"Then you get an infinitely long, circular mountain."
Hmm. I'd like to see the topo map for that one.
 | ||
| The Lagginhorn: It's not circular, but it seemed infinitely long... | (Photo R Berkowitz, July 2009) |
Friday 25 February 2011
Mathematicians.
Fantastic quote from Thursday's seminar on fluid dynamics:
"Then you get an infinitely long, circular mountain."
Hmm. I'd like to see the topo map for that one.
"Then you get an infinitely long, circular mountain."
Hmm. I'd like to see the topo map for that one.
Thursday 24 February 2011
New cell death mechanism has implications for breast cancer treatments
Press release published by Cambridge University, 22 Feb 2011, © 2010 News, University of Cambridge. http://www.admin.cam.ac.uk/news/dp/2011022402
A novel mechanism of cell death that occurs in mammalian organisms has been revealed by researchers at the University of Cambridge.
Billions of damaged or superfluous cells die in our bodies every day. It is thought that most cell death occurs by a process called apoptosis, in which biochemical events lead to cell changes and death.
However, during the course of Peter Kreuzaler's PhD research at the Department of Pathology, the Cambridge team have shown that cells in the breast die following lactation by a process that involves lysosomes - organelles which digest and recycle cellular components.
As the mammary gland regresses, enzymes called cathepsins leak out of the lysosomes into the cell and induce cell death. This is the first time that this type of cell death has been shown to occur in a healthy mammal: the original work was done in vivo in mice. Additionally, the protein Stat3, which is present in high levels in cancers that have poor prognosis, plays a significant role in lysosomal-mediated programmed cell death as it induces high levels of cathepsins while suppressing cathepsin inhibitors.
Describing how the work was done, Professor Christine Watson of the Department of Pathology said: "We found a gene that was hugely down-regulated by Stat3."This gene inhibits lysosomal enzymes, so [we] started looking at these."
The team's findings will cause scientists to think differently about how cells die.
Kreuzaler added, "Our work is the first to show that a lysosomal pathway of cell death occurs in a normal situation in the body. Current cancer research focuses on understanding how cancers evade cell death. The discovery of a novel pathway of cell death is likely to explain a yet unexplained tumour resistance to cell death, while giving researchers new prospective therapeutic targets."
According to Watson, the most exciting thing about this work is that the team have identified a new form of cell death that has major implications for cell death research and for treating people with breast cancer.
The research, recently published in the journal Nature Cell Biology, was funded by studentships from the Department of Pathology and the Breast Cancer Campaign, as well as the Biotechnology and Biological Sciences Research Council and the Medical Research Council.
The next steps will be to take advantage of this as a death pathway in breast cancer in particular, and to see how this pathway actually operates and is controlled. She plans to investigate whether the same process works to kill cancer cells in culture. While a treatment based on this new cell death mechanism is far in the future, Watson thinks that a therapy based on lysosomal-mediated cell death could target very aggressive cancers.
A novel mechanism of cell death that occurs in mammalian organisms has been revealed by researchers at the University of Cambridge.
 |
Section of a mammary gland in which cells have been shed from the lining of the milk-producing structures and are undergoing cell death. (credit: Peter Kreuzaler, Cambridge University Department of Pathology) |
However, during the course of Peter Kreuzaler's PhD research at the Department of Pathology, the Cambridge team have shown that cells in the breast die following lactation by a process that involves lysosomes - organelles which digest and recycle cellular components.
As the mammary gland regresses, enzymes called cathepsins leak out of the lysosomes into the cell and induce cell death. This is the first time that this type of cell death has been shown to occur in a healthy mammal: the original work was done in vivo in mice. Additionally, the protein Stat3, which is present in high levels in cancers that have poor prognosis, plays a significant role in lysosomal-mediated programmed cell death as it induces high levels of cathepsins while suppressing cathepsin inhibitors.
