I have one year left of my PhD!

⏱ One year left, the countdown is on ⏱

Just writing that makes me feel a little bit sick 😅

It’s honestly flown by, I can’t quite actually believe how fast it’s gone. I’ve grown so much as person since I started, I hardly recognise first year Beth. Throw in a global pandemic, two side projects, outreach work, being part of two committees and my actual PhD project (as well as having a life), it’s hardly surprising it’s gone so fast and I’ve changed so much 🤔

When I say I’ve changed, it’s definitely for the better. I definitely feel more like an independent researcher than I did in the beginning. It’s been no secret that I really struggled with my mental health this past year but I’m in a much better place now!

I finally feel in a good place with my research, I feel much more confident and ready to tackle this next year 💪

I’ve developed a good working relationship with my supervisors and my colleagues and believe me it’s made the whole process much more manageable and enjoyable ☺️

Don’t get me wrong there have been some MAJOR lows (that’s sadly part of the PhD journey) BUT there have been some pretty great highs too 😁

Thanks so much for following me on this journey! Time to knuckle down and absolutely take on this final year! I hope to document this final year of my journey to Dr Beth! I’ll share lab life and thesis writing to show the realities of being a final year PhD student coming out of a global pandemic.

Tell me where you see yourself in the next year ⬇️

Thanks for reading, see you in the next one!

Beth x

PhD update: 4 months of 3rd year!

Well, long time no speak!

This year has kinda run away with itself already so I’ve got so much to update you on.

First up, I submitted an abstract for two conferences which were both accepted (I couldn’t believe it). One was for a 3-minute impact statement style presentation, while the other was in the form of an online poster presentation. 

Abstract writing was pretty tough, it seemed to take much longer than I thought it would and found it quite challenging to be so concise. However, I got there in the end. Top tip – always ask for feedback! For more abstract writing tips check out my Instragram account (see below).

This was the first time presenting at a conference since starting my PhD which were both virtual due to covid restrictions. I have to say they were both great but I do really miss in-person conferences. Something about sitting in front of a computer all day just isn’t the same!

For one of the conferences I had to pre-record my impact statement which was a bit weird and the perfectionist in me kept wanting to re-record it but I was strong and managed to do it in two takes! 

The other conference used a really cool platform called GatherTown where you created an avatar and you could “walk” around the “conference centre” and drop in and out of conversations. It was really effective actually! This also made it super fun and easy to look at everyone’s poster and really imitate an in-person conference which I really enjoyed.  

Then to my absolute surprise, I won joint first for my poster at one of the conferences and I couldn’t be prouder!

Next up, my partner and I moved flats! It felt like such an ordeal doing this during a pandemic and at an extremely busy time for us both work-wise. But we managed it in the end and I think we’re pretty settled now. I have a desk now and it’s a massive game-changer!! No more sitting at the tiny kitchen table with my laptop. I also treated myself to a monitor and some fun LED lights so it’s a really nice working set up. Check out my set-up here.

Then a paper I co-authored was published, this was again another really proud moment. It took a while to get to the publication stage with several rounds of review but I’m so pleased we persevered as I really do love this paper (check it out here).

Then finish off, I’ve been super busy in the lab working through important samples for my PhD so needless to say my blog has been neglected. I really want to get back into blogging so I plan to create a bit more of a schedule as I have lots of ideas, it’s just getting around to doing them!

Let me know what you’ve been up in the last couple of months, I’d love to hear.

Thanks for reading, see you in the next one.

Beth x

2020: a year in review

WHAT. A. YEAR!

We friggin’ made it!!

Little did we know what was around the corner when we blissfully stepped into the year 2020!

This year has been difficult for everyone and it really just goes to show how resilient we are as humans. It has been tough. There have been tears, anxiousness, depression, you name it but there have also been some great times. Again, another testament to us human beans, we can see the light if even it’s very dark and we don’t really feel like it. 

Looking back I think I’ve grown a lot as a person, there have been extremely low lows but with that being said there have been some pretty awesome highs. I’ve tried lots of new things, things I wouldn’t have dreamt of doing last year and you know what, I actually really enjoyed them! 

