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Thursday, January 31, 2008

Stanley Miller and Life from Ice

If you are able to get a copy of the latest Discover Magazine, I recommend you pick it up. They have a very interesting article about an up and coming theory that life began in the ice. Stanley Miller seemed to have a preference for an ice cold version of abiogenesis, judging by his book "The Origin of Life on Earth" in which he noted that prebiotic molecules have much longer lifespans in ice than in warm water. Before he passed away, he completed a 25 year experiment that he had tended to everyday. It may be the next big break through in prebiotic research. He had mixed ammonia and cyanide and left it to freeze. When it was done, he took it out, and noticed it had had turned a familiar amber color. Upon analyzation it had seven amino acids and eleven nucleobases (building blocks of RNA). To get an idea of just what advantages a cold origin of life has, be sure and check out the following article:

"Did Life Begin in Ice?"

Maybe they're on to something...

Tuesday, January 29, 2008

Answers in Genesis on UFO's

AiG has offered a very ironic article on Alien Life and UFO's. My views on alien life are that bacteria or some simple life may exist in our solar system, and probably elsewhere in the universe, and I think there may even be intelligent life somewhere out there. I do not think that aliens visit us (or ever have) simply because out of all the citings and reports of abduction, no tangible evidence has ever been found to support this notion. I'd like to see an alien body recovered, or at the least, a ship that we could reasonably conclude was not created on earth. I feel that if there is alien life, we may never discover it, due to the fact that we may never develop the technology to travel far enough to discover it (intelligent alien life may, and probably is, very rare and thus likely to be light years away). Nevertheless, I do admire AiG for admitting that if intelligent alien life were ever discovered, it would constitute a falsification of creationism. Now for the irony:

People often want me to explain a sighting of some unknown flying object which they or often a friend have claimed to see. (Sometimes the implication is that if I can’t explain it, it somehow proves that it must be an alien spacecraft; but such reasoning is completely vacuous.1) These kinds of questions are unreasonable. It is one thing to be asked to interpret evidence that we have, but it is unrealistic to ask someone to interpret undocumented second- or third-hand stories with no actual evidence available for inspection.

This reminds me a lot of creationists using flood myths as evidence of a worldwide flood. People from all civilizations have some form of UFO myth, or at least report UFO citings, and this is taken to be evidence of extra-terrestrials. Yet they take flood myths, some of which speak only of a local flood, and use it as evidence that there was a global flood.

The author states the following in his footnotes:
The argument is that alien spacecraft could not be explained by a natural phenomenon. Therefore, it is suggested that witnessing something that cannot be explained naturally must prove the existence of alien spacecraft.

This reminds me a lot of arguments for irreducible complexity or against abiogenesis. "We can't imagine a natural explanation, therefore it must be a direct act of God!"

Sunday, January 27, 2008

The Dishonesty of John Woodmorappe

A creationist named John Woodmorappe has been caught quoting himself. In a "Revolution Against Evolution" Article entitled "A Hands-on Science Activity that Demonstrates the Atheism and Nihilism of Evolution" He states the following:

"Illinois high school science teacher Jan Peczkis writes: The misconception that evolution works towards a pre-determined goal is held by many high school and college students. This is understandable because evolution is an abstract and generally non-observable phenomenon, and living things do seem well-designed for their environments."

He forgot to mention something: He is Jan Peczkis. He quoted himself under his real name (J.W. is his pen name). Why? (For proof see the CreationWiki profile of J.W.)

The list goes on. In an exchange with Talk Origins author Steven Schimmrich, he states,

I find it amusing to see members of Schimmrich's group complain about the intensity of my responses in view of the scurrility of their own remarks (see below). Then again, perhaps some of these people are bullies/crybabies combined: they love to punch others but run home to mama in tears if someone punches them back. And everyone should know by now that I don't put up with any crap from anti-Creationists.

He goes on to compare his debate opponent to the Nazis... Several Times.

Besides the problems with his character, he's also a very illogical person. He is the creationist who proposed Tectonically Associated Biological Provinces (TABs) to explain the order of the fossil record. My understanding is that he believes different geologic rocks represent different ecosystems, which sank in to the earth and were stacked on top of one another like pancakes. Its far out, and not in a cool 70's-ish way. The problem with it is that it does not explain just why the layers on top contain fossils most similar to today's life. I mean, why can't dinosaurs be found on top and human beings in the middle?

Last, but not least, No Answers in Genesis has posted a devasting critique of his work on radiometric dating and more. It is well worth checking out.

Tuesday, January 22, 2008

Evolvable Robots

Panda's thumb has a really cool article about altruism and evolvable robots right now. Check it out!

Abiogenesis For Creationists Part 1

This was written at an online forum in order to counter creationists' constant attacks on abiogenesis. There is an excellent video on the origin of life which does a great job explaining the basics. And of course, due to creationist attacks, the creator of that video had to address some erronous claims.

First of all, there has been an accusation that there's no evidence for the primordial soup. That's simply not true. The primordial soup is just the ocean, with a small amount of chemicals and amino acids. Experimental evidence shows that amino acids can be synthesized under plausible prebiotic conditions.

And even if amino acids could not form on earth, we know that they are carried on meteorites. We know meteorites hit the early earth.

Amino Acids:

Meteors striking the early earth (This link also discusses evidence for the primordial earth being covered in water)

Now, Amino Acids don't automatically mean life. We need a way to get from the soup to life. And here's the most likely way to do that: Form a replicator. A replicator is something that reproduces itself, just like living things. Its copies are mostly like it, displaying true heredity, yet some of them differ in small ways due to copy errors (mutations). If we have replicator, it can make copies slightly different from itself, and they can do the same, and so on. Eventually, this descent with modification should produce something like primitive cells (We know, by the way, that membrane like barriers can form from simple lipids and fatty acids, see Finding Darwin's God, page 276).

And yes, we have observed replicators forming. A famous example is Spiegelman's monster:

"The Qb virus doesn't need anything as complicated as a cell in order to
replicate: a test tube full of suitable chemicals is enough. The
experiment, conducted by Sol Spiegelman of the University of Illinois,
consisted of introducing the viral RNA into a medium containing the RNA's
own replication enzyme, plus a supply of raw materials and some salts, and
incubating the mixture. When Spiegelman did this, the system obligingly
replicated the strands of naked RNA. Spiegelman then extracted some of the
freshly synthesized RNA, put it in a separate nutrient solution, and let it
multiply. He then decanted some of that RNA into yet another solution, and
so on, in a series of steps.
"The effect of allowing unrestricted replication was that the RNA that
multiplied fastest won out, and got passed on to the 'next generation' in
the series. The decanting operation therefore replaced, in a highly
accelerated way, the basic competition process of Darwinian evolution,
acting directly on the RNA. In this respect it resembled an RNA world.
"Spiegelman's results were spectacular. As anticipated, copying errors
occurred during replication. Relieved of the responsibility of working for
a living and the need to manufacture protein coats, the spoon-fed RNA
strands began to slim down, shedding parts of the genome that were no
longer required and merely proved to be an encumbrance. The RNA molecules
that could replicate the fastest simply out-multiplied the competition.
After seventy-four generations, what started out as an RNA strand with
4,500 nucleotide bases ended up as a dwarf genome with only 220 bases. This
raw replicator with no frills attached could replicate very fast. It was
dubbed Spiegelman's monster.
"Incredible though Spiegelman's results were, an even bigger surprise lay
in store. In 1974, Manfred Eigen and his colleagues also experimented with
a chemical broth containing Qb replication enzyme and salts, and an
energized form of the four bases that make up the building blocks of RNA.
They tried varying the quantity of viral RNA initially added to the
mixture. As the amount of input RNA was progressively reduced, the
experimenters found that, with little competition, it enjoyed untrammeled
exponential growth. Even a single RNA molecule added to the broth was
enough to trigger a population explosion. But then something truly amazing
was discovered. Replicating strands of RNA were still produced even when
not a single molecule of viral RNA was added! To return to my architectural
analogy, it was rather like throwing a pile of bricks into a giant mixer
and producing, if not a house, then at least a garage. At first Eigen found
the results hard to believe, and checked to see whether accidental
contamination had occurred. Soon the experimenters convinced themselves
that they were witnessing for the first time the spontaneous synthesis of
RNA strands form their basic building blocks. Analysis revealed that under
some experimental conditions the created RNA resembled Spiegelman's
monster." Paul Davies, The Fifth Miracle, (New York: Simon and Schuster,
1999), p.127-128

(This was copied from the following:

For the peer reviewed paper on the monster, see:

We also know that protein fragments can replicate. Mad Cow Disease is caused by replicating protein fragments:

And of course, there are self replicating peptides (a peptide is the most likely thing to have formed in the primordial soup):

And, finally, what are the odds of a scenario like this happening? I'm going to quote from 2 NCSE articles:

These investigators observe that the building blocks of life (amino acids and other compounds known to form spontaneously) can link together, and some of the compounds formed are "autocatalytic": they cause other amino acids to link up. Something like a primitive metabolism emerges in these models -- and scientists are testing these models in laboratories. Exciting developments in the production of something very close to RNA, a major chemical of life, have recently been announced. If life is capable of self-organization, the criticisms raised by Meyer against "primal soup" biochemistry are irrelevant.

Scientists do not agree on how life began - yet. And "yet" is a very important word in science. One should not assume that just because something is not currently understood that it never will be understood. Meyer suggests that because some models of the natural origin of life have been disproved, we must give up our search and seek a supernatural explanation.

Creationists seem to be proud of their calculations that supposedly show how thermodynamics and probability prevent the chance formation of biologically useful macromolecules such as enzymes. Their "evidence" usually consists of quotations from such authors as Hubert P. Yockey, who agrees that catalytically active proteins cannot occur by chance. Yockey (1977a and b), looking at fully evolved proteins, says that their information content is too high for their chance formation.