Describing how the work was done, Professor Christine Watson of the Department of Pathology said: "We found a gene that was hugely down-regulated by Stat3."This gene inhibits lysosomal enzymes, so [we] started looking at these."
The team's findings will cause scientists to think differently about how cells die.
Kreuzaler added, "Our work is the first to show that a lysosomal pathway of cell death occurs in a normal situation in the body. Current cancer research focuses on understanding how cancers evade cell death. The discovery of a novel pathway of cell death is likely to explain a yet unexplained tumour resistance to cell death, while giving researchers new prospective therapeutic targets."
According to Watson, the most exciting thing about this work is that the team have identified a new form of cell death that has major implications for cell death research and for treating people with breast cancer.
The research, recently published in the journal Nature Cell Biology, was funded by studentships from the Department of Pathology and the Breast Cancer Campaign, as well as the Biotechnology and Biological Sciences Research Council and the Medical Research Council.
The next steps will be to take advantage of this as a death pathway in breast cancer in particular, and to see how this pathway actually operates and is controlled. She plans to investigate whether the same process works to kill cancer cells in culture. While a treatment based on this new cell death mechanism is far in the future, Watson thinks that a therapy based on lysosomal-mediated cell death could target very aggressive cancers.
The ‘bear’ necessities of hibernation
Published on BlueSci website, 24 Feb 2011, copyright Cambridge University.
http://www.bluesci.org/?p=2124
Black bears display unusual patterns of metabolic and thermal regulation during hibernation as well as when they emerge in the spring, causing some biologists to question whether or not they really hibernate. Hibernation is a powerful way to reduce energy costs; in small mammals it involves lowered body temperatures and metabolic activity interrupted by periods of arousal and increased temperatures. However, a study based at the Institute of Arctic Biology at the University of Alaska found that hibernating black bears lack the periods of arousal. Furthermore the study, which made continuous measurements of oxygen consumption, body temperature and heart, muscle, and brain activities, showed that the bears maintained surprisingly high body temperatures during hibernation yet suppressed their metabolism to 25% of basal rates1.
Upon emerging from hibernation, black bears maintain a reduced metabolic rate for up to three weeks. This suggests that metabolic suppression during hibernation is independent of lowered body temperature, and basal metabolic rate is not a constant but rather is physiologically controlled.
Further research may show that a torpid state via active metabolic inhibition is the primary means by which mammals can conserve energy.
1. Heldmaier, G. (2011). Life on Low Flame in Hibernation. Science, 331(6019), 866 -867. doi:10.1126/science.1203192 [↩]
http://www.bluesci.org/?p=2124
“I wish I could hibernate like a bear this winter!” This sentiment is often expressed by Cambridge University students as they slog through the darkest moments of their degrees. But they might want to reassess what “hibernate like a bear” really means.
Upon emerging from hibernation, black bears maintain a reduced metabolic rate for up to three weeks. This suggests that metabolic suppression during hibernation is independent of lowered body temperature, and basal metabolic rate is not a constant but rather is physiologically controlled.
Further research may show that a torpid state via active metabolic inhibition is the primary means by which mammals can conserve energy.
1. Heldmaier, G. (2011). Life on Low Flame in Hibernation. Science, 331(6019), 866 -867. doi:10.1126/science.1203192 [↩]
Tuesday 22 February 2011
Clegg promises libel law reform
My first story on the ABSW website on Clegg's support for British libel law reform!
Published here: http://www.absw.org.uk/news-events/news/730-clegg-promises-libel-law-reform
© 2009 Association of British Science Writers
Published here: http://www.absw.org.uk/news-events/news/730-clegg-promises-libel-law-reform
© 2009 Association of British Science Writers
This spring the Coalition Government will launch its draft Defamation Bill to reform libel laws that "are having a chilling effect on scientific debate and investigative journalism," according to deputy prime minister and Liberal Democrat leader Nick Clegg in his speech on civil liberties on 7 January.