In the name of being transparent, open and honest I thought I’d run through the highs & lows of this year…

Lows:

  • Suffered quite a bit with my mental health during the first lockdown 
  • Overwhelmed by the media and news
  • PhD research halted for 6 months (this made me worry a lot about the future)
  • Felt lost
  • Realised I didn’t have much happening outside of working (hard pill to swallow)
  • Tinnitus appeared much louder (I really struggled with this)
  • Missed my friends and family incredibly 
  • Missed “freedom’

Highs:

  • Contributed to a paper that was later published (first time my name is on paper yippee)
  • Took part in online outreach activities during lockdown 1.0
  • Set up this blog and Instagram account, and became part of an amazing online science community 
  • Wrote a literature review (hopefully to publish next year)
  • Became a committee member of the Royal Society of Biology Yorkshire branch (I help with social media)
  • Accepted to be part of a scientific society early career researcher working group (remaining unnamed until it’s officially announced)
  • Bought a car and I’ve been building up my driving confidence ever since (this has been quite a big deal for me, I was and to a degree still am a nervous driver so I’m pretty proud of how far I’ve come with it)
  • Tried an array of new hobbies – candle making, drawing, baking, running & lettering (all of which I’d never done before this year, it’s amazing what you can do if you just try)
  • Started a BSL course (been wanting to do this for years and finally got round to it)
  • Read for pleasure 
  • Submitted my 2nd-year annual progress review 
  • Made it through this year 
  • Learnt to appreciate the small things 

My achievements are not in any way to show off, I’m just pretty damn proud of myself for even making it through the year. The rapid change and feeling lost really made me reevaluate a lot of things in my life and that really lead me to try new things. 

What have I learnt this year? 
Well, I’ve learnt that I’m much more resilient than I ever thought I was. I’ve also learnt to take a look at the good stuff and all the things I’m grateful for. Yes, this year has sucked but I have my health, my family, my friends, my amazing partner, a roof over my head and I’m still getting paid to do my PhD. I count myself incredibly lucky given what many people have faced this year. It’s so easy to see the negatives, I know this is something I’m trying really hard to work on. This year did not go as anyone hoped it would but to me, it’s not a total write off because I’ve tried new things, I’ve become closer with my partner, I’ve managed to move my PhD project along slowly but surely and I’m trying not to put pressure on myself to be “on it” all the time. 

Goals for 2021:
I don’t really believe in New Years Resolutions because I think if you want to make a change in your life you can do it whenever you want, not just in January. I also think we end up setting unrealistic and unattainable resolutions that we end of breaking by the time it’s February. I like to split my goals into professional and personal, I think this really helps me with work-life balance too. It’s nice to know that my goals are not just PhD focussed and I have things I want to achieve outside of that. 

Professional:

  • Publish my literature review 
  • Present at a conference (IRL or online)
  • Read more scientific journals – I want to actively carve out time in my week to read more papers, I’ve definitely slacked a lot on this during 2020.
  • Get involved in more outreach activities
  • Achieve the main bulk of data collection for my PhD project – I have 1.5 years until my funding runs out so I really want to get the main bulk of work done this year!

Personal:

  • Put less pressure on myself – this is pretty open and I’m not sure how I’ll measure this but it’s something I’ve tried this year and I want to continue it next year.
  • Journal – I feel like I’ll benefit from journaling and I’ve tried it a bit this year but not built it into my routine which is something I want to achieve next year. 
  • Read more – my goal last year was to read at least 5 books, which I’ve actually managed! I know it’s not much but it’s the most I’ve read for pleasure since starting my PhD. I’d like to try one a month but I think that’s a bit of a stretch for me (aiming high though).
  • Look after my mental and physical health – I’m keeping this open which is in keeping with my first goal. I don’t want to say “I’m gonna run 5k” I just want to move my body regularly and look after my mental health in a way that works for me. 
  • Collaborate with other science bloggers/Instagrammers – I really love the science community we have on Instagram so I’d love to get involved in more collaborations
  • Increase my blog/Instagram following and engagement – I’d like to see these both continue to grow, it’s been great engaging with people online about science, tinnitus and PhD life.
  • Start making more videos (either for YT or IG) – I started making videos at the start of 2020 but I never continued. I’d really like to try again, as I did really enjoy making them. I think I’ll aim for maybe once a month (like the books haha).

Even if you feel like you’ve achieved nothing this year, that’s not true! You have, you made it through an incredibly challenging and unique year so don’t be so hard on yourself! I like to set goals because I find that helps me take the next steps so to speak. I like goals, professional and personal, many don’t and that’s totally ok. You do you! And remember you don’t have to change yourself for the new year, you’re great exactly how you are!

