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- Algae. Not just a soft drink any more. [Greg Laden's Blog]
- Student guest post: Are parasites causing a rise in the global HIV epidemic? [Aetiology]
- What do flies, fish, mice and worms have to do with biomedical science? [Life Lines]
- How high can the sea level rise if all the glacial ice melted? [Greg Laden's Blog]
- Do the creationist shuffle and twist! [Pharyngula]
- Quasi Poll: Most Needed Pop-Science Biography? [Uncertain Principles]
- The Bottleneck Years by H. E. Taylor – Chapter 44 [A Few Things Ill Considered]
- Worth reading: Go bags, water wars, and working while pregnant [The Pump Handle]
- First 4-Wheel Wagon In Swedish East Coast Rock Art [Aardvarchaeology]
- Amazon Throws Tantrum, Screws Minnesota Associates [Greg Laden's Blog]
STUDENT GUEST POST by Carrie Ellsworth
During the summer of 2010 I spent two months in Ghana studying a parasite called schistosomiasis. We worked in a small town called Adasawase to determine prevalence and treat the schoolchildren who were infected. We were told that schistosomiasis was not a major health concern for the people in the town because they were often faced with other diseases that had more immediate and severe health consequences than a parasitic infection. It became apparent that if we wanted the people of this small town to take this health threat seriously, we needed to stress the long term health sequelae that could arise due to schistosome infections.
(Personal photo taken in Ghana in 2010)
Our research group decided to implement an educational portion to our schistosomiasis control program. Through a Knowledge Attitudes and Practices survey, we found that most schoolchildren in the town reported learning about health from their teachers in school. We held a meeting with all teachers and administrators from Adasawase to educate them on the transmission, symptoms, and long term implications of schistosomiasis infections. When the possibility of greater transmission of HIV to individuals with schistosomal infections came up in discussion, we suddenly had everyone’s complete attention. You could have heard a pin drop on the cement floor of the school room.
Recently, the BBC reported that over 25% of schoolgirls between the ages of 10 and 14 in South Africa are infected with HIV. The World Health Organization has shown that HIV prevalence is much higher in females living in urban areas than in any other demographic group. More than 2/3 of the world’s population living with HIV/AIDS lives in Sub-Saharan Africa. Many efforts have been made to decrease the prevalence of HIV in Africa but few people have looked at the possibility of a parasitic infection possibly contributing to the transmission of HIV.
(http://www.who.int/gho/urban_health/outcomes/hiv_prevalence/en/index.html)
Schistosomiasis haematobium is a species of waterborne parasite that specifically affects the urogenital system of infected individuals. When people with S. haematobium urinate in stagnant water, they deposit schistosome eggs. The eggs develop into larvae which then enter a freshwater snail to continue its life cycle and mature. It leaves the snail and matures into its infective stage while in the water. The mature larval form of the parasite burrows through the skin of an individual who has contact with contaminated water. Once inside the body, the mature larva develops into an adult worm and then travels to the blood vessels surrounding the bladder. The male and female will mate to produce eggs which penetrate through the bladder wall and are passed in the urine to continue the cycle.
The treatment for a schistosomiasis infection is an inexpensive anti-helminthic medication called Praziquantel. Common signs of a S. haematobium infection are bloody and cloudy urine. Damage to the bladder wall is inevitable and if the infection becomes chronic, damage to the kidneys can also ensue. Chronic genital sores can develop in females with S. haematobium infections when the schistosome eggs are deposited in the uterus, vulva, cervix, and vagina. These lesions are believed to put the females with S. haematobium infections at a greater risk of contracting HIV. A study conducted in Zimbabwe showed that women ages 20-49, who had genital lesions due to a urogenital schistosomiasis infection, had a 3-fold higher risk of having HIV than women without a schistosomal infection.
There are 207 million cases of Schistosomiasis worldwide, and 112 million of those cases are urogenital Schistosomiasis found in Sub-Saharan Africa. This creates a significant overlap between areas of Africa that are endemic to HIV/AIDS and Schistosomiasis. This has caused many scientists to question whether a greater effort to control S. haematobium infections would be an effective method of decreasing the prevalence and transmission of HIV/AIDS in Africa.
(http://blogs.plos.org/speakingofmedicine/2013/05/06/female-genital-schistosomiasis-fgs-sub-saharan-africas-secret-scourge-of-girls-and-women/)
There is a Schistosomiasis Control Initiative (SCI) based out of London which is attempting to implement schistosome control methods in areas that are endemic. A study done in Burkina Faso showed that a single mass treatment with Praziquantel was shown to decrease the prevalence of S. haematobium by 84% in girls and 78% overall for up to 2 years. The WHO has a strategy of mass drug administration (MDA) in which school aged children in areas that have a greater than 10% prevalence of schistosomiasis would receive Praziquantel on a biannual basis, and areas that have greater than 50% prevalence would receive treatment on an annual basis. Treatment with Praziquantel results in a parasitological cure but will not heal genital lesions that have already developed from a S. haematobium infection. For this reason, prophylactic treatment starting at a young age is crucial in using this method as a means to decrease HIV prevalence.