This reform will make Britain the first country to ask its legislative body to set out its libel laws and provide greater clarity. Clegg is committed to relaxing Britain's libel laws so that academics and journalists are not "bullied into silence" for fear of being sued. Lord Tom McNally, Liberal Democrat minister in the justice department, is preparing the bill.
The draft will be published in late March and the final version will be published this summer according to an interview with Sile Lane, campaigns manager for Sense About Science, a charitable trust and part of the Libel Reform Campaign. Final legislation could be enacted by 2012.
The bill will include restrictions on corporate and public bodies and will bring the law up to date. It will also simplify and strengthen existing defences and restrict libel tourism in which plaintiffs file libel suits in jurisdictions likely to give a more favourable result. A new statutory defence will be provided for journalists and scientists who speak out on important issues.
In his speech, Clegg said that "beyond providing greater access to information, [the government needs] to make sure that, where people discover injustice and bad practice, they can speak out against it too".
Sense About Science conducted a survey which showed that "a third of editors of academic journals said the[y] had been threatened with libel actions," Lane told ABSW. Editors have "asked for changes in how papers were written, to protect themselves from libel actions".
Recent cases bring to light the need for reform. Science writer Simon Singh experienced a lengthy court battle with the British Chiropractic Association over an accusation of libel for an article in which he questioned certain chiropractic practices. Cardiologist Peter Wilmshurst fought a libel case brought against him by an American company after he criticised their research at a medical conference.
"Nobody wants to get rid of libel, but at the moment the law is unfair and entirely hostile to free speech and overly friendly to rich bullies trying to silence criticism," Singh told the ABSW. “The campaign for libel reform is about striking a fairer balance between claimants and defendants.”
John Kampfner, chief executive of the Index on Censorship which is part of the Libel Reform Campaign, wrote in The Independent: "We aim to repair a body of law that has seen countless individuals and voluntary organisations either sued in court or forced into apologising for and retracting comments, articles, and books, even though they have done nothing wrong."
"People who might oppose radical changes [to libel law] would be big libel claimant lawyer firms," said Lane. Libel law is complex and claimant lawyers may argue that it is too specialised to be handled anywhere besides the high courts. This can lead to expensive cases involving long exchanges before trial, according to Tracey Brown, managing director of Sense About Science.
"Why do we assume libel should be a matter for high court?" asked Brown in her post for The Guardian’s OrganGrinder blog. She noted that according to human rights law, all EU member states must provide a remedy for damage to reputation. However, Brown added in her blog, this need not be done "through an arcane, chillingly expensive law in a higher court ... the defamation bill, if it delivers the fundamental reform so many are asking for, will make possible new ways of handling defamation."
Writers, publishers, NGOs, human rights lawyers, clinicians, academics and performers have emphasised different problems with the English libel law. But they all agree that rebalancing libel laws to protect free expression will require fundamental changes to the law and that libel laws are a matter for Parliament as well as the courts.
“Libel law was devised to avoid dragging someone's good name [through] the mud,” Tom Sheldon of the Science Media Centre, an organisation that promotes the views of the scientific community to the national media, told ABSW. "We want to see a law that allows scientists to comment on what evidence tells them, without being concerned whether that will offend shareholders, company directors, etc."
Clegg's said in his speech that "our aim is to turn English libel laws from an international laughing stock to an international blueprint."
This reform will make Britain the first country to ask its legislative body to set out its libel laws and provide greater clarity. Clegg is committed to relaxing Britain's libel laws so that academics and journalists are not "bullied into silence" for fear of being sued. Lord Tom McNally, Liberal Democrat minister in the justice department, is preparing the bill.
The draft will be published in late March and the final version will be published this summer according to an interview with Sile Lane, campaigns manager for Sense About Science, a charitable trust and part of the Libel Reform Campaign. Final legislation could be enacted by 2012.
The bill will include restrictions on corporate and public bodies and will bring the law up to date. It will also simplify and strengthen existing defences and restrict libel tourism in which plaintiffs file libel suits in jurisdictions likely to give a more favourable result. A new statutory defence will be provided for journalists and scientists who speak out on important issues.