Creationists do their own calculations to show that the chance formation of biologically useful proteins is impossible. These calculations almost always involve the erroneous assumption that each of the many amino acid positions in a protein must be filled by the one particular amino acid suitable for that position. Since there are twenty different amino acids available for each position, the chance of randomly getting a string of 200 amino acids all in the right order is (1/20)200. If you plug this expression into a calculator, it will tell you that it equals essentially zero. Thus, the creationists say, you can't get such a protein by a chance ordering of amino acids. As Duane Gish of the Institute for Creation Research (ICR) put it (1976), "The time required for a single catalytically active protein molecule to arise by pure chance would be billions of times the assumed age of the earth."

But proteins, even modern highly evolved specialized proteins, are not built with that degree of specificity. What's more, many proteins show in their structure that they were built of smaller subunit sequences of amino acids (Doolittle, 1981) or they have a simple metalo-organic core that could have functioned alone as a primitive precursor of today's complex enzyme. So the creationist calculations give an answer of zero probability because the creationists make at least two major errors in their assumptions: they assume a degree of specificity that has not been shown to exist in real proteins, and they insist that newly formed proteins must be as efficient as their older and highly evolved counterparts.

We've been trying to explain all this to the protein "experts" at ICR for the last seven years. We have told them that new proteins could indeed form from the random ordering of amino acids. We have warned them that their calculations were based on faulty assumptions and soon someone would document the natural formation of a new protein from the random association of amino acids.

Now it has happened! Not one, but two, new proteins have been discovered. In all probability new proteins are forming by this process all the time, but this seems to be the first documentation of this phenomenon. The newly discovered proteins are enzymes that break down some of the byproducts produced during nylon manufacture. Since nylon first came into commercial production in 1940, we know that the new enzymes have formed since that time.

When the enzymes were first discovered about 1975 (Kino****a, et al, 1981), it was at first thought the new enzymes arose through the modification of preexisting enzymes that had similar functions. To test this notion, the discoverers looked to see if the other enzymes in the same organism would react to antibodies made against the new enzymes. But by this criterion the new enzymes were unique. Antibodies against them found nothing similar with which to react among the array of other enzymes in the organism.

Again it was reasoned that if the new enzymes were just old enzymes with minor changes to allow digestion of nylon byproducts, they should retain at least a slight amount of activity with their original substrates. But the new enzymes had no activity on biologically derived molecules having similar chemical structures. So, by this attribute as well, the new enzymes were seen to be unique.

It seemed that if the new enzymes were indeed derived from randomly ordered amino acids, they would be very inefficient compared to the usual highly evolved enzyme, since the new enzymes would not have had billions of years of natural selection to reach a pinnacle of biological perfection. It has been shown that one of the new enzymes (the linear oligomer hydrolase) has about 2% of the efficiency demonstrated by three other enzymes that perform similar reactions with biologically derived substrates (Kino****a, et al). Thus, by this criterion, as well as the others, the enzyme appears to be newly formed.

More recently, another analysis (Ohno, 1984) added further evidence that at least one of the proteins was formed from an essentially random sequence of amino acids. This evidence is a little bit more difficult to understand since its comprehension involves some understanding of how the genetic code works. I'll just have to refer readers who do not have this background to an explanation such as Suzuki, et. al, 1976. It appears that the DNA that formed the gene was somewhat unusual since it could be "read" without finding a "stop" word in any of the three "reading frames." It can be shown that such DNA sequences could easily occur through the well-known process of duplication. The DNA sequence suggests that a simple "frame-shift" mutation could have brought about the chance formation of at least this one enzyme. "Frame-shift" mutations are known for forming totally new and essentially random arrays of amino acids since the code is "read" in a new reading frame. Usually the proteins that are formed by frame-shift mutations are totally useless sequences of amino acids that have no structural, antigenic, or enzymatic relationship to the original protein. This time, however, the new protein was useful. Being useful, it was retained by natural selection and was finally discovered by biochemists who noticed a bacterium that could live on industrial waste.

All of this demonstrates that Yockey (1977a and b), Hoyle and Wickramasinghe (1981), the creationists (Gish, 1976), and others who should know better are dead wrong about the near-zero probability of new enzyme formation. Biologically useful macromolecules are not so information-rich that they could not form spontaneously without God's help. Nor is help from extraterrestrial cultures required for their formation either. With this information in hand, we can wonder how creationists can so dogmatically insist that life could not have started by natural processes right here on earth.

For more on the odds, please read "Lies, Damned Lies, Statistics and Probability of Abiogenesis"

Keep in mind that there are billions of planets, and out of all the billions of years they orbit their star, and out of all the billions of chemical reactions that take place on them, abiogenesis need only happen once.

Something Irrelevant: Even though cells have not been created in the lab, viruses have!

Sunday, January 20, 2008

The Battle of the Butterflies and the Ants

Reposted from here.

Parasitic caterpillars show local evolution as never before.Butterflies that trick ants into helping to raise their young are driving an evolutionary arms race between the two species, researchers have found. The discovery is important to the conservation of rare Alcon blue butterfies, they say.

Maculinea alcon butterflies infect the nests of Myrmica ants by hatching caterpillars nearby, hoping that the caterpillars will be 'adopted' and cared for by ants that mistake them for their own young. The caterpillars achieve this by mimicking the surface chemistry of the ants. Getting this chemistry right is important: if an ant doesn't recognize a caterpillar as one of its own it will eat it, says David Nash, a zoologist at the University of Copenhagen in Denmark.Successfully adopted caterpillars are bad for the ant colonies, as ants may neglect their own young in favour of the intruders. But the ants are fighting back. "The ant larvae seem to be evolving as a result of being parasitized," says Nash. "It's an ongoing evolutionary arms race."Intruder alert! Intruder alert!Nash and his colleagues tracked the ongoing fight at several sites in Denmark, where caterpillars infiltrate the nests of two types of ants: Myrmica rubra and Myrmica ruginodis . They looked at sites where caterpillars were present and ones where they were absent.M. ruginodis are genetically very similar to each other between populations, the researchers report in Science , and had similar chemical profiles across different populations1. This lack of diversity means that adaptation is difficult: they were relatively consistently susceptible to caterpillar infection, at rates of 8-40%.But M. rubra , the researchers found, had different pockets of colonies with different genetics and different chemical profiles. And there was much more diversity in chemical profiles between colonies that had to deal with the caterpillars than there was outside the area of caterpillar infestation, implying that these colonies were adapting to the presence of the pest.This broad diversity results in a range of susceptibility to caterpillar infection. Infection rates varied widely between 0 and 72% in these ant colonies.And the butterflies are in turn adapting to the different ants. The more ants there are with a specific chemical profile, the more heavily they were infected, showing that the butterflies had adapted to take advantage of the prevalent ants.Running to stay stillThis is a perfect example of a co-evolution between two species, says Jeremy Thomas, a zoologist at the University of Oxford and the Natural Environment Research Council's Centre for Ecology and Hydrology."The study provides a really good and clear cut empirical example of an exciting area of theory," says Thomas. "Local co-evolution has become a really major area of ecology in the last decade. There's a lot of theory on this but there are very few practical examples," he says.

Co-evolutionary battles such as these are examples of what US biologist Leigh Van Valen named Red Queen Theory, after the eponymous character in Lewis Carroll's children's novel Through the Looking Glass . In this book, the Red Queen tells Alice (of Wonderland fame): "Now, here, you see, it takes all the running you can do, to keep in the same place." In evolutionary terms: if the butterflies want to stay where they are, living the high life at the ants' expense, they need to race one step ahead of the evolving ant defences.

Local adaptation such as this has serious implications for the conservation of the butterflies, the researchers say.If a butterfly has evolved to specifically invade the nest of a local ant, it may be chemically different enough to be recognized as a fake by the slightly different ants in other areas.Although the large blue butterfly was successfully reintroduced to the United Kingdom in the 1980s, other reintroductions have failed. It may be that in those cases the ants saw through the disguise, and the would-be nest hijackers instead became dinner.

Thursday, January 17, 2008

Fish out of Water: Your Inner Fish

Retrieved from the University of Chicago:

My knee was swollen to the size of a grapefruit, and one of my colleagues from the surgery department was twisting and bending it to determine whether I had strained or ripped one of the ligaments or cartilage pads inside. This, and the MRI scan that followed, revealed a torn meniscus, the probable result of 25 years spent carrying a backpack over rocks, boulders, and scree in the field. Hurt your knee and you will almost certainly injure one or more of three structures: the medial meniscus, the medial collateral ligament, or the anterior cruciate ligament. So regular are injuries to these three parts of your knee that these three structures are known among doctors as the “Unhappy Triad.” They are clear evidence of the pitfalls of having an inner fish. Fish do not walk on two legs.
Our humanity comes at a cost. For the exceptional combination of things we do—talk, think, grasp, and walk on two legs—we pay a price.
This is an inevitable result of the tree of life inside us. Imagine trying to jerry-rig a Volkswagen Beetle to travel at speeds of 150 miles per hour. In 1933 Adolf Hitler commissioned Dr. Ferdinand Porsche to develop a cheap car that could get 40 miles per gallon of gas and provide a reliable form of transportation for the average German family. The result was the VW Beetle. This history, Hitler’s plan, places constraints on the ways we can modify the Beetle today; the engineering can be tweaked only so far before major problems arise and the car reaches its limit.
In many ways, we humans are the fish equivalent of a hot-rod Beetle. Take the body plan of a fish, dress it up to be a mammal, then tweak and twist that mammal until it walks on two legs, talks, thinks, and has superfine control of its fingers—and you have a recipe for problems. We can dress up a fish only so much without paying a price. In a perfectly designed world—one with no history—we would not have to suffer everything from hemorrhoids to cancer.
Nowhere is this history more visible than in the detours, twists, and turns of our arteries, nerves, and veins. Follow some nerves and you’ll find that they make strange loops around other organs, apparently going in one direction only to twist and end up in an unexpected place. The detours are fascinating products of our past that, as we’ll see, often create problems—hiccups and hernias, for example. And this is only one way our past comes back to plague us.
Our deep history was spent, at different times, in ancient oceans, small streams, and savannahs, not office buildings, ski slopes, and tennis courts. We were not designed to live past the age of 80, sit on our keisters for ten hours a day, and eat Hostess Twinkies, nor were we designed to play football. This disconnect between our past and our human present means that our bodies fall apart in certain predictable ways.
Virtually every illness we suffer has some historical component. The examples that follow reflect how different branches of the tree of life inside us—from ancient humans, to amphibians and fish, and finally to microbes—come back to pester us today. Each of these examples show that we were not designed rationally but are products of a convoluted history.
I. Our hunter-gatherer past: obesity, heart disease, and hemorrhoids.
During our history as fish we were active predators in ancient oceans and streams. During our more recent past as amphibians, reptiles, and mammals, we were active creatures preying on everything from reptiles to insects. Even more recently, as primates, we were active tree-living animals, feeding on fruits and leaves. Early humans were active hunter-gatherers and, ultimately, agriculturalists. Did you notice a theme here? That common thread is the word “active.”
The bad news is that most of us spend a large portion of our day being anything but active. I am sitting on my behind at this very minute typing this, and a number of you are doing the same reading it (except for the virtuous among us who are reading it in the gym). Our history from fish to early human in no way prepared us for this new regimen. This collision between present and past has its signature in many of the ailments of modern life.
What are the leading causes of death in humans? Four of the top ten causes—heart disease, diabetes, obesity, and stroke—have some sort of genetic basis and, likely, a historical one. Much of the difficulty is almost certainly due to our having a body built for an active animal but the lifestyle of a spud.
In 1962 the anthropologist James Neel addressed this notion from the perspective of our diet. Formulating what became known as the “thrifty genotype” hypothesis, Neel suggested that our human ancestors were adapted for a boom-bust existence. As hunter-gatherers, early humans would have experienced periods of bounty, when prey was common and hunting successful. These periods of plenty would be punctuated by times of scarcity, when our ancestors had considerably less to eat.
Neel hypothesized that this cycle of feast and famine had a signature in our genes and in our illnesses. Essentially, he proposed that our ancestors’bodies allowed them to save resources during times of plenty so as to use them during periods of famine. In this context, fat storage becomes very useful. The energy in the food we eat is apportioned so that some supports our activities going on now, and some is stored, for example in fat, to be used later. This apportionment works well in a boom-bust world, but it fails miserably in an environment where rich foods are available 24/7. Obesity and its associated maladies—age-related diabetes, high blood pressure, and heart disease—become the natural state of affairs. The thrifty genotype hypothesis also might explain why we love fatty foods. They are high-value in terms of how much energy they contain, something that would have conferred a distinct advantage in our distant past.
Our sedentary lifestyle affects us in other ways, because our circulatory system originally appeared in more active animals. Our heart pumps blood, which is carried to our organs via arteries and returned to the heart by way of veins. Because arteries are closer to the pump, the blood pressure in them is much higher than in veins. This can be a particular problem for the blood that needs to return to our heart from our feet. Blood from the feet needs to go uphill, so to speak, up the veins of our legs to our abdomen. If the blood is under low pressure, it may not climb all the way. Consequently, we have two features that help the blood move up. The first are little valves that permit the blood to move up, but stop it from going down. The other feature is our leg muscles. When we walk we contract them, and this contraction serves to pump the blood up our leg veins. The one-way valves and the leg-muscle pumps enable our blood to climb from feet to abdomen.
This system works superbly in an active animal, which uses its legs to walk, run, and jump. It does not work well in a more sedentary creature. If the legs are not used much, the muscles will not pump the blood up the veins. Problems can develop if blood pools in the veins, because that pooling can cause the valves to fail. This is exactly what happens with varicose veins. As the valves fail, blood pools in the veins.The veins get bigger and bigger, swelling and taking tortuous paths in our legs.
Needless to say, the arrangement of veins can also be a real pain in the behind. Truck drivers and others who sit for long stretches of time are particularly prone to hemorrhoids, another cost of our sedentary lives. During their long hours of sitting, blood pools in the veins and spaces around the rectum. As the blood pools, hemorrhoids form—an unpleasant reminder that we were not built to sit for too long, particularly not on soft surfaces.
II. Primate past: talk is not cheap.
Talking comes at a steep price: choking and sleep apnea are high on the list of problems we have to live with in order to be able to talk.
We produce speech sounds by controlling motions of the tongue, the larynx, and the back of the throat. All are relatively simple modifications to the basic design of a mammal or a reptile. The human larynx is made up mostly of gill arch cartilages, corresponding to the gill bars of a shark or fish. The back of the throat, extending from the last molar tooth to just above the voice box, has flexible walls that can open and close. We make speech sounds by moving our tongue, by changing the shape of our mouth, and by contracting a number of muscles that control the rigidity of this wall.
Sleep apnea is a potentially dangerous trade-off for the ability to talk. During sleep, the muscles of our throat relax. In most people, this does not present a problem, but in some the passage can collapse so that relatively long stretches pass without a breath. This, of course, can be risky, particularly in people who have heart conditions. The flexibility of our throat, so useful in our ability to speak, makes us susceptible to a form of sleep apnea that results from obstruction of the airway.
Another trade-off of this design is choking. Our mouth leads both to the trachea, through which we breathe, and to our esophagus, so we use the same passage to swallow, breathe, and talk. These three functions can be at odds, for example, when a piece of food gets lodged in the trachea.
III. A hiccup in our tadpole past
This annoyance has its roots in the history we share with fish and tadpoles.
If there is any consolation for getting hiccups, it is that our misery is shared with many other mammals. Cats can be stimulated to hiccup by sending an electrical impulse to a small patch of tissue in their brain stem. This area of the brain stem is thought to be the center that controls the complicated reflex that we call a hiccup. The hiccup reflex is a stereotyped twitch involving a number of muscles in our body wall, diaphragm, neck, and throat. A spasm in one or two of the major nerves that control breathing causes these muscles to contract. This results in a very sharp inspiration of air. Then, about 35 milliseconds later, a flap of tissue in the back of our throat (the glottis) closes the top of our airway. The fast inhalation followed by a brief closure of the tube produces the “hic.”
But we rarely experience only a single hic. Stop the hiccups in the first five to ten hics, and you have a decent chance of ending the bout altogether. Miss that window, and the bout of hiccups can persist for an average of about 60 hics. Inhaling carbon dioxide (by breathing into the classic paper bag) and stretching the body wall (taking a big inhalation and holding it) can end hiccups early in some of us. But not all. Some cases of pathological hiccups can be extremely prolonged. The longest uninterrupted hiccups in a person lasted from 1922 to 1990.
Our tendency to develop hiccups is another influence of our past. There are two issues to think about. The first is what causes the spasm of nerves that initiates the hiccup. The second is what controls that distinctive hic, the abrupt inhalation–glottis closure. The nerve spasm is a product of our fish history, while the hic is an outcome of the history we share with animals such as tadpoles.
First, fish. Our brain can control our breathing without any conscious effort on our part. Most of the work takes place in the brain stem, at the boundary between the brain and the spinal cord. The brain stem sends nerve impulses to our main breathing muscles. Breathing happens in a pattern. Muscles of the chest, diaphragm, and throat contract in a well-defined order. Consequently, this part of the brain stem is known as a “central pattern generator.” This region can produce rhythmic patterns of nerve and, consequently, muscle activation. A number of such generators in our brain and spinal cord control other rhythmic behaviors, such as swallowing and walking.
The problem is that the brain stem originally controlled breathing in fish; it has been jerry-rigged to work in mammals. Sharks and bony fish all have a portion of the brain stem that regulates the rhythmic firing of muscles in the throat and around the gills. The nerves that control these areas all originate in a well-defined portion of the brain stem. We can even see this nerve arrangement in some of the most primitive fish in the fossil record. Ancient ostracoderms, from rocks over 400 million years old, preserve casts of the brain and cranial nerves. Just as in living fish, the nerves that control breathing extend from the brain stem.
This works well in fish, but it is a lousy arrangement for mammals. In fish the nerves that control breathing do not have to travel very far from the brain stem. The gills and throat generally surround this area of the brain. Mammals have a different problem. Our breathing is controlled by muscles in the wall of our chest and by the diaphragm, the sheet of muscle that separates chest from abdomen. Contraction of the diaphragm controls inspiration. The nerves that control the diaphragm exit our brain just as they do in fish, and they leave from the brain stem, near our neck. These nerves, the vagus and the phrenic nerve, extend from the base of the skull and travel through the chest cavity to reach the diaphragm and the portions of the chest that control breathing. This convoluted path creates problems; a rational design would have the nerves traveling not from the neck but from somewhere nearer the diaphragm. Unfortunately, anything that interferes with one of these nerves can block their function or cause a spasm.
If the odd course of our nerves is a product of our fishy past, the hiccup itself is likely the product of our history as amphibians. Hiccups are unique among our breathing behaviors in that an abrupt intake of air is followed by a closure of the glottis. Hiccups seem to be controlled by a central pattern generator in the brain stem: stimulate this region with an electrical impulse, and we stimulate hiccups. It makes sense that hiccups are controlled by a central pattern generator, since, as in other rhythmic behaviors, a typical sequence of events happens during a hic.
It turns out that the pattern generator responsible for hiccups is virtually identical to one in amphibians. And not in just any amphibians—in tadpoles, which use both lungs and gills to breathe. Tadpoles use this pattern generator when they breathe with gills. In that circumstance, they want to pump water into their mouth and throat and across the gills, but they do not want the water to enter their lungs. To prevent it from doing so, they close the glottis, the flap that closes off the breathing tube. And to close the glottis, tadpoles have a central pattern generator in their brain stem so that an inspiration is followed immediately by a closing glottis. They can breathe with their gills thanks to an extended form of hiccup.
The parallels between our hiccups and gill breathing in tadpoles are so extensive that many have proposed that the two phenomena are one and the same. Gill breathing in tadpoles can be blocked by carbon dioxide, just like our hiccups. We can also block gill breathing by stretching the wall of the chest, just as we can stop hiccups by inhaling deeply and holding our breath. Perhaps we could even block gill breathing in tadpoles by having them drink a glass of water upside down.
IV. What’s fishy about hernias
Our propensity for hernias, at least for those hernias near the groin, results from taking a fish body and morphing it into a mammal.
Fish have gonads that extend toward their chest, approaching their heart. Mammals don’t, and therein lies the problem. It is a very good thing that our gonads are not deep in our chest and near our heart (although it might make reciting the Pledge of Allegiance a different experience). If our gonads were in our chest, we wouldn’t be able to have babies.
Slit the belly of a shark from mouth to tail. The first thing you’ll see is liver, a lot of it. The liver of a shark is gigantic. Some zoologists believe that a large liver contributes to the buoyancy of the shark. Move the liver away and you’ll find the gonads extending up near the heart, in the “chest” area. This arrangement is typical of most fish: the gonads lie toward the front of the body.
In us, as in most mammals, this arrangement would be a disaster. Males continuously produce sperm throughout our lives. Sperm are finicky little cells that need exactly the right range of temperatures to develop correctly for the three months they live. Too hot, and sperm are malformed; too cold, and they die. Male mammals have a neat little device for controlling the temperature of the sperm-making apparatus: the scrotum. As we all know, the male gonads sit in a sac. Inside the skin of the sac are muscles that can expand and contract as the temperature changes. Muscles also lie in our sperm cords. Hence, the cold-shower effect: the scrotum will tuck close to the body when it is cold. The whole package rises and falls with temperature. This is all a way to optimize the production of healthy sperm.
The dangling scrotum also serves as a sexual signal in many mammals. Between the physiological advantages of having gonads outside the body wall, and the occasional benefits this provides in securing mates, there are ample advantages for our distant mammalian ancestors in having a scrotum.
The disadvantage is that the plumbing that carries sperm to the penis is circuitous. Sperm travel from the testes in the scrotum through the sperm cord. The cord leaves the scrotum, travels up toward the waist, loops over the pelvis, then goes through the pelvis to travel through the penis and out. Along this complex path, the sperm gain seminal fluids from a number of glands that connect to the tube.
The reason for this absurd route lies in our developmental and evolutionary history. Our gonads begin their development in much the same place as a shark’s: up near our livers. As they grow and develop, our gonads descend. In females the ovaries descend from the midsection to lie near the uterus and fallopian tubes. This ensures that the egg does not have far to travel to be fertilized. In males the descent goes farther.
The descent of the gonads, particularly in males, creates a weak spot in the body wall. To envision what happens when the testes and spermatic cord descend to form a scrotum, imagine pushing your fist against a rubber sheet. In this example, your fist becomes equivalent to the testes and your arm to the spermatic cord. The problem is that you have created a weak space where your arm sits. Where once the rubber sheet was a simple wall, you’ve now made another space, between your arm and the rubber sheet, where things can slip. This is essentially what happens in many types of inguinal hernias in men. Some of these inguinal hernias are congenital—when a piece of the gut travels with the testes as it descends. Another kind of inguinal hernia is acquired. When we contract our abdominal muscles, our guts push against the body wall. A weakness in the body wall means that guts can escape the body cavity and be squeezed to lie next to the spermatic cord.
Females are far tougher than males, particularly in this part of the body. Because females do not have a giant tube running through it, their abdominal wall is much stronger than a man’s.
This is a good thing when you think of the enormous stresses that female body walls go through during pregnancy and childbirth. A tube through the body wall just wouldn’t do. Men’s tendency to develop hernias is a trade-off between our fish ancestry and our mammal present.
V. Mitochondria’s bacterial legacy
Mitochondria exist inside every cell of our bodies, doing a remarkable number of things. Their most obvious job is to turn oxygen and sugars into a kind of energy we can use inside our cells. Other tasks include metabolizing toxins in our livers and regulating different parts of cell function. We notice our mitochondria only when things go wrong. Unfortunately, the list of diseases caused by malfunctioning mitochondria is extraordinarily long and complex. If there is a problem in the chemical reactions in which oxygen is consumed, energy production can be impaired. The malfunction may be confined to individual tissues, say the eyes, or may affect every system in the body. Depending on the location and severity of the malfunction, it can lead to anything from weakness to death.
Many of the processes we use to live reflect our mitochondria’s history. The chain reaction of chemical events that turns sugars and oxygen into usable energy and carbon dioxide arose billions of years ago, and versions of it are still seen in diverse microbes. Mitochondria carry this bacterial past inside of them: with an entire genetic structure and cellular microstructure similar to bacteria, it is generally accepted that they arose from originally free-living microbes over a billion years ago. In fact, the entire energy-generating machinery of our mitochondria arose in one of these kinds of ancient bacteria.
The bacterial past can be used to our advantage in studying the diseases of mitochondria—in fact, some of the best experimental models for these diseases are bacteria. This is powerful because we can do all kinds of experiments with bacteria that are not possible with human cells. One of the most provocative studies was done by a team of scientists from Italy and Germany. The disease they studied invariably kills the infants who are born with it. Called cardioencephalomyopathy, it results from a genetic change that interrupts the normal metabolic function of mitochondria. In studying a patient who had the disease, the team identified a place in the DNA that had a suspicious change. Knowing something about the history of life, they then turned to the microbe known as Paracoccus denitrificans, which is often called a free-living mitochondrion because its genes and chemical pathways are so similar to those of mitochondria. Just how similar was revealed by the European team. They produced the same change in the bacteria’s genes that they saw in their human patient. What they found makes total sense, once we know our history. They were able to simulate parts of a human mitochondrial disease in a bacterium, with virtually the same change in metabolism. This is putting a many-billion-year part of our history to work for us.
The example from microbes is not unique. Judging by the Nobel Prizes awarded in medicine and physiology in the past 13 years, I should have called this book Your Inner Fly, Your Inner Worm, or Your Inner Yeast. Pioneering research on flies won the 1995 Nobel Prize in medicine for uncovering a set of genes that builds bodies in humans and other animals. Nobels in medicine in 2002 and 2006 went to people who made significant advances in human genetics and health by studying an insignificant-looking little worm (C. elegans). Similarly, in 2001, elegant analyses of yeast (including baker’s yeast) and sea urchins won the Nobel in medicine for increasing our understanding of some of the basic biology of all cells. These are not esoteric discoveries made on obscure and unimportant creatures. These discoveries on yeast, flies, worms, and, yes, fish tell us about how our own bodies work, the causes of many of the diseases we suffer, and ways we can develop tools to make our lives longer and healthier.

