t f p g+ YouTube icon

A Faith Journey in a Medical Science Career, Part 3

Bookmark and Share

February 18, 2013 Tags: Lives of Faith

Today's entry was written by John Pohl. Please note the views expressed here are those of the author, not necessarily of The BioLogos Foundation. You can read more about what we believe here.

A Faith Journey in a Medical Science Career, Part 3
Photo courtesy of Alex E. Proimos
As he went along, he saw a man blind from birth. His disciples asked him, “Rabbi, who sinned, this man or his parents, that he was born blind?”

“Neither this man nor his parents sinned,” said Jesus, “but this happened so that the works of God might be displayed in him. As long as it is day, we must do the works of him who sent me. Night is coming, when no one can work. While I am in the world, I am the light of the world.” (John 9:1-5)

In the first part of my essay, I made the argument that one can be a scientist, physician, pastor, or layperson and have no problems with evolution, an ancient universe, or other scientific ideas in respect to one’s Christian faith. I now want to explore some of the interesting aspects of my work as a clinical pediatric gastroenterologist.

You might be asking if a physician is expected to believe in evolution. No, but there is an expectation that evolutionary concepts will be taught in medical school including the ideas surrounding genetic drift, transposons, or small-interfering RNA to name a few. Simply put, one can be a physician and treat infections, stabilize fractures, or treat hypertension without thinking too deeply about how these diseases came into place from a biologic-genetic-evolutionary standpoint. However, as one studies various diseases, the evolutionary impact becomes quite clear, and often further exploration of the genetic history of certain diseases leads to downstream therapeutic benefit, including pharmacologic advancement.

I am a pediatric gastroenterologist, so I deal with children with intestinal, liver, and nutrition issues. Besides patient care, I also participate in medical student teaching as well as clinical research at my academic medical center. I know of many gastrointestinal diseases that have a fascinating evolutionary aspect – celiac disease, Crohn’s disease, and ulcerative colitis – as examples. In fact, my interest in the evolutionary aspect of gastroenterology began early in my career when I was involved in the description of a potential founder effect seen in the Navajo nation regarding a rare disorder known as microvillous inclusion disease. A conversation about that specific disease can occur at another time (it is quite fascinating), but my work on this project allowed me to think about multi-generational genetic mutation effects.

I want to talk about one of my clinical interests, namely cystic fibrosis (CF), its clinical consequences, and its genetics. CF occurs in about 30,000 adults and children in the United States, mainly in Caucasians although all ethnicities can have the disease. When the term “cystic fibrosis” is used, the average person will think about a severe, progressive lung disease resulting in the early death of a child. While lung disease certainly occurs in most cases, its lung presentation can be quite variable with some patients having very mild symptoms such as a mild cough and others having very severe, irreversible lung damage. Many other organs can be affected by CF, including the pancreas, liver, intestine, and gallbladder, bone, and the reproductive organs.

The cause of CF is known. Interestingly, the genetic defect was detected by Dr. Francis Collins of BioLogos and others in 1989. These scientists found a defect on chromosome 7 (the seventh chromosome) in which 3 nucleotide base pairs were deleted in CF patients leading to a loss of the amino acid, phenylalanine. Remember from your biology class in high school or college that DNA consists of four base pairs (adenine, thymine, guanine, and cytosine) that exist by the billions to form the genetic code of DNA. Three base pairs in a row code for one amino acid, and amino acids eventually link up to form proteins that assist in all functions of the cell. In the case of CF, these 3 base pairs were found to affect the formation of this one amino acid (phenylalanine) which leads to downstream disruption of specific protein function. Additionally, these same 3 base pairs belong to a specific gene, CFTR, or the Cystic Fibrosis Transmembrane Conductance Regulator gene.


Figure 2: Diagram of the normal CFTR protein of a cell bringing water and chloride into the environment surrounding the cell, preserving an aqueous layer and allowing for normal cellular and immune functions to occur.

Here is where this genetic mutation leads to fascinating, and at the same time, frankly awful consequences of CF. If both parents carry one CFTR gene mutation (heterozygous) and a child then inherits two such mutations (homozygous) from the parents, the resultant protein made from the CFTR gene malfunctions due to the single amino acid loss. As outlined in my rather crude cartoons included in this essay, the normal mechanism for the CFTR protein (remember the CFTR protein is formed from the CFTR gene) is to pump chloride (Cl-) from the cell to the outside environment while subsequently bringing in sodium (Na+) back into the cell (Figure 2). The positive (+) and negative (-) charges of sodium and chloride, respectively, keep a neutral balance to keep water hypotonic (or at a low concentration of solutes). This water is what you would see in normal body sweat or other body secretions that are inherent for normal physiology to maintain cellular structure, reduce inflammation, and to keep harmful bacteria away from cells.