It only costs about 32 cents to treat one child with Praziquantel. In most developing countries Praziquantel is distributed through bulk sales to the government. From there, the government dispenses its allotted Praziquantel out to different programs. The organizations that supply developing countries with Praziquantel include UNICEF and the World Health Organization among many other international organizations. Data has shown that a schistosomiasis infections increase susceptibility to HIV, elevate viral replication, exacerbate immunosuppression and increase transmission of HIV. Due to these findings, greater emphasis on schistosomiasis control is being pursued as a means of decreasing the ever growing HIV/AIDS prevalence in Africa. Widespread distribution of Praziquantel to schoolchildren in countries endemic to both schistosomiasis and HIV/AIDS could potentially prevent 120,000 new cases of HIV/AIDS in the next decade.
If treatment with Praziquantel for one child costs $0.32, then treating 70 million children would cost $22 million for one year. If a 10 year plan was implemented that treated every one of those 70 million children biannually, that would cost approximately $112 million. Compare that with the $18.8 billion that has been proposed to be spent over the next 5 years by the U.S. President’s Emergency Plan for AIDS Relief (PEPFAR). The cost of treating 70 million children for schistosomiasis over a 10 year span is dwarfed by the projected costs of the PEPFAR and could potentially make a significant change in the rising trend of HIV infections in Africa.
All of the research points towards mass treatment with Praziquantel as being the most cost effective and successful method of decreasing the number of schistosomiasis infections and HIV/AIDS transmission. The cooperation between HIV and schistosomiasis control programs is critical in ensuring the success of such a program. Combatting two of Africa’s top health concerns with one simple low cost medication would do wonders for lowering the morbidity and mortality rates of many African countries.
REFERENCES:
"HIV and AIDS Statistics: Worldwide." Statistics: Worldwide. AmfAR, Nov. 2012. Web. 10 June 2013. .
Temple, Bliss. Schistosoma Haematobium (blood Flukes). Schistosomiasis Haematobium (blood Flukes). Stanford University, May 2004. Web. 10 June 2013. .
(Personal photo taken in Ghana in 2010)
Our research group decided to implement an educational portion to our schistosomiasis control program. Through a Knowledge Attitudes and Practices survey, we found that most schoolchildren in the town reported learning about health from their teachers in school. We held a meeting with all teachers and administrators from Adasawase to educate them on the transmission, symptoms, and long term implications of schistosomiasis infections. When the possibility of greater transmission of HIV to individuals with schistosomal infections came up in discussion, we suddenly had everyone’s complete attention. You could have heard a pin drop on the cement floor of the school room.
Recently, the BBC reported that over 25% of schoolgirls between the ages of 10 and 14 in South Africa are infected with HIV. The World Health Organization has shown that HIV prevalence is much higher in females living in urban areas than in any other demographic group. More than 2/3 of the world’s population living with HIV/AIDS lives in Sub-Saharan Africa. Many efforts have been made to decrease the prevalence of HIV in Africa but few people have looked at the possibility of a parasitic infection possibly contributing to the transmission of HIV.
(http://www.who.int/gho/urban_health/outcomes/hiv_prevalence/en/index.html)
Schistosomiasis haematobium is a species of waterborne parasite that specifically affects the urogenital system of infected individuals. When people with S. haematobium urinate in stagnant water, they deposit schistosome eggs. The eggs develop into larvae which then enter a freshwater snail to continue its life cycle and mature. It leaves the snail and matures into its infective stage while in the water. The mature larval form of the parasite burrows through the skin of an individual who has contact with contaminated water. Once inside the body, the mature larva develops into an adult worm and then travels to the blood vessels surrounding the bladder. The male and female will mate to produce eggs which penetrate through the bladder wall and are passed in the urine to continue the cycle.
The treatment for a schistosomiasis infection is an inexpensive anti-helminthic medication called Praziquantel. Common signs of a S. haematobium infection are bloody and cloudy urine. Damage to the bladder wall is inevitable and if the infection becomes chronic, damage to the kidneys can also ensue. Chronic genital sores can develop in females with S. haematobium infections when the schistosome eggs are deposited in the uterus, vulva, cervix, and vagina. These lesions are believed to put the females with S. haematobium infections at a greater risk of contracting HIV. A study conducted in Zimbabwe showed that women ages 20-49, who had genital lesions due to a urogenital schistosomiasis infection, had a 3-fold higher risk of having HIV than women without a schistosomal infection.