Tuesday, January 15, 2008

Interesting Evolution News

Blind Cave Fish Can Produce Sighted Offspring

It's a miracle! Blind cavefish, despite having adapted to their lightless environment for more than a million years, can produce sighted offspring in just a single generation, a new study reveals.
The ability was discovered when researchers mated fish from distinct populations that had been isolated in separate caves.

In some cases the first-generation offspring of such unions could see.
The find shows that the genetic mutations causing blindness are different in different lineages of the fish.
"Evolution's palette is varied," said study author Richard Borowsky of New York University in a statement.
"Restoration of the ability to see comes in a single generation because the populations residing in different caves are blind for different reasons—i.e., different sets of genes are nonfunctional in the different populations."

Sunday, January 13, 2008

Flood Geology Hanging Out to Dry

I thought this was interesting:

You don't need a Ph.D. in geology to know that desert dunes and other desert deposits do not form under roaring flood waters. These require not only time, but also dry land. The Flood of Noah supplies neither. The Old Red Sandstone, which looks for all the world like a collection of fossilized desert dunes, was formed in Devonian times. It has outcrops extending from the British Isles to Poland and Russia's White Sea, and from Germany to Norway (Gilluly, Waters, and Woodford, 1968). Outcrops have even been found in Greenland and North America. In Devonian times, before North America and Europe drifted apart, these dunes covered an entire semi-arid continent.