Whether you’re into goal setting or not, sometimes it can be really useful to review and reflect on the year to see if you’re doing things that align with your values and what you want out of life!

Thank you so much for reading and following me on this journey! Let me know in the comments what your goals are for 2021 and what you’ve learnt this year, I’d love to hear.

See you in the next one,

 Beth x

Beth talks blood: Part 8

What is cardiovascular disease?
Cardiovascular disease (CVD) is a general term for conditions affecting the heart or blood vessels. It is typically associated with a build of fatty deposits inside blood vessels known as atherosclerosis and an increased risk of blood clots known as thrombosis [1-2]. It can also be associated with damage to arteries in organs such as the brain, heart, kidneys and eyes. 

Unfortunately, CVD is one of the main causes of death and disability in the UK and sadly the number one cause of death globally, more people die annually from CVDs than from any other cause! However, for the most part, CVD can be prevented by following a healthy lifestyle [1-3].

Types of CVD:

Coronary heart disease:
Coronary heart disease occurs when flow blood supplying the heart muscle is blocked or reduced.

Coronary heart disease can put added strain on the heart which can lead to:

  1. Angina – chest pain caused by restricted blood flow to the heart muscle
  2. Heart attack – blood flow to the heart is suddenly blocked
  3. Heart failure – the heart is unable to pump blood around the body properly

CHD develops slowly over time and the symptoms are different for everyone. Some people don’t know they have CHD until they have a cardiovascular event such as a heart attack! [1, 3-4]

Cerebrovascular disease (CeVD) :
A disease of the blood vessels supplying the brain [2]. Ischaemic stroke occurs when blood flow is restricted or cut off in part of the brain which can lead to brain damage and possible death [1-4]. Strokes can also be caused by bleeding from a blood vessel in the brain or from blood clots, this is known as a haemorrhagic stroke. Transient ischaemic attacks (TIAs) or mini-strokes happen when there is an interruption of blood flow to part of the brain for a very short time. TIAs can cause symptoms such as temporary speech loss and they can typically resolve after a few seconds or minutes [1-5].

Peripheral arterial disease (PAD): 
A disease of blood vessels supplying the arms and legs and occurs when there’s a blockage in the arteries to the limbs. This can lead to dull or cramping leg pain when walking which gets better with rest, hair loss on legs and feet, numbness or weakness in the legs and persistent ulcers on the feet and legs [1-3]. PAD is also likely to be a sign of more widespread accumulation of atherosclerosis, which may be reducing blood flow elsewhere i.e. heart or brain. PAD can be managed by quitting smoking and following a healthy diet [6].

Rheumatic heart disease:
A disease which causes damage to the heart muscle and heart valves from rheumatic fever, which caused by streptococcal bacteria [3]. Rheumatic fever is an inflammatory disease that can affect many connective tissues, especially in the heart, joints, skin or brain. During rheumatic fever, the heart valves become inflamed and can scar over time. This results in the narrowing or leaking of the heart valves meaning it is harder for the heart to function normally. It can take years to develop but may result in heart failure [3, 7]. 

Congenital heart disease (CHD): 
A general term for a range of birth defects that affect the normal functioning of the heart. CHD can be due to malformations in the heart structure existing at birth. CHD is one of the most common birth defects, it affects up to 8 in every 1000 babies born in the UK [3, 8].

Types of CHD:

  1. Septal defects – a hole between two of the hearts chambers (referred to as “hole in the heart”)
  2. Coarctation of the aortanarrower aorta than normal
  3. Pulmonary valve stenosispulmonary valve which controls the flow of blood out of the heart to the lungs is lower than normal 
  4. Transposition of the great arteries – the pulmonary and aortic valve and the arteries they’re connected to have swapped positions
  5. Underdeveloped heart – the heart doesn’t develop properly which can make it difficult for it to pump enough blood around the body

It can happen as a result of many things such as Down’s syndrome, issues during pregnancy such as diabetes, medications and family history.

Deep vein thrombosis (DVT) and pulmonary embolism (PE):
Blood clots in the leg veins, which can dislodge and move to the heart and lungs [1-3]. DVT can cause leg pain or swelling but it can also occur without symptoms [9]. DVT can be dangerous if left untreated it can lead to pulmonary embolism (PE). This is where blood blots break loose and travel through the bloodstream and lodge in the lungs blocking blood flow [10].

