Hibernate or hibernot

If the Land Rover advertising campaign is to be believed, us humans should not hibernate, as it is a waste of time during the cold winter months. Although, after reading new research published on the virtues of hibernation for neurodegenerative disorders, I believe this is an ill advised message. Who hasn't considered the concept of hibernation for humans? Just me? Ok, at first glance it doesn't seem a particularly attractive concept, going into a self induced 'coma-like' state during periods of low temperature, in a state of metabolic depression. Interestingly a process called  heterothermy occurs in hibernating mammals, during which they transition from being homeostatic endothermic to being ectothermic organisms, relying on their environment to regulate body heat, allowing for the slowing down of metabolic processes. The more you know right? But let's get back to the crux of this post: does hibernation actually have health benefits? Oh I'm so glad you asked. A UK team from the MRC Toxicology unit in Leicester have discovered the so called 'cold-shock chemicals' that cause mammals to destroy connections in their brains as they enter hibernation. Around 30% of synapses in the brain are destroyed, due to the slower metabolic rate during the winter. But what's truly amazing is that these culled synapses are reformed when the animal awakens in the spring! This obviously has huge implications for the medical profession, because the chemical released in the neural tissue as the animal begins to wake up and needs to repair synapses, RBM3, could be used to treat previously incurable conditions caused by prions, like Creutzfeldt–Jakob disease in humans. By artificially boosting levels of RBM3 in the brain, researchers have found that neurone death due to the misfolding of proteins caused by prions can be significantly reduced, and so we are one step closer to a drug that specifically targets the deadly neurone destroying agents that are prions. Memories are even retained after hibernation, as only the impulse receiving end of the synapses are destroyed (this is pretty obvious if you think about it, as a survival mechanism that wipes the animal's memory clean would be quite detrimental to its survival chances), and there is therefore a strong chance the RBM3 could be tailored into a drug to treat Alzheimer's patients, to slow down or even stop neurone loss during the early stages of the disease. Unfortunately the human body is not adapted to hibernate, as we don't produce enough RBM3 naturally, but I would certainly hibernate if given the chance. You would miss the most depressing months of the year, and reduce the risk of neurodegenerative disorders in later life. Stuff that in your gas-guzzling V8s Land Rover.

The MHCs: the immunological proteins you probably haven't heard of.

When one thinks of immunological proteins, you think of the big players; histamines, cytokines, and B/T cell receptors like CD4. However there are a little known family of proteins, that do play a vital role in the immune response, more specifically in antigen presentation, which make a bold claim in their name; the Major Histocompatability Complexes. In antigen presentation, a phagocyte like a macrophage or dendritic cell displays the antigens, which are specific peptide sequences used by the immune system to identify a pathogen, from the microbe it has just hydrolysed on its cell membrane. The protein the phagocytes use to do this is the MHC II. The phagocyte presenting these antigens will then travel to a lymphoid organ, the thymus or yellow bone marrow for example, through lymph and activate naive T cells. The CD4 receptor on the T cells must be able to dock to the MHC class II protein, so the epitope; the antigenic determinant which is recognised by the immune system, can imprint on the T cell receptor, priming it and therefore forming the effector T cells: the cytokine releasing T helpers which serve to rally the immune response, or the cytotoxic T killers which kill virally infected cells like homicidal spear wielding warriors. This in fact leads me on to the other class of Major Histocompatability Complex: MHC I. I made a passing reference to it as a 'surface marker' used in the immune response during a previous post, most people would stop there and move on to more significant proteins like interferon, but I'm not like most people (hence this blog). MHC I can be expressed on the surface membrane of almost every body cell, and it also displays the epitopes of antigens when, but for an altogether more sinister purpose... Ok that was slightly dramatic, but I doubt most people will read this far into the entry, so I can do what I want down here (whilst still remaining factually correct of course). The cells displaying epitopes on MHC I are virally infected, and can dock with the CD8 glycoprotein and the TCR found on the surface of T killer cells, and so they release cytotoxins like perforin, which destroys the cell membrane thus promoting PCD by apoptosis. How neat. So without this often overlooked protein, there would be no antigen presentation to trigger the adaptive Immune system, or pleasingly efficient destruction of virally infected cells. It just goes to show how interdependent every molecule in our bodies are, a principle that one should both admire and be absolutely petrified about...

Toxoplasma gondii: the parasite with a penchant for felids

If you hadn't already realised, dear readers, I'm a huge nerd. Wipe that look of shock off your faces. Anyway, I've been extremely busy with Pokemon Alpha Sapphire, revision and Fullmetal Alchemist. I'm only human ok! I've also been working tirelessly on my Extended Project, a 5,000 word dissertation of the topic of feline intelligence. Most people chose sensible topics like stem cell research, the UK's involvement in the EU, or the parallels between historical leaders, but I, in an attempt to make my life that little bit more difficult, decided to pick a topic that has very little debate, and even fewer people who are interested in the answer. Whilst I was researching the controversial topic of the intelligence of the domestic cat, I stumbled upon a parasite known as Toxoplasma gondii (T. gondii), as T. gondii's primary host is the domestic cat. T. gondii is a unicellular eukaryotic organism, a protozoan, that causes a disease called Toxoplasmosis in human host cells. Toxoplasmosis is the root of the term 'crazy cat lady' syndrome, as there is a definite link between the disease and mental health issues like schizophrenia, although most hosts are just symptomless carriers. Great. That's what I've got to look forward to.  It is one of the most common parasites found in the human body, and it is estimated that 1/3 of the global population is infected. The parasite can reproduce asexually within virtually all exothermic mammals, however it can only reproduce sexually in the intestines of Felids. This basically means it can only adapt and change its structure to evade our immune systems within cats, making them its definitive host. In order to optimise its chances of infecting cats, T. gondii can alter the behaviour of intermediate hosts like mice, to make them attracted to the scent of cat urine, so they are more likely to be preyed on by a passing feline. To do this the parasite hijacks white blood cells, which seem to be the target for pathogenic attack quite frequently (even parasites have a sense of humour). The WBCs are converted into chemical factories, synthesising neurotransmitters like serotonin, to reduce response of fear and anxiety that usually occurs in the amygdala of the mouse, as soon as it smells a feline nearby. The parasite resides within a membrane known as an oocyst until it passes through the stomach and the membrane is hydrolysed. It then infects epithelial cells, in which it is converted to Tachyzoite cells, speeding up the rate of proliferation, then they are converted to slow dividing Bradyzoites, which form tissue cysts in the host, completing the parasite's lifecycle. It's a feat of biological adaptation that a parasite can become so ultra-specialised to one particular host, but like a lot of evolution and natural selection, this mechanism is kept because it works. It worked during the evolution of the parasite, and so that's what it does to this day, and what it will continue to do until domestic cats develop a resistance to it. T. gondii stubbornly resists change, and that's why I like it...