Previously I have touched on my summer research project on tendinopathy but today I thought I would share a bit of what I have done with you all, enjoy!
The driving force behind my research was due to the fact that soft tissue disorders represent the third most common musculoskeletal condition in the UK with 18 cases per 1000. These primarily affect tendons, accounting for 30% of all rheumatological consultations with a general practitioner. Causes are multifactorial but with an ever increasing number of professional athletes and also an ageing population whose tendons decrease in elasticity; there is an annual estimated cost to the NHS of £250 million. Though molecular pathophysiology of tendinopathy remains incompletely understood key inflammatory mediators such as proinflammatory cytokines are found to play a vital role.
The extracellular matrix molecule tenascin-C is highly expressed during embryonic development, in pathological situations such as chronic inflammation, cancer. By this report it is found to be at significantly higher levels during diseased tendon tissue repair as compared to healthy tendons to carry out its role as an inflammatory mediator and induce inflammation in attempts to repair the diseased tendon. Tenascin-C prolongs inflammation at site of trauma and leads to further tendon damage. These results provide useful insight into the complex cross-regulation of inflammation and tissue remodelling mediated by tenascin-C.
Some background information
Tendons are a band of flexible fibrous connective tissue which connects muscle to bone. They are present in joints and largely inelastic to conserve energy whilst transmitting the contractile movement of muscle to move bone. Despite the frequent mention of tendinopathy, tendons are in fact extremely tough it is found that collagen fibrillogenesis begins as an assembly of collagen molecules in a series of extracellular compartments, progressing through post-depositional maturation leading to thicker and longer fibrils and ending in their coalescence in the final stages of fibre production.
As mentioned in one of my previous posts [click here] this summer I am undertaking a biomedical research project in collaboration with the Nuffield foundation on the topic of: “The role of Tenascin C in tendinopathy”.My main goal for tackling on this ‘challenge’ (I guess) was to engage in some real life science and to better myself in preparation for university. Though I am fortunate to attend a school which go out of their way to provide specialised scientific equipment, I had never experienced university style labs in (as the researchers I worked with called it) the big bad world. I realised that I took for granted the seemingly simple apparatuses such as autoclaves and centrifuges as some undergraduates haven’t even seen one in real life until university, never mind using them. I was overjoyed to leave the world of school bucket chemistry behind which solely consisted of school technicians tirelessly making up solutions only for us to haphazardly throw them all together to see the really tell-tale signs such as a colour change. No, I savoured every moment of making my own discoveries, never again shall I robotically repeat the same boring experiments to end up with a result I already knew.
The term ‘alkaloids’ may be unfamiliar to most of us but if I start naming some examples which fall into this group of ‘nitrogenous bases secondary metabolites’, you will know what I mean. Some of the big names include morphine, quinine, strychnine, nicotine etc. basically a continuous list of –ine’s. The thing to note is that though the alkaloids were attributed to pharmacologically active bases derived from plants however, animals (including us!), insects and microbes also produce them.
For many, the heart is synonymous with passion, personality which is literally at the heart of a person. We even carelessly use the phrase “broke my heart”, however, what does happen when our thick- muscular pump of an organ truly breaks down? The assumed answer would be death; no heart beat=no longer living…right? Well, in reality, a stopped heart can restart, there is no true universal rule in death determination. You are dead when the doctor says you are dead.