Aortic disease:
A group of diseases affecting the aorta which is the largest blood vessel in the body. It carries blood from the heart to the rest of the body. The most common aortic disease is an aortic aneurysm whereby the aorta becomes weakened and bulges [1]. Aortic aneurysm doesn’t have any symptoms and it is very dangerous if not spotted early. There is a chance it could rupture (burst) which can lead to life-threatening bleeding [11]. 

Atherosclerosis 
Atherosclerosis is a very slow process that happens over many years, it can start early in life and results in a build-up of fatty deposits (atheroma) in the lining of blood vessels. If you remember from my previous blog post about fatty acids in the blood, LDL is “bad” cholesterol whereas HDL is “good” cholesterol. These fatty deposits start when the blood vessel lining becomes damaged, which makes it easier for the cholesterol (on LDL) to stick on and build up more rapidly leading to the formation of plaques [12]. HDL however, can remove these fatty deposits. Reducing LDL and increasing HDL as well as reducing other risk factors (such as blood pressure, type 2 diabetes, weight and smoking) can slow down the process of atherosclerosis.

During atherosclerosis plaques can rupture, when this occurs the ruptured plaque can recruit platelets to the rupture site, in a very similar fashion to vascular injury. This causes the platelets to activate and along with clotting factors, form an unwanted blood clot. The problem with a blood clot formed without vascular injury is that it can cause blockage of the affected blood vessel. A result of this blockage in combination with reduced blood flow can cause life-threatening cardiovascular events such as heart attack or stroke [13]. In some cases, the blockage can cause a portion of the heart to die which again can lead to a heart attack.

Fatty acids, atherosclerosis, platelets & CVD – how does it all link? 
Excess fatty acids in the blood can exert a profound effect on blood clotting and can lead to hypercoagulability of the blood, which in turn can lead to thrombosis [14]. LDL attaches to a protein on the surface of platelets called CD36 which causes platelets to become “stickier”. When this happens, platelets release chemicals that cause inflammation and can damage the walls of the blood vessels, contributing to the creation of these atherosclerotic plaques [15].

Risk factors of CVD [1]:

  • high blood pressure
  • smoking
  • high cholesterol 
  • diabetes
  • inactivity 
  • obesity 
  • family history 
  • ethnic background 
  • age
  • gender
  • diet
  • alcohol 

CVDs are likely to be a multifactorial process, which includes interactions between LDLs, platelets, clotting factors, blood vessel walls and inflammation, that together contribute to the development of CVD. In most cases, CVD can be prevented by reducing risk factors and leading a healthy lifestyle. For heart-healthy recipes check out some of the tasty recipes in the BHF’s Heart Matters magazine.

A healthy heart is a happy heart, looking after our cardiovascular health can really help reduce the NHS burden and hopefully one day, CVD won’t be the leading cause of death worldwide! 

As a cardiovascular research scientist, I firmly believe that developing our understanding of the cardiovascular system and what goes wrong at a cellular level during cardiovascular disease will help us to provide improved preventative measures and/or more targeted treatments. 

Thank you for reading, I hope you enjoyed this post!

See you in the next one.

Beth x

References:

[1] nhs.uk. 2020. Cardiovascular Disease. [online] Available at: <https://www.nhs.uk/conditions/cardiovascular-disease/&gt;

[2] http://www.heart.org. 2020. What Is Cardiovascular Disease?. [online] Available at: <https://www.heart.org/en/health-topics/consumer-healthcare/what-is-cardiovascular-disease&gt;

[3] Who.int. 2020. Cardiovascular Diseases (Cvds). [online] Available at: <https://www.who.int/news-room/fact-sheets/detail/cardiovascular-diseases-(cvds)&gt;

[4] British Heart Foundation. 2020. Coronary Heart Disease. [online] Available at: <https://www.bhf.org.uk/informationsupport/conditions/coronary-heart-disease&gt;

[5] British Heart Foundation. 2020. Stroke – Causes, Signs And Symptoms. [online] Available at: <https://www.bhf.org.uk/informationsupport/conditions/stroke&gt;

[6] Mayo Clinic. 2020. Peripheral Artery Disease (PAD) – Symptoms And Causes. [online] Available at: <https://www.mayoclinic.org/diseases-conditions/peripheral-artery-disease/symptoms-causes/syc-20350557&gt;