There are 207 million cases of Schistosomiasis worldwide, and 112 million of those cases are urogenital Schistosomiasis found in Sub-Saharan Africa. This creates a significant overlap between areas of Africa that are endemic to HIV/AIDS and Schistosomiasis. This has caused many scientists to question whether a greater effort to control S. haematobium infections would be an effective method of decreasing the prevalence and transmission of HIV/AIDS in Africa.
(http://blogs.plos.org/speakingofmedicine/2013/05/06/female-genital-schistosomiasis-fgs-sub-saharan-africas-secret-scourge-of-girls-and-women/)
There is a Schistosomiasis Control Initiative (SCI) based out of London which is attempting to implement schistosome control methods in areas that are endemic. A study done in Burkina Faso showed that a single mass treatment with Praziquantel was shown to decrease the prevalence of S. haematobium by 84% in girls and 78% overall for up to 2 years. The WHO has a strategy of mass drug administration (MDA) in which school aged children in areas that have a greater than 10% prevalence of schistosomiasis would receive Praziquantel on a biannual basis, and areas that have greater than 50% prevalence would receive treatment on an annual basis. Treatment with Praziquantel results in a parasitological cure but will not heal genital lesions that have already developed from a S. haematobium infection. For this reason, prophylactic treatment starting at a young age is crucial in using this method as a means to decrease HIV prevalence.
It only costs about 32 cents to treat one child with Praziquantel. In most developing countries Praziquantel is distributed through bulk sales to the government. From there, the government dispenses its allotted Praziquantel out to different programs. The organizations that supply developing countries with Praziquantel include UNICEF and the World Health Organization among many other international organizations. Data has shown that a schistosomiasis infections increase susceptibility to HIV, elevate viral replication, exacerbate immunosuppression and increase transmission of HIV. Due to these findings, greater emphasis on schistosomiasis control is being pursued as a means of decreasing the ever growing HIV/AIDS prevalence in Africa. Widespread distribution of Praziquantel to schoolchildren in countries endemic to both schistosomiasis and HIV/AIDS could potentially prevent 120,000 new cases of HIV/AIDS in the next decade.
If treatment with Praziquantel for one child costs $0.32, then treating 70 million children would cost $22 million for one year. If a 10 year plan was implemented that treated every one of those 70 million children biannually, that would cost approximately $112 million. Compare that with the $18.8 billion that has been proposed to be spent over the next 5 years by the U.S. President’s Emergency Plan for AIDS Relief (PEPFAR). The cost of treating 70 million children for schistosomiasis over a 10 year span is dwarfed by the projected costs of the PEPFAR and could potentially make a significant change in the rising trend of HIV infections in Africa.
All of the research points towards mass treatment with Praziquantel as being the most cost effective and successful method of decreasing the number of schistosomiasis infections and HIV/AIDS transmission. The cooperation between HIV and schistosomiasis control programs is critical in ensuring the success of such a program. Combatting two of Africa’s top health concerns with one simple low cost medication would do wonders for lowering the morbidity and mortality rates of many African countries.
REFERENCES:
"HIV and AIDS Statistics: Worldwide." Statistics: Worldwide. AmfAR, Nov. 2012. Web. 10 June 2013. 
Image of common model organisms from European Molecular Biology Laboratory (EMBL).
There have been times in the past when there was very little ice trapped in glaciers. During this time, sea levels were higher because that water was in the ocean (most of it, anyway). It has been a long time since then. However, with global warming, more and more glacial ice is returning to the sea and this contributes to sea level rise.
The amount of fossil carbon that needs to be released into the atmosphere to cause most of the glacial ice to melt is not known. We can't directly use ancient time periods to assess modern sea level rise by measuring the sea levels from those periods because there has been too much other stuff going on in ocean basins and along current coast lines. But, we can estimate that there was very little glacial ice during, for example, the early Eocene, and the transition of Carbon in the atmosphere to the formation of glaciers might be under 800 ppm. So, if we double the current amount of CO2 in the atmosphere, maybe that would melt all the glaciers. There was more methane in the air at that time as well, but we are releasing plenty of methane as we also release Carbon, so that's not much of a problem. The biggest factor is probably this: The configuration of continents have changed since that time to increase the likelihood of glacial formation at the poles, so returning to some Eocene (or other) atmospheric CO2 value may result in much less melting. But that's OK, because we can certainly increase the amount of carbon to more than around 800 ppm!
If we release CO2 at approximately modern rates (baed on population size), and have population increase up to a point, thus increasing CO2 release (in other words, do nothing significant to mitigate Carbon release, increase the number of people actively releasing it, and population goes up towards 8 or so billion) we can reach over 1000 ppm by 2300 AD, or sooner. That's surely enough to melt most of the glaciers except bits and pieces in the coldest regions of Antarctica.
