they estimate that about 88,000 New Yorkers have HIV infection or AIDS and that an additional 20,000 are infected but unaware of their condition.
Although diagnosed in only one man so far, this mutated version of the virus progresses to AIDS faster than other forms of HIV, officials said. Diagnosed with HIV in mid-October, the unnamed New York City man developed the full-blown form AIDS by mid-January. Normally HIV infection can take up to 10 years to develop into AIDS.
Dr. Ronald O. Valdiserri, the director of HIV/AIDS prevention at the Centers for Disease Control & Prevention (CDC), told the New York Times this new strain of virus is unique because of the rapid progression of the disease and its resistance to multiple AIDS drug regimens. Although the New York case appears to be isolated at this time, the CDC has sent a nation-wide alert to health departments in every state.
"It appears this individual has contracted a new, particularly virulent strain of HIV that swiftly advanced to AIDS in just a few short months," Charles Farthing, MD, AIDS Healthcare Foundation's Chief of Medicine said in a press release. "Unfortunately, it also seems that few of the AIDS treatments currently available today can be used in his case, as this particular strain of infection appears to be resistant to most known AIDS drugs."
Dr. Thomas R. Frieden, commissioner of the New York City Department of Health and Mental Hygiene, urged all newly-diagnosed HIV patients to get tested to see if they have this new form of the virus. He also said all sexually active people should be tested for the HI virus.
New York health officials said they estimate that about 88,000 New Yorkers have HIV infection or AIDS and that an additional 20,000 are infected but unaware of their condition.
Gene Switch turns stem cells into cancer killers
A gene has been discovered that turns stem cells into cancer killers, promising new treatments that boost the body's ability to destroy tumors.
South Korean scientists from the Korea Research Institute of Bioscience and Biotechnology in Daejeon say that the gene, Vitamin D3 Upregulated Protein 1 (VDUP1), spurs stem cells to become natural killer cells.
These components of the immune system can eliminate virus-infected and cancerous cells. Research leader Inpyo Choi says the team observed that VDUP1 plays a decisive role in causing stem cells to become natural killers.
The discovery was made by examining mice bred to lack the gene. The mice had a dramatic reduction in the number and activity of natural killer cells.
Besides determining the gene's importance to the immune system, Choi and colleagues have developed technology needed to spur the creation of natural killers from a person's own bone marrow stem cells.
Choi calls this "the first step toward developing new treatments using our own immune system to fight cancers and other serious diseases."
South Korean scientists from the Korea Research Institute of Bioscience and Biotechnology in Daejeon say that the gene, Vitamin D3 Upregulated Protein 1 (VDUP1), spurs stem cells to become natural killer cells.
These components of the immune system can eliminate virus-infected and cancerous cells. Research leader Inpyo Choi says the team observed that VDUP1 plays a decisive role in causing stem cells to become natural killers.
The discovery was made by examining mice bred to lack the gene. The mice had a dramatic reduction in the number and activity of natural killer cells.
Besides determining the gene's importance to the immune system, Choi and colleagues have developed technology needed to spur the creation of natural killers from a person's own bone marrow stem cells.
Choi calls this "the first step toward developing new treatments using our own immune system to fight cancers and other serious diseases."
Arsenic and Thalidomide may be used to fight cancer
A gathering of more than a thousand medical researchers in Sydney, Australia, has been told that arsenic and Thalidomide — banned in the 1960s after being linked to gross birth abnormalities — held hope as a basis for new treatments, extending the lives of patients with an so-far incurable bone marrow cancer, multiple myeloma.
Diagnosis of the disease has increased by 45% in Australia since 1992. It is the most lethal form of cancer, and the topic of discussion, at the 10th International Myeloma Workshop, continuing until the 16th of April.
The two treatments had advantages over existing chemotherapy treatments, including lessened side-effects, and reducing the need for chemo- and radiotherapy. They may also be usable to treat other illnesses. Both were still under test.
"The development of arsenic dates back many years when it was used for lowering the blood counts in patients, even at the turn of the century," Professor Miles Prince, of the Peter MacCallum Cancer Centre, told Australian Associated Press for the 10th International Myeloma Workshop.
"Subsequently [arsenic] was used in China since the 1960s for treating certain forms of Leukaemia," he said.
It could be used to induce the cell to "commit suicide".
"The side effects with Thalidomide are much less than with chemotherapy because it's not damaging innocent bystander cells - so you don't get low blood counts, you don't lose your hair, you don't get a sore mouth," he said.
"It was originally thought to work because [Thalidomide] blocks the blood vessel growth in tumours, and that is still true, but the research that we've done has shown that one of its major causes of action is to stimulate [ immune system ] T-cells which are directly against the tumour, and these T-cells help patients with myeloma fight their disease," Professor Douglas Joshua, head of Haemotology at Royal Prince Alfred Hospital in Sydney, told Australian radio.
"There's no doubt that with the new combinations of drugs - we've got Thalidomide, the sons of Thalidomide, Velcade and arsenic - we're adding years onto patient's lives and certainly it could add up to five years or more," according to Prof. Prince
Diagnosis of the disease has increased by 45% in Australia since 1992. It is the most lethal form of cancer, and the topic of discussion, at the 10th International Myeloma Workshop, continuing until the 16th of April.
The two treatments had advantages over existing chemotherapy treatments, including lessened side-effects, and reducing the need for chemo- and radiotherapy. They may also be usable to treat other illnesses. Both were still under test.