[7] 2020. Rheumatic Heart Disease. [online] Available at: <https://www.hopkinsmedicine.org/health/conditions-and-diseases/rheumatic-heart-disease&gt;

[8] Bhf.org.uk. 2020. Congenital Heart Disease. [online] Available at: <https://www.bhf.org.uk/informationsupport/conditions/congenital-heart-disease&gt;

[9] Mayo Clinic. 2020. Deep Vein Thrombosis – Symptoms And Causes. [online] Available at: <https://www.mayoclinic.org/diseases-conditions/deep-vein-thrombosis/symptoms-causes/syc-20352557>

[10] Mayo Clinic. 2020. Pulmonary Embolism – Symptoms And Causes. [online] Available at: <https://www.mayoclinic.org/diseases-conditions/pulmonary-embolism/symptoms-causes/syc-20354647&gt;

[11] nhs.uk. 2020. Abdominal Aortic Aneurysm. [online] Available at: <https://www.nhs.uk/conditions/abdominal-aortic-aneurysm/&gt;

[12] Siri-Tarino, P., Sun, Q., Hu, F. and Krauss, R., 2010. Saturated Fatty Acids and RisCoronary Heart Disease: Modulation by Replacement Nutrients. Current Atherosclerosis Reports, 12(6), pp.384-390. http://www.heart.org. 2020. Atherosclerosis. [online] Available at: <https://www.heart.org/en/health-topics/cholesterol/about-cholesterol/atherosclerosis&gt;

[13] http://www.heart.org. 2020. Atherosclerosis. [online] Available at: <https://www.heart.org/en/health-topics/cholesterol/about-cholesterol/atherosclerosis&gt;

[14] HOOK, J., WARNER, E. and CONNOR, W., 1967. Platelets, Fatty Acids and Thrombosis. Circulation Research, 20(1), pp.11-17. <https://www.ahajournals.org/doi/pdf/10.1161/01.RES.20.1.11>

[15] Bhf.org.uk. 2020. How Do Cholesterol And Platelets Team Up To Cause Blood Vessel Damage?. [online] Available at: <https://www.bhf.org.uk/research-projects/characterising-the-thromboinflammatory-roles-of-platelet-cd36&gt;

Beth talks blood: part 7

Blood & the immune system:
The immune system is essential for our survival, without it our bodies would be open to attack from bacteria, viruses, parasites and more. It is made of up of organs, cells and chemicals that fight infection. It can distinguish our tissue from foreign tissue i.e. self from non-self. Dead and faulty cells are also recognised and cleared by the immune system [1-2].

The main parts of the immune system are white blood cells, antibodies, the complement system, the lymphatic system, the spleen, the thymus and the bone marrow. These all work as part of our immune system to actively fight infection [1-3].

Immune response:
To distinguish between self and non-self the immune system detects certain proteins on the surface of cells. It learns to ignore its own proteins from an early stage. An antigen is any substance that can initiate an immune response. It’s worth noting that Antigen is short for ‘antibody generators’ [1-3].

Blood components:
The blood is our main transport system throughout the body so naturally it is heavily involved in our immune system. 

White blood cells (aka leukocytes):
WBCs circulate in the body in blood vessels and the lymphatic vessels that parallel the veins and arteries. WBCs are on constant patrol, looking out for pathogens. When they find a foreign pathogen they begin to multiply and send out signals to other cells to do the same [1-3]. 

WBCs are stored in different places in the body – these are referred to as lymphoid organs [1, 3]:

  • Thymus 
  • Spleen 
  • Bone marrow
  • Lymph nodes

Two types of leukocyte [1, 3]:

  1. Phagocyte – neutrophils, monocytes, macrophages and mast cells
  2. Lymphocyte – B-lymphocytes & T-lymphocytes (also called B-cells and T-cells)

Phagocytes surround and absorb pathogens and break them down, whereas lymphocytes help our bodies to remember previous pathogens and recognise them if they attack again [1, 3].

B-lymphocytes [1-4]

  • Spot the antigen and begin secreting antibodies 
  • Antibodies are proteins that lock onto specific antigens
  • Each B cell makes one specific antibody 

Antibodies are part of a family of chemicals called immunoglobulins (Ig). Immunoglobulins play many roles in the immune system [1-4]:

  • IgG – marks microbes so other cells can recognise and attack
  • IgM – kills bacteria
  • IgA – found in fluids such as tears and salvia 
  • IgE – protects against parasite and is also responsible for allergies
  • IgD – stays bound to B cells, helping to initiate the immune response 

Antibodies lock on to antigens, they don’t kill antigens. They mark the antigens to be killed by other cells such as phagocytes.

