Category: Modern Science

Did This Bird Go Extinct and Re-Evolve? I Doubt It.

A flightless Railbird on the Aldabra atoll in the Indian Ocean (click for credit)

Over the past few days, several people have sent me articles like this one, which makes a rather fantastic claim:

The Aldabra white-throated rail bird was declared extinct, a victim of rising sea levels almost 100,000 years ago.

However, the flightless brown bird has recently been spotted – leaving scientists scratching their heads as to how – and why – the species has come back to life.

What do you conclude from reading that? The article seems to be saying that no one had ever seen this bird before; it was only known from the fossil record. Now, however, living versions of it have been seen, and how they came back from extinction is a mystery. Unfortunately, like many “science news” stories, this one distorts the science to the point that it is deceptive and misleading.

The science that is being distorted comes from a study published last year. A responsible article that describes the study can be found here. While the study and the responsible article don’t distort the science, I do think the conclusion that they draw is not the only one consistent with the data.

Let’s start with the bird that is being discussed. It’s the Aldabra white-throated rail, whose scientific name is Dryolimnas [cuvieri] aldabranus. It lives on the Aldabra atoll in the Indian Ocean and is nearly identical to white-throated rails (Dryolimnas cuvieri) found in other parts of the world, like Madagascar. However, the ones on the Aldabra atoll cannot fly, while the others can. As a result, the flightless birds on the atoll are considered a subspecies of the version that can fly.

While we cannot say for sure, the generally-accepted origin story for the Aldabra white-throated rail is that normal white-throated rails landed on the atoll, and since there were no predators there, they stayed. Since they didn’t need to fly anymore, they evolved into flightless birds over several generations. This makes sense, because when a population of organisms doesn’t need a particular biological trait, mutations can degrade those traits without affecting survivability. In addition, DNA is so incredibly well-designed that over the course of generations, it can “turn off” genes that are no longer used in order to save energy. As a result, it makes sense that these flightless birds are descendants from birds that could originally fly.

Why do these articles discuss the birds being extinct at one point? Because the authors of the scientific study looked at the fossil record of the atoll. Using scientifically-irresponisble dating methods, they came to the conclusion that the atoll was completely underwater about 140,000 years ago. When they looked at fossils they interpreted to be older than 140,000 years, they found two bones that seem identical to the corresponding bones in the Aldabra white-throated rails that currently live on the atoll. Thus, they conclude that these flightless birds lived on the atoll before it went completely underwater.

Well, since the birds couldn’t fly, the authors assume that they all died when the atoll was underwater. However, in fossils that they interpret as being deposited after ocean levels decreased and the atoll was no longer underwater, they found another bone that looks similar to the corresponding bones in white-throated rails that can fly. However, it is heavier and more robust than what is found in those birds, but still lighter than what is found in the flightless Aldabra white-throated rails. In other words, it seems to be “in between” the bone of a normal white-throated rail and a flightless white-throated rail. To them, that gives “irrefutable evidence” (their words) that the Aldabra white-throated rails evolved twice: once before the atoll went underwater, and once after.

While their interpretation of the evidence makes sense and is consistent with all the known data, their case is certainly not “irrefutable.” First, you have to assume that they are interpreting the fossil record correctly. There is a lot of evidence to indicate the earth isn’t anywhere close to 140,000 years old, and if that evidence is correct, then their entire explanation is wrong. Also, even if the earth is as old as these scientists want to believe, the authors’ explanation is not the only one consistent with the data. We know that flightless animals can move from place to place on floating mats of vegetation. This is called “rafting,” and it is used by both evolutionists and creationists to explain the worldwide distribution of certain animals. If the atoll flooded like the authors think, the flightless birds could have survived by rafting. What about that one bone that is “in between” the two subspecies? There are natural variations in all bones. A “more robust” bone from a normal white-throated rail can be explained by natural variation within a population of normal white-throated rails.

The main reason I am writing about this is not to argue with the authors. It’s to point out the deceptiveness of articles like the one I quoted at the beginning of the post. As I have said many times before, do not believe the things you read in the popular press when it comes to science. Most “science journalists” are profoundly ill-equipped to understand science, and usually quite poor journalists as well.

Lichen Hid This Secret From Scientists for More Than 140 Years!