"The development of arsenic dates back many years when it was used for lowering the blood counts in patients, even at the turn of the century," Professor Miles Prince, of the Peter MacCallum Cancer Centre, told Australian Associated Press for the 10th International Myeloma Workshop.
"Subsequently [arsenic] was used in China since the 1960s for treating certain forms of Leukaemia," he said.
It could be used to induce the cell to "commit suicide".
"The side effects with Thalidomide are much less than with chemotherapy because it's not damaging innocent bystander cells - so you don't get low blood counts, you don't lose your hair, you don't get a sore mouth," he said.
"It was originally thought to work because [Thalidomide] blocks the blood vessel growth in tumours, and that is still true, but the research that we've done has shown that one of its major causes of action is to stimulate [ immune system ] T-cells which are directly against the tumour, and these T-cells help patients with myeloma fight their disease," Professor Douglas Joshua, head of Haemotology at Royal Prince Alfred Hospital in Sydney, told Australian radio.
"There's no doubt that with the new combinations of drugs - we've got Thalidomide, the sons of Thalidomide, Velcade and arsenic - we're adding years onto patient's lives and certainly it could add up to five years or more," according to Prof. Prince
South Korean Scientists clone dog for first time
Seoul National University’s Hwang Woo-Suk has reported his findings in the Journal Nature after being involved in producing the first cloned dog.
The dog, named Snuppy, was born on April 24th. He is an Afghan hound. The issue presents a whole host of ethical questions for researchers in the stem cell field.
Companies like Amgen are interested in the technology, as is accounted in Fortune Magazine for making human-safe pharmeceuticals. The business sector relies on technology improvements to make life saving realities.
The Los Angeles Times has reported that Snuppy came from the DNA of the tissue of the ear of the original canine.
According to ABC News Associated Press reporter JI-SOO KIM, Korea has declared that we are still a long way from creating clones of monkeys, which have a great deal more humanlike traits.
Slashdot actually reported an RSS feed yesterday at 4:15PM regarding the BBC and Reuters News articles which told of the 2 successful terms of gestation for Snuppy. "the South Korean team only obtained three pregnancies from more than 1,000 embryo transfers into 123 recipients." (BBC).
Kennel experts, according to the BBC, agree that there will be many moral issues to contend with, especially among pet lovers.
The dog, named Snuppy, was born on April 24th. He is an Afghan hound. The issue presents a whole host of ethical questions for researchers in the stem cell field.
Companies like Amgen are interested in the technology, as is accounted in Fortune Magazine for making human-safe pharmeceuticals. The business sector relies on technology improvements to make life saving realities.
The Los Angeles Times has reported that Snuppy came from the DNA of the tissue of the ear of the original canine.
According to ABC News Associated Press reporter JI-SOO KIM, Korea has declared that we are still a long way from creating clones of monkeys, which have a great deal more humanlike traits.
Slashdot actually reported an RSS feed yesterday at 4:15PM regarding the BBC and Reuters News articles which told of the 2 successful terms of gestation for Snuppy. "the South Korean team only obtained three pregnancies from more than 1,000 embryo transfers into 123 recipients." (BBC).
Kennel experts, according to the BBC, agree that there will be many moral issues to contend with, especially among pet lovers.
Bacteria thrive deep under sea floor
Analysis of sediments taken from hundreds of metres beneath the ocean floor has shown them to contain living microbes. According to a study produced by a team of researchers supported by the International Ocean Drilling Program, this is the first time that microbes have been found in abundance at such depths.
Scientists have long speculated about how much of the bacterial content of the sediments is biologically active. Techniques used to stain the bacteria and identify them could not previously discriminate between live and dead cells. For this study a new technique that could distinguish between alive and dead cells was used.
The results were surprising. The sediments, some of which had been collected from up to 800 metres from beneath the sea floor and are said to be up to 16 million years old, contained between 10-30% living bacteria. Scientists estimate that between 60-70% of all bacteria are living deep beneath the surface, far from any sunlight.
"We didn't have clear evidence that bacteria there were alive until now," said ecologist and team member Lev Neretin of the Max Planck Institute for Marine Biology in Bremen, Germany. According to calculations, the populations of bacteria multiply at the same rate as their surface cousins and contribute significantly to the balance of greenhouse gases, consuming and producing CO2. They also contribute methane via a metabolic process that does not require oxygen.
"Because they play such a major role in the biochemical processes in the subsurface, clearly they are driving lots of reactions that produce the chemical steady state on Earth," said Dr John Parkes, one of the original co-authors of the paper which appeared in Nature magazine, "possibly we might not have oil and gas formations without them."
How could these bacteria get so deep beneath the ocean floor? "The only reasonable way is for them to be buried there," says Bo Thamdrup, a microbiologist from the University of Southern Denmark, Odense. The extremes of temperature and pressures tolerated by these bacteria add weight to the assertion that microbes may flourish in the extreme conditions of other planets.
"It is well known that bacteria living in deep oceans have special adaptations to help them survive," says Thamdrup. "I'm sure these bacteria have special adaptations too." A full genetic analysis may soon reveal them
Scientists have long speculated about how much of the bacterial content of the sediments is biologically active. Techniques used to stain the bacteria and identify them could not previously discriminate between live and dead cells. For this study a new technique that could distinguish between alive and dead cells was used.