In his speech, Clegg said that "beyond providing greater access to information, [the government needs] to make sure that, where people discover injustice and bad practice, they can speak out against it too".
Sense About Science conducted a survey which showed that "a third of editors of academic journals said the[y] had been threatened with libel actions," Lane told ABSW. Editors have "asked for changes in how papers were written, to protect themselves from libel actions".
Recent cases bring to light the need for reform. Science writer Simon Singh experienced a lengthy court battle with the British Chiropractic Association over an accusation of libel for an article in which he questioned certain chiropractic practices. Cardiologist Peter Wilmshurst fought a libel case brought against him by an American company after he criticised their research at a medical conference.
"Nobody wants to get rid of libel, but at the moment the law is unfair and entirely hostile to free speech and overly friendly to rich bullies trying to silence criticism," Singh told the ABSW. “The campaign for libel reform is about striking a fairer balance between claimants and defendants.”
John Kampfner, chief executive of the Index on Censorship which is part of the Libel Reform Campaign, wrote in The Independent: "We aim to repair a body of law that has seen countless individuals and voluntary organisations either sued in court or forced into apologising for and retracting comments, articles, and books, even though they have done nothing wrong."
"People who might oppose radical changes [to libel law] would be big libel claimant lawyer firms," said Lane. Libel law is complex and claimant lawyers may argue that it is too specialised to be handled anywhere besides the high courts. This can lead to expensive cases involving long exchanges before trial, according to Tracey Brown, managing director of Sense About Science.
"Why do we assume libel should be a matter for high court?" asked Brown in her post for The Guardian’s OrganGrinder blog. She noted that according to human rights law, all EU member states must provide a remedy for damage to reputation. However, Brown added in her blog, this need not be done "through an arcane, chillingly expensive law in a higher court ... the defamation bill, if it delivers the fundamental reform so many are asking for, will make possible new ways of handling defamation."
Writers, publishers, NGOs, human rights lawyers, clinicians, academics and performers have emphasised different problems with the English libel law. But they all agree that rebalancing libel laws to protect free expression will require fundamental changes to the law and that libel laws are a matter for Parliament as well as the courts.
“Libel law was devised to avoid dragging someone's good name [through] the mud,” Tom Sheldon of the Science Media Centre, an organisation that promotes the views of the scientific community to the national media, told ABSW. "We want to see a law that allows scientists to comment on what evidence tells them, without being concerned whether that will offend shareholders, company directors, etc."
Clegg's said in his speech that "our aim is to turn English libel laws from an international laughing stock to an international blueprint."
Saturday 19 February 2011
I don't think we're in Kansas anymore.
I've been living in the UK long enough that it feels like home. Perhaps more so than America. Hell, I've even been accused of having lost a bit of my accent (what accent? Washingtonians don't have an accent, we're perfect just as we are!). But there are just a few things that keep reminding me that this place is foreign.
1. My supervisor's pronunciation of "capillary." It's CAPillary!
2. Using "u" in honour and colour and an "o" in foetus. I do this now too, but with a wee(!) bit of hesitation.
3. British musical note values: quarter notes are crotchets, eighths are quavers, half notes are minims. I can do this fluently now, but I still think about it.
4. Thinking that I can go to London at the drop of a hat. I told my Dad that I wanted to get away from work for the day and just do something different that doesn't involve being cold and wet and in pain (my normal choice of weekend activities), so I might head down and check out some museums and snoop for story ideas to pitch to journals. And he pointed out how fabulous it is, from the point of view of our little town in eastern WA, to be able to do that so casually. He's very right.
And it's still a little exciting to be able to drive to France in a day.
A Plume of Gas and Public Interest
 | ||
| Deepwater Horizon oil spill: 24 May 2010, NASA image (photo from Wikimedia Commons, NASA Goddard Space Flight Center) |
The Deepwater Horizon blowout left an oily taste in the mouths of a lot of environmental groups. But the taste is worse when you add in the extent of hydrocarbon gas release.