Figure 3: In this diagram, I have included a red “X” over the CFTR protein region, suggesting malfunction. Chloride transport with water into the environment surrounding the cell is impaired, leading to thickened secretions and the clinical phenotype of cystic fibrosis.

However, this mechanism changes drastically in CF. A mutation in the CFTR gene disrupts this entire function (Figure 3). In CF, chloride transport is impaired; hence, chloride and water moving from the cell to the outside environment become stuck inside the cell. This transport defect causes secretions to thicken. Now, the cell senses that chloride is not being secreted, and it will bring more sodium (as well as water) into the cell, further reducing the amount of water in the extra-cellular environment. This perturbed mechanism affects many of cells in the body, billions of them, leading to organ dysfunction essentially from thickened secretions as cells have an impaired release of fluid. As a result of thickened pulmonary secretions that cannot clear, bacteria can enter the lungs to cause inflammation which further decreases secretions.


Figure 4: This chest X-ray demonstrates the classic findings of cystic fibrosis in the lungs of a child. Due to thickened lung secretions, bacteria begin to colonize lung tissue as the lung’s ability to clear bacteria is impaired. Progressive and irreversible lung disease occurs, which can ultimately lead to death over months or years.

Most people are familiar with the lung problems associated with CF (Figure 4). These children often are breathing quickly and may require supplemental oxygen due to poor air exchange due to thickened pulmonary secretions. However, all organs utilizing a water gradient can become diseased and progress to organ damage as a result of this mutation. Organs such as the pancreas (Figure 5), liver, intestine, stomach, and the reproductive organs will undergo significant injury that affects quality of life and decreases lifetime survival.


Figure 5: No, this is not a sonar reading from a deep part of Lake Michigan. This is an abdominal ultrasound of a child with cystic fibrosis. In a manner similar to the lungs, pancreatic secretions become trapped in the pancreas, leading to inflammation and irreversible fibrosis. The clinical consequences are fat malabsorption, and in some cystic fibrosis patients, diabetes. The pancreas changes from a somewhat smooth shape to a hard, nodular appearance as demonstrated in this image (a phenotypic change of an organ as a result of a genetic mutation).

Today, there are thousands of described CFTR gene mutations although the most common is the one initially described by Dr. Collins and others—this mutation involves the abnormal coding for the amino acid, phenylalanine, at position 508 of the CFTR gene (called “delta” or ∆F508). Some mutations, such as ∆F508, cause significant disease, while others are barely noticeable so that some patients with mild CFTR gene mutations may not be diagnosed with CF for many decades. The growing knowledge of these genetic mutations and their downstream organ effects have allowed CF medical teams to better determine treatment options and prolong lifespans while also improving the quality of life of these patients.

One would think that these mutations are pointless, cause needless suffering, and have nothing but chronic, tragic consequences. However, we need to evaluate this mutation again—remember that a parent of a CF child typically will have one CFTR gene mutation, not two mutations as in the affected child. Would a heterozygote mutation have an evolutionary advantage?

It turns out the answer is “Yes…probably” (remember that good science is always full of qualifiers). Genomic research has shown that the mutation for ∆F508 probably started as a one-time occurrence 58,000 to 173,000 years ago. ∆F508 mutations may have protected against infections in Paleolithic Europe, including Salmonella typhi (typhoid) and influenzae. One infection, Vibrio cholerae (cholera) may have, in particular, been influenced by this heterozygous inheritance. Cholera infection occurs through drinking a contaminated water supply, leading quickly to profound, massive, watery diarrhea with resultant dehydration, shock, and death. However, research has suggested that CFTR protein mutations may cause V. cholerae to have difficulty adhering to the lining of the small intestine while causing less fluid to be secreted during an active infection. It would make sense that a mutation of the CFTR protein would be protective in situations where there was a contaminated water supply, poor hygiene, and a poor understanding of disease transmission.

