Category: Biology

Autotrophic Humans

(I’m going to have a highly controversial foray into the world of biology today, so do bear with me)

Could autotrophic humans bring an end to the need for chocolate cake, bacon and pasta? Or could there be something better in it for everyone?

In the world of biology, the huge range and diversity of Biota (living things) can be broadly broken down into two main groups, autotrophs and heterotrophs. An autotroph, like plants and many bacteria, are organisms that can produce complex organic compounds, such as carbohydrates, fats, and proteins from simple substances present in its surroundings, generally using energy from light (by photosynthesis) ,and carbon dioxide and water from the air and soil . Heterotrophs, like you and me, on the other hand can’t make these complex molecules, and so need to ingest them, most usually through the eating of many delicious foods. But in today’s world, where space is at a premium and food prices are sky rocketing, surely there are better ways of gaining energy from the world, rather than eating its flora and fauna? What if, like plants, we had evolved differently and could create our own energy and proteins using chloroplasts in our skin? For one, we would most probably all turn green from the amount of chlorophyll, but what about the practical side of it? To start, could we actually survive on nothing but sun light, carbon dioxide and water? And what effects would this have on our environment as land use and populations move and change?

Well, first, let’s have a look at the maths (I’m going to make a point here as many people have brought it up with me; ALL of these numbers are optimal numbers, they don’t take into account bad weather, questionable dress sense or how well aligned with the sun you are, they are simply the best and most favourable estimates for this strictly hypothetical experiment). First things first, let’s have a look at our subject; an average adult British male has a usable surface area of about 1.88m2. This is actually not a lot, but we’ll talk about that later. Now, the average solar power absorbed by the entire earth’s surface is roughly equivalent to 164 petawatts, so the amount absorbed by your average male of 1.88 m2 is in the order of 564 Watts (about half a toasters worth of power). So over the course of the day, with six hours of strong, good quality sunlight, our subject would absorb nearly 12,000,000 joules of energy. This does sound like a lot, but do remember, all this solar energy has to go through the chloroplast first, before becoming usable energy. Chloroplasts are deceivingly inefficient, only turning around 6% of the absorbed light energy into actual, usable energy. For plants and bacteria this is more than enough but for humans this means only 720,000 joules of that glorious sunshine becomes usable energy. This value is far short of our bodies recommended energy intake of 10.5 million joules, in fact it’s just under 7% of what we need.

So that’s a no then to running on sunlight. The problem is that humans just aren’t big enough; we have a lot of mass (and therefore a lot of things that need energy) and not much surface area to go along with it. This, however, is the opposite for plants, who have very little respective mass, yet are given a very large surface area due to all their leafy bits.

But it’s not all doom and gloom. Although 7% doesn’t sound like much it all adds up. Just think 13,800,000 km2 of the earth’s surface is taken up by crops and farmland, 7% of this is nearly 1 million square kilometres, an area about the size of Egypt! This land could be put to use as housing to ease the worlds crippling over population and lack of space, or even as extra public parks and spaces.

But what if we kept this land as farm land? What if we used it to a better purpose? 1,000,000 km 2 of farm land equates to a lot of food. If we take the example of wheat, the world’s staple food and one of the most important grains in production. In the year of 2010 the world wheat production was 651 megatons. If 7% of this was going spare, 45.5 megatons, we would have enough grain to feed nearly half a billion people (assuming average consumption of 100kg per annum).  But then again, there are around 1 billion malnourished people in the world, so would this 45.5 megatons of wheat stretch that far? Let’s look at the human body’s most essential micronutrient, iron. Iron is needed to allow the oxygen we breathe in to bond to the haemoglobin in our blood, without which, we simply wouldn’t be able to live. Iron deficiency is defined as having less than 55% of our recommended daily intake of iron. So if we assume that less than 55% of any food stuff equates to malnourishment, or a food deficiency, our ½ billion people worth’s of food could feed every malnourished child, adult and homeless person in the world (within the realms of statistical error).

To conclude, the idea of individuals running off of sunlight and chloroplast may not be viable, but if we add up the small positives, they make a very large difference

Alex Davis


A calculator




1. not mortal; not liable or subject to death; undying.

2. remembered or celebrated through all time.

3. not liable to perish or decay; imperishable; everlasting.

Immortality; the legendary state that humans have been striving for a very long time. But it is impossible to achieve; nothing organic can live forever. Or can it?