The results were surprising. The sediments, some of which had been collected from up to 800 metres from beneath the sea floor and are said to be up to 16 million years old, contained between 10-30% living bacteria. Scientists estimate that between 60-70% of all bacteria are living deep beneath the surface, far from any sunlight.
"We didn't have clear evidence that bacteria there were alive until now," said ecologist and team member Lev Neretin of the Max Planck Institute for Marine Biology in Bremen, Germany. According to calculations, the populations of bacteria multiply at the same rate as their surface cousins and contribute significantly to the balance of greenhouse gases, consuming and producing CO2. They also contribute methane via a metabolic process that does not require oxygen.
"Because they play such a major role in the biochemical processes in the subsurface, clearly they are driving lots of reactions that produce the chemical steady state on Earth," said Dr John Parkes, one of the original co-authors of the paper which appeared in Nature magazine, "possibly we might not have oil and gas formations without them."
How could these bacteria get so deep beneath the ocean floor? "The only reasonable way is for them to be buried there," says Bo Thamdrup, a microbiologist from the University of Southern Denmark, Odense. The extremes of temperature and pressures tolerated by these bacteria add weight to the assertion that microbes may flourish in the extreme conditions of other planets.
"It is well known that bacteria living in deep oceans have special adaptations to help them survive," says Thamdrup. "I'm sure these bacteria have special adaptations too." A full genetic analysis may soon reveal them
Study claims to show the difference between male and female brains
Michael Gurian, psychologist and author of "What Could He Be Thinking?", has claimed to identify approximately one hundred structural differences between male and female brains in a recent study.
Gurian comments:
"Men, because we tend to compartmentalize our communication into a smaller part of the brain, we tend to be better at getting right to the issue, the more female brain (will) gather a lot of material, gather a lot of information, feel a lot, hear a lot, sense a lot."One major structural difference that Gurian has made clear is that males generally have more activity in the mechanical centers of the brain, while women have more activity in centers of the brain dedicated to verbal communication and emotion. A clear example of this is the hypothetical situation of giving a child a toy.
"Men, because we tend to compartmentalize our communication into a smaller part of the brain, we tend to be better at getting right to the issue, the more female brain (will) gather a lot of material, gather a lot of information, feel a lot, hear a lot, sense a lot."One major structural difference that Gurian has made clear is that males generally have more activity in the mechanical centers of the brain, while women have more activity in centers of the brain dedicated to verbal communication and emotion. A clear example of this is the hypothetical situation of giving a child a toy.
He explains it as such:
"That doll becomes life-like to that girl, but you give it to a two-year-old boy and you are more likely, not all the time, but you are more likely than not to see that boy try to take the head off the doll. He thinks spatial-mechanical. He's using the doll as an object."Another expert, Dr. Marianne Legato, says it all boils down to genetics, noting that the Y chromosome (which only males carry) has "at least 21 unique genes unique to males which control many of the body's operations down to the level of the cells."
"That doll becomes life-like to that girl, but you give it to a two-year-old boy and you are more likely, not all the time, but you are more likely than not to see that boy try to take the head off the doll. He thinks spatial-mechanical. He's using the doll as an object."Another expert, Dr. Marianne Legato, says it all boils down to genetics, noting that the Y chromosome (which only males carry) has "at least 21 unique genes unique to males which control many of the body's operations down to the level of the cells."
Gurian agrees that culture is significant in brain development, but argues that biology plays an equally important role. He makes a point of how the MRI scans show that the female corpus callosum, the center of the brain which regulates communication between the brain's hemispheres, is larger than the male's. On the other hand, the scans also show that information flows more freely between the hemispheres of the male brain.
The exact role that brain structure plays in behavior, however, has been an area of considerable contention in science for literally hundreds of years. Early studies in craniometry conducted by Paul Pierre Broca were used to attempt to distinguish differences between human races, though have now been dismissed as scientific racism. The nature-nurture debate has raged for centuries in a variety of forms, without yet any clear resolution as to the role in which innate biological tendencies interact with environmental conditions or willed behavior. As such, studies relating to brain structure and claims to innate behavior often generate substantial controversy.
MIT anthropologist of science Joseph Dumit's study of brain imaging in his book Picturing Personhood: Brain Scans and Biomedical Identity, noted that the apparent "transparency" of such pictures (the appearance that they can be easily interpreted by laymen, when they are often the source of ambiguity and dispute by even highly-trained neurosurgeons) has led to their proliferation as indicators of objective truth in media and in courts of law, and that such conclusions are often knowingly exaggerated by the specialists creating the images for better visual effect.
The timing of Gurian's book comes on the heels of another controversy over gender differences sparked by comments made by Harvard president Lawrence Summers, who blamed low numbers of women in the sciences on genetic differences. Summers has been criticized by a large number of academics and scientists, as well as by many news publications, in the wake of what he was reported as saying during a conference on January 14.
Prions
Prions are infectious proteinaceous particles or, more simply, proteins that lack nucleic acid. They were discovered by Stanley Prusiner, who received the Nobel Prize in medicine in 1997 for his work on them. Prions are biologically unique, existing somewhere in the border zone between living things and nonliving matter. Although they show none of the characteristics associated with life, such as the need to metabolize and the capacity to reproduce, they are in some manner capable of replication in the body of a human or certain other mammals.
