The Molecule Of Life, Part I

Many people live under the false pretext that life on Earth comes down to the presence of the nucleus and its DNA. If we were to abide by this assumption, we would presume that an enucleate cell (lacking a nucleus) would not be able to function as it does normally. However, this is not the case. Experiments were performed whereby the nucleus of a cell was removed in order to see what would happen. The cell not only survived but also continued to carry out its normal living functions and processes. So the brain of the cell had to be present elsewhere.

Now consider humans. Without our brains we die. This leads us to question what it is exactly that the brain does to keep us alive. Well, it assesses our surroundings, taking in environmental information and transforming this data into signals that can be understood and acted upon in the body. It is also potent in its omission of some environmental signals as well as with the emission of messages sent by the body. Does the brain’s function sound familiar? Think back to GCSE biology, and the role of the cell membrane: “The cell membrane controls the movement of substances into and out of the cell”. So essentially, the human brain has the same role as the cell surface membrane.

This links back to one of my previous articles on the impact of genetics versus that of epigenetics. Naturally, the genetics of a cell comes from its DNA information in the nucleus. The influences of the environment, however, enter the cell via the cell surface membrane. Does that not validate the importance of epigenetics over that of genetics, now that we have established that the cellular brain is in fact the plasma membrane and not the nucleus?

Let’s now go back to the title – the molecule of life. What is it that triggers life processes to occur? And once the occurrence of a reaction has been triggered, what is it that enables the process to be carried out? Surely not the DNA as it does not leaves the nucleus, and we well know that reactions do not occur in the nucleus of the cell. Rather, they occur in the cytoplasm, where hundreds of proteins are present.

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Bad Science By Ben Goldacre – The Truth About Media Science Stories

“The media is game-like world of blurry truths, where the vague narrative shape of a story matters more than clarity, accuracy and evidence.”

In this book Ben Goldacre, doctor and author of the weekly Bad Science columns in The Guardian, extends his columns which criticise reports done on science and medicine in media nowadays. This book takes the reader through some of the aspects media misrepresentation of science which he disapproves of via clear-cut sections, making it very easy to understand.

Throughout the book, the most common theme noticeable will be Goldacre’s frustration at the lack of evidence-based science these days, commonly known as pseudoscience (collection of beliefs mistakenly regarded as being based on scientific methods). This means that the accounts reported as news don’t provide any substantial evidence for that result. Usually, the only people who are curious about these stories are those who have an interest in science of medicine and you can, therefore, presume that they’ll have the basic knowledge about the subject yet these articles are dumbed down to such an extent that it leaves out most of the crucial information, mostly because the journalists themselves don’t have any understanding of the matter.

The book takes you through 16 features of what’s thought to be “bad science”, starting off with detoxification processes which can be proved to be rubbish by some simple experiments (what I liked was that he would show you how to do the experiment at home so you get your own results, rather than taking his word for it). The more serious issues in the book comprise of homeopathy, where it is thought that a person can be cured by small doses of the substance that caused that disease, the placebo effect and the MMR vaccine deception, all of which is has the underlying message of how statistical facts to back up the hypothesis is lacking.

What I found particularly funny was how Gillian McKeith had her own personal chapter where Goldacre just completely tore her down with his ridicule (he really is not fond of nutritionists). An amusing quote which he’s used many times in any talks he gives is how she believes that dark-leaved vegetables, as they have a lot of chlorophyll in them, will “reoxygenate your blood”. I’m hoping that anyone with the basic GCSE education doesn’t need any explanation (watch the video above if you do but be warned, he speaks extremely fast).

What I’ve mentioned above is only some of the things talked about, read this book which reached #1 in the UK non-fiction charts to find out the rest!

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Will the Chytrid Fungus Kill All Our Frogs?

Scientists in Australia first discovered the chytrid fungus – scientifically referred to as Chytridiomycosis dendrobatitis – in the late 1970’s. However it is believed to have first occurred in Africa.

The chytrid fungus enters the amphibian’s body through the skin where it begins to multiply and spread in the middle layers. This becomes an increasing problem for the frog, as it breathes and drinks through its skin. In order to combat the fungus, the frog produces more skin cells. However, this only allows the fungus to spread further and the skin to thicken. The frog loses its ability to breath and drink, causing it to become weaker and eventually die of suffocation.

As a result of this chytrid fungus, 120 of Central America’s amphibian species have become extinct since 1980, with many more in grave danger at present.

So what can be done in order to stop the extinction of many more amphibian species? Veterinarians and researchers are ensuring that infected species around the world are being taken in under care. The fungus is then eradicated from their bodies, as this is possible to do in a controlled environment. The species are taken into zoos. However this poses another problem. Frogs and amphibians cannot continue to live in zoos permanently. Their natural habitat is the wild and our hope is that someday they may be released back into the wild with no worry that the fungus will attack again. But how to stop the chytrid fungus? Scientists need to find a way of completely eradicating it from the wild. Alternatively, a breeding program (selective breeding) could be put into place, whereby the frogs would not only become resistant to the fungus, but also reproduce to enlarge the number of individuals in their species back to their original size.