There also appears to be an advantage to having a CFTR protein mutation in tuberculosis prevention. Epidemiologic evidence from British mortality records in the 1800s followed by modeling has suggested that CFTR protein mutations protect from tuberculosis (the reason is not entirely clear), and that the number of patients with cystic fibrosis may be declining in those parts of the world where tuberculosis becomes an irrelevant pathogen. These evolutionary aspects are fascinating and provocative, but we have to be very careful to make sure we are not making the genetics history of CF a “just so story” (or an ad hoc fallacy).

Theological Reflections

Now that we have gone into quite a bit of detail about one specific disease, I want to describe certain aspects of a Creator related to what we have learned about CF genetics.

  1. God is smarter than me (or you). It is amazing what He has done in regards to the complexity of life and inheritance.
  2. Disease and death are a part of reality, which is justified in a reading of the Bible. The blind man, just like a child with CF, had no sin which caused a debilitating illness. Much of the suffering that we see in the world of medicine is due to environmental and genetic consequences.
  3. Besides our immune system, there appear to be other mechanisms for protection against disease that are often difficult to observe in a first-world setting. We see this idea in how CFTR protein mutations may protect against certain infectious diseases. Whether God did this through a divine purpose or allowed a random mechanism to occur (or for what appears to be random to us, in our limited scientific understanding) is irrelevant. I can see that the process of mutation occurs, and I believe in a God that allows it.
  4. Finally, I am thankful that “modern” medicine has developed therapies in the basic science and clinical realms to allow an improved quality of life in CF patients, as well as for patients with other diseases. It is now common for patients with ∆F508 mutations to live into their 30s or 40s. At the beginning of the 20th century, most CF children died well before 2 years of age. I use quotation marks around this word – modern - as 20 years from today, much of our current CF treatments will have changed, leading to even longer life for these patients. I am thankful that God has allowed us the capacity to investigate our world at an ever-advancing state through the use of the scientific method. That, in itself, is a gift for humanity for which we should always be thankful.

In my next installment of this essay, I will discuss ways for Christians to reach out and show mutual respect to each other based on an understanding of how many scientists and physicians work, think, and feel.


John F. Pohl MD is a pediatric gastroenterologist and a professor of pediatrics at the University of Utah in Salt Lake City, Utah. He went to medical school at the University of Texas Medical Branch in Galveston, Texas and completed his pediatric residency at Phoenix Children’s Hospital / Maricopa Medical Center (University of Arizona) in Phoenix, Arizona. His fellowship in pediatric gastroenterology was completed at Children’s Hospital Medical Center in Cincinnati, Ohio (University of Cincinnati). His clinical and research interests include cystic fibrosis and pediatric pancreatic disease. He attends Missio Dei church with his wife (a family physician) and two daughters in Salt Lake City. You can follow John on Twitter (@Jfpohl ) where he rambles about theology, science, gastroenterology, and his weekend activities.

< Previous post in series Next post in series >


View the archived discussion of this post

This article is now closed for new comments. The archived comments are shown below.

Loading...
Page 1 of 1   1
GJDS - #76785

February 19th 2013

Dr John F. Pohl,

I find your treatment of these matters regarding diseases and how we may rationalise them within a scientific and theological context most refreshing and agree with your four points in this essay. I want to add this simple point, that God’s creation also includes men and women who are motivated to serve in whatever capacity they can, to improve the well being of their fellow human beings and also to add beneficially to the planet we live in. These practical matters speak much more loudly than perhaps debates and quarrels about what this or that may mean. I am also greatly heartened by another simple observation, and that is such people are found in every walk of life, and include those of faith, and those who may not profess faith. A marvellous observation, and one that has IMO, considerable theological relevance.


Chip - #76792

February 19th 2013

Thanks for a fascinating presentation. 

People in such forums are often asked if they “believe in/accept evolution,” to which I respond with an overwhelming yes.  I would further agree with Dr Pohl that “as one studies various diseases, the evolutionary impact becomes quite clear,” although perhaps not in the way he may have intended.