Meet Turritopsis nutricula. This little hydrozoan has achieved what no other multicellular organism (that we know of) has ever achieved before; it is the immortal jellyfish. Well to be precise, the biological immortal jellyfish. This means that theoretically, one of these little creatures could quite happily live for an indefinite period of time, except that most of them are likely to succumb and die off due to predation or disease, especially in the plankton stage.

The immortal jellyfish, in the flesh



So how does the immortal stinger do it? Well let’s start from the beginning:

The male and female jellyfish release gametes (sex cells) and the eggs become planula larvae that seek out a surface to rest on before becoming a polyp (which is the first form jellyfish take). These hydrozoan polyps are called hydroids. They make up a hydroid colony, with polyps all connected to each other by a tube known as a stolon.

The hydroid colony then buds and releases tiny jellyfish (which are scientifically known as medusoids) that are only a few millimetre across. The tiny jellyfish feed on plankton and grow to a maximum size of about 4.5 millimetres (0.18 in) after 2 to 4 weeks where they take their second form and are now known as ‘medusa’. They are now sexually mature and can reproduce in the usual way, but if the conditions get a little dire, such as starvation, changes in temperature or drops in salinity, they switch up the style and carry out something amazing.

The hydroid colony













An adult will actually revert back into a polyp, by absorbing the tentacles and the jellyfish bell as it reattaches itself to the ground. It then extends those its stolons and begins making a whole new hydroid colony. What’s even better is that they can perform this cool trick at any time during jellyfish development.

The immortal jellyfish does this by going through a process known as cell ‘transdifferentiation’. Cell transdifferentiation is when an already differentiated cell is altered and transformed into a completely new cell. This is one organism that the Grim Reaper doesn’t have an easy time dealing with!

It’s a stinging sensation!



Now imagine if humans could harness that potential. We could use the process to heal or replace damaged tissue without any adverse effects. Immortality may not as far out of our reach as we had once thought.


By Myles Scott – The Demotivator

One Nasty Bacteria

Good news everyone!


Group A streptococcus is a bacterium that causes many illnesses from strep throat to scarlet fever. The Group A streptococcus bacterium is able to cause so many diseases and dodge the bodies immune responses because of certain factors. One is that it has M proteins on its surface, which give it acid and heat resistance, an advanced ability to attach to its host and resist phagocytosis (being engulfed by white blood cells). It is chemically similar to the body’s connective tissue meaning it can go unrecognized by the body thus avoiding phagocytosis. Another factor is that it can produce three types of exotoxins, such as streptokinase – a toxin that digests blood clots, allowing the bacteria to invade the body – allowing it to cause numerous diseases. One of the most shocking of the diseases it causes is Necrotising Fasciitis.

Necrotizing Fasciitis

If Group A streptococcus manages to pass through the throat lining or an opening in the skin then you have most probably contracted Necrotizing Fasciitis and practically zero chance of getting out unaffected. There are two types of Necrotizing Fasciitis:

  • Type 1 – polymicrobial; the infection consists of more than just one type of bacteria
  • Type 2 – monomicrobial; the infection consists of only one type of bacteria, this is the most common type of the disease

Group A streptococcus is only one of many bacteria that cause Necrotizing Fasciitis but is the main cause of type 2 infections.

At first you start off with minor symptoms that you would put down to either an allergy or a normal common flu, maybe inflammation/ irritation at the area of infection meaning it is easy for the doctor to misdiagnose the patient.

If your lucky the doctor will have heard of the disease and has a suspicion that you are infected, he will carry out several tests on factors such as your haemoglobin, liver proteins and white blood cell count. Once it has been confirmed that you are infected, the doctor will perform surgery and aggressively remove the infected tissue to stop the spreading, however it is likely you will be severely disfigured.

If you’re unlucky then you’ll carry on normally until it becomes too painful or you end up passing out and the doctor performs exploratory surgery and discover most of your tissue gone. You will not get out of this unchanged; disfigured or dead (to put it bluntly). It is sad to know that this disease only has around a 30% survival rate.

It’s noteworthy that the bacterium does not physically eat your tissue but releases exotoxins. One of the toxins known as a Superantigen causes some T-Cells to activate which in turn causes an overproduction of cytokines (proteins used for cell signaling) and possibly Toxic Shock Syndrome – a whole other thing on its own.

Do not fret however as it is unlikely that it will infect people with a generally healthy life style. 70% of cases occur in those with health problems such as diabetes, alcoholism and drug use. A way to make sure that you don’t get infected is to always clean cuts thoroughly.

So if you don’t have enough to worry about already such as work, paying the bills and having to listen to a Connor Maynard song then feel free to concern yourself with flesh eating bacteria.