A Panamanian Golden Frog

In Panama, the Golden Frog is under threat. Thankfully, measures are being taken: the frogs are being put under quarantine and then into an enclosed space referred to as the “clean room”. In this room they are rid of the fungus, fed and looked after. Space is limited, hence why they are providing the frogs with a new space in one of Panama’s zoos. This is just one example of the amphibian crises that are occurring and being dealt with as a result of the chytrid fungus.

Personally, I believe that although this is a worrying issue at the moment, it is something that can be managed and eventually resolved. How long the process will take I cannot say, however the surveillance and care of the endangered species is already a big step forward. The next, as mentioned earlier, is to find a solution, which will allow these frogs and other amphibians to be released back into the wild without risk of infection and extinction once more.

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Are We Losing The Fight Against Superbugs?

First of all, let us define the word ‘superbug’. More scientifically known as multi-resistant bacteria, superbugs are bacteria that contain several resistance genes. These genes can code either for enzymes which destroy or alter the antibiotic, or for the production of the efflux pump which can transport antibiotic compounds out of the cell. The genes tend to be found in the plasmids (rings of DNA) in the bacterial cells. This makes it easier for lateral gene transfer to occur, whereby genes have the ability to jump from species to species within the bacterial kingdom, and is one of the reasons that superbugs arise in the first place. Lateral gene transfer takes place via three different mechanisms: conjugation, transformation, and transduction. However, we shall not go into the details, as they do not concern us. It also allows antibiotic resistant genes to spread at an alarmingly fast rate, making it hard for scientists and researchers to find the appropriate drugs to kill off the bacteria quickly enough.

A specific type of bacteria will have many different strains, each carrying very subtle genetic mutations. This makes some of them more resistant to an antibiotic than others, and hence natural selective breeding between the bacterial colonies in the infected organism occurs, leading to increased germ resistance. This concept is known as survival of the fittest (one of the basic principles of Darwinian evolution). For example, if MRSA was present in a patient, and the patient was treated with the penicillin antibiotic, some of the bacteria would be destroyed, while other strains would be more able to cope with the drug and create resistance to it. These strains would then reproduce and spread, so that a new antibiotic would be needed in order to kill the bacterium.

The problem nowadays is that antibiotics are being overused and prescribed without being needed. This is as a result of the majority of the public who are under the false impression that all viral infections should be treated with antibiotics. Some doctors who feel they do not have the time to explain why and how it would not help may just prescribe it to the patient despite the consequences. So what are the consequences? In what way could a useless antibiotic prescription be harmful and potentially dangerous? Well, instead of killing off the bacteria present in the organism, the antibiotic would be solely helping it become resistant, in many cases leading to the development of the infamous superbugs. Day-to-day commodities such as antibacterial hand wash are essentially doing the same thing and making it more difficult for us to win this so-called fight against multi-resistant bacteria.

According to the World Health Organisation (WHO), around 10 million people die each year as a result of antibiotics that no longer work. 10 years ago, the pneumococcus bacterium – the cause of most cases of pneumonia, meningitis and ear infections – could be treated using any of 10 antibiotics. Nowadays, 1 or 2 of these antibiotics is left fully functioning. Even more recent, NDM-1 bacteria – a new superbug – is becoming of increasing concern. Even though there have only been 50 cases in the UK, scientists fear that it will become global. Why? NDM-1 bacteria carry a gene, which encodes an enzyme called NDM-1. This enzyme can fight and destroy the antibiotic(s) working against it, making it resistant to even the most powerful antibiotics (namely carbapenems). It can exist inside different bacteria, and so we fear that lateral gene transfer will occur. Consequently, this would allow bacteria that are already resistant to certain antibiotics to carry the gene for NDM-1 enzyme. In other words, the antibiotics that could be effective against these NDM-1 superbugs would decrease hugely as the gene spread and more NDM-1 bacterial communities formed.

So, are we losing the fight against superbugs? Well, as it is today, our only solution to the problem also seems to be one of its principal causes – antibiotics. Although their aim is essentially to fight the infection and kill off the bacteria, they are also unintentionally strengthening the resistance of many bacterial communities. To make matters worse, bacterial genes are constantly mutating, creating many different strains of just one type of bacterium. Not only does this mean that different antibiotics are needed for different strains, this also means that the naturally more resistant strains will survive the antibiotic course, thereby spreading and reproducing. And once the antibiotic made to fight off that particular strain has been put into practise, yet another strain may have been produced as a result of these subtle genetic mutations. Lastly, as you might already know, bacteria love to divide and replicate, and are very efficient at doing so. They can double their numbers in just 20 minutes. Meanwhile, lateral gene transfer may be occurring and causing other types of bacteria to become a threat too.