Several lines of evidence derived from this great geologic formation create difficulties for the flood geology model. For instance, the interfingering of these sandstones with marine sediments shows that the shoreline of this continent advanced and retreated several times. Thus the desert rocks are entangled with rocks that the flood geology model says were formed within the one-year-long flood. Also, redbeds, consisting partly of rust formed above sea level, are also
found in this formation. These would not have been formed in any catastrophic flood. The Old Red Sandstones also contain typical playas, complete with their characteristic cubic salt crystal deposits. These are desert salt-pan deposits formed after the rainy-season lakes evaporate. Today, in the Mojave Desert, playas can become lakes for a couple of weeks, only to dry out again, leaving a crust of salt deposits like those found in the Red Sandstone. Although a few freshwater ponds did exist on this ancient semi-arid continent, they dried up from time to time. So, we find fossil mud cracks in the shales that came from the dried-up pond bottoms, and we find fossil lungfish, a type of fish that can survive drought by building a mud cocoon in the pond bottom and breathing air. Hundreds of square miles of fossil sand dunes in these deposits contain cross-bedding and sand-blasted pebbles (ventifacts) of the sort found in modern desert sand dunes, and in no other kind of modern sediment. These different independent lines of evidence converge to show that the Old Red Sandstones almost certainly formed over thousands of years in a dry climate, not in any kind of flood catastrophe.
The Grand Canyon contains fossil desert dunes and other sediments that to all appearances were deposited on dry land. The Permian Coconino Sandstones in the upper walls of the Grand Canyon have the frosted well-sorted wellrounded sand grains found only in land-deposited sand dunes (Shelton, 1966). Furthermore, many of the laminae of the cross-bedding contain fossil footprints that could only have come from reptiles or other quadrupeds climbing up the face of a slightly damp sand dune in the open air. (Those climbing down the slopes left no tracks because they simply slid.) ICR geologist Dr. Steve Austin has taught the theory that amphibians resting between underwater dunes made the tracks. His theory is very interesting, but rather implausible since the Flood must have been violently dumping several meters' worth of sediment per day. The Canyon's Supai and Hermit Shales, found today beneath the Coconino Sandstones, look exactly like river deltas that formed above sea level (Shelton, 1966). Back in Permian times, many quadrupeds (probably reptiles) left their footprints in the soft delta mud. As the mud baked hard in the sun, it formed cracks. The hardness of the baked mud preserved the footprints and mudcracks until the flooded rivers of the rainy season buried them in fresh mud. These fossil prints and mudcracks are found today, as well as iron oxides that form in the open air, showing that these shales formed above sea level.
The pure quarz Navajo Sandstones of Triassic and Jurassic times in Zion National Park, Utah, also look exactly like desert sand dunes (Gilluly, Waters, and Woodford, 1968). They contain extensive cross bedding of the type found in sand dunes, and the frosted sand grains and sand-blasted pebbles found only in dunes formed on the land.

Certain formations in western Wyoming look exactly like deserts that bordered a fitfully receding sea in Carboniferous times (Houlik, 1973). In particular, the Mississippian Lodgepole Formation contains the type of carbonate deposits and evaporites found forming in tidal flats today. The Amsden formation consists of sabkhas and desert dunes. Sabkhas are a kind of hardpan that forms in deserts after hard water seeps up through the ground by capillary action and evaporates leaving nodules of calcite, andhydrite, and other salts. They are seen forming extensively in Saudi Arabia today. Unless Houlik has grossly erred, these sabkhas, casts of evaporite crystals, and fossil dunes show that these Carboniferous deposits formed in a desert, not a flood.

Several times at the end of the Miocene epoch (six to eight million years ago), the Mediterranean Sea dried up, leaving extensive desert deposits on the sea bottom (Hsu, 1972). The Straits of Gibraltar opened and closed, causing these complex changes, as the Glomar Challenger discovered in 1970 by using echo soundings and deep-sea core samples. Each time the Mediterranean slowly dried up, first calcite precipitated around the rim of the basin of the Balearic abyssal plain, then anhydrites and gypsum further in, and finally rock salt in the center at the deepest point. This is just the order that these salts would precipitate if you set out a large saucer of sea water to dry. Successive dryings of the Mediterranean produced hundreds of meters of evaporites. Not only did evaporites form, but also land deposits like sun-baked mud cracks, wind-blown sand, and sabkha anhydrite nodules. Since algae can only grow where sunlight reaches, the stromatolites (a common algae deposit) found in deep sea core samples show that the Mediterranean sea floor, now two miles deep, was once dry land. The Rhone and Nile rivers cut their canyons thousands of feet below current sea level to feed the desiccated Mediterranean basin. Desert-style alluvial fans accumulated from debris washed by cloudbursts down the slopes of Sardinia; now these deposits lie far under the water. After the Mediterranean refilled with water for the last time, at the beginning of the Pliocene, sediments began to accumulate over the evaporites; the weight of these sediments forced evaporites up through weak spots in the sediments to form salt domes. Some of these salt domes are a few miles across, and hundreds to thousands of feet high. Even though such structures may not be forming today, a dried-up Mediterranean could have easily formed them, whereas flood geology is hard pressed to account for such things.

Friday, January 11, 2008

Apologetics Press: Final Round (I promise)

This is an email I got from our old buddy at AP, Kyle Butt (real name):

Hello Ryan, Thanks for writing. No, I am not wrong. Every experiment ever doneverifies that life does not arise from non-living chemicals. You mightnot be convinced, but that is not because the evidence is notconvincing. It is because you are choosing to deny the truth. And you are choosing to apply different standards to your thoughts on Abiogenesis than you apply to almost every other area in your life. Fora refutation of the abiogenesis idea you might check out Anthony Flew's new book "There is a God" or you could read:(link deleted)

If you are honest, youwell know that the "self-replicating" entities projected by many stillfall far short of life, as Robert Hazen has shown in his variouswritings and lectures on the origins of life. You would lose your money.Thanks for writing.
Kyle Butt

I did not send him an email back. I think it is important for us to note the dishonesty. I hand him his ass about vestigial organs, he goes off into the origin of life. This is very typical of creationists: swing from one subject to another until you can find something your opponent doesn't know. When that happens say, "Aha! God must've done it!"

What bothers me even more is that he referenced Anthony Flew. Anthony Flew is a Deist, not a christian. Even so, he was a very vigilant atheist from his youth. I once read that he ran away from home to get away from religion. He wrote several books and spent a great deal of his life defending atheism. And now, in his later years, he has converted to deism: believing in a god who set the world in motion, never to be heard from again. What is disturbing is that it seems christian apologists are using him in his old age and writing books through him. See the New York Times Article for more. Flew said that he converted because abiogenesis was improbable, but later conceded, "I now realize that I have made a fool of myself by believing that there were no presentable theories of the development of inanimate matter up to the first living creature capable of reproduction." Richard Carrier added, in his article about Flew, "Nor has he examined any of the literature of the past five or ten years on the science of life's origin, which has more than answered his call for "constructing a naturalistic theory" of the origin of life. This is not to say any particular theory has been proven--rather, there are many viable theories fitting all the available evidence that have yet to be refuted."

Well, I've gone off topic enough. I'm sure everyone sees what dishonest zealots creationists are, especially those at AP.

Tuesday, January 8, 2008

Debunking Creationist Myths About Woolly Mammoths

I got involved in a debate with a creationist on a site called "Why Won't God Heal Amputees". He brought up Woolly Mammoths and the flood, and cited Answers in Genesis. The Following Questions come from an article at Answers in Genesis, while the answers come from an article at the National Center for Science Education.

How could the animals have endured the extremely cold winters? What would they eat?

William R. Farrand (1961) has investigated claims like these, and laid many of the exaggerations to rest. In particular, he proves that these animals were arctic animals, and he proves that the Berezovka mammoth was really rather putrified. He gives a chart of the plants found in the stomach of the Berezovka mammoth: they are all arctic plants like conifers, tundra grasses, and sedges. The mammoths had a thick insulating underwool beneath their shaggy coat of hair to shield them from the arctic cold. Ice age cave artists painted pictures of mammoths in their caves, a fact that should settle once and for all that the mammoths were arctic creatures.

Most puzzling of all is how did the mammoths and their companions die en masse and how could they have become encased in the permafrost?

The cold Siberian rivers could easily wash carcasses of the mammoths to the river deltas during the spring thaw. I'm sure there were thousands of spring thaws which could cause this. But it should be noted that there is really very little frozen mammoth flesh lying around in Siberia. Farrand points out how only 39 mammoths have been found with some of their flesh preserved; of these, only four have been found more or less intact, including the Berezovka mammoth.

Strangely, scientists investigating three woolly mammoths and two woolly rhinos, including the Beresovka mammoth, found they all died by suffocation. For a live animal to die of suffocation, it had to be buried rapidly or drowned.

Here is some additional evidence that a literal Flood of Noah could not have deposited these mammoth remains:
Farrand points out that we find no other species of frozen animals in Siberia except mammoths and wooly rhinoceri. Since these animals were so big and clumsy, they had trouble crossing crevices in the earth's surface, just as modern elephants do. This evidence fits well with the theory that mammoths fell off cliffs and were killed, fell into holes, were buried in landslides, or were caught and buried in ways that more mobile animals like horses and bison were able to avoid. Yet, if the Flood of Noah were literal history, we would expect to find many different species of frozen animals, not just the mammoth and wooly rhinoceros. Also, the radiocarbon dates taken from various frozen mammoth remains span the time period from 11,450 to 39,000 years before the present, and I dare say, 27,000 years is a little long for Noah's Flood. (Click here to read an article about the accuracy of radiocarbon dating).

Farrand shows that the Berezovka mammoth took several days to freeze. Predators had had a chance to mutilate it before this happened. The excavators found the stench of the partially rotted Berezovka mammoth unbearable; even the earth in which it was buried stank. Histological studies of the flesh showed "deep penetrating chemical alterations as the result of very slow decay."

Sunday, January 6, 2008

What Every Creationist Must DENY

Hello, my fellow bloggers and blog readers alike!

Youtuber CDK007 has just dropped another excellent video, entitled "What Every Creationist Must DENY". One of my favorite parts in it was when he mentioned the volcanic ash layers found between strata. This is an excellent disproof of the flood, since it would require the rushing waters to stop depositing sediment, dry up so the volcanic ash could be laid down, and then go back to depositing sediment. I just can't picture ash somehow settling to the bottom of those supposedly turbulent flood waters without being mixed in with a LOT of sediment.