Prions apparently gain entry to the body mainly by ingestion, or else in contaminated human growth hormone, or, possibly, in contaminated blood or blood products. They selectively attack the central nervous system, causing a relentless and progressive destruction of neural tissue, leaving in its place microscopic vesicular globules. The pathological name for this is spongiform encephalopathy. Conditions in this category, all of them invariably fatal, are all transmissible. They include kuru, Creutzfeldt-Jakob disease, scrapie (a degenerative neural disease of sheep), bovine spongiform encephalopathy (mad cow disease), and variant Creutzfeldt-Jakob disease, which appears to be acquired by ingesting beef contaminated by the prions that cause mad cow disease.
As of September 2000, it remains unknown what other mammalian species are vulnerable to prions; in research laboratories they have been shown to infect rodents and primates. It is possible that all domestic farm animals are at risk, though so far only sheep, beef and dairy cattle, and wild ungulates such as deer and elk have been confirmed as vulnerable. There is no vaccine or serum to protect against infection, and no agent that can arrest or retard the progress of the spongiform degeneration once it begins
Prions apparently gain entry to the body mainly by ingestion, or else in contaminated human growth hormone, or, possibly, in contaminated blood or blood products. They selectively attack the central nervous system, causing a relentless and progressive destruction of neural tissue, leaving in its place microscopic vesicular globules. The pathological name for this is spongiform encephalopathy. Conditions in this category, all of them invariably fatal, are all transmissible. They include kuru, Creutzfeldt-Jakob disease, scrapie (a degenerative neural disease of sheep), bovine spongiform encephalopathy (mad cow disease), and variant Creutzfeldt-Jakob disease, which appears to be acquired by ingesting beef contaminated by the prions that cause mad cow disease.
As of September 2000, it remains unknown what other mammalian species are vulnerable to prions; in research laboratories they have been shown to infect rodents and primates. It is possible that all domestic farm animals are at risk, though so far only sheep, beef and dairy cattle, and wild ungulates such as deer and elk have been confirmed as vulnerable. There is no vaccine or serum to protect against infection, and no agent that can arrest or retard the progress of the spongiform degeneration once it begins
Cancer antidote in the attic
Researchers have discovered that “junk” RNA, which has the power to check unbridled cell growth, can help in developing anti-cancer treatments
A scientist born in India and his colleagues at Oxford seem to have unearthed an antidote to cancer from the “junkyards” of the human genome.
Aroul Ramadass and his associates in Alexandre Akoulitchev’s lab at Sir William Dunn School of Pathology, University of Oxford , have discovered RNA (ribonucleic acid) that is capable of stopping the runaway proliferation of cells. The amazing control that this particular RNA — whose role was previously unknown — showed of genes involved in cell division may lead to tools that can prevent the growth of tumour cells, the scientists hope. Their findings were published on January 21 in the online edition of the journal, Nature.
Cancer is a class of diseases characterised by uncontrolled cell division and the ability of these cells to invade tissues of neighbouring or faraway organs. Normally, unregulated growth is caused by damage to DNA, resulting in mutations in genes that encode for proteins controlling cell division. Thus, intervention at the genetic level could offer a lasting solution — present-day therapy revolves mainly around the destruction of malignant cells — feel experts.
Typically, RNA plays an important and direct role in the synthesis of proteins, the building blocks of our bodies. But the RNA that the Oxford scientists studied belongs to the type of RNA not directly involved in protein synthesis.
Significantly, the RNA was located in that part of the genome which scientists once considered “junk”. The Human Genome Project completed early this century found that some 34,000 genes, constituting just three per cent of the genome, are responsible for producing proteins. The rest of the genome does not seem to have any function. According to the latest estimates, this “junk” DNA produces around half a million varieties of RNA of unknown functions. And to be politically correct, scientists have of late dropped the word “junk” and are instead using “non-coding”, meaning the parts of the genome which do not encode for proteins useful to the host genome.
Explaining the mechanisms involved in the process, Ramadass said that the RNA molecule is capable of shutting down the gene dihydrofolate reductase (DHFR). The DHFR gene produces an enzyme that controls the production of thymine, one of the four bases of DNA. Thymine is necessary for cell multiplication.
“By slowing down the replication process, it prevents any ordinary cell from becoming cancerous,” Ramadass, who completed his master’s degree in molecular biology and biotechnology in 2000 from New Delhi ’s Indian Agricultural Research Institute, told KnowHow.
To demonstrate this, the scientists applied the technique “RNA silencing” which won two US scientists — Andrew Fire and Craig Mello — the 2006 Nobel Prize for physiology and medicine.
They specifically targeted the “interfering” RNA and nullified its effect on the DHFR gene. This, in turn, prevented the DHFR gene shutdown, leading to rapid cell multiplication.
“There’s been a quiet revolution taking place over the last few years regarding the role of RNA,” says Dr Alexandre Akoulitchev. “Scientists have begun to see ‘junk’ DNA as having a very important function. The variety of RNA types produced from this ‘junk’ is staggering and the functional implications are huge.”
Inhibiting the DHFR gene could help prevent the growth of neoplastic cancerous cells, ordinary cells which develop into tumour cells, such as in prostate cancer cells,” explains Dr Akoulitchev. “In fact, the first anti-cancer drug, Methotrexate, acts by binding and inhibiting the enzyme produced by this gene,” he says.
