Is Engaging in Science Outreach Damaging to Scientists?A few years ago, I started posting about science publicly on Google+. I did it in my spare time because as a scientist, it was obviously a topic I was interested in. I also found the public ignorance about science particularly depressing. This, coupled with a woeful misrepresentation of science on the part of many science journalists on popular media meant that even if the public cared enough to read about science, they would be ill-informed by sensationalised over-hyped articles. There was only one solution, as I saw it - the scientists themselves should engage directly with the public. This has always been my personal motto when it came to doing science outreach (http://goo.gl/Ts8oYf and http://goo.gl/W1XKHT). So it is with dismay that I read this ‘joke’ article on Genome Biology by Neil Hall (http://goo.gl/oX52dI). In it, he defines the K-index (Kardashian Index) as:“a measure of discrepancy between a scientist’s social media profile and publication record based on the direct comparison of numbers of citations and Twitter followers.”  A high K-index indicates that the scientist may have built their reputation on a shaky foundation, while a low K- index indicates that the scientist is not being given credit where credit is due.An unfortunate consequence of the K-index is that it is damaging to other scientists who genuinely engage in science outreach on social media. Scientists are evaluated by their publication records. People who have a low K-index will likely be older and well-established. Someone who started publishing 30 years ago and just joined Twitter will have a very low K-index. On the other hand, early career researchers who haven’t published a lot but engage in outreach can appear to have a high K-index. The author also advises people that "if your K-index gets above 5, then it’s time to get off Twitter and write those papers". Never mind that only 1% of scientists regularly publish one paper a year (http://goo.gl/yvd1Yv). Do we really want the other 99% of scientists to stop writing about science on social media?I understand that this paper was ‘semi-serious’. I understand that there are certain science outreach ‘personalities’ on social media who regularly over-estimate their popularity and importance. But I can already imagine how this index can be used to patronise young researchers who engage in outreach. I can imagine the smirks from senior scientists at job interview panels and evaluation committees. This ‘joke’ article is only funny if you are a senior tenured professor with lots of papers and yet have a low follower count on social media. "Ha ha, let’s laugh at those silly scientists doing social media outreach when they should be writing papers!" The K-index trivialises those of us who work hard to communicate science with the public. I don’t earn anything from doing outreach. It doesn’t benefit me professionally. I don’t have better job prospects because I have an audience. I do it because as a scientist, I feel I have a duty to directly engage with the public. Doing outreach doesn’t harm me either. I hate to think that someday, it might. I hate to think that I might be taken less seriously because I do this. I especially hate to think that other young researchers might be discouraged from engaging in outreach because of this. Thanks to +Tommy Leung for the discussion that inspired this post. Image: Twitter followers versus number of scientific citations for a sort-of-random sample of researcher tweeters. Individuals with a highly overinflated number of followers (when compared with the number predicted by the trendline) are highlighted by the area labeled Kardashians. (from: http://goo.gl/oX52dI) #ScienceEverydayhttp://click-to-read-mo.re/p/8tSO/5221820b

Is Engaging in Science Outreach Damaging to Scientists?

A few years ago, I started posting about science publicly on Google+. I did it in my spare time because as a scientist, it was obviously a topic I was interested in. I also found the public ignorance about science particularly depressing. This, coupled with a woeful misrepresentation of science on the part of many science journalists on popular media meant that even if the public cared enough to read about science, they would be ill-informed by sensationalised over-hyped articles. There was only one solution, as I saw it - the scientists themselves should engage directly with the public. This has always been my personal motto when it came to doing science outreach (http://goo.gl/Ts8oYf and http://goo.gl/W1XKHT). 

So it is with dismay that I read this ‘joke’ article on Genome Biology by Neil Hall (http://goo.gl/oX52dI). In it, he defines the K-index (Kardashian Index) as:

“a measure of discrepancy between a scientist’s social media profile and publication record based on the direct comparison of numbers of citations and Twitter followers.”  A high K-index indicates that the scientist may have built their reputation on a shaky foundation, while a low K- index indicates that the scientist is not being given credit where credit is due.

An unfortunate consequence of the K-index is that it is damaging to other scientists who genuinely engage in science outreach on social media. Scientists are evaluated by their publication records. People who have a low K-index will likely be older and well-established. Someone who started publishing 30 years ago and just joined Twitter will have a very low K-index. On the other hand, early career researchers who haven’t published a lot but engage in outreach can appear to have a high K-index. The author also advises people that "if your K-index gets above 5, then it’s time to get off Twitter and write those papers". Never mind that only 1% of scientists regularly publish one paper a year (http://goo.gl/yvd1Yv). Do we really want the other 99% of scientists to stop writing about science on social media?

I understand that this paper was ‘semi-serious’. I understand that there are certain science outreach ‘personalities’ on social media who regularly over-estimate their popularity and importance. But I can already imagine how this index can be used to patronise young researchers who engage in outreach. I can imagine the smirks from senior scientists at job interview panels and evaluation committees. 

This ‘joke’ article is only funny if you are a senior tenured professor with lots of papers and yet have a low follower count on social media. "Ha ha, let’s laugh at those silly scientists doing social media outreach when they should be writing papers!" The K-index trivialises those of us who work hard to communicate science with the public. 

I don’t earn anything from doing outreach. It doesn’t benefit me professionally. I don’t have better job prospects because I have an audience. I do it because as a scientist, I feel I have a duty to directly engage with the public. Doing outreach doesn’t harm me either. I hate to think that someday, it might. I hate to think that I might be taken less seriously because I do this. I especially hate to think that other young researchers might be discouraged from engaging in outreach because of this. 