A University of Georgia-led study co-authored by Florida State University oceanographer Ian MacDonald found that up to 500,000 tons of gaseous hydrocarbons were emitted into the deep ocean. This generated concentrations of 75,000 times the norm and could result in zones of oxygen depletion as microbes degrade the gaseous hydrocarbons.
The amount of gas released by the blowout is critical for determining potential impacts on deep oceanic systems. The depth of the blowout (nearly 1 mile) is significant because the hydrocarbon gases become trapped in the water column.
Then, microbes consume the gases which leads to low-oxygen waters. And the timescale for replenishing oxygen is many decades.
It's difficult to separate oxygen depletion due to gas from that due to liquid hydrocarbons. Therefore, documenting the total mass of discharged hydrocarbons is important for understanding the long-term implications for the Gulf's microbial communities and food chain.
The team calculated the gas discharge to be equivalent to 1.6 to 3.1 million barrels of oil. This figure encompasses a lot of uncertainty, but even the lowest is a significant increase in total discharge.
Where exactly has all of the gas gone? Also difficult to say, as the shifting small-scale currents in the Gulf have probably dissipated the plumes and the associated low oxygen zones. And it will take a long time for the microbes to consume all the gases released: they need other nutrients which are in scarce supply, and once these nutrients are depleted, the microbes won't be able to grow.
The opportunities for multi-disciplinary modeling of fluid dynamics and microbiology and economic and social effects are endless.
It's been nearly a year since the blowout. The plume of upset and urgency seems to have diffused quite a bit since then; with stories like this cropping up reasonably frequently but without nearly the publicity that they would have had nearer to the event. It might be interesting to model public interest in a particular disastrous event (I'd hate to call it a "natural disaster") as a source plume. Now that's a PhD thesis waiting to happen.
Wednesday 16 February 2011
How the hell do you do a science PhD?!
In a state of desperation after weeks of failed and broken lab experiments, I asked my friend who is allowed to use the title 'Doctor:'
"How the hell do you do a PhD?! Because I just don't seem to be getting it!"
He replied,
"I guess when you've done every possible mistake, [there] remains the beautiful truth..."
(followed by some sarcastic comments about how "beautiful" is relative).
Well, fine. I understand that there is meant to be beauty and simplicity underlying all of the faff of spilled fluids and scribbled equations. But why, then, do my current experiments seem to involve finding the most complex way to do something that should be obvious?!
"How the hell do you do a PhD?! Because I just don't seem to be getting it!"
He replied,
"I guess when you've done every possible mistake, [there] remains the beautiful truth..."
(followed by some sarcastic comments about how "beautiful" is relative).
Well, fine. I understand that there is meant to be beauty and simplicity underlying all of the faff of spilled fluids and scribbled equations. But why, then, do my current experiments seem to involve finding the most complex way to do something that should be obvious?!
Tuesday 8 February 2011
Immune interaction optimises foetal nourishment during pregnancy
My first PR written for Cambridge University Science Communications Office!
Published here:
http://www.admin.cam.ac.uk/news/dp/2011020801
© 2010 News, University of Cambridge, The Old Schools, Trinity Lane, Cambridge, CB2 1TN
Paternal genes advise maternal immune cells on how to build the best womb for developing foetuses.
Researchers at the University of Cambridge and the Babraham Institute have identified a mechanism by which specific combinations of genes can lead to miscarriage and other complications in pregnancies.
The research revealed that paternal immune genes (MHC) in the placenta provide information to uterine natural killer (NK) cells to ensure that the foetus receives sufficient blood supply. Unlike their blood counterpart NK cells, which kill infectious and cancerous cells, uterine NK (uNK) cells actually help placental cells adapt the blood vessels in the womb to nourish the foetus.