The challenge (or one of them, at least) is to believe that evolutionary processes are capable of doing what people claim they are.  Consider again what Dr Pohl says about the effect of  the evolutionary process in the case of CF (emphasis and edits are mine): 

A mutation in the CFTR gene disrupts this entire function (Figure 3). In CF, chloride transport is impaired;  chloride and water become stuck inside the cell. This transport defect causes secretions to thicken. further reducing the amount of water in the extra-cellular environment. This perturbed mechanism affects many of cells in the body leading to organ dysfunction as cells have an impaired release of fluid. As a result of thickened pulmonary secretions that cannot clear, bacteria can enter the lungs to cause inflammation which further decreases secretions… Most people are familiar with the lung problems associated with CF (Figure 4). These children may require supplemental oxygen due to poor air exchange due to thickened pulmonary secretions. However, all organs utilizing a water gradient can become diseased and progress to organ damage as a result of this mutation. Organs such as the pancreas (Figure 5), liver, intestine, stomach, and the reproductive organs will undergo significant injury that affects quality of life and decreases lifetime survival.

What does such an analysis tell us, or what conclusions can we draw?  While it doesn’t necessarily close the deal in any particular direction, the data does seem pretty compelling: In the case under consideration, a mutation-driven evolutionary process left to its own devices clearly damages, degrades or even destroys existing complex function. 

Does evolution occur?  Absolutely.  But in this case—and presumably in all cases in which “diseases came into place from a biologic-genetic-evolutionary standpoint”— the effect is overwhelmingly deleterious.  In such cases when evolutionary change can be directly observed, it doesn’t make the organism more fit, but rather weakens or even kills it. 


melanogaster - #76821

February 20th 2013

“Consider again what Dr Pohl says about the effect of the evolutionary process in the case of CF (emphasis and edits are mine):”

When I consider it, I note that you omitted the part that followed about the advantages enjoyed by heterozyotes, which greatly outnumber the homozygotes.

“What does such an analysis tell us, or what conclusions can we draw?”

I conclude that you are very selective in the evidence you choose to cite.

“But in this case—and presumably in all cases in which “diseases came into place from a biologic-genetic-evolutionary standpoint”— the effect is overwhelmingly deleterious.”

No, as the heterozygotes are much more numerous than the homozygotes, the effect of the allele in the population as a whole is overwhelmingly advantageous.

“In such cases when evolutionary change can be directly observed, it doesn’t make the organism more fit, but rather weakens or even kills it.”

No, heterozygosity makes carriers more fit than homozygous wild-type noncarriers. Dr. Pohl understated what we know about that.

Individual organisms don’t evolve, Chip, populations evolve.


Chip - #76829

February 20th 2013

Guilty as charged. I elected to emphasize the content that has been demonstrated, and that the expert expressed in definitive language (a consistent weakness I have when I write about things I read… sorry). Namely, that in this particular example, the effect of the mutation included significant injury, organ damage, a decrease in lifetime survival and other similar conseqences. All of it without any hint of qualification.

melanogaster, on the other hand, wants to plant his flag on the content heavily peppered with “probably,” “may have been,” the academically-ubiquitous “research has suggested….,” and my personal favorite, the admonition that we should “be very careful to make sure we are not making the genetics history of CF a ‘just so story.’”

Hmmm…. I’m wondering what sort of person might be at risk taking this kind of data and making it into a just so story. I dunno… Well, anyway, I guess that doesn’t matter.  Thanks to melanogaster taking the time to set me straight. 


melanogaster - #76862

February 22nd 2013

“… that the expert expressed in definitive language (a consistent weakness I have when I write about things I read… sorry).”

But he’s not an expert in genetics. The only demonstration here was pure hearsay.

“Namely, that in this particular example, the effect of the mutation included significant injury, organ damage, a decrease in lifetime survival and other similar conseqences. All of it without any hint of qualification.”

You’re dead wrong in two ways, Chip.

1) Those are the effects only when the mutant allele is homozygous. What are the effects when it is heterozygous? What is the ratio of heterozygotes to homozygotes?

2) These are not effects of “the mutation,” which you are implicitly framing as new mutations, because the frequency of the allele is far too high (in only some populations) to be produced by new mutations. How do you explain these facts, Chip? The frequency and the ethnic differences?

“melanogaster, on the other hand, wants to plant his flag on the content heavily peppered with “probably,” “may have been,” the academically-ubiquitous “research has suggested….,” and my personal favorite, the admonition that we should “be very careful to make sure we are not making the genetics history of CF a ‘just so story.’””