Thanks to +Tommy Leung for the discussion that inspired this post. 

Image: Twitter followers versus number of scientific citations for a sort-of-random sample of researcher tweeters. Individuals with a highly overinflated number of followers (when compared with the number predicted by the trendline) are highlighted by the area labeled Kardashians. (from: http://goo.gl/oX52dI)

#ScienceEveryday

http://click-to-read-mo.re/p/8tSO/5221820b

Cambridge DelightsThere is a quaint little ice cream stand attached to a bicycle that can be found around Cambridge. Jack’s Gelato has very quirky flavours, my favourites so far being Earl Grey Tea and Jordanian Orange Flower. This afternoon they were at a farm shop so it was nice to sit under the trees and enjoy some ice cream. Trying this again because mobile app is being a pita.http://click-to-read-mo.re/p/8qKY/5221820b

Cambridge Delights

There is a quaint little ice cream stand attached to a bicycle that can be found around Cambridge. Jack’s Gelato has very quirky flavours, my favourites so far being Earl Grey Tea and Jordanian Orange Flower. This afternoon they were at a farm shop so it was nice to sit under the trees and enjoy some ice cream. 

Trying this again because mobile app is being a pita.

http://click-to-read-mo.re/p/8qKY/5221820b

Egg-cellent breakthrough in Parasite ResearchThere is a recent paper in PLOS Pathogens (  #OpenAccess  ) which represents a really interesting development in parasite control. You can read the full paper here: http://goo.gl/E06mMo✤ Schistosomiasis is a disease caused by parasitic worms of the Schistosoma genus. It affects over 200 million people worldwide, and kills an estimated 300,000 people each year.✤ Currently there is only one drug (Praziquantel) to treat infections caused by all the different species of Schistosoma. Use of this drug does not prevent reinfection and is not effective against juvenile worms. Understandably, the development of drug resistance is a big worry. Therefore any alternative methods for controlling infections would be very useful.✤ The life cycle of the parasite is somewhat complex; eggs are eliminated with faeces into the environment, and they hatch under optimal conditions. Once the eggs hatch, the larvae (known as miracidia) swim and infect specific snail intermediate hosts. Once inside the snail they grow further into another larval stage known as cercaria. The cercariae are infective, and are able to penetrate the skin of the human host. Once inside humans, they develop into adult worms, and migrate into the organs to have lots of sexy time. This produces up to 300 eggs per day per reproductive pair.✤ Obviously, egg production is therefore important in the life cycle of the Schistosoma. Could this be a way to control Schistosome infections? Researchers focused on the mechanism of eggshell development at the molecular level. They found that one of the key proteins involved in eggshell development is Smp14. The gene for Smp14 is the most abundant RNA transcript in sexually mature females.✤ Remember that generally speaking, DNA makes RNA makes protein (for a more detailed explanation of this pathway, see http://goo.gl/qqOqa5). Preventing the translation of Smp14 RNA transcript into Smp14 protein would therefore be a valid approach for disrupting egg production.✤ Indeed, this was the case. Inhibiting the production of Smp14 protein resulted in disrupted eggshell formation. The eggs that were produced had severe defects - they had holes on their surface, which resulted in the egg contents ‘leaking’ out (see image).✤ By decreasing the number of viable eggs deposited in the environment, it is possible to limit the transmission of the parasites. This work therefore represents a very attractive route for the development of more effective treatments for the disease. Image credit: Marcelo Rosado Fantappie (http://goo.gl/E06mMo) #ScienceSundayhttp://click-to-read-mo.re/p/8jek/5221820b

Egg-cellent breakthrough in Parasite Research

There is a recent paper in PLOS Pathogens ( #OpenAccess ) which represents a really interesting development in parasite control. You can read the full paper here: http://goo.gl/E06mMo

✤ Schistosomiasis is a disease caused by parasitic worms of the Schistosoma genus. It affects over 200 million people worldwide, and kills an estimated 300,000 people each year.

✤ Currently there is only one drug (Praziquantel) to treat infections caused by all the different species of Schistosoma. Use of this drug does not prevent reinfection and is not effective against juvenile worms. Understandably, the development of drug resistance is a big worry. Therefore any alternative methods for controlling infections would be very useful.

✤ The life cycle of the parasite is somewhat complex; eggs are eliminated with faeces into the environment, and they hatch under optimal conditions. Once the eggs hatch, the larvae (known as miracidia) swim and infect specific snail intermediate hosts. Once inside the snail they grow further into another larval stage known as cercaria. The cercariae are infective, and are able to penetrate the skin of the human host. Once inside humans, they develop into adult worms, and migrate into the organs to have lots of sexy time. This produces up to 300 eggs per day per reproductive pair.

✤ Obviously, egg production is therefore important in the life cycle of the Schistosoma. Could this be a way to control Schistosome infections? Researchers focused on the mechanism of eggshell development at the molecular level. They found that one of the key proteins involved in eggshell development is Smp14. The gene for Smp14 is the most abundant RNA transcript in sexually mature females.

✤ Remember that generally speaking, DNA makes RNA makes protein (for a more detailed explanation of this pathway, see http://goo.gl/qqOqa5). Preventing the translation of Smp14 RNA transcript into Smp14 protein would therefore be a valid approach for disrupting egg production.

✤ Indeed, this was the case. Inhibiting the production of Smp14 protein resulted in disrupted eggshell formation. The eggs that were produced had severe defects - they had holes on their surface, which resulted in the egg contents ‘leaking’ out (see image).