By mating mice whose only genetic difference was in the MHC genes of the mother and father (1% of the genome), the researchers found that uNK cells would sense the difference in highly variable MHC genes. When faced with mismatched MHC genes from the father's immune system, uNKs were presumably not switched off and could focus on optimising the blood flow of the womb.
Francesco Colucci of the University of Cambridge Department of Obstetrics and Gynaecology had previously identified the particular genes expressed by mouse uNK cells and Ashley Moffett of the University of Cambridge's Department of Pathology had pioneered the research relevant to human uNK cells and MHC genes. But up until now, it was not clear which paternal MHC genes were expressed by mouse placentae.
"What is most exciting," Colucci says, "is that by revealing the similarities between human and mouse immunology of pregnancy, the [teams] lay new foundation for using mouse genetics to test new ideas and hypotheses informed by human genetics data."
The interaction of MHC and NK genes is also key in foetal programming of adult diseases such as diabetes and hypertension which are known to have early developmental origins
Colucci's work, published in Proceedings of the National Academy of Sciences of the United States of America (PNAS) yesterday, was funded by the BBSRC and the Wellcome Trust, along with the Centre for Trophoblast Research, Medical Research Council, and NIHR Cambridge Biomedical Research Centre.
Colucci describes the next steps of where this research is leading, saying, "We are now well positioned to explore how the inherent variability of these immune system genes affects reproductive success by comparing NK receptors and MHC in normal pregnancy to those with disorders."
In the future research, the 'good' and 'bad' combinations in humans will be mimicked in mice to examine uterine blood vessels and foetus/placenta growth. The results of these experiments should help provide an understanding of how to prevent pregnancy disorders.
"This paradox has puzzled scientists for decades and understanding how the foetus evades rejection, except in severe pregnancy complications, has remained elusive," said Dr Myriam Hemberger of the Babraham Institute, the senior co-author who is an expert in mouse placental development. "Our findings show that paternal antigens on foetal trophoblast cells, which form the placenta and are therefore in direct contact with maternal tissue, help to transform the uterus for robust placental and foetal growth. This is essential for reproductive success."
Published here:
http://www.admin.cam.ac.uk/news/dp/2011020801
© 2010 News, University of Cambridge, The Old Schools, Trinity Lane, Cambridge, CB2 1TN
Paternal genes advise maternal immune cells on how to build the best womb for developing foetuses.
 |
| Mouse placental cells (red) and uterine natural killer cells (green). Note the close intermingling of placental cells with maternal immune cells at this early developmental stage - 8.5 days after conception. Credit: Myriam Hemberger and Francesco Colucci |
Researchers at the University of Cambridge and the Babraham Institute have identified a mechanism by which specific combinations of genes can lead to miscarriage and other complications in pregnancies.
The research revealed that paternal immune genes (MHC) in the placenta provide information to uterine natural killer (NK) cells to ensure that the foetus receives sufficient blood supply. Unlike their blood counterpart NK cells, which kill infectious and cancerous cells, uterine NK (uNK) cells actually help placental cells adapt the blood vessels in the womb to nourish the foetus.
By mating mice whose only genetic difference was in the MHC genes of the mother and father (1% of the genome), the researchers found that uNK cells would sense the difference in highly variable MHC genes. When faced with mismatched MHC genes from the father's immune system, uNKs were presumably not switched off and could focus on optimising the blood flow of the womb.
Francesco Colucci of the University of Cambridge Department of Obstetrics and Gynaecology had previously identified the particular genes expressed by mouse uNK cells and Ashley Moffett of the University of Cambridge's Department of Pathology had pioneered the research relevant to human uNK cells and MHC genes. But up until now, it was not clear which paternal MHC genes were expressed by mouse placentae.
"What is most exciting," Colucci says, "is that by revealing the similarities between human and mouse immunology of pregnancy, the [teams] lay new foundation for using mouse genetics to test new ideas and hypotheses informed by human genetics data."