Saturday, January 5, 2008

"Science, Evolution, and Creationism"

National Acadamies Press has released a new book entitled, "Science, Evolution, and Creationism." You can read the PDF version for free here. One of my favorite passages in the book was,

"In late 2002 several hundred people in China came down with a severe form of pneumonia
caused by an unknown infectious agent. Dubbed “severe acute respiratory syndrome,” or SARS, the disease soon spread to Vietnam, Hong Kong, and Canada and led to hundreds of deaths. In March 2003 a team of researchers at the University of California, San Francisco, received samples of a virus isolated from the tissues of a SARS patient. Using a new technology known as a DNA microarray, within 24 hours the researchers had identified the virus as a previously unknown member of a particular family of viruses — a result confirmed by other researchers using different techniques. Immediately, work began on a blood test to identify people with
the disease (so they could be quarantined), on treatments for the disease, and on vaccines to
prevent infection with the virus. An understanding of evolution was essential in the identification
of the SARS virus. The genetic material in the virus was similar to that of other
viruses because it had evolved from the same ancestor virus. Furthermore, knowledge of the evolutionary history of the SARS virus gave scientists important information about the disease, such as how it is spread. Knowing the evolutionary origins of human pathogens will be critical in the future as existing infectious agents evolve into new and more dangerous forms."

Thursday, January 3, 2008

Updating the Resources

Updates to Evolution Resources:

Added Youtuber Nethius. He's posted a lot of lectures from the Howard Hughes Medical Institute, and they are well worth watching. The 'Selection in Action' series is especially good.

Added an article on Vestigial Organs. This is a very neat article, I encourage everyone to check it out! Here's an excerpt:

In the first chapter of The Descent of Man, Charles Darwin identified roughly a dozen anatomic traits that he gleefully described as “useless, or nearly useless, and consequently no longer subject to natural selection.” The list included body hair, wisdom teeth, and the coccyx—superfluous features that served as Exhibit A in his argument that humans did not descend from “demigods” but rather from a long line of fur-insulated, plant-chewing creatures that sported tails.

A set of cervical ribs—possibly leftovers from the age of reptiles—still appear in less than 1 percent of the population. They often cause nerve and artery problems.

This small muscle stretching under the shoulder from the first rib to the collarbone would be useful if humans still walked on all fours. Some people have one, some have none, and a few have two.

This long, narrow muscle runs from the elbow to the wrist and is missing in 11 percent of modern humans. It may once have been important for hanging and climbing. Surgeons harvest it for reconstructive surgery.

Our closest cousins, chimpanzees and gorillas, have an extra set of ribs. Most of us have 12, but 8 percent of adults have the extras.

    More than 20 percent of us lack this tiny, triangular pouchlike muscle that attaches to the pubic bone. It may be a relic from pouched marsupials.

    These fused vertebrae are all that’s left of the tail that most mammals still use for balance and communication. Our hominid ancestors lost the need for a tail before they began walking upright.

While some have suggested that the coccyx helps to anchor minor muscles and may support pelvic organs, surgically removing it has no discernible effect on health.

(One Minor Note: The lady who authored this article lists the appendix as vestigial. It is vestigial, even though a minor use for it was recently discovered. And by the way, the scientists who discovered it said that in sanitary countries the appendix would probably not be needed.)

An Update to the Creationism Resources:

The NCSE's Evolution/Creation Archives

This is an archive of the Creation/Evolution Journal from 1980 through 1990. It is very good, easy to read, and overall a nice resource.

Wednesday, January 2, 2008

The Debate with Apologetics Press Continues...

Hey Everyone! Do you guys remember the debate I had started with Apologetics Press? Well, I got a couple of messages in my mailbox, so I'll share them with you- with my responses, naturally:

Hello Ryan,
I am now back in the office and can respond
to your statements. There is an excellent
book on the subject of vestigial organs.
It is written by Jerry Bergman, Ph.D. and
George Howe, Ph.D. They quote Alfred Kinsey,
a respected author from the 1920s. I will
give you the entire quote: "is the collection
of small and useless structures which are always to be
found in species. Vestiges we call them.
They appear to be remnants of things that
were well developed and had some use among ancestral
organisms, but which have now almost
disappeared in more devoloped forms. . . .
Vestiges are similar to G's in English words
as reign and sign. The latter is not pronounced
in those words, and is now useless, but it is
positive evidence of their origin from the older
Latin words, regnum and signum" The authors also quote
Arthur Thompson, from 1958 in Riddles of Science:
"In our body we carry about several scores of
useless relics which tell us some things about the past."
It is an undeniable fact that many evolutionists
have taught that vestigial organs are "useless."
Those who attempt to alleviate the evolutionary
vestigial argument by changing the definition to
"not as good, but not useless" have been forced
to do so by the overwhelming evidence that
the organs are quite useful. In fact, the
"not as good" argument is false as well, which
doctors Bergman and Howe artfully show.
I hope you will post this on your blog,
as well as the title of Bergman and Howe's book:
"Vestigial Organs are Fully Functional." Thanks for writing.

Kyle Butt

My response:

Hi Kyle,

I realize some people do think/thought vestigial
organs are totally useless. However, the quote I gave
you from Darwin supports the fact that evolutionists
have always realized vestigial organs aren't totally
useless. Talk Origins' 29 Evidences for MacroEvolution
discusses several definitions given in encyclopedias
and reference books from many time periods, from the
1980's to the 1950's and even before then.

Besides this, there are organs that we know of that
appear to serve no function, and are even COMPLETELY
GONE from large portions of the population. This is
what we would expect if the organ was useless and
beginning to "evolve away". Here are some examples:
A set of cervical ribs—possibly leftovers from the age
of reptiles—still appear in less than 1 percent of the
population. They often cause nerve and artery

This small muscle stretching under the shoulder from
the first rib to the collarbone would be useful if
humans still walked on all fours. Some people have
one, some have none, and a few have two.

This long, narrow muscle runs from the elbow to the
wrist and is missing in 11 percent of modern humans.
It may once have been important for hanging and
climbing. Surgeons harvest it for reconstructive

Often mistaken for a nerve by freshman medical
students, the muscle was useful to other primates for
grasping with their feet. It has disappeared
altogether in 9 percent of the population.

Our closest cousins, chimpanzees and gorillas, have an
extra set of ribs. Most of us have 12, but 8 percent
of adults have the extras.

The Debate with Apologetics Press Continues... Part 2

His second email:

Hey Ryan,
One more thing. I can prove the negative
that the human body has not evolved.
Here is the argument. The Law of Biogenesis
says that life in the material Universe
comes only from previous life of its own kind.
According to evolution, life had to
spontaneously generate from non-living
chemicals, then change into millions of
different kinds. Evolution would violate
the Law of Biogenesis. Thus, the human body did
not evolve.

Kyle Butt

My reply:

Hey Kyle,

You're wrong. Abiogenesis is not
within the province of evolution.
It is (barely) in the province of
biology (It's almost closer to
chemistry). Even if God created
the first cell, it is still very
possible that that cell evolved
into all the life we see around us.

I'm not convinced that abiogenesis
is impossible. Even though seems
like a trivial observation that life
doesn't come from non-life, we have
to stop and think. Are the lines
between life and non-life solid or
blurry? I say blurry, because we
have discovered things that meet
some definitions of life and do not
satisfy others. The virus is one
example. Another example is the
replicating entities formed in the
laboratory. If I could, I'd
put my money on life beginning
as a simple, self replicating entity. A
peptide or something like that.
Here are some of the experiments:

The Replicating Peptide
Self Replicating DNA


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text:
Mennock Pass 16.07.17

7:00 am

ACC club ride for Sunday will be Mennock Pass pictures and report to follow

G1 07.00 leaving from Peters Barbers Shop, Airdrie

G2 07.45 Carluke Tesco (A73) ML12 5AL

G3 09.15 @ junction of B7078/B740

if all riders can be ready for the depart @ times stated this will save riders waiting Thanks