It is estimated (see this web page) that there is about 80 meters of ocean trapped in glacial ice. There are plenty of web sites out there that allow you to add ocean height to see how coastal regions would change, but the ones I know about don't go to 80 meters. So, to find out what North America would look like, I found a map that has pixels to indicate altitude, with different colors representing topography, at a fine enough level to work with. This is the map, from here:
This map has a color coded key with elevations of 8, 54, 114, etc. labeled but there are color transitions half way between these marks, so there is a mark at 60 meters. I therefore will go ahead and assume that if most of the glacial ice melted, there would be a 60 meter rise in sea level. Therefore, a first approximation of what North America would look like with major glacial melting can be obtained by deleting all the bluish colors from 60 meters on down and converting them to ocean. The resulting map looks like this:
There are several caveats. First, sea level would not rise uniformly, but rather, it would go up more in some places than in others. In the US, I think there would be more sea level rise along the east coast, father to the south, because of a number of these effects, so where you see a coastal plain remaining along the eastern mountains, maybe delete that; perhaps the shores of the Atlantic would wash against the Appalachians or Piedmont in Virginia and North and South Carolina. Also, as sea level rises, the land will be pushed down various amounts by the weight of the water, so this might be considered a minimum estimate of rise in some areas. Also, erosion would cause important changes. If you look at, say, a 60 meter topo line in a region made of something other than hard rock, you have to assume that transgression of the sea including the effects of erosion would move way inland in some cases. Also, this map has the edge of the continent all rough and wiggly. This would only be true where hard bedrock meets the sea. Other places, there would be smoothing off, formation of linear barrier beaches, and the rise of deltas.
But putting all that aside, there are some amazing effects. For one thing, the Atlantic extends to and engulfs Lake Erie. Also, it appears that the Hudson and Champlain valleys merge and join the Saint Lawrence Seaway, so New England and adjoining regions of Canada become a big rocky island. The region of New Orleans and the Lower Mississippi become a large embayment, with the southern end of the Appalachians and nearby mountains forming a peninsula.
El Centro and the Salton Sea become part of the much enlarged Baja (Sea of California). Hudson Bay gets huger. Ignore Greenland; that big ocean in the middle of Greenland would mostly rise up and become land, as this area is currently depressed by glacial mass. Also, gee, there seems to be a big ocean in Mexico.
This is a VERY ROUGH approximation. Just for fun.
____________________
The image at the top of the post is from NOAA and shows, I think 10 meter sea level rise from a different angle.
This map has a color coded key with elevations of 8, 54, 114, etc. labeled but there are color transitions half way between these marks, so there is a mark at 60 meters. I therefore will go ahead and assume that if most of the glacial ice melted, there would be a 60 meter rise in sea level. Therefore, a first approximation of what North America would look like with major glacial melting can be obtained by deleting all the bluish colors from 60 meters on down and converting them to ocean. The resulting map looks like this:
There are several caveats. First, sea level would not rise uniformly, but rather, it would go up more in some places than in others. In the US, I think there would be more sea level rise along the east coast, father to the south, because of a number of these effects, so where you see a coastal plain remaining along the eastern mountains, maybe delete that; perhaps the shores of the Atlantic would wash against the Appalachians or Piedmont in Virginia and North and South Carolina. Also, as sea level rises, the land will be pushed down various amounts by the weight of the water, so this might be considered a minimum estimate of rise in some areas. Also, erosion would cause important changes. If you look at, say, a 60 meter topo line in a region made of something other than hard rock, you have to assume that transgression of the sea including the effects of erosion would move way inland in some cases. Also, this map has the edge of the continent all rough and wiggly. This would only be true where hard bedrock meets the sea. Other places, there would be smoothing off, formation of linear barrier beaches, and the rise of deltas.
But putting all that aside, there are some amazing effects. For one thing, the Atlantic extends to and engulfs Lake Erie. Also, it appears that the Hudson and Champlain valleys merge and join the Saint Lawrence Seaway, so New England and adjoining regions of Canada become a big rocky island. The region of New Orleans and the Lower Mississippi become a large embayment, with the southern end of the Appalachians and nearby mountains forming a peninsula.
El Centro and the Salton Sea become part of the much enlarged Baja (Sea of California). Hudson Bay gets huger. Ignore Greenland; that big ocean in the middle of Greenland would mostly rise up and become land, as this area is currently depressed by glacial mass. Also, gee, there seems to be a big ocean in Mexico.
This is a VERY ROUGH approximation. Just for fun.
____________________
The image at the top of the post is from NOAA and shows, I think 10 meter sea level rise from a different angle.
Don't you hate it when you get up in the morning and the first thing you read on the internet is that the news that your entire career has been a waste of time, your whole field of study has collapsed, and you're going to have to rethink your entire future? Happens to me all the time. But then, I read the creationist news, so I've become desensitized to the whole idea of intellectual catastrophes.