Interestingly, Methotrexate, the first-ever cancer drug to be approved by the US Food and Drug Administration in 1953, was designed and developed by the late Indian scientist, Yellapragada SubbaRow, who is often hailed as the “miracle man of miracle drugs”.
“This is not the first non-coding RNA originated from the non-coding part of the genome. But it is likely to be the first one to control the promoter (the gene that expresses the enzyme) in such a direct way,” Dr Akoulitchev told KnowHow.
Understanding how we can use the RNA to switch off or inhibit DHFR and other genes may help derive important therapeutic insights for developing new anti-cancer treatments, concludes the University of Oxford researcher
A scientist born in India and his colleagues at Oxford seem to have unearthed an antidote to cancer from the “junkyards” of the human genome.
Aroul Ramadass and his associates in Alexandre Akoulitchev’s lab at Sir William Dunn School of Pathology, University of Oxford , have discovered RNA (ribonucleic acid) that is capable of stopping the runaway proliferation of cells. The amazing control that this particular RNA — whose role was previously unknown — showed of genes involved in cell division may lead to tools that can prevent the growth of tumour cells, the scientists hope. Their findings were published on January 21 in the online edition of the journal, Nature.
Cancer is a class of diseases characterised by uncontrolled cell division and the ability of these cells to invade tissues of neighbouring or faraway organs. Normally, unregulated growth is caused by damage to DNA, resulting in mutations in genes that encode for proteins controlling cell division. Thus, intervention at the genetic level could offer a lasting solution — present-day therapy revolves mainly around the destruction of malignant cells — feel experts.
Typically, RNA plays an important and direct role in the synthesis of proteins, the building blocks of our bodies. But the RNA that the Oxford scientists studied belongs to the type of RNA not directly involved in protein synthesis.
Significantly, the RNA was located in that part of the genome which scientists once considered “junk”. The Human Genome Project completed early this century found that some 34,000 genes, constituting just three per cent of the genome, are responsible for producing proteins. The rest of the genome does not seem to have any function. According to the latest estimates, this “junk” DNA produces around half a million varieties of RNA of unknown functions. And to be politically correct, scientists have of late dropped the word “junk” and are instead using “non-coding”, meaning the parts of the genome which do not encode for proteins useful to the host genome.
Explaining the mechanisms involved in the process, Ramadass said that the RNA molecule is capable of shutting down the gene dihydrofolate reductase (DHFR). The DHFR gene produces an enzyme that controls the production of thymine, one of the four bases of DNA. Thymine is necessary for cell multiplication.
“By slowing down the replication process, it prevents any ordinary cell from becoming cancerous,” Ramadass, who completed his master’s degree in molecular biology and biotechnology in 2000 from New Delhi ’s Indian Agricultural Research Institute, told KnowHow.
To demonstrate this, the scientists applied the technique “RNA silencing” which won two US scientists — Andrew Fire and Craig Mello — the 2006 Nobel Prize for physiology and medicine.
They specifically targeted the “interfering” RNA and nullified its effect on the DHFR gene. This, in turn, prevented the DHFR gene shutdown, leading to rapid cell multiplication.
“There’s been a quiet revolution taking place over the last few years regarding the role of RNA,” says Dr Alexandre Akoulitchev. “Scientists have begun to see ‘junk’ DNA as having a very important function. The variety of RNA types produced from this ‘junk’ is staggering and the functional implications are huge.”
Inhibiting the DHFR gene could help prevent the growth of neoplastic cancerous cells, ordinary cells which develop into tumour cells, such as in prostate cancer cells,” explains Dr Akoulitchev. “In fact, the first anti-cancer drug, Methotrexate, acts by binding and inhibiting the enzyme produced by this gene,” he says.
Interestingly, Methotrexate, the first-ever cancer drug to be approved by the US Food and Drug Administration in 1953, was designed and developed by the late Indian scientist, Yellapragada SubbaRow, who is often hailed as the “miracle man of miracle drugs”.
“This is not the first non-coding RNA originated from the non-coding part of the genome. But it is likely to be the first one to control the promoter (the gene that expresses the enzyme) in such a direct way,” Dr Akoulitchev told KnowHow.
Understanding how we can use the RNA to switch off or inhibit DHFR and other genes may help derive important therapeutic insights for developing new anti-cancer treatments, concludes the University of Oxford researcher
Leptospirosis
Leptospirosis [lep-to-spy-RO-sis] is a potentially serious bacterial illness that is most common in the tropics. Leptospirosis can affect many parts of the body.Infected wild and domestic animals pass leptospirosis-causing bacteria in their urine.People get leptospirosis by contact with fresh water, wet soil, or vegetation that has been contaminated by the urine of infected animals.Leptospirosis is treatable with antibiotics.To prevent leptospirosis, minimize contact with fresh water and mud that might be contaminated with the urine of infected animals.
What is leptospirosis?
Leptospirosis is a potentially serious illness that can affect many parts of the body.
What is the infectious agent that causes leptospirosis?
Leptospirosis is caused by Leptospira interrogans, a corkscrew-shaped bacterium (spirochete).
Where is leptospirosis found?
Leptospirosis-causing bacteria are common worldwide, especially in tropical countries with heavy rainfall. Infected rodents and other wild and domestic animals pass the bacteria in their urine. The bacteria can live for a long time in fresh water, damp soil, vegetation, and mud. Flooding after heavy rainfall helps spread the bacteria in the environment.
How is leptospirosis spread?