The colorful splotches on this rock are lichens, which we now know are a mutualistic association between THREE different organisms (photo copyright Kathleen J. Wile)

For more than 140 years, scientists have taught that lichens are the result of a relationship between a fungus and an alga (singular of algae). The fungus gives the lichen most of its visible characteristics and provides a protected place for the alga to grow. In exchange, the alga does photosynthesis and shares what it makes with the fungus. In other words, the fungus provides housing for the alga, and the alga provides food for the fungus. This is a form of symbiosis, in which organisms of different species exist in a long-term relationship. Since both organisms benefit in this symbiosis, it is called a mutualistic symbiosis, one of the most fascinating aspects of the biological world (see here, here, here, here, here, here, and here, for example).

Despite the fact that lichens have been studied for more than 140 years, there has always been one nagging mystery: The relationship cannot be recreated in a lab. Lichens can be found in all sorts of ecosystems, but no matter what you do with the fungus and the alga, you cannot get them to form the same relationship in a laboratory setting. A recent study might explain why. The authors of the study analyzed two different species of lichen, Bryoria fremontii and Bryoria tortuosa. They are easily distinguished from each other, since the first is dark brown, while the second is yellow. However, recent studies have indicated that the fungus and alga in each are the same. How is it that two lichens can be so different when their fungus and alga are the same? That’s what the authors wanted to find out.

They decided to look at the specific genes that were actually being used by the two species. After all, even if both lichens have the same fungus DNA and the same alga DNA, it’s possible that one lichen uses one set of genes more than the other lichen, and perhaps that could explain the differences between them. However, their initial analysis indicated that both lichens used essentially the same set of genes. That’s when they decided to think “outside the box.”

When doing a study like this, you have to decide what gene products you are looking for. They had limited themselves to the genes found in the fungus and the alga that were known to exist in the lichens. They decided to change their analysis to include all known fungus genes. When they did that, they found that genes from an entirely different fungus were also being used by the lichens! That fungus is a type of yeast (specifically from genus Cyphobasidium), which is very different from the fungus that was already known. The authors did some very difficult microscope work and confirmed the presence of the yeast in the lichen. In addition, they did the same genetic tests on many different species of lichen, and they found the yeast genes in the vast majority of the lichens that they studied. As a result, the authors suggest that the vast majority of lichens are made up of at least three different species. Here is how they conclude their paper:

The assumption that stratified lichens are constructed by a single fungus with differentiated cell types is so central to the definition of the lichen symbiosis that it has been codified into lichen nomenclature. This definition has brought order to the field but may also have constrained it by forcing untested assumptions about the true nature of the symbiosis. We suggest that the discovery of Cyphobasidium yeasts should change expectations about the potential diversity and ubiquity of organisms involved in one of the oldest known and most recognizable symbioses in science.

While this discovery in and of itself is remarkable, it is also an excellent illustration of how assumptions can put blinders on science. Why haven’t these yeasts been discovered in more than 140 years of lichen study? Partly, because they are well-hidden. To confirm the presence of the yeast in the lichen required some rather detailed microscopic analysis. In addition, when you are doing genetic analysis, you have to decide what to search for, which means your results will be limited by that decision. However, here’s the main reason: No one was looking for them. Since the assumption that lichens are mutualistic symbioses between two different species was so ingrained in biological thought, no one ever considered looking for a third, until these authors decided to “think outside the box.”

I wonder how many more scientific discoveries are waiting on other scientists who are willing question old paradigms and look for things that no one else has been looking for!

Please…Discard the Dogma!

Evolutionists have dogmatically insisted that pseudogenes are genes that were broken by mutation and are now useless. Some are now pleading with their colleagues to actually look at the data.

It always troubles me when I read other scientists who ignore the data in order to cling to their cherished dogmas. As a scientist, I know that this holds back the progress of science. As a result, I was heartened to read three scientist calling on their colleagues to abandon evolutionary dogma when it comes to pseudogenes. If others heed their call, we will most certainly learn more about DNA.

What am I talking about? Let’s start with what a pseudogene is. It is a region of DNA that looks like a known gene, but is different enough that it can’t do what the known gene does. As a result, it has become evolutionary dogma that pseudogenes are “broken” genes – genes that became non-functional due to duplication and mutation. Here, for example, is how the Encyclopedia of Genetics definitively describes a pseudogene:

A pseudogene is a nonfunctional genomic region that originated by duplication of, and is still homologous to, an ancestral gene.