Today's fresh demolition of the whole of evolutionary theory comes via Christian News, which reports on a paper in the journal Molecular Biology and Evolution which challenges the ape to human evolutionary theory. Wait, that's a journal I read regularly. What did I miss?
With one exception. What if there is a crossover event, that is, an exchange of DNA strands, within the inversion? It can get ugly. In the diagram below, there has been a crossover or recombination event between the _ro_ and _ca_ genes. Try tracing the effects on each DNA strand with your finger -- you'll see that some of the strands are going to be really messed up.
Or just look below. The four DNA strands that result from this process are separated to make it clear what happens.
A crossover event involves two strands of DNA out of the total of four, so you still get two uninvolved bystanders, the two NONCROSSOVER PRODUCTS. They're fine and will lead to two normal, healthy gametes with a full genetic complement.
The crossover strands are totally screwed up. One is now dicentric, having two centromeres -- when they're separated at cell division, it will be like a little tug-of-war. This is a gross abnormality in the chromosomes, and will be read as a problem that leads to suppression of division and cell death. The other crossover chromosome is acentric, no centromere at all, as well as being severely truncated and lacking most of the genes present on the chromosome. It will most likely be lost completely during cell division, leading to a genetic deficiency.
The net result of all this finagling is an apparent suppression of crossovers in the progeny. The alleles present at the _e_, _ro_, and _ca_ genes on each chromosome are locked in to each other and aren't easily reshuffled around.
That's all basic genetics. What does evolutionary theory think about inversions?
They are mechanisms that could _reduce_ gene flow between two populations, one that carries the inversion and another that doesn't. It's a process that could contribute to _genetic isolation_ between those populations, and could therefore be part of _speciation_.
I'm not making this up, and I'm not relying on esoteric knowledge to know this: the paper states it clearly in the _opening paragraph_!
Fresh findings in the field of genetics have directly challenged yet another key evolutionary hypothesis by showing that the differences between humans and apes cannot be easily accounted for under the theory of evolution. A recent 12-page journal article, written by three scientists in Spain and published in Molecular Biology and Evolution, details the results of careful analysis of human and chimpanzee DNA. After comparing and contrasting thousands of orthologous genes from humans and chimps, the scientists found their final data to be very much at odds with evolutionary theory. [Oh, _reeeally_?] In fact, they even titled their article “Recombination Rates and Genomic Shuffling in Human and Chimpanzee—A New Twist in the Chromosomal Speciation Theory.”I knocked over my bowl of oatmeal in my haste to track down this "groundbreaking genetic discovery," and got the paper downloaded and read while I sipped my morning tea. Hey, it's from Aurora Ruiz-Herrera's lab -- I know her work. Good stuff. Nice to know she's going to be winning the Nobel prize for toppling evolutionary theory, even if it means I'm going to have to find something new to study. But there's a little contradiction here. The creationist account continues:
Why are these findings seen as a “new twist” to the evolutionary theory? In short, because many scientists have claimed that genetic differences between humans and apes can be attributed to a process known as “genetic recombination,” [They do? News to me.] which is a phenomenon that generates slight genetic variation via meiosis. However, this new journal article seriously calls this proposition into question. In their research, the three Spanish scientists scrutinized differences between human and chimp genes, expecting to find higher genetic recombination rates in these areas of dissimilarity [Are you sure about that, Christian News?]. Even though studies of human-chimp similarities have been conducted in years past, this particular research was unprecedented because the scientists took advantage of new, high-resolution genome maps. Ultimately, the study results were contradictory to what evolutionists had theorized [Really?]. Not only were genetic recombination rates markedly low in areas of human-chimp DNA differences (“rearranged” chromosomes), but the rates were much higher in areas of genetic similarity (“collinear” chromosomes) [Correct.]. This is the reverse of what evolutionists had predicted. [Uh, what?] “The analysis of the most recent human and chimpanzee recombination maps inferred from genome-wide single-nucleotide polymorphism data,” the scientists explained, “revealed that the standardized recombination rate was significantly lower in rearranged than in collinear chromosomes.” [Yes.] Jeffrey Tomkins, a Ph.D. geneticist with the Institute for Creation Research (ICR), told the Christian News Network that these results were “totally backwards” from what evolutionists had predicted, since genetic recombination is “not occurring where it’s supposed to” under current evolutionary theory. [Now, you see, this is where I lose all respect for you, Mr Tomkins.]The problem here is that while the creationists got the main result right, they tried to wedge it into a bungled, fallacious version of evolutionary theory. Ruiz-Herrera has refuted _creationist evolution_ all right, but not the real science that the rest of us study. In fact, it goes the other way and uses detailed genomic maps to _confirm_ a hypothesis about evolution. You didn't expect anything else, did you? This is the way it always turns out. Creationist makes claim, creationist interpretation is bullshit. Let's look at what the paper actually says. But first, a little background. There are a number of common genetic changes that affect rates of recombination -- inversions and translocations. These changes can _suppress_ recombination. For example, look at this pair of complementary chromosomes. One of them carries an inversion: that is, the chunk of DNA that carries the _e_, _ro_, and _ca_ genes is flipped around on one strand, so that the sequence _e_--_ro_--_ca_ on the white strand reads _ca_--_ro_--_e_ on the black strand. This is not a problem for the organism. It still carries two copies of each of the genes, as it should, they're just arranged in different ways on the two chromosomes. This rearrangement does not inhibit pairing during meiosis, either. As you can see in the bottom illustration, the two chromosomes have to get all twisty and kama-sutraey to line up all the genes, but they can do it just fine. So meiosis, the process by which the organism produces gametes like sperm and egg, can work out with no problem. So this is a rearrangement that doesn't affect viability or fertility in any significant way.
