We are an ecosystem!!

Viruses in the faecal microbiota of monozygotic twins and their mothers. 
Reyes A, Haynes M, Hanson N, Angly FE, Heath AC, Rohwer F, Gordon JI.

Abstract

Viral diversity and life cycles are poorly understood in the human gut and other body habitats. Phages and their encoded functions may provide informative signatures of a human microbiota and of microbial community responses to various disturbances, and may indicate whether community health or dysfunction is manifest after apparent recovery from a disease or therapeutic intervention. Here we report sequencing of the viromes (metagenomes) of virus-like particles isolated from faecal samples collected from healthy adult female monozygotic twins and their mothers at three time points over a one-year period. We compared these data sets with data sets of sequenced bacterial 16S ribosomal RNA genes and total-faecal-community DNA. Co-twins and their mothers share a significantly greater degree of similarity in their faecal bacterial communities than do unrelated individuals. In contrast, viromes are unique to individuals regardless of their degree of genetic relatedness. Despite remarkable interpersonal variations in viromes and their encoded functions, intrapersonal diversity is very low, with >95% of virotypes retained over the period surveyed, and with viromes dominated by a few temperate phages that exhibit remarkable genetic stability. These results indicate that a predatory viral-microbial dynamic, manifest in a number of other characterized environmental ecosystems, is notably absent in the very distal intestine.

Nature. 2010 Jul 15;466(7304):334-8.

Why is this cool?
Viruses. 'Nuff said.

 If that isn't enough for you, let me explain. The researchers collected fecal matter three times a year from three people: identical twins and the mother of those twins. Then they isolated the DNA from that feces and sequenced it (did they sequence it all? Or just the 16S ribosomal RNA sequences? I don't know yet). They determined what each sequence was and then compared the sequences from each person to each other person. As you know, identical twins have the exact same genome sequence, but mothers only share ~50% genome sequence.

The results show that each person regardless of genetic similarity has their own unique combination of phages (bacterial viruses). In case you didn't know, our intestines are filled with bacteria that provide us many benefits. Amazing, right?
 I find this immensely amazing because if you look at the human with an eye towards our parasites or passengers, it seems to me that WE ARE AN ECOSYSTEM!! Bacteria fill our bowels. Bugs eat our eyelashes. Our skin is covered in bacteria that provide many benefits as well. I don't know the literature at all, but I wonder if someone has done work on determining the number of human, not bacterial, viruses in us at any time. Also, how many bacteria float in our blood?
 I'm starting to see the world as a nesting doll of ecosystems (what constitutes an ecosystem?). First, we have planet Earth! Next, we have North America! Then, we have Alabama! Smaller, we have Huntsville! Smaller, we have a guy eating at a Subway! Next, we have his bowels! In his bowels are bacteria waving the American flag!!

DNA is our genetic material!!!

STUDIES ON THE CHEMICAL NATURE OF THE SUBSTANCE INDUCING TRANSFORMATION OF PNEUMOCOCCAL TYPES : INDUCTION OF TRANSFORMATION BY A DESOXYRIBONUCLEIC ACID FRACTION ISOLATED FROM PNEUMOCOCCUS TYPE III.

Avery OT, Macleod CM, McCarty M.

Abstract

1. From Type III pneumococci a biologically active fraction has been isolated in highly purified form which in exceedingly minute amounts is capable under appropriate cultural conditions of inducing the transformation of unencapsulated R variants of Pneumococcus Type II into fully encapsulated cells of the same specific type as that of the heat-killed microorganisms from which the inducing material was recovered. 2. Methods for the isolation and purification of the active transforming material are described. 3. The data obtained by chemical, enzymatic, and serological analyses together with the results of preliminary studies by electrophoresis, ultracentrifugation, and ultraviolet spectroscopy indicate that, within the limits of the methods, the active fraction contains no demonstrable protein, unbound lipid, or serologically reactive polysaccharide and consists principally, if not solely, of a highly polymerized, viscous form of desoxyribonucleic acid. 4. Evidence is presented that the chemically induced alterations in cellular structure and function are predictable, type-specific, and transmissible in series. The various hypotheses that have been advanced concerning the nature of these changes are reviewed.

J Exp Med. 1944 Feb 1;79(2):137-58.

Why is this cool?

 I have posted a lot about DNA and it only recently occurred to me that I was blank on exactly when DNA was discovered to be our genetic material. This the paper that is credited with ending the debate. Also, notice that it took nine years before the structure of DNA was published after DNA was found to be the genetic material. Previously, people thought that our genetic material could be protein in nature! It seems silly now, but just imagine!

 You find yourself thrust into the world, you know nothing, how do you go about creating the current edifice of SCIENCE? Well, you do so incrementally. For this line of research, (it seems to me) you start with what are organisms made of: cells. Is there something heritable in those cells? Yes. What are those cells made of: proteins, lipids, DNA, RNA, and sugars. Which of those is important for passing along genetic information? Turns out that is it DNA.
 A line of research that I think will be seen in the future if not now, is using other molecules for genetic material in biological life! Creatures maybe could use steroids, estrogen, androgens as the units for the code! How would this change the resulting morphology? What about life with different necessary minerals? Total random thoughts, but I think a human with steroids as genetic material and selenium for maintaining osmotic pressure would probably look something like this:

MOSQUITO ANNIHILATION ATTACK!!!

Genetic elimination of dengue vector mosquitoes.

Wise de Valdez MR, Nimmo D, Betz J, Gong HF, James AA, Alphey L, Black WC 4th.