In other words, a pseudogene is the result of a gene being copied and then broken. Creationists have long argued that pseudogenes are functional; they just don’t function the way evolutionists expect them to. The three authors of the paper I mentioned above have arrived at that same conclusion (at least for many pseudogenes), and they are asking their colleagues to pay attention to the data and do the same.

To emphasize the point that this evolution-inspired dogma is wrong, they list many pseudogenes that have been demonstrated to have an important function. They then make this important statement:

The examples of pseudogene function elaborated on here should not imply that pseudogene functionality is likely to be confined to isolated instances.

In other words, you can’t say that the known functional pseudogenes are exceptions to the rule. There are enough functional pseudogenes to call into question the assumption that they are mostly non-functional.

At the same time, however, these authors are cautious:

The purpose of this article is not to discard the pseudogene concept or to suggest that all pseudogenes are functional. The majority of currently annotated pseudogenes are neither robustly transcribed nor translated. Such regions fit well the original descriptions of pseudogenes as ‘similar, but defective’. Rather, we argue that their labelling as pseudogenes is not constructive for advancement of understanding of genome function and misdirects experimental design.

In other words, the authors are simply telling their colleagues to follow the data. Do not assume that a pseudogene is non-functional just because it has been identified as a pseudogene. Instead, investigate it to find out whether or not it actually is. The progress of science is hindered when you assume non-functionality because of the way the sequence has been identified.

I not only completely agree with that sentiment, I would also add this: following any dogma (evolutionist, creationist, or other) hinders the progress of science. Scientists should be willing to follow the data wherever they lead. Unfortunately, such scientists tend to be the exception, not the rule.

Are Hydroxychloroquine and Azithromycin Effective Against COVID-19?

Dr. Didier Raoult, French physician and microbiologist who thinks he has an effective treatment for COVID-19 (click for image source)
Two weeks ago I wrote about a possible treatment for COVID-19, the pandemic disease that is affecting most of our lives. It has been championed by French physician and microbiologist Dr. Didier Raoult. So far, he has written two papers about it (here and here). I was excited about his initial report, and I was hoping for a serious follow-up study. When I saw that he had written a second paper, I eagerly read it. Unfortunately, it wasn’t the serious study that I had hoped for. Nevertheless, it has gotten some media attention and seems to have influenced the FDA, so I decided to share my thoughts on it.

The results seem very exciting. He and his colleagues treated 80 patients with the malaria-fighting drug hydroxychloroquine and the antibiotic azithromycin. They note that they saw “clinical improvement” in 78 of them. One of the other two (an 86 year-old patient) died, and the other (a 74 year-old patient) was still in intensive care when the paper was written. While that sounds really good, there are a couple of “red flags” that make me hesitant to think that the treatment is as effective as it seems.

The first problem is that there is no control group. In a serious medical study, there needs to be a similar group of patents who do not receive the treatment. The treated group can be then measured against the untreated (control) group. Without that, it is very difficult to determine what the actual effect of the treatment is. Of course, I understand why there is no control group. Dr. Raoult wants to save lives. He thinks his treatment is effective, so he wants to give it to as many people as he can. He would have to “withhold” his life-saving treatment from some people so that he could have a control group, and that could lead to more deaths. I can understand why a physician would shudder at that idea.

However, the control group is important, because we really have no idea what would have happened to the 78 people who recovered had they not been given the treatment. While we still don’t know, the fatality rate of this disease is thought to be 1-2%. In 80 people, then, you would expect only one or two (0.8-1.6 to be precise) deaths, so this group of patients has the fatality outcome we expect had there been no treatment at all.

Now, of course, Dr. Raoult and his colleagues did more than just track whether or not the patients died. They tracked the amount of virus in each patient’s nasal cavity and found that the amount of virus dropped significantly for most of them. Once again, that sounds nice, but without a control group, we simply don’t know whether or not that was because of the treatment.

The second problem is the profile of patients who got the treatment. They mostly seemed to have a mild case of the disease. Only 15% had fever. Only 53% showed signs of lower respiratory tract infection. Worse, 5% showed no symptoms at all. Once again, it isn’t surprising that most of these patients recovered – most of them fit the profile of people who are expected to recover.

There is a third problem. A scientific study has been done in China with a control group. It is very small, and I can’t read it, since it is in Chinese. However, based on a Forbes article, the study had 30 patients. Half were given hydroxychloroquine, and half were not. That study showed no significant difference between the control group and the treatment group. Thus, if that study is correct, hydroxychloroquine is not an effective treatment for COVID-19.