That’s false, because unlike you, I didn’t limit myself to one bit of hearsay. I’m going with the facts:

Salmonella typhi uses CFTR to enter intestinal epithelial cells.
Pier GB, Grout M, Zaidi T, Meluleni G, Mueschenborn SS, Banting G, Ratcliff R, Evans MJ, Colledge WH.
Department of Medicine, Brigham and Women’s Hospital, Harvard Medical School, Boston, Massachusetts 02115, USA. .(JavaScript must be enabled to view this email address)

“Homozygous mutations of the cystic fibrosis transmembrane conductance regulator (CFTR) cause cystic fibrosis (CF). In the heterozygous state, increased resistance to infectious diseases may maintain mutant CFTR alleles at high levels in selected populations. Here we investigate whether typhoid fever could be one such disease.”

Try to open your eyes to see that they are stating is the hypothesis to be tested, so stating it as a certainty would be dishonest.

Now, the facts:

The disease is initiated when Salmonella typhi enters gastrointestinal epithelial cells for submucosal translocation. We found that S. typhi, but not the related murine pathogen S. typhimurium, uses CFTR for entry into epithelial cells. Cells expressing wild-type CFTR internalized more S. typhi than isogenic cells expressing the most common CFTR mutation, a phenylalanine deleted at residue 508 (delta508). Monoclonal antibodies and synthetic peptides containing a sequence corresponding to the first predicted extracellular domain of CFTR inhibited uptake of S. typhi. Heterozygous deltaF508 Cftr mice translocated 86% fewer S. typhi into the gastrointestinal submucosa than wild-type Cftr mice; no translocation occurred in deltaF508 Cftr homozygous mice. The Cftr genotype had no effect on the translocation of S. typhimurium. Immunoelectron microscopy revealed that more CFTR bound to S. typhi in the submucosa of Cftr wild-type mice than in deltaF508 heterozygous mice.

Did you see any “probably,” “may have been,” etc. in the facts?

And now the conclusion, which is far more modest than your accusation about me:

“We conclude that diminished levels of CFTR in heterozygotes may decrease susceptibility to typhoid fever.”

“Hmmm…. I’m wondering what sort of person might be at risk taking this kind of data and making it into a just so story. I dunno…”

You? What’s your explanation for the high frequency of mutant CFTR alleles then? God doesn’t like white people, particularly of Western European ancestry? Or God likes them more (increased heterozygote fitness), and is willing to sacrifice the homozygotes to a lifetime of misery and an early death?

“Well, anyway, I guess that doesn’t matter.”

Why not? Which one of us is using just so stories and hearsay? Why do you reject the most important sentence Dr. Pohl wrote about science?


Chip - #76866

February 22nd 2013

What’s your explanation for the high frequency of mutant CFTR alleles then?

Take a deep breath mel.  As I said previously, evolution.  No objections. 

If I may, my view is that the good doctor made his “just-so story” reference because of people’s tendency to take a legitimate observation and subsequently extrapolate it beyond the limits of what the observed data will support. Namely, that we are subject to the effects of such evolutionary processes causes me no angst at all.  That we owe our existence to such processes is highly questionable.  This was the point of my original response. 


melanogaster - #76877

February 23rd 2013

Chip,

What you’re missing is that this is population genetics, not evolution itself. My point is that those who claim that evolution is not the mechanism God put in place to produce diversity are also denying the sciences that underly it, such as population genetics, without ever admitting it publicly.

If you think it’s “highly questionable,” do you also think that paternity testing is highly questionable? How can any thinking person question one and not the other?

Why do you apparently disagree with the good doctor’s reminder, “remember that good science is always full of qualifiers”?


Chip - #76886

February 25th 2013

Mel,

What you’re missing is that this is population genetics, not evolution itself.

Ah, the shifting sands of the malleable definition—a sadly common phenomenon in all these discussions.  When his language is taken at face value, the good doctor certainly seems to think this is about “evolution itself”:

In the first part of my essay, I made the argument that one can be a scientist, physician, pastor, or layperson and have no problems with evolution, …You might be asking if a physician is expected to believe in evolution. No, but there is an expectation that evolutionary concepts will be taught in medical school … how these diseases came into place from a biologic-genetic-evolutionary standpoint. However… the evolutionary impact becomes quite clear, … I know of many gastrointestinal diseases that have a fascinating evolutionary aspect – celiac disease, Crohn’s disease, and ulcerative colitis – as examples. In fact, my interest in the evolutionary aspect of gastroenterology…

.

If you think it’s “highly questionable,” do you also think that paternity testing is highly questionable? How can any thinking person question one and not the other?