People get leptospirosis by contact with fresh water, damp soil, or vegetation contaminated by the urine of infected animals. People who canoe, raft, wade, or swim in contaminated lakes, rivers, and streams can get leptospirosis. Leptospirosis is also a problem for people who work in contaminated flood plains or wet agricultural settings.
Leptospirosis bacteria can enter the body through broken skin and mucous membranes. The bacteria can also enter the body when a person swallows contaminated food or water, including water swallowed during water sports. Once in the bloodstream, the bacteria can reach all parts of the body and cause signs and symptoms of illness.
What are the signs and symptoms of leptospirosis?
Most infected persons have a mild to moderate illness that is like many other tropical diseases. Symptoms include fever, headache, chills, nausea and vomiting, eye inflammation, and muscle aches. In more severe cases, the illness can result in liver damage and jaundice (yellowing of the skin and whites of the eyes), kidney failure, and internal bleeding. People who are seriously ill with leptospirosis often need to be hospitalized.
How soon after exposure do symptoms appear?
Symptoms usually begin about 10 days after infection.
How is leptospirosis diagnosed?
Leptospirosis is diagnosed by a special blood test that is available through state health departments.
Who is at risk for leptospirosis?
People who take part in freshwater recreational activities in areas where leptospirosis is common, especially during the rainy season or in times of floodingFarmers, workers in rice fields, sewer workers, and others whose jobs involve contact with water or mud that is contaminated by animal urine, especially the urine of rodentsVeterinarians and others in contact with leptospirosis-affected animals
What complications can result from leptospirosis?
Severe or untreated leptospirosis can lead to organ system damage and, in rare cases, death.
What is the treatment for leptospirosis?
Leptospirosis is treatable with antibiotics. Treatment should be started as soon as possible. Severely ill persons might need intravenous antibiotic treatment and other supportive care.
How common is leptospirosis?
Mild leptospirosis is common in tropical countries where people have regular contact with fresh water and animals. The disease is under-diagnosed in the United States. The 50 to 150 cases reported each year are probably only a fraction of the total number of infections.
Is leptospirosis an emerging infectious disease?
Yes. Increased awareness of the disease has led to increased recognition. In 1995, after widespread flooding in Nicaragua, a leptospirosis epidemic killed at least 13 persons and made more than 2,000 others sick. In 1997, nine whitewater rafters from the United States were infected during a river trip in Costa Rica. Leptospirosis is also a problem in deteriorating inner cities that are infested with rats.
How can leptospirosis be prevented?
Minimize contact with fresh water, mud, and vegetation that might be contaminated with the urine of infected animals, especially rodents.Wear protective clothing, such as waterproof boots or waders, when participating in recreational or work activities that might result in contact with contaminated water.If your travel plans might put you at risk for leptospirosis, consider taking antibiotics before and during travel to help prevent infection from short-term, high-risk exposures.
What is leptospirosis?
Leptospirosis is a potentially serious illness that can affect many parts of the body.
What is the infectious agent that causes leptospirosis?
Leptospirosis is caused by Leptospira interrogans, a corkscrew-shaped bacterium (spirochete).
Where is leptospirosis found?
Leptospirosis-causing bacteria are common worldwide, especially in tropical countries with heavy rainfall. Infected rodents and other wild and domestic animals pass the bacteria in their urine. The bacteria can live for a long time in fresh water, damp soil, vegetation, and mud. Flooding after heavy rainfall helps spread the bacteria in the environment.
How is leptospirosis spread?
People get leptospirosis by contact with fresh water, damp soil, or vegetation contaminated by the urine of infected animals. People who canoe, raft, wade, or swim in contaminated lakes, rivers, and streams can get leptospirosis. Leptospirosis is also a problem for people who work in contaminated flood plains or wet agricultural settings.
Leptospirosis bacteria can enter the body through broken skin and mucous membranes. The bacteria can also enter the body when a person swallows contaminated food or water, including water swallowed during water sports. Once in the bloodstream, the bacteria can reach all parts of the body and cause signs and symptoms of illness.
What are the signs and symptoms of leptospirosis?
Most infected persons have a mild to moderate illness that is like many other tropical diseases. Symptoms include fever, headache, chills, nausea and vomiting, eye inflammation, and muscle aches. In more severe cases, the illness can result in liver damage and jaundice (yellowing of the skin and whites of the eyes), kidney failure, and internal bleeding. People who are seriously ill with leptospirosis often need to be hospitalized.
How soon after exposure do symptoms appear?
Symptoms usually begin about 10 days after infection.
How is leptospirosis diagnosed?
Leptospirosis is diagnosed by a special blood test that is available through state health departments.
Who is at risk for leptospirosis?
People who take part in freshwater recreational activities in areas where leptospirosis is common, especially during the rainy season or in times of floodingFarmers, workers in rice fields, sewer workers, and others whose jobs involve contact with water or mud that is contaminated by animal urine, especially the urine of rodentsVeterinarians and others in contact with leptospirosis-affected animals
What complications can result from leptospirosis?
Severe or untreated leptospirosis can lead to organ system damage and, in rare cases, death.
What is the treatment for leptospirosis?
Leptospirosis is treatable with antibiotics. Treatment should be started as soon as possible. Severely ill persons might need intravenous antibiotic treatment and other supportive care.
How common is leptospirosis?
Mild leptospirosis is common in tropical countries where people have regular contact with fresh water and animals. The disease is under-diagnosed in the United States. The 50 to 150 cases reported each year are probably only a fraction of the total number of infections.