Now, of course, that study didn’t include the antibiotic, so it’s possible that Dr. Raoult’s treatment is better than the treatment assessed by the study. It’s also possible that because of problems with the Chinese study’s design (small number of patients and no placebo, for example), the Chinese study is wrong. From a scientific point of view, then, we simply do not know whether or not Dr. Raoult’s treatment (or hydroxychloroquine by itself) is effective against COVID-19.

Nevertheless, the FDA has approved using hydroxychloroquine and other, similar drugs to treat COVID-19. This is probably a good plan, since the risks of using the drugs are low. However, until serious, controlled studies are done, we have no idea whether or not they are doing any good.

A Possible Treatment for COVID-19

A transmission electron microscope image of the coronavirus SARS-CoV-2. The spikes surrounding the virus make it look like a crown, which is where it gets its name. (click for credit)

While countries are scrambling to prevent the spread of COVID-19 (the disease caused by the new coronavirus), doctors are trying to find the best treatment for it. In three separate studies, a surprising candidate has been found: the anti-malarial drug chloroquine. In a letter that was published on February 19th, three Chinese scientists reported that more than 100 patients were given the drug. Based on the patients’ responses, they write:

…chloroquine phosphate is superior to the control treatment in inhibiting the exacerbation of pneumonia, improving lung imaging findings, promoting a virusnegative conversion, and shortening the disease course…

The authors also report that there were no adverse side effects noted in the patients.

A report in Spanish (translation here) concurs. It discusses both the results seen in patients and the results of experiments where primate cells are infected with the virus and then treated with chloroquine. The conclusion is as follows:

Chloroquine can both prevent and treat coronavirus in primate cells…According to South Korean and China human treatment guidelines, chloroquine is effective in treating COVID-19. Given chloroquine’s human safety profile and existence, it can be implemented today in the U.S., Europe and the rest of the world.

Finally, a study published in the journal Nature confirms that when primate cells are infected by the virus that causes COVID-19, both chloroquine and an antiviral drug known as remdesivir were effective at fighting it. The researchers state:

Our findings reveal that remdesivir and chloroquine are highly effective in the control of 2019-nCoV infection in vitro. Since these compounds have been used in human patients with a safety track record and shown to be effective against various ailments, we suggest that they should be assessed in human patients suffering from the novel coronavirus disease.

Now, of course, these studies are far from conclusive. However, I expect that doctors will judiciously test the treatment on patients who volunteer for it. Hopefully, that will allow us to learn more. Perhaps an effective treatment is on the horizon!

More Thoughts on the New Coronavirus

An infographic adapted from one produced by the CDC (click for larger version)

A few readers have sent me questions regarding the coronavirus that is spreading across the world, so I thought I would make a post answering those questions and providing some resources you can use to deal with the issue. Please note, however, that I am neither a medical doctor nor a biologist. As a result, I don’t claim any expertise on the matter. However, there are some misconceptions about the virus that are easily cleared up, and there are some facts that anyone who can understand the scientific literature should share.

First, a few facts. The term “coronavirus” refers to a very large group of viruses that circulate mostly among mammals and birds. However, some are able to infect people. Most coronaviruses that infect people produce mild illnesses, but some (like this one) produce potentially fatal ones. The coronavirus that is in the news right now is one that has not been seen before. This is not unusual. When an animal is infected with two different versions of the coronavirus, they can mix together, producing a new (usually called “novel”) coronavirus. This particular novel coronavirus has been charmingly named SARS-CoV-2, and it causes the disease referred to as COVID-19. Because of that, it is sometimes referred to as the “COVID-19 virus.”

The reason it has been given the name SARS-CoV-2 is that its genetic sequences indicate it is very similar to the virus that caused the SARS outbreak of 2003. Based on that sequence, it is thought that the virus originated in bats, but it might have passed through another animal (possibly a scaly anteater) before infecting people. Most importantly, there is strong evidence against the idea that it was genetically engineered. This is because the way it infects people is quite different from what would have been predicted given our current knowledge about these viruses. In other words, it is very hard to believe that anyone knowledgable enough to engineer a virus would purposefully make the genetic sequences that end up allowing the virus to be so good at infecting people.