The interaction of MHC and NK genes is also key in foetal programming of adult diseases such as diabetes and hypertension which are known to have early developmental origins
Colucci's work, published in Proceedings of the National Academy of Sciences of the United States of America (PNAS) yesterday, was funded by the BBSRC and the Wellcome Trust, along with the Centre for Trophoblast Research, Medical Research Council, and NIHR Cambridge Biomedical Research Centre.
Colucci describes the next steps of where this research is leading, saying, "We are now well positioned to explore how the inherent variability of these immune system genes affects reproductive success by comparing NK receptors and MHC in normal pregnancy to those with disorders."
In the future research, the 'good' and 'bad' combinations in humans will be mimicked in mice to examine uterine blood vessels and foetus/placenta growth. The results of these experiments should help provide an understanding of how to prevent pregnancy disorders.
"This paradox has puzzled scientists for decades and understanding how the foetus evades rejection, except in severe pregnancy complications, has remained elusive," said Dr Myriam Hemberger of the Babraham Institute, the senior co-author who is an expert in mouse placental development. "Our findings show that paternal antigens on foetal trophoblast cells, which form the placenta and are therefore in direct contact with maternal tissue, help to transform the uterus for robust placental and foetal growth. This is essential for reproductive success."
Sunday 6 February 2011
Questions on genetic engineering
Scientists have recently been able to genetically engineer chickens to render them unable to transmit avian flu.
This all sounds good for the poultry industry, but it brings to mind a few questions about genetic engineering, to which I certainly don't have any good answers.
What are the ethical implications of human beings trying to genetically change a creature with a central nervous system, whether genetically engineering chickens to avoid avian flu, or engineering pigs to synthesise omega-3 rather than omega-6 fatty acids thus providing healthier pork?
Would the ethics of the situation be different if these genetic changes were done with the goal of providing a better life for the birds/pigs themselves, rather than the goal of more profit to the people that were doing the genetic engineering?
What about the evolutionary side? Genetic traits evolve over time. Is human beings' interference with other species' genetics changing the course of evolution, or is our ability to do this simply a product of evolution and thus completely natural?
Suppose a family member had an incurable disease such as chronic leukemia or diabetes. If this individual's parents had, before birth, chosen to have their offspring's genes engineered so that this disease would not have been able to happen (if the technology were available), would this be a different case to genetic engineering in chickens or pigs? Would there be anything wrong with that?
In the chickens or pigs, nobody could ever explain to the chicken or pig what had happened nor why. But in the would-have-been chronically ill person, presumably the child would grow up and understand that his parents had done something helpful for him. The parents would have effectively provided the consent for medical treatment (genetic modification) on behalf of the child. So effectively, there would be consent within the family. For chickens and pigs, there's not even consent within the species.
As an afterthought: could this ever lead to genetically engineering groups of people to fill certain roles in society? Pre-programming the genes of, say, non-university educated groups, to be really good at farming so that they could crank out productive 14 hour-days on a farm every day? And genetically engineering another group to be really good at truck-driving? And another group to be really good at politics? As though selectively breeding a certain type of dog or horse to accentuate a trait associated with that variety of animal, this would be genetically programming people to accentuate traits associated with different roles in society. Humans trained in genetic engineering would become the ruling class and ultimately control the function of all other groups of people. I'd hate to see what would happen.
http://www.sciencemag.org/content/331/6014/132.1.full?sid=5b36e31e-5329-41e4-927d-6e8a266bc6f3
This all sounds good for the poultry industry, but it brings to mind a few questions about genetic engineering, to which I certainly don't have any good answers.
What are the ethical implications of human beings trying to genetically change a creature with a central nervous system, whether genetically engineering chickens to avoid avian flu, or engineering pigs to synthesise omega-3 rather than omega-6 fatty acids thus providing healthier pork?
Would the ethics of the situation be different if these genetic changes were done with the goal of providing a better life for the birds/pigs themselves, rather than the goal of more profit to the people that were doing the genetic engineering?