Ah, I see.  Because paternity testing is reliable, it is therefore not possible to be a “thinking person” and still have doubts about the grand evolutionary creation epic. Well, let’s see.  Paternity testing: is limited to a single generation; is always and by definition limited to a single species; is concerned with two distinct individuals (child and alleged father) within that species—and you yourself have reminded me that individuals don’t evolve, populations do; can be tested rigorously in the here and now; can be observed in the here and now; can be falsified. 

In other words, apples and oranges—actually, much further apart than that, but I’ll stick with the standard metaphor.  As i stated way back at the beginning, this whole series demonstrates that we are subject to evolutionary pressures; it in no way demonstrates that we owe our existence to them.  Certainly, you can grasp the difference. 

Finally,

Why do you apparently disagree with the good doctor’s reminder, “remember that good science is always full of qualifiers”?

What is “questionable” or even “highly questionable” if not a qualifier? 

 


melanogaster - #77141

March 5th 2013

“Ah, I see.”

Possibly, but your response suggests anything but.

“Because paternity testing is reliable, it is therefore not possible to be a “thinking person” and still have doubts about the grand evolutionary creation epic.”

That’s quite a misrepresentation of my position, Chip, but I’ll play along. My point is much more limited than that, but I can see why you’d avoid acknowledging that reality.

“Well, let’s see.”

You keep using visual metaphors when your eyes are closed!!!

“Paternity testing: is limited to a single generation;…”

False right out of the box! It’s quite easy to use the suspected grandfather or grandmother’s DNA. The father’s DNA isn’t needed.

Do you understand what difference that would make in the probabilities? It’s a very simple formula.

“…is always and by definition limited to a single species;”

But I’m talking about the principles involved, and you clearly don’t understand them or you wouldn’t have started out with a false claim.

“… is concerned with two distinct individuals (child and alleged father) within that species—”

See above. You’re utterly wrong on principle, as you don’t need the alleged father’s DNA.

“…and you yourself have reminded me that individuals don’t evolve, populations do;…”

That’s true, but I’m talking about the evidence establishing relationship and you are closing your eyes to talk about anything but.

“… can be tested rigorously in the here and now;…”

So can evolution, and it is. Do you not see that we are rigorously testing for an event that we did not witness and occurred in the past?

“… can be observed in the here and now;…”

No, we don’t need to observe conception to establish paternity, just like we don’t need fossils to use sequences to establish the relationship between you and baker’s yeast.

“… can be falsified.”

That’s an identity, not a difference.

“In other words, apples and oranges—actually, much further apart than that, but I’ll stick with the standard metaphor.”

Why? Almost everything you wrote is wrong, so what does that do to your conclusion?

“As i stated way back at the beginning, this whole series demonstrates that we are subject to evolutionary pressures; it in no way demonstrates that we owe our existence to them. Certainly, you can grasp the difference.”

Certainly, I can, just as certainly as you can grasp the flaming hypocrisy of using DNA to establish paternity while closing your eyes to its utility in establishing more distant relationships with incredible rigor.


beaglelady - #76919

February 26th 2013

Melanogaster,

Would the situation in this article be an example of “heterozygote advantage” aka “overdominance”?  It sounds similar to the case of the sickle cell mutation:   the person who is heterozygous for the mutation has a lower chance of getting malaria than the homozogous person with no copy of the defect, while a person who is homozygous with 2 copies of the defect gets sickle cell disease?


melanogaster - #77142

March 5th 2013

Yes, that’s exactly what it is. CF mutant alleles are fixed in the population at a very high frequency. If the CF alleles were simply deleterious when homozygous, their frequency should be much lower and asymptotically declining.


beaglelady - #77185

March 6th 2013

Hooray,  and thank you! My course is helping me understand a lot. You see, I’m taking the Coursera course “Introduction to Genetics and Evolution” taught by Mohamed Noor at Duke.  I’m sure you’ve heard of him and his research. I really love the course.

The course is free, and I’ve pointed it out to people here, but nobody is interested.  Are you surprised? Neither am I.


melanogaster - #77187

March 6th 2013

Not surprised at all.  People who have no faith in their positions tend to demand that all of their “information” be filtered as hearsay from those they have predecided to follow.


beaglelady - #77194

March 7th 2013

Wouldn’t you think that BioLogos would list all the great relevant courses from Coursera and other mooc sites?   Everything is free, and it’s a wonderful opportunity to learn from top professors and schools.


Page 1 of 1   1