Abstract

An approach based on mosquitoes carrying a conditional dominant lethal gene (release of insects carrying a dominant lethal, RIDL) is being developed to control the transmission of dengue viruses by vector population suppression. A transgenic strain, designated OX3604C, of the major dengue vector, Aedes aegypti, was engineered to have a repressible female-specific flightless phenotype. This strain circumvents the need for radiation-induced sterilization, allows genetic sexing resulting in male-only releases, and permits the release of eggs instead of adult mosquitoes. OX3604C males introduced weekly into large laboratory cages containing stable target mosquito populations at initial ratios of 8.5-101 OX3604Ctarget eliminated the populations within 10-20 weeks. These data support the further testing of this strain in contained or confined field trials to evaluate mating competitiveness and environmental and other effects. Successful completion of the field trials should facilitate incorporation of this approach into area-wide dengue control or elimination efforts as a component of an integrated vector management strategy.

Proc Natl Acad Sci U S A. 2011 Mar 22;108(12):4772-5. Epub 2011 Mar 7.

Why is this cool? 
 First, what is it? The researchers mutated a mosquito so that females became flightless leading to their death and the impossibility of them producing offspring. They did this in a mosquito that is responsible for spreading dengue fever. Their laboratory cage experiment shows that by adding mutated mosquitoes they saw elimination of the targeted population within 10-20 weeks. Does that mean there were no mosquitoes at the end? I don't know. I will need to read the paper.

 Now , back to the question at hand, why is this cool? Let's step back and see what they did: they made a mutant line and systematically introduced that line back into a somewhat wild population for the result of annihilating that wild population. For any organism that can be mutated, this is a viable plan for shifting the population in a desired direction. It doesn't have to be annihilation, it could be something more interesting like intelligence.

 Let's pretend for a second that the genes responsible for group cooperation and intelligence were discovered for octopus. Maybe some quack would make some change in the octopus genome so that these genes cause more of an effect, ultimately making intelligent, team-working octopi. Now, imagine said quack re-introduced super octopus back into the wild with the end result being super octopus taking over. They would naturally run into man and hide and develop intelligence to battle man! Then we would have to battle for the seas as octopi learn to farm!

The Double Helix!!

Molecular structure of nucleic acids; a structure for deoxyribose nucleic acid.

WATSON JD, CRICK FH.

Nature. 1953 Apr 25;171(4356):737-8.

Why is it cool?

 Today's paper is the seminal work of James Watson and Francis Crick where they present their model of the structure of DNA!! Everyone knows the double helix and the shape has become ingrained in our cultural psyche that references to it abound in any movie about biology. This research may have ushered in the era of biological investigation that currently rules our mindset (or so I think)!
 If you are my age, then you can really get a feel for how close 1953 is to right now. My parents were both born before 1953 and that means that for a brief (2 years) period my parents did not know the structure of DNA! Of course, they didn't know anything at that time because they were both toddlers. It may not seem very close, but we have only known the structure of our genetic material for 58 years! If you have grandparents, they probably don't understand what all the fuss is about.
 If you don't know the structure of the double helix, just imagine twisting a ladder.

REVIEW: Unidentified curved bacilli in the stomach of patients with gastritis and peptic ulceration

 Your stomach hurts from ulcers? Drink milk. Where did those ulcers come from? Stress. This is what I heard all my life before I went to undergrad. It was only then that I learned the vicious truth: my mom is a liar. She spread insidious lies about where christmas gifts come from, where my baby teeth went, and where ulcers come from. It turns out that christmas gifts came from them, my baby teeth went onto a necklace that she wears to this day, and ulcers come from bacteria, Helicobacter pylori to be exact.

 For a long time, people thought that stress was this magical thing that could just destroy your body with plenty of warning, but no scientific basis. Today's paper, published in the Lancet in 1984 showed a correlation between bacteria presence and ulcer incidence. Let me explain.

Despotellis fought Leezle Pon and could definitely take down a sentient H. pylori.

 Prior to the researchers' research, there was a lot of evidence that bacteria were found repeatedly in ulcers, but they were mis-identified and forgotten. The researchers decided to confirm the presence of bacteria in patients with ulcers and then to identify those bacteria. They took 100 patients and questioned them about their lifestyles to determine how the bacteria got in the body. There seemed to be no consistent routes, but burping was more common in patients with bacteria than those without.

 Of these patients, cells were removed from several areas within the gastrointestinal tract and tested for the presence of bacteria. The test for presence of bacteria being smearing on blood agar or chocolate agar plates and waiting for growth, in this case four days. Their data show that duodenal ulcers are always correlated with bacteria and, overall, all ulcers are 87% likely to involve bacteria! Their cultures showed a spiral bacteria with 36 % GC content of the DNA and unique flagella. They initially called it Campylobacter pyloridis, but later it would be changed to Helicobacter pylori.

Polyploidy rocks!!

Polyploidy and ecological adaptation in wild yarrow. 
Ramsey J.

Abstract

Chromosome evolution in flowering plants is often punctuated by polyploidy, genome duplication events that fundamentally alter DNA content, chromosome number, and gene dosage. Polyploidy confers postzygotic reproductive isolation and is thought to drive ecological divergence and range expansion. The adaptive value of polyploidy, however, remains uncertain; ecologists have traditionally relied on observational methods that cannot distinguish effects of polyploidy per se from genic differences that accumulate after genome duplication. Here I use an experimental approach to test how polyploidy mediates ecological divergence in Achillea borealis (Asteraceae), a widespread tetraploid plant with localized hexaploid populations. In coastal California, tetraploids and hexaploids occupy mesic grassland and xeric dune habitats, respectively. Using field transplant experiments with wild-collected plants, I show that hexaploids have a fivefold fitness advantage over tetraploids in dune habitats. Parallel experiments with neohexaploids-first-generation mutants screened from a tetraploid genetic background-reveal that a 70% fitness advantage is achieved via genome duplication per se. These results suggest that genome duplication transforms features of A. borealis in a manner that confers adaptation to a novel environment.