We are trapped in a vicious cycle, which at present, does not seem to be coming to an end.

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Stop Crying, That’s Why You’re Still Single

Everyone knows how men can’t bear a woman crying but actual evidence was found a few months ago to prove there is a special chemical in tears that result in men actually being “turned off”.

I read an article which described a study carried out which proved the theory that men are less sexually aroused when women shed tears when upset. Six women who could cry with ease watched films like Terms Of Endearment and My Sister’s Keeper (the usual chick flicks, I’m surprised The Notebook wasn’t on here) which, as expected, caused them to weep uncontrollably and these tears were then preserved by absorbing them with pads. Young men then sniffed these pads whilst looking at arousing pictures of women but there was also a control (anyone who does biology should be familiar with this) in the form of a saline solution (water and salt) being inhaled for comparison. The sexual excitement was measured by their heart rate, skin and brain responses and testosterone levels. The results, as you can guess, were that the emotional tears triggered a decrease in all of the criteria. One of the researchers (Israel Weizmann Institute) stated “Basically what we’ve found is the chemo-signaling word for ‘no’ — or at least ‘not now’.”

The message behind this type of behaviour that the tears induce is unclear at the moment. One hypothesis is an evolutionary protection against rape or deterring men from sex when PMSing/menstruating.

Don’t you think the experiment’s a bit biased? Only testing the effects women’s tears have on men? What about the other side? Well, it was initially going to both but the reply to the advertisement searching for male criers was too low. One.

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Phobia Of The Day: Cyberphobia

Those with this phobia can’t even read this post or google it..

This is a persistent, irrational fear of computers and technology.

Treatment:

Behaviour therapy or psychotherapy




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Epigenetics vs. Genetics

Epi – meaning over/above – genetics is the study of factors that affect DNA blueprint and gene expression, other than changes in the DNA sequence. The science of genes (genetics) is completely disregarded in epigenetics.

People tend to think that we are born with a concrete and unchanging DNA blueprint. This is untrue. Scientists and epigenesists have shown us, through experiments, that mechanisms other than those within the DNA sequence (known as epigenetics) will affect the activity of a gene and override some of the principles of genetics. For example – put simply – that our genes determine our physiology and chemical behavior.

Consider the following experiment:

The agouti mouse has a specific gene, which sources the reason for the mouse’s yellow fur and its obesity. Agouti mice are therefore very prone to diseases such as cardiovascular disease and diabetes.

This particular gene is passed onto future generations through reproduction, and therefore so are the agouti mouse’s traits. Hence, all agouti mice will have yellow fur and be obese.

The above represents the conclusion drawn from geneticists.

However, mechanisms such as methylation[1] can cause gene suppression, without altering the underlying DNA sequence. They do this by changing the positioning of regulator proteins[2] on the DNA, and can consequently activate or deactivate genes in the DNA strand. From the viewpoint of an epigenesist, this would stop the effect of the agouti gene, thereby overruling the genetic ideals involved.

The scientists performing the experiment took two groups of agouti mothers. One group was given methyl-rich supplements; the other was given nothing.

The offspring of the agouti mice that had not been given anything was as expected – yellow fur and overweight. The young of the agouti mice that took the supplement and underwent methylation differed to the other group in physiology and appearance. They had a normal brown coat, and were very lean. Nevertheless the gene responsible for agouti traits had been inherited.

 

This experiment helps to explain and to prove to us how our DNA blueprint is variable and changing, according to environmental factors (sometimes ambiguous). The methyl supplement given to one of the two groups of mothers altered their DNA blueprint, causing the deactivation of the agouti gene. So effectively, yes, the gene was passed on to their offspring, and yes, the offspring also inherited their DNA blueprint. However it was not the original blueprint, and the expected characteristics that usually follow the presence of the gene were not observed.

Humans and mice contain approximately the same number of genes – 24 000. Yet we are far more complex organisms than mice. Therefore, the answer as to why that is cannot lie in the make up and abundance of the genes, but rather what genes inside us are activated that perhaps are not in mice (and vice versa). From this we can draw that genes cannot be the structures that control us; we should focus instead on understanding how they are or aren’t put into play.

On a separate note (relevant nonetheless), the supposed big breakthrough when the two genes responsible for breast cancer (BRCA1 & BRCA2) were discovered proved to be less helpful than we thought – only 5% of breast cancers are hereditary. The other 95% occur as a result of environmentally induced mechanisms involved in epigenetics.


[1] The addition of a methyl-rich supplement to a substrate, or the substitution of an atom by a methyl group. In this case, we are referring to the methylation of DNA.

[2] Regulator proteins are a particular type of protein found on the DNA. When they cover a specific strand of the DNA molecule (a gene), that gene is tightly bound and latent. Methylation causes the shifting of the regulator proteins, thus activating the gene underneath.

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