✤ By decreasing the number of viable eggs deposited in the environment, it is possible to limit the transmission of the parasites. This work therefore represents a very attractive route for the development of more effective treatments for the disease. 

Image credit: Marcelo Rosado Fantappie (http://goo.gl/E06mMo)

#ScienceSunday

http://click-to-read-mo.re/p/8jek/5221820b

Can Dogs Detect Cancer?+Nick Kai Nielsen  tagged me about a recent article on the Guardian about a story where a woman’s assistance dog detected her breast cancer (http://goo.gl/WXkfJj). The story is remarkable."One evening in November 2011, I was at my computer when Mia leapt on to my lap and nuzzled into the flesh at the top of my left breast. She closed her eyes and licked furiously. That frightened me because it’s what she does when I have a bruise or cut. I had an ultrasound within a week and, sure enough, there was a lump that a biopsy later confirmed was grade 2a breast cancer"Cancer detection through dogs is not unheard of. What is the theory behind this approach? We know that dogs have extremely sensitive noses, and it has been reported that bloodhounds have upto 4 billion olfactory receptor cells, compared to just 5 million in a human. What this means is that our canine friends can discern the presence of a molecule, even when it is greatly diluted. We also know that cancer cells have abnormal metabolic pathways to generate energy, and it is possible that tumours can give off specific volatile chemicals that could be detected by dogs with extremely sensitive noses. But, we do not yet know what these molecules are, much less if and how they are produced by cancers. Clearly, this is a topic that needs to be researched.In the UK there is a charity called Medical Detection Dogs (http://medicaldetectiondogs.org.uk/), and a quick search through Pubmed indicates that there are several studies to evaluate the efficacy of this novel detection method. However, they are a bit hit-and-miss, and some of the studies seem poorly designed. I’ll summarise a couple below:In 2013, a retrospective study was carried out (http://goo.gl/CKjPrx) where the dogs were trained to detect ovarian cancer in blood samples taken from patients. They compared patients that had clinical remission after undergoing chemotherapy with healthy controls. Generally, we do not know how many patients will have residual cancer cells after complete clinical remission is declared. We also do not know if the dogs were detecting residual chemotherapy drugs in the patient blood samples, or actual cancer cells. I am struck by how the study design did not include another control where the patients were diagnosed with cancer but had not undergone chemotherapy yet, to ensure that the dogs actually detected cancer as opposed to chemo drugs.Another study looking at prostate cancer (http://goo.gl/KKg5gQ), used dogs that learned to positively identify prostate cancer samples from controls. But when the dogs were tested under double-blind conditions (where neither the dog, nor the handlers, nor the scientists know which samples belong to the control group vs the test group), they did not identify prostate cancer samples more frequently than expected by chance. The study warns that “it is possible that the dogs may memorise the individual odours of large numbers of training samples rather than generalise on a common odour”. As tempting as it is to look at stories such as the Guardian article with optimism, it is critical to approach them with a degree of realism. These are anecdotal stories. Compelling yes, but still anecdotal. There are so many questions we still need to answer: ✤ Are there molecules produced by cancer cells that can be detected by dogs? ✤ How is it produced by the cancer cells? ✤ Can dogs actually smell it? ✤ Can the dogs be trained to indicate that they smell it? ✤ How reliable are the dogs at smelling it? Until this approach has been rigorously tested, we cannot abandon traditional cancer screening and detection programs in favour of cancer sniffing dogs.Image: Emilie Clark with Mia.Photograph: Mark Chilvers for the Guardian #cancer     #fidofridayhttp://click-to-read-mo.re/p/7Uww/5221820b

Can Dogs Detect Cancer?

+Nick Kai Nielsen  tagged me about a recent article on the Guardian about a story where a woman’s assistance dog detected her breast cancer (http://goo.gl/WXkfJj). The story is remarkable.

"One evening in November 2011, I was at my computer when Mia leapt on to my lap and nuzzled into the flesh at the top of my left breast. She closed her eyes and licked furiously. That frightened me because it’s what she does when I have a bruise or cut. I had an ultrasound within a week and, sure enough, there was a lump that a biopsy later confirmed was grade 2a breast cancer"

Cancer detection through dogs is not unheard of. What is the theory behind this approach? We know that dogs have extremely sensitive noses, and it has been reported that bloodhounds have upto 4 billion olfactory receptor cells, compared to just 5 million in a human. What this means is that our canine friends can discern the presence of a molecule, even when it is greatly diluted. We also know that cancer cells have abnormal metabolic pathways to generate energy, and it is possible that tumours can give off specific volatile chemicals that could be detected by dogs with extremely sensitive noses. But, we do not yet know what these molecules are, much less if and how they are produced by cancers. Clearly, this is a topic that needs to be researched.

In the UK there is a charity called Medical Detection Dogs (http://medicaldetectiondogs.org.uk/), and a quick search through Pubmed indicates that there are several studies to evaluate the efficacy of this novel detection method. However, they are a bit hit-and-miss, and some of the studies seem poorly designed. I’ll summarise a couple below:

In 2013, a retrospective study was carried out (http://goo.gl/CKjPrx) where the dogs were trained to detect ovarian cancer in blood samples taken from patients. They compared patients that had clinical remission after undergoing chemotherapy with healthy controls. Generally, we do not know how many patients will have residual cancer cells after complete clinical remission is declared. We also do not know if the dogs were detecting residual chemotherapy drugs in the patient blood samples, or actual cancer cells. I am struck by how the study design did not include another control where the patients were diagnosed with cancer but had not undergone chemotherapy yet, to ensure that the dogs actually detected cancer as opposed to chemo drugs.