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Abbreviation : ADSCs
Long Form : adipose-derived stem cells
No. Year Title Co-occurring Abbreviation
2021 In vitro cartilage differentiation of human adipose-derived mesenchymal stem cell spheroids cultured in porous scaffolds. ---
2021 Nature-inspired topographies on hydroxyapatite surfaces regulate stem cells behaviour. HAP
2020 "Improving In Vitro Cartilage Generation by Co-Culturing Adipose-Derived Stem Cells and Chondrocytes on an Allograft Adipose Matrix Framework". AAM, ACs
2020 3D Culture Facilitates VEGF-Stimulated Endothelial Differentiation of Adipose-Derived Stem Cells. PEG
2020 A bioengineering approach to Schlemm's canal-like stem cell differentiation for in vitro glaucoma drug screening. HSC, HTM
2020 A novel 3D indirect co-culture system based on a collagen hydrogel scaffold for enhancing the osteogenesis of stem cells. ---
2020 A possible injectable tissue engineered nucleus pulposus constructed with platelet-rich plasma and ADSCs in vitro. GAG, PRP
2020 Adipocyte-progenitor cell communication that influences adipogenesis. ---
2020 Adipose derived stem cells and platelet rich plasma improve the tissue integration and angiogenesis of biodegradable scaffolds for soft tissue regeneration. PRP
10  2020 Adipose mesenchymal stem cell-derived extracellular vesicles containing microRNA-26a-5p target TLR4 and protect against diabetic nephropathy. CCK-8, DN, EVs, HG, miRs, MSCs, TLR4, VEGF-A
11  2020 Adipose Tissue From Type 1 Diabetes Mellitus Patients Can Be Used to Generate Insulin-Producing Cells. IPCs, PDL1, T1DM
12  2020 Adipose tissue-derived mesenchymal stem cells and chitosan/poly (vinyl alcohol) nanofibrous scaffolds for cartilage tissue engineering. CS, FE/SEM, FTIR, OA
13  2020 Adipose Tissue-Derived Stem Cell Sheet Improves Glucose Metabolism in Obese Mice. CM, HF/HSD, TNF-alpha
14  2020 Adipose Tissue-derived Stem cells in Plastic and Reconstructive Surgery: A Bibliometric Study. ---
15  2020 Adipose tissue-derived stem cells modulate immune function in vivo and promote long-term hematopoiesis in vitro using the aGVHD model. aGVHD, BMSCs, IL, INF
16  2020 Adipose tissue-derived stem cells suppress coronary arteritis of Kawasaki disease in vivo. KD, PBS
17  2020 Adipose tissue-derived stem cells upon decellularized ovine small intestine submucosa for tissue regeneration: An optimization and comparison method. OSIS, SDS
18  2020 Adipose tissue-derived stromal cells stimulated macrophages-endothelial cells interactions promote effective ischemic muscle neovascularization. BMDCs
19  2020 Adipose-Derived Biogenic Nanoparticles for Suppression of Inflammation. EVs, Lipo-NPs
20  2020 Adipose-Derived Mesenchymal Stem Cell Treatments and Available Formulations. ---
21  2020 Adipose-derived mesenchymal stem cells alleviate TNBS-induced colitis in rats by influencing intestinal epithelial cell regeneration, Wnt signaling, and T cell immunity. CD, GFP, IECs, TNBS
22  2020 Adipose-derived mesenchymal stem cells and extracellular vesicles confer antitumor activity in preclinical treatment of breast cancer. ADSC-EVs, EVs, MSCs
23  2020 Adipose-derived mesenchymal stem cells protect against CMS-induced depression-like behaviors in mice via regulating the Nrf2/HO-1 and TLR4/NF-kappaB signaling pathways. CMS, LPS, Nrf2
24  2020 Adipose-derived mesenchymal stem cells-derived exosome-mediated microRNA-342-5p protects endothelial cells against atherosclerosis. HUVECs, miRNAs
25  2020 Adipose-derived mesenchymal stromal cells promote corneal wound healing by accelerating the clearance of neutrophils in cornea. CWH
26  2020 Adipose-derived mesenchymal stromal cells suppress osteoclastogenesis and bone erosion in collagen-induced arthritis. CIA, CII/CFA, M-CSF, RA, RANKL, TRAP
27  2020 Adipose-derived stem cell sheet under an elastic patch improves cardiac function in rats after myocardial infarction. ---
28  2020 Adipose-derived stem cell therapy shows promising results for secondary lymphedema. ---
29  2020 Adipose-derived stem cell-conditioned medium protects fibroblasts at different senescent degrees from UVB irradiation damages. ADSC-CM, HDFs, PDGF-AA
30  2020 Adipose-Derived Stem Cells (ADSCs) Loaded Gelatin-Sericin-Laminin Cryogels for Tissue Regeneration in Diabetic Wounds. ADSC, GS, ROS
31  2020 Adipose-derived stem cells and cancer cells fuse to generate cancer stem cell-like cells with increased tumorigenicity. BCCs, CSC
32  2020 Adipose-Derived Stem Cells Can Replace Fibroblasts as Cell Control for Anti-Tumor Screening Assay. DFs, SEIs
33  2020 Adipose-Derived Stem Cells for Regenerative Wound Healing Applications: Understanding the Clinical and Regulatory Environment. ---
34  2020 Adipose-derived stem cells integrate into trabecular meshwork with glaucoma treatment potential. IOP, TM
35  2020 Adipose-derived stem cells modified by BDNF gene rescue erectile dysfunction after cavernous nerve injury. lenti-rBDNF
36  2020 Adipose-Derived Stem Cells Modulate BV2 Microglial M1/M2 Polarization by Producing GDNF. GDNF, MG, PI3K
37  2020 Adipose-Derived Stem Cells Primed with Paclitaxel Inhibit Ovarian Cancer Spheroid Growth and Overcome Paclitaxel Resistance. CM, OvCa, PTX, PTX
38  2020 Adipose-Derived Stem Cells Promote Intussusceptive Lymphangiogenesis by Restricting Dermal Fibrosis in Irradiated Tissue of Mice. LEC, LYVE-1, VEGF
39  2020 Adipose-Derived Stem Cells Protect Ischemia-Reperfusion and Partial Hepatectomy by Attenuating Endoplasmic Reticulum Stress. ERS, IR, IRI, MSCs
40  2020 ADSC-Exos containing MALAT1 promotes wound healing by targeting miR-124 through activating Wnt/beta-catenin pathway. ---
41  2020 ADSCs inhibit photoaging- and photocarcinogenesis-related inflammatory responses and extracellular matrix degradation. UV
42  2020 Ameliorated healing of biliary anastomosis by autologous adipose-derived stem cell sheets. ---
43  2020 Analysis of Adipose-Derived Stem Cells from Different Donor Areas and Their Influence on Fibroblasts In Vitro. ---
44  2020 Angiotensin receptor subtypes regulate adipose tissue renewal and remodelling. RAS
45  2020 Application and prospect of adipose stem cell transplantation in treating lymphedema. ---
46  2020 Aspiration-assisted bioprinting of the osteochondral interface. AAB, OC
47  2020 Assessment of ability of human adipose derived stem cells for long term overexpression of IL-11 and IL-13 as therapeutic cytokines. ---
48  2020 Astragaloside IV Promotes Antiphotoaging by Enhancing the Proliferation and Paracrine Activity of Adipose-Derived Stem Cells. ASI, ELISA, MMP1
49  2020 AURKA Enhances Autophagy of Adipose Derived Stem Cells to Promote Diabetic WoundRepair via Targeting FOXO3a. ---
50  2020 Autologous fat graft assisted by stromal vascular fraction improves facial skin quality: A randomized controlled trial. CAL, SVF
51  2020 Autologous Fractionated Adipose Tissue as a Natural Biomaterial and Novel One-Step Stem Cell Therapy for Repairing Articular Cartilage Defects. MF
52  2020 Autologous transplantation of adipose-derived stromal cells combined with sevoflurane ameliorates acute lung injury induced by cecal ligation and puncture in rats. ALI, CLP
53  2020 Beneficial Effect of IL-4 and SDF-1 on Myogenic Potential of Mouse and Human Adipose Tissue-Derived Stromal Cells. ---
54  2020 Biocompatible Crosslinked Nanofibers of Poly(Vinyl Alcohol)/Carboxymethyl-Kappa-Carrageenan Produced by a Green Process. CMKC, PVA
55  2020 Bone marrow- and adipose tissue-derived mesenchymal stem cells from donors with coronary artery disease; growth, yield, gene expression and the effect of oxygen concentration. BMSCs, MSCs
56  2020 Bone regeneration in rabbit calvarial defects using PRGF and adipose-derived stem cells: histomorphometrical analysis. BBM, PRGF
57  2020 Bone regeneration of minipig mandibular defect by adipose derived mesenchymal stem cells seeded tri-calcium phosphate- poly(D,L-lactide-co-glycolide) scaffolds. TCP
58  2020 Bone tissue engineering using adipose-derived stem cells and endothelial cells: Effects of the cell ratio. ALP, HUVECs
59  2020 Cardiac Differentiation of Adipose Tissue-Derived Stem Cells Is Driven by BMP4 and bFGF but Counteracted by 5-Azacytidine and Valproic Acid. 5'-aza, bFGF, BMP4, RT-PCR, VPA
60  2020 Cell-Free Fat Extract Increases Dermal Thickness by Enhancing Angiogenesis and Extracellular Matrix Production in Nude Mice. ---
61  2020 Chitosan modified Fe3O4/KGN self-assembled nanoprobes for osteochondral MR diagnose and regeneration. KGN, MR
62  2020 CircHivep2 contributes to microglia activation and inflammation via miR-181a-5p/SOCS2 signalling in mice with kainic acid-induced epileptic seizures. circRNA, KA
63  2020 CircRNA-vgll3 promotes osteogenic differentiation of adipose-derived mesenchymal stem cells via modulating miRNA-dependent integrin alpha5 expression. circRNAs, CPC, ITGA5
64  2020 Co-culture of Adipose-Derived Stem Cells and Chondrocytes With Transforming Growth Factor-Beta 3 Promotes Chondrogenic Differentiation. ---
65  2020 Co-overexpression of VEGF and GDNF in adipose-derived stem cells optimizes therapeutic effect in neurogenic erectile dysfunction model. ADSC-V, BCNI, ED, MPG
66  2020 Co-transplantation with adipose-derived cells to improve parathyroid transplantation in a mice model. EYA1, FGF, SVFs, VEGF
67  2020 Combination of low intensity electromagnetic field with chondrogenic agent induces chondrogenesis in mesenchymal stem cells with minimal hypertrophic side effects. EMF, PRP
68  2020 Combinational therapy with antibiotics and antibiotic-loaded adipose-derived stem cells reduce abscess formation in implant-related infection in rats. ---
69  2020 Combined Transplantation of Adipose Tissue-Derived Stem Cells and Endothelial Progenitor Cells Improve Diabetic Erectile Dysfunction in a Rat Model. DED, ED, EPCs, ICP, MAP, PBS, SDF-1, VEGF
70  2020 Comparative Analysis of Adipose-Derived Stromal Cells and Their Secretome for Auricular Cartilage Regeneration. IGF-1, TGF-beta1
71  2020 Comparative impact of platelet rich plasma and transforming growth factor-beta on chondrogenic differentiation of human adipose derived stem cells. ALP, PRP, TGF-beta, TNF-alpha, VEGF
72  2020 Comparison of the proteome patterns of adipose-derived stem cells with those treated with selegiline using a two dimensional gel electrophoresis analysis. BLAST, NF68, NP, PKC-eta
73  2020 Constructing a Sr2+-Substituted Surface Hydroxyapatite Hexagon-Like Microarray on 3D-Plotted Hydroxyapatite Scaffold to Regulate Osteogenic Differentiation. HA
74  2020 Controlling the Poly(epsilon-caprolactone) Degradation to Maintain the Stemness and Function of Adipose-Derived Mesenchymal Stem Cells in Vascular Regeneration Application. DP, PCL
75  2020 Cryopreservation of lipoaspirates: in vitro measurement of the viability of adipose-derived stem cell and lipid peroxidation. CFU
76  2020 Cystine transporter expression is a marker to identify a subpopulation of canine adipose-derived stem cells. xCTLo
77  2020 Cytoprotective Effects of Mesenchymal Stem Cells During Liver Transplantation From Donors After Cardiac Death in Swine. DCDs, HB, MSCs
78  2020 Data supporting exosome laden oxygen releasing antioxidant and antibacterial cryogel wound dressing OxOBand alleviate diabetic and infectious wound healing. DLS, P. aeruginosa, PUAO, S. aureus, SEM
79  2020 Depletion of the diabetic gut microbiota resistance enhances stem cells therapy in type 1 diabetes mellitus. MSC, T1DM
80  2020 Differences in the Inflammatory Response of White Adipose Tissue and Adipose-Derived Stem Cells. L-WAT, TNF-alpha
81  2020 Differential gene expression by lithium chloride induction of adipose-derived stem cells into neural phenotype cells. DMEM, FBS, LiCl, NFH, NfL, NLCs, qRT-PCR
82  2020 Differentiated adipose-derived stem cells promote peripheral nerve regeneration. dADSCs, PGA-c
83  2020 Dual delivery of stem cells and insulin-like growth factor-1 in coacervate-embedded composite hydrogels for enhanced cartilage regeneration in osteochondral defects. Coa, GFs, IGF-1, IPN, PEAD, PEGDA
84  2020 Dual functional nanoparticles containing SOX duo and ANGPT4 shRNA for osteoarthritis treatment. ANGPT4, DEX PEI, MC, MMPs, OA, SOX
85  2020 Effect of ascorbic acid on morphology of post-thawed human adipose-derived stem cells. DMEM, FBS, LAA2P
86  2020 Effect of Breast Cancer and Adjuvant Therapy on Adipose-Derived Stromal Cells: Implications for the Role of ADSCs in Regenerative Strategies for Breast Reconstruction. PMBR
87  2020 Effect of cAMP Signaling Regulation in Osteogenic Differentiation of Adipose-Derived Mesenchymal Stem Cells. cAMP, Id2, MSCs, OM, PKA
88  2020 Effect of Collagen Scaffold With Bcl-2-Modified Adipose-Derived Stem Cells on Diabetic Mice Wound Healing. ---
89  2020 Effect of exosomes from adipose-derived stem cells on the apoptosis of Schwann cells in peripheral nerve injury. ADSC-Exo, PNI, SCs
90  2020 Effect of Intracorporeal Human Adipose-Derived Stem Cells (hADSCs) on Corpora Cavernosa Transforming Growth Factor beta1 (TGFbeta1) and Collagen Type I Concentration in Wistar Rat Priapism Model. hADSC, hADSCs, TGF-beta1
91  2020 Effect of Mineral Pitch on the Proliferation of Human Adipose Derived Stem Cells on Acellular Scaffold. DAPI, ECM, FESEM, HMGB1, RT-PCR, SDF1
92  2020 Effect of the deuterium on efficiency and type of adipogenic differentiation of human adipose-derived stem cells in vitro. ---
93  2020 Effects of scaffold geometry on chondrogenic differentiation of adipose-derived stem cells. ---
94  2020 Efficacy of adipose derived stem cells on functional and neurological improvement following ischemic stroke: a systematic review and meta-analysis. SMD
95  2020 Efficient isolation and proliferation of human adipose-derived mesenchymal stromal cells in xeno-free conditions. hADSCs
96  2020 Encapsulation of troglitazone and AVE0991 by gelation microspheres promotes epithelial transformation of adipose-derived stem cells. ---
97  2020 Engraftment potential of maternal adipose-derived stem cells for fetal transplantation. i.c.v, MSC
98  2020 Enhanced Adipose Mesenchymal Stem Cells Proliferation by Carboxymethyl-Chitosan Functionalized Polycaprolactone Nanofiber. CMC, PCL
99  2020 Enhanced Bone Formation in Osteoporotic Mice by a Novel Transplant Combined with Adipose-derived Stem Cells and Platelet-rich Fibrin Releasates. BMD, OP, PRFr
100  2020 Enhanced protection against lipopolysaccharide-induced acute lung injury by autologous transplantation of adipose-derived stromal cells combined with low tidal volume ventilation in rats. AFC, ALI/ARDS, IL, KGF, LPS, LVT, siRNA