Is leptospirosis an emerging infectious disease?
Yes. Increased awareness of the disease has led to increased recognition. In 1995, after widespread flooding in Nicaragua, a leptospirosis epidemic killed at least 13 persons and made more than 2,000 others sick. In 1997, nine whitewater rafters from the United States were infected during a river trip in Costa Rica. Leptospirosis is also a problem in deteriorating inner cities that are infested with rats.
How can leptospirosis be prevented?
Minimize contact with fresh water, mud, and vegetation that might be contaminated with the urine of infected animals, especially rodents.Wear protective clothing, such as waterproof boots or waders, when participating in recreational or work activities that might result in contact with contaminated water.If your travel plans might put you at risk for leptospirosis, consider taking antibiotics before and during travel to help prevent infection from short-term, high-risk exposures.
Playstation 3 will be used to help cure cancer and Alzheimer's
The upcoming Sony PlayStation 3 game console is going to assist scientists in finding cures for cancer and Alzheimer's disease using the Folding@home distributed computing program.
Folding@home is run by the Pande group of Stanford University (America) to research protein folding, this is the process whereby proteins build themselves inside the cells in the body.
Analyisis of how proteins fold (specifically how the folding goes wrong) can give insights into how diseases form. The simulation processes used in the research take months just for a single protein so the data is split into small packets (called workunits by the community) and distributed to volunteers around the world. By downloading a program called a 'client' users can receive units and perform the simulations on them - results are then sent back to the Stanford servers.
Currently more than 150,000 computers run the folding 'client' worldwide. The new client can be downloaded to the users PlayStation 3 console and will then begin to calculate "work units" when users are not playing games. Since the PS3 has a 'Cell' processor with a total of 8 cores the calculations should be performed faster than on a PC. With this new program scientists aim to create a super computer faster than IBM's BlueGene/L System (which currently calculates more than 280.6 trillion bits of information per second). The new calculations are expected to process a thousand trillion bits of information across the whole project every second.
A statement on Folding@home's website explained further: "Using the Cell processor of the PS3, we should be able to do more folding than what one could do on a PC. Also, since the PS3 has a powerful GPU, the PS3 client will offer real time visualization for the first time."
The new program is part of an expansion of the project and the first of 2 new clients that have been developed. The second, scheduled for release later on, will utilise a computer's graphics card (supporting only ATI graphics cards at first) to perform folding calcualtions.
"We will release more details on all of this as the new software rolls out," said the statement, "We are beta testing the ATI GPU client software internally at the moment and will likely announce an open beta in four to five weeks (end of September)."
The Pande group noted their ultimate aim as being to create an even faster super computer, with the ability to process over a million trillion bits of data every second: "The PS3 client and GPU client are together part of our new broader goals to push Folding@Home to the next stage, reaching calculations on the petaflop to 10 petaflop scale."
Folding@home is run by the Pande group of Stanford University (America) to research protein folding, this is the process whereby proteins build themselves inside the cells in the body.
Analyisis of how proteins fold (specifically how the folding goes wrong) can give insights into how diseases form. The simulation processes used in the research take months just for a single protein so the data is split into small packets (called workunits by the community) and distributed to volunteers around the world. By downloading a program called a 'client' users can receive units and perform the simulations on them - results are then sent back to the Stanford servers.
Currently more than 150,000 computers run the folding 'client' worldwide. The new client can be downloaded to the users PlayStation 3 console and will then begin to calculate "work units" when users are not playing games. Since the PS3 has a 'Cell' processor with a total of 8 cores the calculations should be performed faster than on a PC. With this new program scientists aim to create a super computer faster than IBM's BlueGene/L System (which currently calculates more than 280.6 trillion bits of information per second). The new calculations are expected to process a thousand trillion bits of information across the whole project every second.
A statement on Folding@home's website explained further: "Using the Cell processor of the PS3, we should be able to do more folding than what one could do on a PC. Also, since the PS3 has a powerful GPU, the PS3 client will offer real time visualization for the first time."
The new program is part of an expansion of the project and the first of 2 new clients that have been developed. The second, scheduled for release later on, will utilise a computer's graphics card (supporting only ATI graphics cards at first) to perform folding calcualtions.
"We will release more details on all of this as the new software rolls out," said the statement, "We are beta testing the ATI GPU client software internally at the moment and will likely announce an open beta in four to five weeks (end of September)."
The Pande group noted their ultimate aim as being to create an even faster super computer, with the ability to process over a million trillion bits of data every second: "The PS3 client and GPU client are together part of our new broader goals to push Folding@Home to the next stage, reaching calculations on the petaflop to 10 petaflop scale."
BOB MARLEY
I love the development of our music, that's what Ireally dig about the whole thing. How we've triedto develop, y'know? It grows. That's why every daypeople come forward with new songs. Music goes onforever."
--Bob Marley, August 1979
--Bob Marley, August 1979
We remember the brilliant and evocative music Bob Marley gave the world; music that stretches back over nearly two decades and still remains timeless and universal. Marley has been called "the first Third World superstar," "Rasta Prophet," "visionary," and" "revolutionary artist." These accolades were not mere hyperbole. Marley was one of the most charismatic and challenging performers of our time.