Another study looking at prostate cancer (http://goo.gl/KKg5gQ), used dogs that learned to positively identify prostate cancer samples from controls. But when the dogs were tested under double-blind conditions (where neither the dog, nor the handlers, nor the scientists know which samples belong to the control group vs the test group), they did not identify prostate cancer samples more frequently than expected by chance. The study warns that “it is possible that the dogs may memorise the individual odours of large numbers of training samples rather than generalise on a common odour”. 

As tempting as it is to look at stories such as the Guardian article with optimism, it is critical to approach them with a degree of realism. These are anecdotal stories. Compelling yes, but still anecdotal. 

There are so many questions we still need to answer: 

✤ Are there molecules produced by cancer cells that can be detected by dogs? 
✤ How is it produced by the cancer cells? 
✤ Can dogs actually smell it? 
✤ Can the dogs be trained to indicate that they smell it? 
✤ How reliable are the dogs at smelling it? 

Until this approach has been rigorously tested, we cannot abandon traditional cancer screening and detection programs in favour of cancer sniffing dogs.

Image: Emilie Clark with Mia.
Photograph: Mark Chilvers for the Guardian

#cancer   #fidofriday

http://click-to-read-mo.re/p/7Uww/5221820b

The Fires of HatredThis is one of those posts that I’m not sure I should publish, because it’s personal, and the topic is complicated, and I don’t feel that I have the historical/political expertise to do this any justice. But staying silent is harder so…here goes.I am a Sri Lankan citizen, and I am ethnically a Sinhalese. A few years ago, Sri Lanka ended a brutal civil war that some of you may have heard about on the news. Sometimes I get asked about the war in Sri Lanka, and what it was like growing up with it. Answering that question is always hard for me. I suspect it’s hard for a lot of people in my position, because the answer, the right answer, consists of a lot of words, and the person asking the question tends to want answers in the form of an easily digestible summary: "well, you have your Nazis on the one side, doing bad things like killing unicorns, and the daring pure-hearted heroes on the other saving those unicorns with their laser-beams" If it took less than five minutes to explain, it’s all bullshit, no matter which side of the story you’re hearing. Not to mention the fact that the person asking the question usually doesn’t have a clue about the ethnic and geopolitical background that led to the whole mess, because who really cares about a tiny island in the middle of the Indian ocean?But here is a simplified background on what happened, over thirty years ago.So there is this country, Sri Lanka. Most of the people there are Sinhalese. Less people are Tamil. After becoming a semi-proper democracy back around 60 years ago, the majority Sinhalese began the standard democratic practice of treating the minorities like shit. Not nearly as badly as white America screwed over black America, I mean, we’re not barbarians, but still there were some major disparities. So eventually, about 30 years ago, a small group of Tamils decided enough was enough, and made a fuss. A couple of soldiers died in that fuss. The Sinhalese population thought that was rather bad form, and rioted. Much chaos ensued, many Tamil-owned houses were burned to a crisp (sometimes with Tamils in them), and a lot of Tamils had to flee the country for their lives.In the ensuing 30 years, a war was waged that resulted in a massive loss of life on both sides. It’s difficult for me to explain how I feel about this part in an unbiased manner because seeing the results of a suicide-bombing first hand tends to hamper one’s sympathy for the cause espoused by the bomber, as I’m sure you’ll understand. Either way, the bloody war drew to an end a few years ago, with Sri Lanka declaring loud and proud that they truly ‘defeated terrorism’. The loudest and proudest voices were of course, the Sinhalese Buddhists.Since the End of the War, the Sinhalese Buddhists have become even more xenophobic than before. A few of them, led by Buddhist monks no less, have organised themselves into Sri Lanka’s version of the Ku Klux Klan known as The Bodhu Bala Sena (BBS). They are on the brink of instigating yet another civil war. History is repeating itself, except this time it is the Muslims that are being targeted, since the ‘Tamils’ have already been ‘defeated’. Why am I writing about this now? Last weekend, Aluthgama, a small town on the southern coast of Sri Lanka witnessed riots. Several people have been killed, and many more injured. The town is burning, and a curfew is in place. The people are running out of food because of the curfew, and the BBS is blocking any food parcels being sent in. The police are apathetic observers at best, because they are mostly Sinhalese Buddhists. Ignoring the violence is a matter of policy. The politicians are staunchly pro-Buddhists and racists against the Muslims. It is a jungle out there, and the violence is escalating. This incident is but one in a long series of events that rarely get reported on because of the atmosphere of silence. But disturbing snippets leak out. YouTube has a speech in which the leader of the BBS (a Buddhist monk) is heard saying that if even one ‘marakkalaya’ (a derogatory Sinhala word for Muslim) so much as laid a hand on a Sinhalese, that it would mean the end of all of them (Bodu Bala Sena Meeting - Aluthgama). The speech, in Sinhalese, makes me shiver because it is so reminiscent of the type of rhetoric that precedes communal and ethnic war. The sort of people who listen to racist priests and politicians.The media in Sri Lanka is predictably silent. The ‘adults’ are predictably silent. The old hatred runs deep. But it is heartening to see commentary on social media condemning these incidents. I have seen many of my Sri Lankan friends, speak out against these events. Perhaps there is still hope. To paraphrase another article on this topic, it feels like “the war never ended, we just took some time off” (http://goo.gl/jpZFFe)Image: Fire services struggling to control another Muslim shop on fire in  #Aluthgama   (via http://goo.gl/X0hmeY)http://click-to-read-mo.re/p/7HwR/5221820b

The Fires of Hatred

This is one of those posts that I’m not sure I should publish, because it’s personal, and the topic is complicated, and I don’t feel that I have the historical/political expertise to do this any justice. But staying silent is harder so…here goes.