Proc Natl Acad Sci U S A. 2011 Mar 14. [Epub ahead of print]

Why is this cool?

  First off, what does polyploidy mean? What is a ploid? It is a suffix that means chromosome (a loose summary, but whatever). Humans are diploids meaning that we have two copies of our genome/chromosomes in each cell. Most bacteria are monoploids meaning that they got just one copy of their genome/chromosome. Plants are fantastically unique because they can have many copies of their genome/chromosomes in each cell. 

 Today's paper seeks to understand the effects of polyploidy by comparing plants that have differing numbers of genome copies. The researcher compare six copy plants (hexaploids) against four copy plants (tetraploids) in two different environments and sees differences in growth between the two types. The results of the experiments is that hexaploids are better adapted for their environment than tetraploids, but didn't the hexaploid evolve to survive in that environment? Well, the researcher was able to isolate a hexaploid plant from the tetraploid population and it had increased growth than the tetraploid!

 Some of you might be thinking that since plants have so much genetic material, shouldn't they be super intelligent or absurdly complex like humans? Good thoughts, but the answer is no. Plants have a different evolutionary history that doesn't depend on intelligence. Imagine a plant as Helm's Deep, a stationary fortress to hold off any kind of attack. Now consider humans as tanks, they move around and just blow everything up. These are two different strategies necessary to accomplish these goals. As for complexity, I think the better question is: can humans ever be as complex as plants? Plants can communicate with one another. Some can live hundreds of years. Many are entrenched in a vital process that is indispensable to life on Earth. Where do the humans stand?

 What about a human plant hybrid? Which is your favorite?

 My favorite: Man-Thing.

Population genetics of cockroaches!!!

Population genetic structure of the German cockroach (Blattodea: Blattellidae) in apartment buildings.

Crissman JR, Booth W, Santangelo RG, Mukha DV, Vargo EL, Schal C.

Abstract

The German cockroach, Blattella germanica (L.) (Blattodea: Blattellidae), is a major residential pest with the potential to vector various pathogens and produce and disseminate household allergens. Understanding population genetic structure and differentiation of this important pest is critical to efforts to eradicate infestations, yet little is known in this regard. Using highly polymorphic microsatellite markers, we investigated patterns of genetic diversity and differentiation within and among 18 apartments from six apartment complexes located in Raleigh, NC. No departure from panmixia was found between rooms within apartments, indicating that active dispersal resulting in gene flow may occur among rooms within apartment units. Alternatively, aggregations within apartments may exist in relative isolation under a metapopulation framework, derived from a recent, common source. Thus, in the event of population control practices leading to incomplete cockroach eradication within an apartment, recolonization of shelters and rooms is likely to occur from a genetically similar aggregation. A pattern of isolation-by-distance across the six apartment complexes indicated that dispersal was more common within complexes than among them, and F statistics suggested greater genetic similarity between apartments in a single building than between separate buildings of an apartment complex. Similarly, neighbor-joining tree and Bayesian clustering analyses were able to cluster only those apartments that were within a single building, indicating higher dispersal with associated gene flow within buildings than between them. The lack of any broader connectivity, as indicated by significant F(ST) and G-tests suggests that human-mediated dispersal of B. germanica between buildings of an apartment complex or between complexes occurs infrequently enough to have negligible effects on gene flow.

J Med Entomol. 2010 Jul;47(4):553-64.

Why is this cool?

 Humans are thought to have started out as small tribes with little environmental impact. As time progressed and technology improved, it became possible for large masses of humans to congeal into cities and towns. A lot of research has been devoted to understanding the effects in terms of pollution from cities on less developed land, but I think a new line of research will involve determining the genetic changes in organisms to survive life in the city.
Today's article is a push that direction even though it is for disease prevention. The researchers sought to understand the genetic differences between several populations of roaches all within the same city, but located in different apartment complexes. They found that each apartment complex had its own distinct roach as measured by genetic differences at certain positions on the cockroach genome.
 There are a myriad of reasons I think that studying organisms adapting to city survival is amazing. Let me give a quick list:
1. These organisms are acquiring all their nutrients from things we brought into the city and as such it might be a crude estimate of the necessary components of an ecosystem. This may be completely whack, but I don't know better just yet.
2. The city houses most of humanity and that number will only increase over time. As such it is important to understand what our uninvited guests are doing to stay with us.
3. If we can understand what these roaches, bedbugs, and squirrels are doing we can start thinking about constructing the city to invite the kinds of organisms that will make the city healthier or livable.

 Man, squirrels and roaches are serious issues to me. Did you know that a roach will eat dead skin and hair. They have been documented to eat the eyelashes off of babies. Squirrels are more stupendous because they get all their nutrients from our trees and trash. This is a testament to our wastefulness and to a possible genetic difference between forest squirrels and city squirrels. A similar line of thinking goes for roaches, city ones must be different from wild roaches. Where do roaches even occur naturally?
 Imagine that roaches are becoming more intelligent, but a crowd intelligence where a larger group means a larger group! It would be like Exterminators! Have you read that? It is about the ROACH REVOLUTION!!

Binge drinking cure....possibly!!!!

Binge alcohol drinking is associated with GABAA {alpha}2-regulated Toll-like receptor 4 (TLR4) expression in the central amygdala.

Liu J, Yang AR, Kelly T, Puche A, Esoga C, June HL Jr, Elnabawi A, Merchenthaler I, Sieghart W, June HL Sr, Aurelian L.