Christian Tuckwell-Smith – Farnsworth


Bill Bryson: A Short History of Nearly Everything

Climate change is one of the most common topics discussed in the news. The weather and climate play a huge role in affecting our health, for example, a large flood can destroy people’s homes and lead to the increase in many water-borne diseases like cholera or an increase in temperature and humidity in an area could enhance the spread of some diseases, such as malaria.

Although some people may believe there are health benefits – fewer cold-related deaths in winter – the disadvantages definitely outweigh the advantages. There are predicted to be many heatwaves (though the weather this July doesn’t seem to agree!) and these can be deadly particularly to elderly and sick people. In the USA, heatwaves kill more people than all other natural disasters put together. Higher temperatures also increase the risk of food-borne diseases, above average temperatures in Europe contribute to around 30% more reported cases of Salmonella poisoning.

There is likely to be an increased number of droughts and floods, mainly in poorer countries, due to the increase in temperatures. Crop yields are predicted to fall by 50% by 2020 and variable precipitation, along with higher temperatures, will lead to a decrease in the production of staple foods, making more people malnourished. Climate change will also cause sea levels to rise and the seawater which flows onto the land due to loss of ice sheets will contaminate low-lying agricultural land.

In my view, the most serious problem is that the spread of infectious diseases, such as malaria, will increase to countries that at the moment are not at risk. Warmer weather is also likely to speed up the vector’s life cycles and provide more opportunities for breeding. Mosquitoes are responsible for more human deaths than any other single organism. Due to mosquitoes spreading malaria, around 1 million people are killed a year from the disease. Malaria is only prevalent in areas where a particular species of mosquito lives. So if climate change changes the distribution of mosquitoes, the spread of malaria will also move to. This is a serious worry for the populations in the highlands of Kenya where scientists have found that for an increase in temperature by 1°C leads to at least a ten-fold increase in mosquito numbers. This leads to a prediction that somewhere between 220 million and 400 million more people will be at risk from malaria.

All in all, it is clear that climate change will have a great impact on our health in many different ways, affecting all countries around the world with diverse consequences.

Steph White

First of all, this is a more advanced expansion on “You ate a peanut? Quick, block the airways!”, so I warn you now this may get a little complicated. For further reference, here is a table to show the differences between each Immunoglobulin (antibody) class, credit to

‘Allergic’ reactions, or hypersensitive reactions as they will be referred to for the rest of this post, are divided into the 4 main assortments: ‘Type I’, ‘Type II’, ‘Type III’ and finally ‘Type VI’; generally all allergy-based reactions fall into these groups.  All of these involve immunoglobin antibodies (G/E), minus type IV, which works on a series of T-cells assisting to stimulate a cytotoxic response. The science behind the reaction is listed below, along with features that provoke the response, the underlying effectors’ mechanism, and the nature of the ailment caused.

Allergies are type I hypersensitive reactions: type I hypersensitive reactions result from the binding of the antigen to the immunoglobin E (to be referred to as IgE), already bound to its FC receptor (the cell receptor on mast cells); FCεRI receptors, typically associated with hypersensitive reactions, and whose surface receptors have an exceptionally high affinity to the IgE (A measure of the strength from which the molecules bind to, in this case, the receptor). The binding transmits a signal encoded by proteins  within the mast cell to the nucleus, and this then leads swiftly onto the degranulation process of the mast cell, and its ultimate release of inflammatory mediators, causing potential anaphylactic symptoms when the mediators disperse. In the mast-cell based hypersensitive reaction, cross linkage of FCεRI by the antigens and immunoglobin causes mast cell activation and degranulation; primary mediators (e.g. Proteases, histamine and heparin) cause a standard inflammatory reaction, while secondary mediators -such as platelet allowing factor (or P.A.F for short)- have side effects which cause ‘heavier’ internal stimulation: the symptoms of Anaphylaxis. An example of type one would be the recipient inhaling flower pollen, these particulates are spotted by the IgE and grouped into clumps; which binds to the FCԑRI receptors (FC receptor). These then begins an inflammatory response, depending of the severity of the hypersensitive reaction.