I am a Sri Lankan citizen, and I am ethnically a Sinhalese. A few years ago, Sri Lanka ended a brutal civil war that some of you may have heard about on the news. Sometimes I get asked about the war in Sri Lanka, and what it was like growing up with it. Answering that question is always hard for me. I suspect it’s hard for a lot of people in my position, because the answer, the right answer, consists of a lot of words, and the person asking the question tends to want answers in the form of an easily digestible summary: "well, you have your Nazis on the one side, doing bad things like killing unicorns, and the daring pure-hearted heroes on the other saving those unicorns with their laser-beams" If it took less than five minutes to explain, it’s all bullshit, no matter which side of the story you’re hearing. Not to mention the fact that the person asking the question usually doesn’t have a clue about the ethnic and geopolitical background that led to the whole mess, because who really cares about a tiny island in the middle of the Indian ocean?

But here is a simplified background on what happened, over thirty years ago.

So there is this country, Sri Lanka. Most of the people there are Sinhalese. Less people are Tamil. After becoming a semi-proper democracy back around 60 years ago, the majority Sinhalese began the standard democratic practice of treating the minorities like shit. Not nearly as badly as white America screwed over black America, I mean, we’re not barbarians, but still there were some major disparities. So eventually, about 30 years ago, a small group of Tamils decided enough was enough, and made a fuss. A couple of soldiers died in that fuss. The Sinhalese population thought that was rather bad form, and rioted. Much chaos ensued, many Tamil-owned houses were burned to a crisp (sometimes with Tamils in them), and a lot of Tamils had to flee the country for their lives.

In the ensuing 30 years, a war was waged that resulted in a massive loss of life on both sides. It’s difficult for me to explain how I feel about this part in an unbiased manner because seeing the results of a suicide-bombing first hand tends to hamper one’s sympathy for the cause espoused by the bomber, as I’m sure you’ll understand. Either way, the bloody war drew to an end a few years ago, with Sri Lanka declaring loud and proud that they truly ‘defeated terrorism’. The loudest and proudest voices were of course, the Sinhalese Buddhists.

Since the End of the War, the Sinhalese Buddhists have become even more xenophobic than before. A few of them, led by Buddhist monks no less, have organised themselves into Sri Lanka’s version of the Ku Klux Klan known as The Bodhu Bala Sena (BBS). They are on the brink of instigating yet another civil war. History is repeating itself, except this time it is the Muslims that are being targeted, since the ‘Tamils’ have already been ‘defeated’. 

Why am I writing about this now? Last weekend, Aluthgama, a small town on the southern coast of Sri Lanka witnessed riots. Several people have been killed, and many more injured. The town is burning, and a curfew is in place. The people are running out of food because of the curfew, and the BBS is blocking any food parcels being sent in. The police are apathetic observers at best, because they are mostly Sinhalese Buddhists. Ignoring the violence is a matter of policy. The politicians are staunchly pro-Buddhists and racists against the Muslims. It is a jungle out there, and the violence is escalating. This incident is but one in a long series of events that rarely get reported on because of the atmosphere of silence. But disturbing snippets leak out. YouTube has a speech in which the leader of the BBS (a Buddhist monk) is heard saying that if even one ‘marakkalaya’ (a derogatory Sinhala word for Muslim) so much as laid a hand on a Sinhalese, that it would mean the end of all of them (Bodu Bala Sena Meeting - Aluthgama). The speech, in Sinhalese, makes me shiver because it is so reminiscent of the type of rhetoric that precedes communal and ethnic war. The sort of people who listen to racist priests and politicians.

The media in Sri Lanka is predictably silent. The ‘adults’ are predictably silent. The old hatred runs deep. But it is heartening to see commentary on social media condemning these incidents. I have seen many of my Sri Lankan friends, speak out against these events. Perhaps there is still hope. To paraphrase another article on this topic, it feels like “the war never ended, we just took some time off” (http://goo.gl/jpZFFe)

Image: Fire services struggling to control another Muslim shop on fire in #Aluthgama   (via http://goo.gl/X0hmeY)

http://click-to-read-mo.re/p/7HwR/5221820b

French Apple TartI’ve been craving apple tart for quite a few days now so a relatively free Sunday was an ideal opportunity to get baking again. The recipe is fairly straightforward, and the results are worth the wait. Best consumed with some vanilla ice cream, or some custard, while watching the football :)Click through the photos for recipe with quantities (in metric!) and instructions!http://click-to-read-mo.re/p/7FJE/5221820b

French Apple Tart

I’ve been craving apple tart for quite a few days now so a relatively free Sunday was an ideal opportunity to get baking again. The recipe is fairly straightforward, and the results are worth the wait. Best consumed with some vanilla ice cream, or some custard, while watching the football :)

Click through the photos for recipe with quantities (in metric!) and instructions!