Abstract

Binge drinking (blood-alcohol levels ≥ 0.08 g% in a 2-h period), is a significant public health burden in need of improved treatment. Gene therapy may offer beneficial alternatives to current psychosocial and pharmacotherapeutic interventions, but identification of the target genes is a clinical challenge. We report that a GABA(A) α2 siRNA vector (pHSVsiLA2) infused into the central nucleus of the amygdala (CeA) of alcohol-preferring (P) rats caused profound and selective reduction of binge drinking associated with inhibition of α2 expression, decreased GABA(A) receptor density, and inhibition of Toll-like receptor 4 (TLR4). CeA infusion of a TLR4 siRNA vector (pHSVsiLTLR4a) also inhibited binge drinking, but neither vector functioned when infused into the ventral pallidum. Binge drinking was inhibited by a GABA(A) α1 siRNA vector (pHSVsiLA1) infused into the ventral pallidum, unrelated to TLR4. The vectors did not alter sucrose intake and a scrambled siRNA vector was negative. The data indicate that GABA(A) α2-regulated TLR4 expression in the CeA contributes to binge drinking and may be a key early neuroadaptation in excessive drinking.


Proc Natl Acad Sci U S A. 2011 Mar 15;108(11):4465-70. Epub 2011 Feb 28.

Why is this cool?

 Like many of you, I drink and sometimes, not often, I drink too much. As a younger lad, I drank profusely and constantly. People suggested that I lay off the sauce, but what did they know?

 

 Well, it turns out that those people told some people and those people outsourced the research to this group. Most alcohol drinkers are calm and relaxed, but there are those (mostly under 25 years old) that just can't stop themselves. It is some sort of mental disorder (total guess on my part) that prevents someone from enjoying drinks in moderation. How do you treat a mental disorder (again, total guess) with such a physical manifestation? These researchers did it by pumping special RNA straight into a rat brain. This may seem trivial, but this is really astounding! The RNA was targeted towards transcription of specific receptors in a specific region of the brain.
 What is RNA? Well, everyone knows that DNA is where our genetic heritage lies, but how does that create us? The DNA is transcribed to RNA, which is essentially a messenger system, and that RNA is translated into protein. Well, it turns out that RNA can do a great many things in the cell, such as inhibit the translation of other RNAs, this RNA is called "short inhibitory RNA" (siRNA). This paper uses specially designed siRNAs  to inhibit receptors associated with binge drinking.
 If you think about far flung future applications, we have ripe story telling potential! Let us say that the treatment here gets translated into pill form or patch or oral liquid form. Sneaky parents would use this treatment on their children to prevent them from binge drinking at bonfires.

Caring bartenders might use the treatment to prevent problem drinkers from getting completely hammered.
 Now, let's consider different problems that may be explained by similar compulsions as found in binge drinking, specifically: binge eating. What if the obesity epidemic that is strangling the highly developed countries could be cured with an orally administered pill?
What if the government mandated that everyone took the pill as a means of ensuring food security? What if controlling the amount of food we eat is the next civil liberty to be taken from us? I think that the government should stop telling me to be skinny and healthy, because my fatness is an expression of FREEDOM!!! 

REVIEW: Inactivation of Organophosphorus Nerve Agents by the Phosphotriesterase from Pseudomonas diminuta

Inactivation of organophosphorus nerve agents by the phosphotriesterase from Pseudomonas diminuta.
Dumas DP, Durst HD, Landis WG, Raushel FM, Wild JR.

Arch Biochem Biophys. 1990 Feb 15;277(1):155-9.

 Let's say that you want to remove a native population, but you do not want to destroy the valuable infrastructure, what do you do? Immediately you should think: chemical weapons! A representation of the potent, chemical weapon sarin is shown below:

 Since these molecules have a fluorine attached (F connected to the P), they degrade very rapidly in water. Given that sarin degrades rapidly in water, it is odd that there exists an enzyme that can degrade this POISONOUS TOXIN!!! So, that is where today's paper comes in, these researchers identified an enzyme that can degrade this compound. To illustrate the fact that this molecule is toxic, you should know that the LD50 is approximately 0.01 mg/kg. Converting that to real numbers, to kill five out of ten Tom Sellecks each Tom Selleck (at 205 lbs) needs to break a single Ritz cracker into 3000 pieces and then eat just one piece.

Enzymes? What are they and what do they do? Enzymes are long strings of molecules with a defined fold that catalyzes some reaction. What molecules is are enzymes composed of? Amino acids, of course. These strings of amino acids fold into many different structures, one of which is shown below.

 The functions catalyzed are amazingly varied and each enzyme is not limited to a single reaction, which comes back to the paper. The enzyme investigated was first identified as a phosphotriesterase, meaning that it can break three bonds on phosphate.  Turns out that it can also break the bonds on sarin and many other herbicides and poisons. Where did they get the enzyme? They took the bacteria Pseudomonas diminuta and isolated the enzyme and then purified it. This enzyme could be have been used to inoculate soldiers in preparation for a chemical attack, but SADLY, USE OF SARIN WAS OUTLAWED IN 1993!!

 This paper is a fine example of typical papers in science: technical and boring. the best papers are from Science or Nature or more prestigious journals because those are the places that entire stories can be told. This is why you will see many papers from Science or Nature here.
 After purifying the enzyme, the researchers added the purified enzyme to some buffer and then added the molecule to be tested. They monitored the progress of the reaction by use of a fluoride electrode which told them the amount of fluoride present over the course of the reaction. They did this for several other molecules, which were also organophosphorus nerve agents.

DOLLY!!!

Sheep cloned by nuclear transfer from a cultured cell line. 
Campbell KH, McWhir J, Ritchie WA, Wilmut I.