With one exception. What if there is a crossover event, that is, an exchange of DNA strands, within the inversion? It can get ugly. In the diagram below, there has been a crossover or recombination event between the _ro_ and _ca_ genes. Try tracing the effects on each DNA strand with your finger -- you'll see that some of the strands are going to be really messed up.
Or just look below. The four DNA strands that result from this process are separated to make it clear what happens.
A crossover event involves two strands of DNA out of the total of four, so you still get two uninvolved bystanders, the two NONCROSSOVER PRODUCTS. They're fine and will lead to two normal, healthy gametes with a full genetic complement.
The crossover strands are totally screwed up. One is now dicentric, having two centromeres -- when they're separated at cell division, it will be like a little tug-of-war. This is a gross abnormality in the chromosomes, and will be read as a problem that leads to suppression of division and cell death. The other crossover chromosome is acentric, no centromere at all, as well as being severely truncated and lacking most of the genes present on the chromosome. It will most likely be lost completely during cell division, leading to a genetic deficiency.
The net result of all this finagling is an apparent suppression of crossovers in the progeny. The alleles present at the _e_, _ro_, and _ca_ genes on each chromosome are locked in to each other and aren't easily reshuffled around.
That's all basic genetics. What does evolutionary theory think about inversions?
They are mechanisms that could _reduce_ gene flow between two populations, one that carries the inversion and another that doesn't. It's a process that could contribute to _genetic isolation_ between those populations, and could therefore be part of _speciation_.
I'm not making this up, and I'm not relying on esoteric knowledge to know this: the paper states it clearly in the _opening paragraph_! More recently, a number of related studies have proposed an alternative explanation by which chromosomal rearrangements could reduce gene flow and potentially contribute to speciation by the suppression of recombination (Noor et al. 2001; Rieseberg 2001). According to this “suppressed recombination” model, chromosome rearrangements could have a minimal influence on fitness, but would suppress recombination leading to the reduction of gene flow across genomic regions and to the accumulation of incompatibilities.That's the part of evolutionary theory the scientists are addressing. It's the idea that regions of DNA that differ, that lead to the differences between two related species, might also be accompanied by genetic changes like inversions that reduced gene flow between the founding populations. It's a component of the speciation process that allowed novel polymorphisms to accumulate in one group without spreading to the other group. Let me try to make this even simpler. THE PREDICTION OF THIS HYPOTHESIS IS THAT REGIONS OF DNA THAT CONTRIBUTE SIGNIFICANTLY TO THE DIFFERENCES BETWEEN TWO SPECIES OUGHT TO ALSO SHOW _HIGHER_ FREQUENCIES OF CHROMOSOMAL REARRANGEMENTS AND _LOWER_ FREQUENCIES OF RECOMBINATION. Master that one sentence and you'll have the gist of this part of evolutionary theory. So, in this paper, what did they find? They used high resolution genomic data to compare recombination rates in regions of the human and chimpanzee genome, predicting _low_ recombination in those areas that are significantly different. Here's the summary:
Overall, our data provide compelling evidence for the existence of low recombination rates within genomic regions that have been rearranged in the chromosomal evolution of human and chimpanzee.Allow me to repeat what creationist geneticist Jeffrey Tomkins said.
Jeffrey Tomkins, a Ph.D. geneticist with the Institute for Creation Research (ICR), told the Christian News Network that these results were “totally backwards” from what evolutionists had predicted, since genetic recombination is “not occurring where it’s supposed to” under current evolutionary theory.Huh. Did he not read that paragraph I quoted from the introduction, that clearly stated the expectation of evolutionary theory, and that the results fit that expectation? Perhaps he skipped over the introduction, knowing it all already. So did he miss this statement in the results?