http://click-to-read-mo.re/p/7FJE/5221820b

Pulling a Fast One on CancerThere is a report making the rounds on social media that really needs to be explained, because as usual the media hype is distorting the findings. The article in question was published in the Cell Stem Cell journal, and is #OpenAccess (http://goo.gl/pnoiwa). I will explain the background, what these results mean, and more importantly, what they don’t mean.✤ Traditional chemotherapy is toxic to cells. The only reason traditional chemotherapy works is because it kills cancer cells faster than it kills normal cells. The side effects from chemo often happen because normal cells are also affected. One such side effect is the suppression of the immune system. This happens because chemo damages adult stem cells too, which impairs tissue repair and regeneration. ✤ Blood stem cells (known as hematopoietic stem cells) are responsible for replacing our blood cells; these reside in the bone marrow. In this study, scientists investigated the effect of prolonged fasting on hematopoietic stem cells.✤ Mice used in this study were fasted for 48 hours, which the scientists defined as prolonged fasting. These mice received no food, only water. They then treated the mice with cyclophosphamide, a common chemotherapy drug. They found that cycles of prolonged fasting reduced the damage caused to hematopoietic stem cells when the mice were treated with cyclophosphamide. They also found that prolonged fasting cycles promoted the regeneration of blood cells through the protection of hematopoietic stem cells. ✤ Next, the scientists tested whether the effects of prolonged fasting were independent of the toxic side effects of chemotherapy. Could prolonged fasting alone stimulate hematopoietic stem cells to self-renew? Indeed, it could. ✤ What is the molecular mechanism for this process? A growth factor known as Insulin-like Growth Factor-1 (IGF-1) seemed to be involved. Growth factors are proteins that control the multiplication of cells. To examine this mechanism, the scientists used mice that were deficient in IGF-1.  If you’re curious about how these ‘knockout mice’ are generated, read http://goo.gl/jdbqbk. When these IGF-1 deficient mice were treated with cyclophosphamide, they showed similar results to the prolonged fasting mice; reduced levels of hematopoietic stem cell damage. So getting rid of IGF-1 induced the same protective effects on hematopoietic stem cells.  ✤ How does IGF-1 signalling protect hematopoietic stem cells? They found that the activity of an enzyme known as PKA was also reduced in these prolonged fasting/IGF-1 deficient mice. PKA controls the pathway involved in stem cell regeneration. So inhibiting IGF-1 or PKA signalling mimics the effect of prolonged fasting; it promotes the regeneration of hematopoietic stem cells, thereby reducing the immuno-suppressive side effect of chemotherapy. ✤ This is really interesting data - this research has identified one of the signalling pathways in the intricate network of reactions controlling the behaviour of hematopoietic stem cells. The mechanism involves PKA and IGF-1 signalling.  WHAT THE DATA DOESN’T SHOWWhat this doesn’t show is that fasting is magically a cure-all for cancer. There isn’t a single study that shows lowered incidence of cancer in human populations that fast regularly. The fasting that these mice underwent also did not include the feasting that goes on every night as seen with human populations either. The scientists also conducted a small Phase I clinical trial in which patients undergoing chemotherapy fasted for 72h - the results are promising; their hematopoietic stem cells were protected when compared with the non-fasting control group. But obviously more data is needed, and it is highly inadvisable to fast before undergoing chemo, without the explicit guidance of a physician.To summarise, fasting is not a cure for cancer. If anything, fasting does “cure” everything, eventually; this pathway involves a mechanism known as ‘death’. Image: fasting causes a major reduction in white blood cells followed by their replenishment after refeeding. These effects of prolonged fasting can result in the reversal of chemotherapy-induced immunosuppression. Image source: http://goo.gl/pnoiwa #ScienceMediaHype    #ScienceEverydayhttp://click-to-read-mo.re/p/7BvA/5221820b

Pulling a Fast One on Cancer

There is a report making the rounds on social media that really needs to be explained, because as usual the media hype is distorting the findings. The article in question was published in the Cell Stem Cell journal, and is #OpenAccess (http://goo.gl/pnoiwa). I will explain the background, what these results mean, and more importantly, what they don’t mean.

✤ Traditional chemotherapy is toxic to cells. The only reason traditional chemotherapy works is because it kills cancer cells faster than it kills normal cells. The side effects from chemo often happen because normal cells are also affected. One such side effect is the suppression of the immune system. This happens because chemo damages adult stem cells too, which impairs tissue repair and regeneration. 

✤ Blood stem cells (known as hematopoietic stem cells) are responsible for replacing our blood cells; these reside in the bone marrow. In this study, scientists investigated the effect of prolonged fasting on hematopoietic stem cells.

✤ Mice used in this study were fasted for 48 hours, which the scientists defined as prolonged fasting. These mice received no food, only water. They then treated the mice with cyclophosphamide, a common chemotherapy drug. They found that cycles of prolonged fasting reduced the damage caused to hematopoietic stem cells when the mice were treated with cyclophosphamide. They also found that prolonged fasting cycles promoted the regeneration of blood cells through the protection of hematopoietic stem cells. 

✤ Next, the scientists tested whether the effects of prolonged fasting were independent of the toxic side effects of chemotherapy. Could prolonged fasting alone stimulate hematopoietic stem cells to self-renew? Indeed, it could. 

✤ What is the molecular mechanism for this process? A growth factor known as Insulin-like Growth Factor-1 (IGF-1) seemed to be involved. Growth factors are proteins that control the multiplication of cells. To examine this mechanism, the scientists used mice that were deficient in IGF-1.  If you’re curious about how these ‘knockout mice’ are generated, read http://goo.gl/jdbqbk. When these IGF-1 deficient mice were treated with cyclophosphamide, they showed similar results to the prolonged fasting mice; reduced levels of hematopoietic stem cell damage. So getting rid of IGF-1 induced the same protective effects on hematopoietic stem cells.  