Abstract

Nuclear transfer has been used in mammals as both a valuable tool in embryological studies and as a method for the multiplication of 'elite' embryos. Offspring have only been reported when early embryos, or embryo-derived cells during primary culture, were used as nuclear donors. Here we provide the first report, to our knowledge, of live mammalian offspring following nuclear transfer from an established cell line. Lambs were born after cells derived from sheep embryos, which had been cultured for 6 to 13 passages, were induced to quiesce by serum starvation before transfer of their nuclei into enucleated oocytes. Induction of quiescence in the donor cells may modify the donor chromatin structure to help nuclear reprogramming and allow development. This approach will provide the same powerful opportunities for analysis and modification of gene function in livestock species that are available in the mouse through the use of embryonic stem cells.



Nature. 1996 Mar 7;380(6569):64-6.

Why is this cool?
 The 90s were awesome for many scientific reasons: the sequencing of the human genome project was started, the first crystal structure of farnesyl pyrophosphate synthase was solved, and cloning became something serious. In 1996 at the Roslin Institute, researchers cloned a sheep.

What exactly does it mean to "clone" something? To understand that, we need to know that unlike bacteria, sheep cells have a defined and segregated structure for containing the genetic material called the "nucleus." For constructing Dolly, the researchers removed the nucleus from a sheep cell line which they they had cultured and then they inserted that into an embryo that had its nucleus removed previously. This embryo was then inserted into a ewe and they waited until their MIRACLE OF SCIENCE BIRTHED A NEW ERA OF HUMAN POSSIBILITY!!!! To culture a cell line means that they took cells from some random sheep (actually it was not completely random) and grew them.
 A few thoughts on transferring genetic material to embryos. I would like to reveal some of my own ignorance and speak outside my comfort zone, so correct me if I am wrong.

When you are born, your genetic material is "fresh" and "clean" meaning that it has not accumulated the many deadly mutations that cause horrible things like cancer. you may ask "But the genetic material that went into making me came from someone who had the time to accumulate deadly mutations that cause cancer, why am I not born with it?" I just don't know why that is not the case, but years of clean doctor visits have assured me that I and all young people are not born with cancer. So, when you transfer genetic material that has had time to accumulate deadly mutations into an embryo, you would would expect that organism to be prone to cancer. Is this why Dolly was taken from us while she was so young? I don't know. There are many ideas. The techniques that make Dolly possible open a new avenue for studying aging on a genetic level in higher order organisms.
 With all this in mind, we can finally look at Michael Keaton's seminal work Multiplicity (1996) and answer some real questions:

Could he suddenly have full grown clones? No, Dolly was born and raised.
Would clones have to leave and get new jobs as pizza makers? Most likely, pizza making is a challenging line of work and it requires the skills of a sassy gay man, a butch macho man, and some whack job.

THERE WILL BE BLOOD...slowly converted to oil!!!!

THE ORIGIN OF PETROLEUM.
Science. 1889 Oct 4;14(348):228-30.

A PROBABLE ORIGIN OF PETROLEUM.
Roger J.
Science. 1927 Aug 12;66(1702):152.

ORIGIN OF PETROLEUM.
Brooks BT.
Science. 1935 Feb 15;81(2094):176.

ARE FISHES THE PRINCIPAL SOURCE OF PETROLEUM?
Henderson J.
Science. 1935 Feb 15;81(2094):176-7.


The Origin of Petroleum: Effects of Low Temperature Pyrolysis on the Organic Extract of a Recent Marine Sediment.
Whitehead WL, Breger IA.
Science. 1950 Mar 31;111(2883):335-7.

Why is this cool?
 Like many things, we take this simple fact that we take for granted. Imagine finding the black gold one day and building an industry on it. Later, someone would ask "Hey, where did that come from?" How would you as a scientist or thinker even go about figuring out the problem? You would first characterize everything in petroleum. You might look around and see where all those things exist now. Truth be told, I haven't read these articles yet so I'm not privy to the exact random path taken to discover the origin of petroleum. As far as I understand, things die and accumulate on the ground. As these dead things get covered up with dirt and crap like that they find themselves BENEATH THE SURFACE OF THE EARTH!! Under the intense pressure of geological forces (I have the vaguest of vague ideas exactly how that works) those carbon based life forms are converted into power and industry!
 Curiously, whenever I think of oil, I always think of two creatures: 
that black thing from Phantoms

 
and

Hexxus from Ferngully.

  This may be PTSD from Ted Turner's personal war on pollution.

Fungus may have killed the dinosaurs!!!

Fungal virulence, vertebrate endothermy, and dinosaur extinction: is there a connection?

Casadevall A.

Abstract

Fungi are relatively rare causes of life-threatening systemic disease in immunologically intact mammals despite being frequent pathogens in insects, amphibians, and plants. Given that virulence is a complex trait, the capacity of certain soil fungi to infect, persist, and cause disease in animals despite no apparent requirement for animal hosts in replication or survival presents a paradox. In recent years studies with amoeba, slime molds, and worms have led to the proposal that interactions between fungi and other environmental microbes, including predators, select for characteristics that are also suitable for survival in animal hosts. Given that most fungal species grow best at ambient temperatures, the high body temperature of endothermic animals must provide a thermal barrier for protection against infection with a large number of fungi. Fungal disease is relatively common in birds but most are caused by only a few thermotolerant species. The relative resistance of endothermic vertebrates to fungal diseases is likely a result of higher body temperatures combined with immune defenses. Protection against fungal diseases could have been a powerful selective mechanism for endothermy in certain vertebrates. Deforestation and proliferation of fungal spores at cretaceous-tertiary boundary suggests that fungal diseases could have contributed to the demise of dinosaurs and the flourishing of mammalian species.

Fungal Genet Biol. 2005 Feb;42(2):98-106. Epub 2005 Jan 5.

Why?