These data suggest that those chromosomes that have been maintained collinear during evolutionary history retained higher recombination rates than those that have been altered during evolution in each particular lineage.That's the flip side: collinear regions between chimp and human chromosomes retain a conserved arrangement, and have a higher recombination rate. So he didn't read or understand the introduction or the results. Did he comprehend this statement from the discussion?
Using this approach, we provide evidences of a reduction of recombination within genomic regions that have been implicated in the chromosomal evolution between human and chimpanzee.I daresay Mr Tomkins failed to read the whole damned paper! Or stared at it with glazed eyes and struggled to find some imaginary objection he could use to distort it into a rejection of evolution. I'm sorry to say that Dr Ruiz-Herrera will not be winning a Nobel prize for refuting evolution, but she has still made a useful and interesting contribution to the evidence _for_ evolution. ------------------------- Farré M, Micheletti D, Ruiz-Herrera A (2012) Recombination Rates and Genomic Shuffling in Human and Chimpanzee—A New Twist in the Chromosomal Speciation Theory. Mol Biol Evol 30(4):853-864.
I've got a ton of stuff that needs to get done this week, but I don't want the blog to be completely devoid of new content, so here's a quasi-poll question for my wise and worldly readers:
What scientist is most in need of a good popular biography?By "popular biography," I mean things like Norton's Great Discoveries books, several of which Ive reviewed here, including Krauss on Feynman and Reeves on Rutherford, two books that I keep coming back to for useful tidbits. These aren't deep works of historical scholarship, and don't necessarily attempt to be definitive, but focus on being accessible and readable. There are only a small number of these out there, though, and many important scientists don't have this kind of bio yet. So, the question to be answered in comments is: who should get one of these sorts of books that doesn't already have one? I've been reading a lot of history of physics recently for the book-in-progress, specifically about the history of QED, and I think at this point, I'd probably vote for a Wolfgang Pauli biography. This may seem odd, as Pauli was a theorist's theorist, who was so inept in the laboratory that some experimentalists once attributed a lab failure to the fact that Pauli was changing trains in their city at the time that their apparatus broke. At the same time, though, the histories I've been reading put Pauli at or near the center of physics in the mid 20th Century- he contributed to all the major problems, and more importantly seems to have been a key communications nexus. Everybody working on quantum physics appears to have written to and gotten responses from Pauli. And he was pretty entertaining, in a witheringly sarcastic, quirky sort of way. The photo at the top, taken from Roy Glauber's autobiography at the Nobel Prize website is a pretty good indication: Pauli was kicking a soccer ball around, and when he saw Glauber about to take a photo of this, he turned and kicked the ball directly into the camera… So, I bet it'd be fun to read a good popular bio of Pauli. Somebody should get on writing one of those. Who's your favorite scientist who ought to get a good popular biography?
THE BOTTLENECK YEARS
by H.E. Taylor
Chapter 43
Table of Contents
Chapter 45
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CHAPTER 44
AN UNSETTLING MEETING, JULY 19, 2056
With the summer trimester, my schedule changed. Peter cut the UNGETF meetings down to once a month. I no longer had classes on Wednesday, the regular UNGETF meeting day. Usually I went in to work in the lab, but occasionally I stayed at home.
As I walked downtown to the meeting that day, the sun was burning hot. I was sweating within a block. It was uncomfortable and I was thirsty, but mainly I was troubled by my membrane design. My artificial biology project was going nowhere. I kept generating new sequences that ought to work, but which for one reason or another didn't. And I couldn't see why. Some of them went to seed inappropriately. Some curled around, creating a carbon shell that either killed the plant or stifled all growth. Plants had never grown flat and continuously in the fashion I imagined and their genes seemed to know it.
I was distracted when I arrived at the conference. Peter had gone ahead and posed the question: what was going to work? There were several reports. A forensic team from the USSA reported that the initial damage to the Chile balloon was caused by lightning. Makeba greeted this news with a shrug, even though it meant no electronics would have been functioning onboard.
When he was wrapping up, Rhamaposa was particularly blunt. "Methane levels are still rising.
"Group 2 was our best bet in the short term. A new contract has been awarded to a Japanese company with a higher level of quality assurance, although that fact is not being advertised.
"Group 6 is at best a publicity campaign, in my opinion.
"Group 4 is busy planting trees. Industrial scale sequestration is still too expensive.
"Group 5 is being funded, but is still in the early stages."
"And it is unproven technology," objected Barnes.
"I know, I know," Peter held up his hands placatingly. "I'm feeling a little hard pressed here. I don't know how we are going to pull this out of the fire."
His frank admission struck the group. People looked at each other, shifting uneasily.
"Unless one of you happens to have a cheap and easy way to suck more CO2 or methane from the atmosphere…" Rhamaposa looked around the table.
Nobody said a word and I felt impelled to speak up. "I have been trying to create an artificial membrane that will do just that…"
Rhamaposa snapped to attention. "Yes, and…?"