Type II Hypersensitive reactions are due to small molecules that bond to the surface components of internal Human cells, producing modified cells that are seen as ‘foreign’ by the immune system. The immune system’s B-cell response produces immunoglobin G (to be referred to as IgG) via a MHC/HLA class I molecular stimulation (molecules bind to the B-cell’s receptor, causing the cell to release its immunoglobin G, and bind to the FC receptor on mast cells, beginning the release of primary inflammatory mediators). A MHC class I cell’s  function is to display fragments of proteins -as a bacterial antigen- from within the cell to T-cells; healthy cells will be ignored, while cells containing foreign proteins will be attacked by the immune system, a process initiated by the Immune system once the T-cells recognise the protein. T-cells cause B-cells, whose only purpose is to create antibodies, to track down this foreign protein. These antibodies bond onto the modified complexes, causing their destruction via phagocytosis and complement activation (initiation of a series of reactions involving components of the Plasma [liquid in the blood], leading to the elimination of the cell now seen as a ‘pathogen’ modified complex). The body is attacking its own cells. A hypersensitive reaction to Penicillin is described as ‘Type II’, and such is the reason doctor’s will often ask (before being prescribed drugs) if the recipient is ‘allergic’ to any drugs, often led by “such as penicillin?”, as penicillin is prescribed often, and is one of the more popularized drugs to hold an sensitivity to.

Type III Hypersensitive reactions are due to tiny complexes formed by soluble antigens binding to the IgG/IgA made to combat them. Some of these complexes become deposited in the walls of blood vessels and alveoli of the lungs. This leads on to cause a response (generally inflammatory) that mainly damages tissue, impairing its function (impairing the lung’s function for example, the ability to breath). When other proteins from a non-human species are given to a human patient in medical issuing, or when mould spores are inhaled, type III is to be expected.

The molecules described as ‘effectors’ in type I, type II and type III are all antibodies (immunoglobin G/E/A). Type IV hypersensitive reactions, however, are cell-mediated instead, involving T-helper cells (CD4 Th1 cells): T-cells that –in this case– bind to the molecules on the antigen and acts as a receptor, in order to augment the T-cell’s response to the antigen; usually inflammatory.The helper T-cells response is usually due to the introduction of cytotoxic molecules that come into contact with the skin; these lipid soluble molecules (molecules that can easily access through cell membranes in the skin) covalently bond to human proteins, causing them to appear chemically modified. These chemically modified proteins degradate (the process involving the chemical breakdown of organic substances by living organisms) to reveal –to what the body sees as– foreign peptides (a chain of amino acids, packaged into a small[er] space). They bind to MHC/HLA class I molecules and stimulate a cytotoxic, destructive response caused by T-cells. The cytotoxic response causes inflammation, and is commonly associated with an ‘itch’ or ‘sting’, but usually nothing further, as where type-I/II/III can be found –more commonly- in fatal circumstances.

Leaves of three? Leave it be!” – Old saying to avoid Poison Ivy.

Examples of a type IV hypersensitive reaction are both nettle and poison ivy stings, which inject chemicals such as the long-winded ‘pentadecacatechol’ into tissue, bypassing the skin as its lipid soluble nature allows it to diffuse through plasma membranes, consisting largely of phospholipids.

– Cole Holroyd, Sources:

The Immune System by Peter Parham,

To summarise:

    Hypersensitivity             type                                                   PROPERTIES
  I Antibodies (IgE), bond with the FC receptors on the mast cell. This causes mast cells to start the process of degranulation: eventually releasing their primary and secondary mediators, which cause symptoms.
  II Small, foreign molecules chemically modify cells. The body then views and recognises the cell as a pathogen, and proceeds to inflict the process of phagocytosis (destruction of the cell) upon it. This is commonly seen as the body ‘attacking’ its own cells.
  III Minute complexes formed by soluble antigens bind to the IgG designed to combat them. These complexes are then deposited in the walls of small blood vessels/alveoli in the lungs, that damages tissue and are the central cause of other internal symptoms (e.g. difficulty to breathe).
  IV Lipid soluble molecules bond to human proteins, causing them to appear chemically modified. They yield abnormal peptides, which binds to HLA/MHC class I molecules and cause a cytotoxic and ultimately destructive response from the immune system.

A ten year old Swedish girl has become the world’s first patient to receive a vein which was donated by a cadaver and treated with stem cells.

The girl required the transplant after suffering from chronic blockages of her hepatic portal vein. The hepatic portal vein is a large vein (roughly 8cm long in adults) in the body which carries out the role of transporting blood from the gastrointestinal system (spleen, gut) into the inferior surface of the liver. The vein is called a ‘portal vein’ as it cannot truly be considered a vein. This is because it carries blood to the liver, not the heart.

In order to be transplanted, the 9cm section of vein, removed from the groin of the cadaver, was chemically ‘stripped’ of the cadaver’s DNA. The next step was to take endothelial and smooth muscle cells from the recipient’s bone marrow and culturing these cells in the lab. The surface of the vein was then coated in the cultured cells and transplanted into the recipient. As the vein contained no trace of the donor’s DNA and was already coated in the recipient’s DNA, there was no need for the girl to take immunosuppressive drugs.