Today's article is a truly amazing idea! Everyone pretty much believes that a meteorite struck the Earth a long time ago and this caused the extinction of the dinosaurs. The dirt thrown into the air darkened the sky for years and plants could not grow and plant eaters can't flourish with no plants and predators can't live with dwindling food supplies. The author, who I heard speak some years ago, proposes that when the dirt was thrown in the air the normal fungus in the dirt was also thrown and ultimately breathed in by dinosaurs. A word about body temperature, mammals maintain a body temperature of 98.6 F (37 C) no matter the temperature outside. Reptiles, amphibians, and insects do not regulate their body temperature and that is why they are generally restricted to warmer climates or warmer seasons. Fungus can't grow at mammalian body temperature, but it can grow at a slightly reduced normal temperature. Connecting all that, fungus in the air that was breathed in by dinosaurs, who have the perfect temperature for fungal growth, grew inside of the dinosaurs!

The fungal infection killed the dinosaurs! Mammals with their higher body temperature survived and become conquerors of the Earth! Those conquerors went on to produce the greatest human ever born: Lee Marvin.

High altitude adaptation in humans!!

Genetic variations in Tibetan populations and high-altitude adaptation at the Himalayas.
Peng Y, Yang Z, Zhang H, Cui C, Qi X, Luo X, Tao X, Wu T, Ouzhuluobu, Basang, Ciwangsangbu, Danzengduojie, Chen H, Shi H, Su B.

Abstract

Modern humans have occupied almost all possible environments globally since exiting Africa about 100,000 years ago. Both behavioral and biological adaptations have contributed to their success in surviving the rigors of climatic extremes, including cold, strong ultraviolet radiation, and high altitude. Among these environmental stresses, high-altitude hypoxia is the only condition in which traditional technology is incapable of mediating its effects. Inhabiting at >3,000-m high plateau, the Tibetan population provides a widely studied example of high-altitude adaptation. Yet, the genetic mechanisms underpinning long-term survival in this environmental extreme remain unknown. We performed an analysis of genome-wide sequence variations in Tibetans. In combination with the reported data, we identified strong signals of selective sweep in two hypoxia-related genes, EPAS1 and EGLN1. For these two genes, Tibetans show unusually high divergence from the non-Tibetan lowlanders (Han Chinese and Japanese) and possess high frequencies of many linked sequence variations as reflected by the Tibetan-specific haplotypes. Further analysis in seven Tibetan populations (1,334 individuals) indicates the prevalence of selective sweep across the Himalayan region. The observed indicators of natural selection on EPAS1 and EGLN1 suggest that during the long-term occupation of high-altitude areas, the functional sequence variations for acquiring biological adaptation to high-altitude hypoxia have been enriched in Tibetan populations.

Mol Biol Evol. 2011 Feb;28(2):1075-81. Epub 2010 Oct 28.

Why?
 There is an ongoing debate and a sort of naive feeling among people that humans have stopped evolving and all humans are inherently alike, the differences being superficial like skin color. This paper is an illustration that our glorious simian heritage has been adapted to living in the oxygen poor environment of the high mountains. I like thinking about impossible experiments, like ethically impossible experiments. One that I constantly imagine is cross breeding humans Kwisatz Haderach style!

I would start with sickle cell anemic Africans to make the superman malaria proof. I would breed him with a Tibetan to create a high altitude adapted being. This cross would then be breed with a descendant of the black plague, preferably from Germany. Lastly, I would breed this with a Chinese to make it so my superbeing would not be so sweaty. Maybe not so last. I have heard of humans that are predisposed towards massive muscle growth, I need to find a reference, but it would certainly be in there. I can only imagine the copulation between my anemic African, black plague descended German, sweatless Chinese uberbeing and the beef filled monster to finally produce my ANNIHILATION BEAST!!!

P.S. If you haven't seen Dune, you need to join us in the Future.

FISH RESISTANCE!!

Mechanistic Basis of Resistance to PCBs in Atlantic Tomcod from the Hudson River
Isaac Wirgin1,*, Nirmal K. Roy1, Matthew Loftus1, R. Christopher Chambers2, Diana G. Franks3, and Mark E. Hahn3

Abstract

The mechanistic basis of resistance of vertebrate populations to contaminants, including Atlantic tomcod from the Hudson River (HR) to polychlorinated biphenyls (PCBs), is unknown. HR tomcod exhibited variants in the aryl hydrocarbon receptor 2 (AHR2) that were nearly absent elsewhere. In ligand-binding assays, AHR2-1 protein (common in the HR) was impaired as compared to widespread AHR2-2 in binding TCDD (2,3,7,8-tetrachlorodibenzo-p-dioxin) and in driving expression in reporter gene assays in AHR-deficient cells treated with TCDD or PCB126. We identified a six-base deletion in AHR2 as the basis of resistance and suggest that the HR population has undergone rapid evolution, probably due to contaminant exposure. This mechanistic basis of resistance in a vertebrate population provides evidence of evolutionary change due to selective pressure at a single locus.

Science 11 March 2011: Vol. 331 no. 6022 pp. 1322-1325 


Why?

 This paper says that it will show rapid evolution of a higher order organism and that the evolution seen is in response to human actions! It is one of my major interests to do research in how organisms are evolving to fit into our human world. I wonder what the flavor impact of this resistance will be when the fish is prepared. I also wonder, more for the science fiction value, if new organs will develop in the far future to deal with the vast human pollution. I doubt it ever will, but the idea fascinates me!