"It's not working. I can't stop it curling."
Peter's face fell and he took a deep breath. "In that case, unless anyone has an objection, I will declare this meeting adjourned."
Nobody said a word and slowly the holograms began to wink out. Dr. Makeba and I locked eyes across the table -- person to hologram for each of us -- then she too disappeared.
Unusually, Peter Barnes' holo lingered and I looked at him curiously.
"Have you looked into using algae?" he asked.
"No."
"I just thought with your background it would be a natural."
I shrugged and his hologram disintegrated.
As I walked home, Rhamaposa's air of dejection lingered with me. I replayed the whole short meeting in my mind. "Algae," Barnes had suggested.
Suddenly I wondered why not?
The more I thought about it, the more sense working with algae made. I wouldn't be trying to replicate millions of years of evolution at the drop of a hat; instead, I could apply my hard won photosynthesis knowledge directly.
The trouble with algae, as the old failed attempts at ocean iron fertilization had shown, was that, like in any dynamic system, as soon as you removed one bottleneck, another one showed up. Give the algae plenty of iron and they ran out of calcium or nitrates, phosphorus or silicon. If only they were on land where they were within easy reach.
Then it hit me. There were algae on land! In the form of lichen! A symbiosis of algae and fungus. Maybe that would work. It was time to to read up on lichen.
-------------------------
Excerpted from _The Bottleneck Years_ by H.E. Taylor
For further information see:
A Gentle Introduction.
Last modified June 11, 2013
A few of the recent pieces I've liked:
NPR Staff on All Things Considered: Water Wars: Who Controls the Flow?
Maryn McKenna at Superbug: The Risks You Don’t Think of: A Plea to Pack a ‘Go Bag’
Dwyer Gunn at Gothamist: Why Working Class Women Are Better Off Injured Than Pregnant
Jay Hancock at Kaiser Health News: Hospital CEO Bonuses Reward Volume and Growth
Brad Plumer at Wonkblog: Why does the government encourage people to build homes in wildfire zones?
Bronze Age rock art along Sweden's south-east coast is rich but not as varied as that of the famous west-coast region. One motif that we have been missing is the four-wheel wagon. It isn't common anywhere except on one site, Frännarp in inland Scania (below right), but we have had none whatsoever where I am.
Wagons at Frännarp in ScaniaThe other day we got our first wagon: at the rich classical site of Himmelstalund on the outskirts of Norrköping in Östergötland province. According to period convention, it is depicted in a flattened perspective with the wheels seen from the sides and the carriage from the top. The drawbar is cut by a later ship (off camera), and it appears that there were never any draught animals. The wagon probably dates from the centuries about 800 BC.
This rock art is carved into the smooth surfaces left by the inland ice. The paint and chalk is recent. The red-painted figure above the Himmelstalund wagon is a pair of incomplete foot soles or shoes. The thin chalk lines represent two ships that appear to have been mostly weathered away before the wagon was carved. People returned to these panels and made additions for centuries.
Note that the person who painted the foot soles didn't see the wagon or the faint ships! This shows how important it is to return to rock art panels regularly with skilled personnel for renewed study. In this case I can take a small amount of avuncular pride in the find, because Theres Furuskog is a long-time collaborator of mine who has done GPS surveying, fieldwalking and metal-detecting with me on many sites in Östergötland and Södermanland. She has also worked for years with cleaning and painting rock art. Her find is a prime example of how important it is to employ educated, intelligent and experienced people for such tasks.
_Another fine first in east-coast rock art was the sun horse of nearby Gärstad, found in 2011._
Wagons at Frännarp in Scania
Amazon has sent a letter to all of its associates based in Minnesota. All Minnesota based associates are being thrown out of the Amazon Associates program as of July 1st. This is because the State of Minnesota passed a bill that Amazon does not like. Amazon may well have a good reason to not like this (or any other) bill, but I'm shocked and dismayed that the response is to strike out against its loyal associates.
This is where fine print rears its ugly head. If the contract between associates and Amazon was a normal business contract, it would not likely be possible to terminate it with just a few days notice. At the moment, Minnesotans who use the Associates program, collectively, have a gazillion links on their web sites and blogs pointing to Amazon, and Amazon will continue to reap the benefits of those links (or force Minnesotan web developers and bloggers to spend considerable effort undoing the links), while Amazon will not be holding up their end of the bargin.
This affects me a little … I've got some Amazon Associate links, though the total income they bring in for me is very small. Still, that is how I was paying the server fee for The X Blog (or at least most of it most months).
I'd love to change the associates links to Barnes and Nobel, but the last time I looked at their associates program it sucked and was difficult to use. Maybe I'll have another look.
This, by the way, is why THIS IS TRUE even though I appear to the the only person on the planet who sees the impending end of civilization as we know it!