✤ How does IGF-1 signalling protect hematopoietic stem cells? They found that the activity of an enzyme known as PKA was also reduced in these prolonged fasting/IGF-1 deficient mice. PKA controls the pathway involved in stem cell regeneration. So inhibiting IGF-1 or PKA signalling mimics the effect of prolonged fasting; it promotes the regeneration of hematopoietic stem cells, thereby reducing the immuno-suppressive side effect of chemotherapy. 

✤ This is really interesting data - this research has identified one of the signalling pathways in the intricate network of reactions controlling the behaviour of hematopoietic stem cells. The mechanism involves PKA and IGF-1 signalling.  

WHAT THE DATA DOESN’T SHOW

What this doesn’t show is that fasting is magically a cure-all for cancer. There isn’t a single study that shows lowered incidence of cancer in human populations that fast regularly. The fasting that these mice underwent also did not include the feasting that goes on every night as seen with human populations either. The scientists also conducted a small Phase I clinical trial in which patients undergoing chemotherapy fasted for 72h - the results are promising; their hematopoietic stem cells were protected when compared with the non-fasting control group. But obviously more data is needed, and it is highly inadvisable to fast before undergoing chemo, without the explicit guidance of a physician.

To summarise, fasting is not a cure for cancer. If anything, fasting does “cure” everything, eventually; this pathway involves a mechanism known as ‘death’. 

Image: fasting causes a major reduction in white blood cells followed by their replenishment after refeeding. These effects of prolonged fasting can result in the reversal of chemotherapy-induced immunosuppression. 

Image source: http://goo.gl/pnoiwa

#ScienceMediaHype   #ScienceEveryday

http://click-to-read-mo.re/p/7BvA/5221820b

The Cancer-resistant Blind Mole Rat: Clues from the GenomeAlthough the Naked Mole Rat and the Blind Mole Rat have similar sounding names, they are not close relatives. The two species diverged over 70 million years ago, and blind mole rats are more closely related to rats and mice than to naked mole rats. But both these species are resistant to cancer; in over 40 years of studying blind mole rats, not a single spontaneous tumour was recorded among thousands of captive animals. Intriguingly, the two animals have evolved this resistance independently. Studying the mechanisms for cancer resistance in these two animals can therefore provide a deeper understanding of how cancer arises at the cellular level. The recent publication of the blind mole rat’s genome sequence (http://goo.gl/CxlnDH) provides some intriguing hints about these mechanisms.✤ The blind mole rat lives underground. Life underground requires several evolutionary adaptations. Of these, one of the most remarkable is its adaptation to low oxygen (highly hypoxic) environments found in underground burrows; O2 as low as 7.2% and CO2 as high as 6.1% have been reported. Low oxygen environments are also found inside tumours, and tumours are able to survive this environment through mechanisms I have explained here: http://goo.gl/8LWVXq✤ Hypoxic environments typically cause cells to undergo apoptosis - a type of programmed cell suicide. This process is regulated by an important protein known as p53 (see here for more information about apoptosis and: http://goo.gl/lYJRdm). Hypoxia-induced apoptosis would be disastrous for an underground-dwelling blind mole rat, so their p53 protein has a mutation that prevents the induction of apoptosis. Even more interestingly, this mutation is almost identical to a similar p53 mutation found in many human cancers. Both mutations seem to encourage the cells to stop dividing, rather than to self-destruct.✤ Understandably, the massive loss of cells due to hypoxia-induced apoptosis is undesirable for the blind mole rat, so the p53 mutation can be explained that way. But mutant p53 also means cancer, as many human cancers have a similar mutation. It sounds counter-intuitive that a cancer resistant animal has nearly the same mutation that actual cancers do. How does this work? Clearly, the blind mole rat has other mechanisms in place to compensate for this ‘weakened’ p53 status. But what are they?✤ Instead of apoptosis, the blind mole rat relies on a different mechanism for guarding its cells against cancer. This mechanism is necrotic cell death; messier than apoptosis, it is a mechanism that involves the immune system and inflammation. The genome sequence of the blind mole rat has an extra copy of the gene Ifnb1 which encodes a protein known as interferon beta 1. In comparison, the mouse, rat and naked mole rat genomes have only one copy of Ifnb1. The blind mole rat has extra copies of this gene, which results in extra amounts of this protein, leading to a stronger necrotic cell death response. This compensates for the ‘weakened’ p53. Supporting this hypothesis is the fact that several other genes from the interferon signalling pathway, along with other genes that regulate cell death and inflammation are also expanded in the blind mole rat genome, indicating that this immuno-inflammatory response is heightened in the blind mole rat.✤ In summary, the blind mole rat genome has acquired a mutant version of p53 (i.e. weakened) as an adaptation to underground hypoxic conditions. This would normally lead to a lowered ability to resist cancer, as p53 is vital for tumour suppression. Therefore as compensation, the blind mole rat genome has extra copies of genes involved in necrotic cell death in order to remain cancer resistant.✤ It might seem a bit disconnected to study an underground dwelling blind mole rat that is so different from us, in order to understand our own cancers. But as these findings show, understanding the evolution of cancer resistance mechanisms can increase our knowledge of cancer; with this knowledge comes the power to someday develop therapies against cancer, or measures for cancer prevention.Image credit: Blind mole rat (http://goo.gl/IE5wT3). #ScienceSundayhttp://click-to-read-mo.re/p/7wZ5/5221820b

The Cancer-resistant Blind Mole Rat: Clues from the Genome

Although the Naked Mole Rat and the Blind Mole Rat have similar sounding names, they are not close relatives. The two species diverged over 70 million years ago, and blind mole rats are more closely related to rats and mice than to naked mole rats. But both these species are resistant to cancer; in over 40 years of studying blind mole rats, not a single spontaneous tumour was recorded among thousands of captive animals. Intriguingly, the two animals have evolved this resistance independently. Studying the mechanisms for cancer resistance in these two animals can therefore provide a deeper understanding of how cancer arises at the cellular level. The recent publication of the blind mole rat’s genome sequence (http://goo.gl/CxlnDH) provides some intriguing hints about these mechanisms.