Bob Marley's career stretched back over twenty years. During that time Marley's growing style encompassed every aspect in the rise of Jamaican music, from ska to contemporary reggae. That growth was well reflected in the maturity of the Wailers' music.
Bob's first recording attempts came at the beginning of the Sixties. His first two tunes, cut as a solo artist, meant nothing in commercial terms and it wasn't until 1964, as a founding member of a group called the Wailing Wailers, that Bob first hit the Jamaican charts.
The record was "Simmer Down," and over the next few years the Wailing Wailers -- Bob, Peter Mclntosh and Bunny Livingston, the nucleus of the group -- put out some 30 sides that properly established them as one of the hottest groups in Jamaica. Mclntosh later shortened his surname to Tosh while Livingston is now called Bunny Wailer.
Despite their popularity, the economics of keeping the group together proved too much and the two other members, Junior Braithwaite and Beverley Kelso, left the group. At the same time Bob joined his mother in the United States. This marked the end of the Wailing Wailers, Chapter One.
Marley's stay in America was short-lived, however, and he returned to Jamaica to join up again with Peter and Bunny. By the end of the Sixties, with the legendary reggae producer Lee "Scratch" Perry at the mixing desk, The Wailers were again back at the top in Jamaica. The combination of the Wailers and Perry resulted in some of the finest music the band ever made. Tracks like "Soul Rebel," "Duppy Conquerer," "400 Years," and "Small Axe" were not only classics, but they defined the future direction of reggae.
It's difficult to properly understand Bob Marley's music without considering Rastafari. His spiritual beliefs are too well known to necessitate further explanation. It must be stated, however, that Rastafari is at the very core of the Wailers' music.
In 1970 Aston Familyman Barrett and his brother Carlton (bass and drums, respectively) joined the Wailers. They came to the band unchallenged as Jamaica's HARDEST rhythm section; a reputation that was to remain undiminished during the following decade. Meanwhile, the band's own reputation was, at the start of the Seventies, an extraordinary one throughout the Caribbean. However, the band was still unknown internationally.
That was to change in 1972 when the Wailers signed to Island Records. It was a revolutionary move for an international record company and a reggae band. For the first time a reggae band had access to the best recording facilities and were treated in the same way as a rock group. Before the Wailers signed to Island, it was considered that reggae sold only on singles and cheap compilation albums. The Wailer's first album, Catch A Fire broke all the rules: it was beautifully packaged and heavily promoted. And it was the start of a long climb to international fame and recognition.
The Catch A Fire album was followed a year later by Burnin', an LP that included some of the band's older songs, such as "Duppy Conquerer," "Small Axe," and "Put In On," together with tracks like "Get Up Stand Up" and "I Shot The Sheriff" (which was also recorded by Eric Clapton, who had a #1 hit with it in America).
In 1975 Bob Marley & The Wailers released the extraordinary Natty Dread album, and toured Europe that summer. The shows were recorded and the subsequent live album, together with the single, "No Woman No Cry," both made the UK charts. By that time Bunny and Peter had officially left the band to pursue their own solo careers.
Rastaman Vibration, the follow-up album in 1976, cracked the American charts. It was, for many, the clearest exposition yet of Marley's music and beliefs, including such tracks as "Crazy Baldhead," "Johnny Was," "Who The Cap Fit" and, perhaps most significantly of all, "War," the Iyrics of which were taken from a speech by Emperor Haile Selassie.
In 1977 Exodus was released, which established Marley's international superstar status. It remained on the British charts for 56 straight weeks, and netted three UK hit singles, "Exodus," "Waiting In Vain," and "Jamming."
In 1978 the band released Kaya, which hit number four on the UK chart the week of its release. That album saw Marley in a different mood -- Kaya was an album of love songs, and, of course, homages to the power of ganja.
There were two more events in 1978, both of which were of extraordinary significance to Marley. In April that year he returned to Jamaica (he had left in 1976 after the shooting that had almost cost him his life), to play the One Love Peace Concert in front of the Prime Minister Michael Manley, and the then Leader of the Opposition Edward Seaga. And at the end of the year he visited Africa for the first time, going initially to Kenya and then on to Ethiopia, spiritual home of Rastafari.
Marley returned to Africa in 1980 at the official initation of the Government of Zimbabwe to play at that country's Independence Ceremony. It was the greatest honor afforded the band, and one which underlined the Wailers' importance in the Third World.
In 1979 the Survival LP was released. A European tour came the following year: the band broke festival records throughout the continent, including a 100,000 capacity show in Milan. Bob Marley & the Wailers were now the most important band on the road that year and the new Uprising album hit every chart in Europe. It was a period of maximum optimism and plans were being made for an American tour, an opening slot with Stevie Wonder for the following winter.
At the end of the European tour, Bob Marley & The Wailers went to America. Bob played two shows at Madison Square Garden but, immediately afterwards he was seriously ill. Cancer was diagnosed.
Marley fought the disease for eight months. The battle, however, proved to be too much. He died in a Miami Hospital on May 11,1981.
A month before the end Bob was awarded Jamaica's Order of Merit, the nations' third highest honor, in recognition of his outstanding contribution to the country's culture.
On Thursday, May 23,1981, the Honorable Robert Nesta Marley was given an official funeral by the people of Jamaica. Following the funeral -- attended by both the Prime Minister and the Leader of the Opposition -- Bob's body was taken to his birthplace where it now rests in a mausoleum. Bob Marley was 36 years old. His legend lives on.
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