Immunosuppressive drugs are given to patients receiving donated organs which have not been treated with stem cells in order to prevent the body’s immune system from attacking the donated organ. This process is known as rejection. There are three main types of immunosuppressive drugs currently being used for transplant patients:

cyclosporins – these prevent or inhibit the production of T-lymphocyte cells, thus preventing the organ from being ‘attacked.’

azathioprines – these disrupt and prevent the synthesis of RNA and DNA, thus disrupting cell division.

corticosteriods – these suppress the inflammation caused by the immune response which occurs when an organ is being rejected.

Many transplant patients are required to take drugs like those previously mentioned for the rest of their lives. This can lead to other health complications, so there is hope that the new process of stripping donated organs of the donor’s DNA and recoating with stem cells with reduce the use of immunosuppressive drugs in transplant patients. This method has been previously used in 2009, when a woman received a windpipe transplant using the same method. In the future, doctors and research hope to increase the potential of this transplant method by the use of animal organs or synthetically created organs.


by Laura Cherry

In the midst of an anaphylactic / allergic reaction, your body perceives a molecule (antigen) as a threat, or scientifically an ‘allergen’. With the onslaught of Hay Fever drawing ever so closer as we approach summer, pollen will act as the allergen that your body wrongly recognises as a threat. Inhaled allergens can cause asthmatic attacks, or start to close airways in the worse case scenarios, while chemicals which come in contact with the skin and are absorbed and can cause hives, rashes, muscular pains and aches, nausea and pounding headaches.

This process is to do with a degranulation of Mast Cells. Mast cells (cells which occur in the tissue surrounding blood vessels and nerves) have the same interior composition as Endothelial cells for A level students, or the basic cell model for GCSE students, but have the properties of remaining inactive until they release (degranulate) their mediator molecules to take inflammatory action. Degranulate is a term for the mast cells releasing these ‘cyto-toxic’ (cell-toxic) molecules to destroy the allergen. Within the cell, visually, the molecules appear as a series of granules within the bigger, visual granules (actually called vescicles) and are released out of the granule through the membrane by binding to it, where the vescicle releases its contents.

These ‘granules’ are released when IgE (for A level students, this is immunoglobin E, an antibody produced by B cells that have become predisposed via T cells to the allergen) binds to the allergen and cross links with a FCεRI receptor on the cell plasma membrane, alerting the mast cell to the presence of the allergen. This signals the start of the degranulation process; releasing their inflammatory mediators (proteins: histamine, proteases, chekomines and heparin) which tend to cause Inflammation. Inflammation is important for several reasons:

– It helps to remove infectious agents from the site

– Plasma dilutes the pathogen, making them easier to deal with

– The extra white blood cells arriving at the site help to fight the infection

– The slight increase in heat can denature proteins and kill pathogenic cells.

This is followed by the introduction of newly formed mediators within the mast cells which attempt to regulate the level of foreign chemicals by directly destroying them. These new mediators include prostaglandins, leukotrienes, thromboxanes and platelet allowing factor (PAF): proteins which can cause:

-Airflow obstruction

-Increased secretion of mucus

-Constriction of the Bronchi.

-Infiltration of inflammatory cells in the airway wall


ImageImageImageImage – Cole Holroyd

In all healthy cells there is a protein called Procaspase-3, if for some reason there is a problem with the cell this protein can be actives intrinsically or extrinsically to form a digestive enzyme ; Caspase-3. This is a destructive enzyme used in apoptosis (programmed cell death), however when a cell becomes cancerous this process is removed preventing the cell from controlling its mitotic division thus producing a tumour. This is relevant to all cancers but some have higher Procaspase-3 levels than others, giving the problem of how do we stop the cancer? The answer may be closer than expected as researchers from the University of Illinois (after studying around 20,000 compounds ) have discovered a molecule which triggers the Procaspase-3 activation called PAC-1. After testing on mice and human tumours they have shown that PAC-1 caused cancer cells to apoptose whilst leaving the healthy cells unaffected., as it turned out the more Procaspase-3 a cell contained the less PAC-1 was needed; leukaemia needed very little. The healthy cells were unaffected due to the significantly smaller amounts of Procaspase-3 (when compared to the healthy cells, the cancerous cells were about 2000x as sensitive). If the safety tests are successful then we may be one step closer to a cure for cancer

Christian Tuckwell-Smith