✤ The blind mole rat lives underground. Life underground requires several evolutionary adaptations. Of these, one of the most remarkable is its adaptation to low oxygen (highly hypoxic) environments found in underground burrows; O2 as low as 7.2% and CO2 as high as 6.1% have been reported. Low oxygen environments are also found inside tumours, and tumours are able to survive this environment through mechanisms I have explained here: http://goo.gl/8LWVXq

✤ Hypoxic environments typically cause cells to undergo apoptosis - a type of programmed cell suicide. This process is regulated by an important protein known as p53 (see here for more information about apoptosis and: http://goo.gl/lYJRdm). Hypoxia-induced apoptosis would be disastrous for an underground-dwelling blind mole rat, so their p53 protein has a mutation that prevents the induction of apoptosis. Even more interestingly, this mutation is almost identical to a similar p53 mutation found in many human cancers. Both mutations seem to encourage the cells to stop dividing, rather than to self-destruct.

✤ Understandably, the massive loss of cells due to hypoxia-induced apoptosis is undesirable for the blind mole rat, so the p53 mutation can be explained that way. But mutant p53 also means cancer, as many human cancers have a similar mutation. It sounds counter-intuitive that a cancer resistant animal has nearly the same mutation that actual cancers do. How does this work? Clearly, the blind mole rat has other mechanisms in place to compensate for this ‘weakened’ p53 status. But what are they?

✤ Instead of apoptosis, the blind mole rat relies on a different mechanism for guarding its cells against cancer. This mechanism is necrotic cell death; messier than apoptosis, it is a mechanism that involves the immune system and inflammation. The genome sequence of the blind mole rat has an extra copy of the gene Ifnb1 which encodes a protein known as interferon beta 1. In comparison, the mouse, rat and naked mole rat genomes have only one copy of Ifnb1. The blind mole rat has extra copies of this gene, which results in extra amounts of this protein, leading to a stronger necrotic cell death response. This compensates for the ‘weakened’ p53. Supporting this hypothesis is the fact that several other genes from the interferon signalling pathway, along with other genes that regulate cell death and inflammation are also expanded in the blind mole rat genome, indicating that this immuno-inflammatory response is heightened in the blind mole rat.

✤ In summary, the blind mole rat genome has acquired a mutant version of p53 (i.e. weakened) as an adaptation to underground hypoxic conditions. This would normally lead to a lowered ability to resist cancer, as p53 is vital for tumour suppression. Therefore as compensation, the blind mole rat genome has extra copies of genes involved in necrotic cell death in order to remain cancer resistant.

✤ It might seem a bit disconnected to study an underground dwelling blind mole rat that is so different from us, in order to understand our own cancers. But as these findings show, understanding the evolution of cancer resistance mechanisms can increase our knowledge of cancer; with this knowledge comes the power to someday develop therapies against cancer, or measures for cancer prevention.

Image credit: Blind mole rat (http://goo.gl/IE5wT3).

#ScienceSunday

http://click-to-read-mo.re/p/7wZ5/5221820b

Searching for Sugar ManIf you watch just one documentary this year (or month, or week -depending on how often you watch them), make it this one. In the late 1960s, amidst the height of the apartheid in South Africa, a bootleg recording of an album titled ‘Cold Fact’ by a mysterious American artist known as Rodriguez suddenly became a phenomenon. But his album failed miserably in America, and there were rumours about a gruesome onstage suicide - one in which he set fire to himself. After that, he disappeared into oblivion. But two South African fans turned into musical detectives to find out more about what really happened to him. The story is incredible, with an unbelievable plot-twist. I won’t give it away, but it is a humbling, poignant story that was gripping from start to finish. And it goes without saying, but the soundtrack is amazing - all original music from Rodriguez. For those in the UK, you can watch this on BBC iPlayer: http://goo.gl/e313nIFor those outside the UK, this link should work: Sugar ManFull album ‘Cold Fact’ on YouTube: Sixto Rodriguez- Cold Fact full albumhttp://click-to-read-mo.re/p/7tOT/5221820b

Searching for Sugar Man

If you watch just one documentary this year (or month, or week -depending on how often you watch them), make it this one. In the late 1960s, amidst the height of the apartheid in South Africa, a bootleg recording of an album titled ‘Cold Fact’ by a mysterious American artist known as Rodriguez suddenly became a phenomenon. But his album failed miserably in America, and there were rumours about a gruesome onstage suicide - one in which he set fire to himself. After that, he disappeared into oblivion. But two South African fans turned into musical detectives to find out more about what really happened to him. The story is incredible, with an unbelievable plot-twist. I won’t give it away, but it is a humbling, poignant story that was gripping from start to finish. 

And it goes without saying, but the soundtrack is amazing - all original music from Rodriguez. 

For those in the UK, you can watch this on BBC iPlayer: http://goo.gl/e313nI
For those outside the UK, this link should work: Sugar Man
Full album ‘Cold Fact’ on YouTube: Sixto Rodriguez- Cold Fact full album

http://click-to-read-mo.re/p/7tOT/5221820b