Review: Transfer of carbohydrate-active enzymes from marine bacteria to Japanese gut microbiota

 When people think about human evolution they usually consider big changes like multiple arms or extra eyes, but the reality is that there are many small changes long before any major change. These small changes occur in our genetic material and can have numerous effects, such as allowing us to process alcohol faster as is the case in alcohol dehydrogenase in peoples of European descent versus peoples of Asian descent. This paper is interesting because evolution is occurring and is opening new food sources to humans, but the thing changing is the genetic material of the microorganisms that live in our gut.
 So, a few words about microorganisms. They are single celled and the term "microorganism" can apply to archaea or bacteria, but for this paper it is bacteria. Humans have 23 chromosomes and two of each of them in each cell except for red blood cells, which don't have any genetic material. The totality of these chromosomes is the human genome. Bacteria only have one chromosome, but some, possibly many, can accept small pieces of DNA from other bacteria. These transferable pieces of DNA are called "plasmids." The transfer of plasmids is responsible for antibiotic resistant strains of Staphylococcus aureus which plague hospitals. This process of transferring plasmids is called "horizontal gene transfer." Many types of bacteria have an outer barrier which is composed of long strings of sugars usually D-galactose or some variation of it. Lastly, bacteria exist everywhere. Every square inch of everything has something growing on it or ready to grow on it should nutrients become available on aforementioned it.
 Now to the paper at hand. The researchers were initially interested in finding enzymes that can breakdown seaweed to its component sugars. By the way, seaweed is a collection of bacteria that grow together and their sugar barriers blend together. The researchers wanted to see what bacteria can eat that sugar barrier and what enzymes are used in that task. To do this they took the sequenced genome of Zobellia galactanivorans and used a computer program to search for genes which code for enzymes most likely to degrade the long sugar chains of seaweed. There search found five genes. Enzymatic analysis showed that only two could degrade seaweed, with Porphyra, commonly known as "nori," being preferentially degraded. These are the first "beta-porphyranases described so far" and represent "a new class of glycoside hydrolases."
 From here, the researchers crystallized those enzymes and identified the features that would allow them to find other enzymes that can degrade nori using the many publicly available sequence databases. During this data mining, they found that all beta-porphyranases were found in marine microorganisms except Bp1689, which is found in the human gut bacterium Bacteroides plebeius.  Curiously, all sequences of B. plebeius are from bacteria collected from Japanese individuals. Genomic sequences of B. plebeius strains collected from western people didn't contain the beta-porphyranase.
 I should give an additional word about microorganisms and their genetic material, they have operons. Operons are genes in very close proximity (<100 basepairs apart) that are part of a metabolic pathway. When studying bacteria, operons are very convenient because they can provide valuable clues about an enzyme's function. The paper, under discussion now, compared the operon of the beta-porphyranase from B. plebeius from Japanese individuals to B. plebeius from western individuals and found many of the former genes to be missing in the latter. Interestingly, the operon from B. plebeius from Japanese individuals is situated between conserved genes coding for "conjugative DNA transfer," suggesting horizontal gene transfer.
 Summing it all up, Z. galactanivorans evolved a beta-porphyranase to degrade nori. Nori is eaten by Japanese people who initially could not digest it. Over the years, the plasmid containing the operon that codes for nori degradation was transferred to B. plebeius in the gut of Japanese people. This allowed Japanese people to eat nori and get some nutritional value out of it. "Tax records from the eighth century list seaweeds as payments to the Japanese government" and since seaweed is not cooked this allows for live bacteria to enter the system.

Second hand smoking and cancer!!!

Non-smoking wives of heavy smokers have a higher risk of lung cancer: a study from Japan.
Hirayama T.

Abstract

In a study in 29 health centre districts in Japan 91 540 non-smoking wives aged 40 and above were followed up for 14 years (1966-79), and standardised mortality rates for lung cancer were assessed according to the smoking habits of their husbands. Wives of heavy smokers were found to have a higher risk of developing lung cancer and a dose-response relation was observed. The relation between the husband's smoking and the wife's risk of developing lung cancer showed a similar pattern when analysed by age and occupation of the husband. The risk was particularly great in agricultural families when the husbands were aged 40-59 at enrolment. The husbands' smoking habit did not affect their wives' risk of dying from other disease such as stomach cancer, cervical cancer, and ischaemic heart disease. The risk of developing emphysema and asthma seemed to be higher in non-smoking wives of heavy smokers but the effect was not statistically significant. The husband's drinking habit seemed to have no effect on any causes of death in their wives, including lung cancer. These results indicate the possible importance of passive or indirect smoking as one of the causal factors of lung cancer. They also appear to explain the long-standing riddle of why many women develop lung cancer although they themselves are non-smokers. These results also cast doubt on the practice of assessing the relative risk of developing lung cancer in smokers by comparing them with non-smokers.


Br Med J (Clin Res Ed). 1981 Jan 17;282(6259):183-5.

Three Domains of LIFE!!

An ancient divergence among the bacteria.

Balch WE, Magrum LJ, Fox GE, Wolfe RS, Woese CR.

Abstract

The 16S ribosomal RNAs from two species of methanogenic bacteria, the mesophile Methanobacterium ruminantium and the thermophile Methanobacterium thermoautotrophicum, have been characterized in terms of the oligonucleotides produced by digestion with T1 ribonuclease. These two organisms are found to be sufficiently related that they can be considered members of the same genus or family. However, they bear only slight resemblance to "typical" Procaryotic genera; such as Escherichia, Bacillus and Anacystis. The divergence of the methanogenic bacteria from other bacteria may be the most ancient phylogenetic event yet detected--antedating considerably the divergence of the blue green algal line for example, from the main bacterial line.

J Mol Evol. 1977 Aug 5;9(4):305-11.

Pandemics new and old!!!

Structural basis of preexisting immunity to the 2009 H1N1 pandemic influenza virus.

Xu R, Ekiert DC, Krause JC, Hai R, Crowe JE Jr, Wilson IA.

Department of Molecular Biology, Scripps Research Institute, 10550 North Torrey Pines Road, La Jolla, CA 92037, USA.