What about the evolutionary side? Genetic traits evolve over time. Is human beings' interference with other species' genetics changing the course of evolution, or is our ability to do this simply a product of evolution and thus completely natural?
Suppose a family member had an incurable disease such as chronic leukemia or diabetes. If this individual's parents had, before birth, chosen to have their offspring's genes engineered so that this disease would not have been able to happen (if the technology were available), would this be a different case to genetic engineering in chickens or pigs? Would there be anything wrong with that?
In the chickens or pigs, nobody could ever explain to the chicken or pig what had happened nor why. But in the would-have-been chronically ill person, presumably the child would grow up and understand that his parents had done something helpful for him. The parents would have effectively provided the consent for medical treatment (genetic modification) on behalf of the child. So effectively, there would be consent within the family. For chickens and pigs, there's not even consent within the species.
As an afterthought: could this ever lead to genetically engineering groups of people to fill certain roles in society? Pre-programming the genes of, say, non-university educated groups, to be really good at farming so that they could crank out productive 14 hour-days on a farm every day? And genetically engineering another group to be really good at truck-driving? And another group to be really good at politics? As though selectively breeding a certain type of dog or horse to accentuate a trait associated with that variety of animal, this would be genetically programming people to accentuate traits associated with different roles in society. Humans trained in genetic engineering would become the ruling class and ultimately control the function of all other groups of people. I'd hate to see what would happen.
http://www.sciencemag.org/content/331/6014/132.1.full?sid=5b36e31e-5329-41e4-927d-6e8a266bc6f3
Tuesday 1 February 2011
Musings on "Cornell Dots" clinical trial and radioactive iodine
 |
| Schematic representation of a Cornell Dot, with several molecules of dye encapsulated in the center (Image (c) Cornell University) |
Cornell researchers' efforts at tagging tumors has been approved by the US Food and Drug Administration for a clinical trial in humans.
"Cornell Dots" are silica spheres less than 8 nanometers in diameter that enclose several dye molecules and attach to tumor cells. The glass-like shell is chemically inert and coated with polyethylene glycol to avoid being treated as a foreign substance by the body. Organic molecules that bind to tumor surfaces are attached to the shell so the dots stick to tumors and flouresce much more brightly than unencapsulated dyes.
This can show the extent of a tumor’s blood vessels, cell death, treatment response and invasive or metastatic spread to lymph nodes and distant organs. In the new clinical trials, the dots will be labeled with radioactive iodine so they're visible in PET scans and can show how many attach to tumors and where else in the body they go.
The dots will hopefully stay in the body (and attached to the tumor) during surgery, thus providing a useful visual for the surgeon. They also may be useful for delivering radioactivity or drugs to tumors. Other potential applications include biological imaging, optical computing, sensors and microarrays such as DNA chips.
But what about the radioactive iodine? Is this going to be particularly relevant to the clinical trial which has five melanoma patients as subjects?
Now, to treat chronic lymphocytic leukemia (CLL), monoclonal antibodies that bind to particular structures on leukemic cells can be used to deliver payloads of radioactive iodine to the tumor cells. The radioactive iodine-antibody combination is a drug called Bexxar. The antibody identifies the targeted cell for destruction by the immune system, but also zaps it with radiation just to be sure.
The Cornell Dots trial seems to use radioactive iodine as a label. But given that the trial involves skin cancer patients, could the radioactive iodine not actually be used to kill the melanoma cell in the same way that Bexxar attacks CLL cells with radiation?
If the organic molecule on the dots' shells is able to identify and attach to melanoma cells, whether or not it singles out the cells for immune destruction, it seems that this clinical trial could shed new light on a possible radioimmunotherapy treatment.
Ow, Hooiswing et al., Bright and Stable Core-Shell Fluorescent Silica Nanoparticles. Nano Letters Vol. 5, No. 1., 113-117, 2005.
http://www.newswise.com/articles/view/572923/?sc=dwhr&xy=10005433
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