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Death and Life

Photo: Donut Diva

Now Mary stood outside the tomb crying. As she wept, she bent over to look into the tomb and saw two angels in white, seated where Jesus’ body had been, one at the head and the other at the foot.

They asked her, “Woman, why are you crying?”

“They have taken my Lord away,” she said, “and I don’t know where they have put him.” At this, she turned around and saw Jesus standing there, but she did not realize that it was Jesus.
He asked her, “Woman, why are you crying? Who is it you are looking for?”
Thinking he was the gardener, she said, “Sir, if you have carried him away, tell me where you have put him, and I will get him.”
Jesus said to her, “Mary.”
She turned toward him and cried out in Aramaic, “Rabboni!” (which means “Teacher”).
Jesus said, “Do not hold on to me, for I have not yet ascended to the Father. Go instead to my brothers and tell them, ‘I am ascending to my Father and your Father, to my God and your God.’”
Mary Magdalene went to the disciples with the news: “I have seen the Lord!” And she told them that he had said these things to her.
John 20:11-18

I’ve never experienced a Lenten season quite like this one. A little over 40 days ago days ago, I gave up blogging (except for this one post) so I would focus more on Jesus. My plan was to pray diligently, read the Bible every day, and try to look for signs of Jesus in every day life.

That lasted three days.

Turns out, instead of using my time wisely while not writing, I was on Facebook a lot more. That’s why, on March 19, I saw the message right away. My friend’s son posted asking all loved ones to come say goodbye to his mother.

Wait. What?

Karen was just diagnosed with cancer, right? Wasn’t she just supposed to beat this thing? Isn’t that what my friends do? They get cancer. Then they get a lot of crappy poison in their bodies. Then they get better.

Unless, like my dear friend Teresa, they get lung cancer.
Or, unless like Karen, they get pancreatic cancer.

I never got to say goodbye to Teresa. There is no way I was letting Karen go without one last hug.

Karen’s son, Tim, requested visits to be limited to five minutes. Five minutes. How do you say goodbye to someone you won’t see again,
get advice from again,
hug again,
laugh with again,
in five minutes?

I told my daughters what was going on, grabbed my keys, and headed to the hospital. Karen’s three kids were inside her room. A few friends were there. It was a small party.

Screw five minutes. I stayed for an hour.

Karen lie in the hospital bed under a homemade quilt. She wasn’t speaking. She was barely breathing. But she was listening. I’m sure of it.

I love you Karen. I sat down on her hospital bed and whispered close to her ear. Where would I be without you? You were supposed to help me get my girls through their teenage years! You’re really going to bail on me? Just kidding. Sort of.

You deserve peace. You have spent your entire life helping others. So many live today because of you. [Karen was a popular pediatrician in town. She made house calls. She worked on her days off.] There is a piece of my heart that will always be yours, friend. Now there is a hole no one else can fill.”

I stroked her hair, now grey and limp. I touched her forehead, her skin almost the same color as her tresses. She was ready to see Jesus.

Goodbye, friend.

I exited the room, but instead of going to my car, I searched the directory for the hospital chapel. I needed to have words with Someone.

What. The. Hell, God? Are you freaking kidding me right now? She gets through a tough marriage, finally finding independence through divorce. Then her son gets a brain tumor, which after remission, came back. She gets him through that and THEN YOU TAKE HER WITH CANCER?!? Was it not enough she had to suffer with her son, through all of the children she’s cared for over the years, all the while remaining EXTREMELY faithful to You. Now her body deteriorates before she leaves this earth. Where is the justice?
Where are Your miracles?
Can’t you pull a “Lazarus” and save her?

The next day, just after noon, my question was answered.

God didn’t save her. At least for us, here, the ones left on earth. He did save her from her pain, from her cancer.

I miss my friend.

On this Easter Sunday, we celebrate the day Jesus Christ resurrected from the dead. 3 days earlier, his mother watched him murdered. His friends could not help him. They lamented, What the freaking hell, God? (I’m sure that’s in scripture somewhere.)

Still in deep mourning, Mary Magdalene, probably the woman closest to Jesus,went to take care of his body. The body wasn’t there. At least, not a dead body.

A very much alive Jesus showed himself to her and later to the rest of his friends, his followers, and family. The dead man was alive. Eating with them. Talking with them. Praying with them.

I can only imagine the elation I would feel if Karen came back to life. I would drop everything to spend as much time as possible with her. I would blast the news all over Facebook and Twitter. There would be no way to silence me. For a second, I can sense the disciples reaction when Jesus came back.

I rejoice in Jesus’ resurrection. I know Karen is up there, pain free, with him. Most likely she’s already found the celestial orchestra and she is first chair for oboe. (That’s a thing, right? Obviously I did not share her passion for instruments.) If the wind has a melodic tune today, you’ll know it’s her.

Andee Zomerman Nature of a Servant

Today, because of Jesus, I will take comfort believing death is not an end, but the beginning of new life.

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