The illness caused by this virus is flu-like, but it is much more serious than the flu. The death rate caused by the flu changes from year-to-year, depending on the strains that circulate. However, on average, the flu has a death rate of about 0.1%. That means for every 1,000 people who get the flu, 1 will die. Even though that is a low death rate, a lot of people get the flu. As a result, millions of people die from the flu every year. We don’t know the death rate for this new virus, since we don’t really know how many people have actually been infected, but the best estimate so far is that the death rate is about 2%. That means this virus is thought to be 20 times more deadly than the flu virus.

Second, the resources. The infographic above has been adapted from one that was produced by the CDC. The university at which I teach has asked all its professors to post this electronically as well as wherever students might be found. It is basic, but nevertheless, it does contain some helpful information. This link will take you to the latest information regarding where the virus has been detected, how many people have been infected, and how many people have died.

In general, the best way to avoid being infected by this virus is to avoid other people and avoid going to places where it has been found. The virus spreads most effectively when an infected person is within a few feet of an uninfected person. However, it might also be transferred by surfaces. If someone sneezes on a surface and someone else touches that surface, the virus can be transferred to the hand. Then, if that person touches his or her mouth, nose, or eyes, it is possible for the virus to begin an infection. Thus, you need to wash your hands a lot and avoid touching your eyes, nose, and mouth in between washings.

The most important thing to remember is that while the illness caused by this virus has a death rate that is thought to be about 2% on average, it is significantly higher for elderly people, people who are already sick with something else, and people with weakened immune systems. Thus, if you show any of the signs of the illness (fever, cough, shortness of breath) and think you might have been in contact with someone who has the virus, you should seek medical help.

While there are several groups working on a vaccine to prevent the spread of the virus, the earliest a vaccine could possibly be ready would be at least a year from now. My guess, given that I am anything but an expert about these things, is that it will not be needed. The disease seems to have already plateaued in China, and I expect other countries to be a bit better at reducing the spread. Thus, I expect that the spread of the disease will slow down significantly before a vaccine can be approved for use. I could easily be wrong about that, however.

No Other Explanation: Dinosaur DNA!

Cells In two different stages of mitosis. The dark areas represent DNA, which is most likely damaged but still at least partially arranged in chromosomes.
(image from paper being discussed)

Despite the overwhelming evidence, there are some who are skeptical that soft tissue can be found in dinosaur fossils. Even among those who think that there may be soft tissue in some dinosaur fossils, there are those who think that there is no way complex molecules like DNA could possibly be found in that tissue. Well, Dr. Mary Schweitzer and her colleagues have recently published a study that, as far as I am concerned, should put all doubts to rest. Yes, dinosaur fossils do contain soft tissue and original dinosaur biomolecules, including DNA.

The study involves a detailed investigation of fossils from duck-billed dinosaur (Hypacrosaurus stebingeri) nestlings that are supposed to be 75 million years old. The authors examined cartilage tissue under the microscope and found what were obviously cells. Of course, that’s nothing unusual. The Dinosaur Soft Tissue Research Institute has some really great examples of dinosaur cells and other delicate structures from dinosaur fossils. They also have evidence for RNA in the fossils (see here, here, and here).

What’s new (and in my mind definitive) about this study is that they applied two different DNA stains to the tissue. The stains are designed to bind only to DNA, and when you use two different stains and see them both bind to the same structures, you have doubly confirmed the presence of DNA. Of course, what they saw could be DNA stains binding to DNA that contaminated the fossil, right? Wrong! The image at the top of the post indicates why. If I ask anyone who has taken a good high school biology class what the red box is drawn around, he or she should be able to tell me.

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A Newly-Discovered Component of Blood!

This transmission electron microscope image shows the structure of the newly-discovered blood component: functional mitochondria enclosed in vesicles.
(click for credit)

I have been teaching science for 34 years. I have been writing science textbooks for 27 years. I can’t tell you how many times I have written about blood and its components. Indeed, I am writing a 7th-grade textbook right now (Science in the Atomic Age), and it has a couple of sections on the properties and characteristics of human blood. As usual, I discuss the cellular components of blood (red blood cells, white blood cells, and blood platelets) as well as the chemical components of blood (blood clotting factors, water, electrolytes, various proteins, etc.). I honestly thought we understood blood pretty well. However, God’s creation is so complex and intricate, it still surprises us. In a recently-published paper, scientists have found that blood contains something no one ever noticed before, and it is neither cellular nor chemical. It is something in between!