Abstract

The 2009 H1N1 swine flu is the first influenza pandemic in decades. The crystal structure of the hemagglutinin from the A/California/04/2009 H1N1 virus shows that its antigenic structure, particularly within the Sa antigenic site, is extremely similar to those of human H1N1 viruses circulating early in the 20th century. The cocrystal structure of the 1918 hemagglutinin with 2D1, an antibody from a survivor of the 1918 Spanish flu that neutralizes both 1918 and 2009 H1N1 viruses, reveals an epitope that is conserved in both pandemic viruses. Thus, antigenic similarity between the 2009 and 1918-like viruses provides an explanation for the age-related immunity to the current influenza pandemic.



Science. 2010 Apr 16;328(5976):357-60. Epub 2010 Mar 25.

Mass Extinction!!

Has the Earth's sixth mass extinction already arrived?

Barnosky AD, Matzke N, Tomiya S, Wogan GO, Swartz B, Quental TB, Marshall C, McGuire JL, Lindsey EL, Maguire KC, Mersey B, Ferrer EA.

Abstract

Palaeontologists characterize mass extinctions as times when the Earth loses more than three-quarters of its species in a geologically short interval, as has happened only five times in the past 540 million years or so. Biologists now suggest that a sixth mass extinction may be under way, given the known species losses over the past few centuries and millennia. Here we review how differences between fossil and modern data and the addition of recently available palaeontological information influence our understanding of the current extinction crisis. Our results confirm that current extinction rates are higher than would be expected from the fossil record, highlighting the need for effective conservation measures.



Nature. 2011 Mar 3;471(7336):51-7.

HORSES!!

Dietary Change and Evolution of Horses in North America

Matthew C. Mihlbachler1,2,*, Florent Rivals3, Nikos Solounias1,2, and Gina M. Semprebon4

Abstract

The evolution of high-crowned molars among horses (Family Equidae) is thought to be an adaptation for abrasive diets associated with the spread of grasslands. The sharpness and relief of the worn cusp apices of teeth (mesowear) are a measure of dietary abrasion. We collected mesowear data for North American Equidae for the past 55.5 million years to test the association of molar height and dietary abrasion. Mesowear trends in horses are reflective of global cooling and associated vegetation changes. There is a strong correlation between mesowear and crown height in horses; however, most horse paleopopulations had highly variable amounts of dietary abrasion, suggesting that selective pressures for crown height may have been weak much of the time. However, instances of higher abrasion were observed in some paleopopulations, suggesting intervals of stronger selection for the evolution of dentitions, including the early Miocene shortly before the first appearance of Equinae, the horse subfamily in which high-crowned dentitions evolved.

Science 4 March 2011: Vol. 331 no. 6021 pp. 1178-1181 

Epigenetics!!

Epigenetic differences arise during the lifetime of monozygotic twins.

Fraga MF, Ballestar E, Paz MF, Ropero S, Setien F, Ballestar ML, Heine-Suñer D, Cigudosa JC, Urioste M, Benitez J, Boix-Chornet M, Sanchez-Aguilera A, Ling C, Carlsson E, Poulsen P, Vaag A, Stephan Z, Spector TD, Wu YZ, Plass C, Esteller M.

Abstract

Monozygous twins share a common genotype. However, most monozygotic twin pairs are not identical; several types of phenotypic discordance may be observed, such as differences in susceptibilities to disease and a wide range of anthropomorphic features. There are several possible explanations for these observations, but one is the existence of epigenetic differences. To address this issue, we examined the global and locus-specific differences in DNA methylation and histone acetylation of a large cohort of monozygotic twins. We found that, although twins are epigenetically indistinguishable during the early years of life, older monozygous twins exhibited remarkable differences in their overall content and genomic distribution of 5-methylcytosine DNA and histone acetylation, affecting their gene-expression portrait. These findings indicate how an appreciation of epigenetics is missing from our understanding of how different phenotypes can be originated from the same genotype.

Proc Natl Acad Sci U S A. 2005 Jul 26;102(30):10604-9. Epub 2005 Jul 11.

Bacteria that degrade nerve agents!!!

Inactivation of organophosphorus nerve agents by the phosphotriesterase from Pseudomonas diminuta.

Dumas DP, Durst HD, Landis WG, Raushel FM, Wild JR.

Department of Chemistry, Texas A&M University, College Station 77843.

Abstract

The phosphotriesterase from Pseudomonas diminuta was tested as a catalyst for the hydrolysis of phosphofluoridates. The purified enzyme has been shown to hydrolyze the phosphorus-fluorine bond of diisopropyl fluorophosphate, isopropyl methylphosphonofluoridate, and 1,2,2-trimethylpropylmethylphosphonofluoridate at pH 7.0, 25 degrees C, with turnover numbers of 41, 56, and 5 s-1, respectively. The enzymatic rate enhancement for the hydrolysis of sarin at pH 7.0 is 2.2 X 10(7). The turnover number for paraoxon hydrolysis is 2100 s-1. The enzyme does not hydrolyze methanesulfonyl fluoride, phenylmethylsulfonyl fluoride, or O-p-nitrophenyl phenylsulfonate nor do these compounds inactivate or inhibit the ability of the enzyme to hydrolyze diethyl p-nitrophenyl phosphate. The breadth of substrate utility and the efficiency of the hydrolytic reaction exceed the more limited abilities of other prokaryotic and eukaryotic enzymes that catalyze similar reactions. The substantial rate enhancement exhibited by this enzyme for the hydrolysis of a wide variety of organophosphorus nerve agents make this enzyme the prime candidate for the biological detoxification of insecticide and mammalian acetylcholinesterase inhibitors.



Arch Biochem Biophys. 1990 Feb 15;277(1):155-9.