To understand what was found, you need to know that cells in fungi, plants, animals, and people contain small structures that are responsible for burning chemicals from your food and packaging the resulting energy into small units that the cells can use. Those structures are called mitochondria. While most of a cell’s DNA is held in the nucleus of the cell, there is some DNA found in the mitochondria. Not surprisingly, it is called mitochondrial DNA (mtDNA) to distinguish it from the DNA found in the nucleus, which is called nuclear DNA (nDNA).

I had learned quite some time ago that there was a lot more mtDNA in blood than nDNA, but that always made sense to me. Red blood cells have neither, because they eject their nucleus and mitochondria when they mature. However, white blood cells have both. When someone extracts DNA from blood, he or she is getting the nuclear DNA from the white blood cells. Well, each cell has several mitochondria and only one nucleus, so the white blood cells will contribute more mtDNA than nDNA to blood. In addition, blood platelets have mitochondria but no nucleus, so they are contributing a lot of mtDNA and no nDNA.

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Our Best Computer is Positively PRIMITIVE Compared to the Human Brain

A small selection of the connections in the human brain (left) and the world’s most powerful supercomputer (right).
Image on left by the PIT Bioinformatics Group. Image on right by the OLCF at ORNL.
Creative commons licensing. Click for specifics.

I have been working on my new book, Science in the Atomic Age, which (Lord willing) will be published this summer. In the section where I cover the nervous system, I compare a mouse brain and a human brain to computers. It’s rather fascinating. Below, you will find a slightly-edited excerpt from that discussion. Please note that the students have already learned that neurons are cells found in nervous tissue and that the integumentary system is the system of organs that makes your skin:

The brain has three major divisions: the cerebrum (suh ree’ brum), the cerebellum (sehr’ uh bell’ uhm), and the brain stem. The cerebrum is in charge of most of the really complicated things that the brain does. For example, it receives signals from your eyes and interprets them so that you can see. It receives signals from your ears and interprets them so you can hear. It receives signals from all the nervous tissue in your integumentary system so that you can figure out what you are touching as well as things like whether you are too warm, too cold, or comfortable. It also helps you learn, and it stores your memories. All this takes a lot of work, so it requires a lot of neurons.

How many neurons? The average adult cerebrum contains about 20 billion neurons. That number doesn’t mean very much by itself, so by comparison, the average adult mouse cerebrum contains about 2.5 million neurons. So the human cerebrum contains about 10,000 times as many neurons as a mouse’s cerebrum. Of course, a mouse is much smaller than a person. By weight, a person is about 3,000 times as heavy as a mouse. At least part of the difference between a mouse’s cerebrum and a person’s cerebrum is due to that. But people are much more intelligent than mice, and the number of neurons in the cerebrum must also be related to that.

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68% of the Universe May Not Exist!

The history of the universe, according to the standard model of cosmology (click for credit)

Unsuspecting students are often taught “facts” that are anything but actual facts. Consider, for example, what NASA says about the nature of the universe:

It turns out that roughly 68% of the universe is dark energy. Dark matter makes up about 27%. The rest – everything on Earth, everything ever observed with all of our instruments, all normal matter – adds up to less than 5% of the universe. Come to think of it, maybe it shouldn’t be called “normal” matter at all, since it is such a small fraction of the universe.

What is this thing called “dark energy” that supposedly makes up more than half of the universe? NASA honestly says that no one has any idea. However, NASA assures students that we know that 68% of the universe is made up of it.

Of course, what NASA (and most astrophysicists) neglect to tell students is that the entire existence of dark energy, including its amount in the universe, is based on a myriad of assumptions, some of which are almost certainly not true. Nevertheless, they assure students that they know dark energy exists and that most of the universe is made up of it. The cold, hard truth, however, is that everything we know about dark energy is based on models, and those models are built on assumptions. If the assumptions are wrong, the models could be wrong, and if the models are wrong, the whole idea of dark energy could be wrong.

This issue was brought front and center with the recent publication of a paper that challenges one of the assumptions that is instrumental in the conclusion that dark energy exists. If the results of this paper are confirmed, dark energy will be thrown into the same trash bin as phlogiston, luminiferous ether, and the impossibility of quasicrystals.

Continue reading “68% of the Universe May Not Exist!”