T-lymphocytes [1-5]

  • T Helper cells (Th cells) – orchestrate the immune response. Some stimulate B cells, some communicate with other cells, while some attract more T cells or phagocytes.
  • T Killer cells (cytotoxic T cells)– they attack other cells and useful for fighting viruses. They recognise small parts of the virus on the outside of infected cells and destroy the already infected cells.

Immunity:
Immunity is the capability of our bodies to resist harmful pathogens. Everyones immune system is different but it considered to become stronger during adulthood as we are likely to have been exposed to more pathogens and as a result, more immunity. 

Once an antibody is produced a copy then remains in the body so that if the same antigen appears again it can be dealt with much more quickly. 

There are three types of immunity in humans called innate, adaptive and passive [1-3].

Innate:
Our innate immune system is with us from birth, its response is more general and non-specific but it protects us from foreign invaders from day one. The innate immune response is the first rapid response to a foreign invader, when this system recognises a pathogen it goes into action immediately. The cells of the innate immune system called phagocytes, surround and engulf the pathogen where it is then killed. The innate immune system includes external barriers such as the skin and mucous membranes. If a pathogen manages to get past the innate immune system, the adaptive immune response kicks in [1-2, 6-7].

Adaptive (acquired):
The adaptive immune system, with help from the innate system, produces antibodies to protect us from specific invaders. If we are exposed to diseases or get vaccinated then we build up a bank of antibodies to different pathogens. The adaptive immune system “remembers” previous pathogens and can respond quickly if they return [1-2, 6-7]. 

Passive immunity:
Passive immunity is “borrowed” from another source and does not last. For example, a baby receives antibodies from the mother through the placenta before birth and in breast milk after birth. This passive immunity protects the baby from some infections during the early years of their life. These antibodies disappear between ages 6 and 12 months [1, 7]. 

Our bodies have other important defence mechanisms such as [3]:

  • Skin
  • Lungs
  • Digestive Tract
  • Other defences: bodily fluids like skin oil, saliva and tears (all contain bacterial enzymes that help reduce the risk of infection)


Inflammation:

Another important part of our immune response is the inflammatory response (inflammation). Inflammation occurs when tissues are damaged by bacteria, trauma, toxins, heat or any other cause. Damaged cells release chemicals which include, histamine, bradykinin and prostaglandins. These chemicals can lead to blood vessel leakage into the tissues, which in turn causes swelling. This helps to isolate the foreign substance from further contact with other body tissues [7]. 

The chemicals also attract phagocytes that “eat” the germs, dead or damaged cells. This process is known as phagocytosis [8].

Complement system:
The complement system is another key part of our immune system that enhances or complements the ability of antibodies and phagocytes to clear microbes and damaged cells from our bodies. The complement system also promotes inflammation and attacks the cell membranes of pathogens. 

Blood coagulation, complement and the fibrinolytic systems are highly interactive, when one system becomes dysregulated, activation of the others are altered and processes such as thrombosis and chronic inflammation can occur. This is why in cases like sepsis (infection and inflammation) we see severe changes in the blood coagulation cascade whereby it becomes activated resulting in disseminated intravascular coagulation (DIC) resulting in a higher mortality rate [9-11].

Platelets:
Platelets were originally deemed to only play a role in prevention of bleeding but in the last decade or so they have been recognised for their activities independent of thrombosis. Platelets are capable of storing and releasing bioactive mediators and express a wide range of functional immunoreceptors [12] . 

Platelets in innate immunity:
Platelets have the ability to release inflammatory and bioactive molecules stored within granules (dense and alpha granules) or that can synthesised upon activation. These mediators attract and modulate effector cells of the innate immune system. Platelets themselves also demonstrate direct effector function and therefore are regarded as cells in the innate immune system [12-13].

Platelets are the first to detect endothelial injury and microbial pathogens as they gain access or invade the bloodstream or tissues. Injury to the endothelium exposes collagen and other membrane proteins allowing platelets to adhere. Stable adhesion to collagen leads to platelet aggregation and causes the release of platelet agonists such as ADP, thrombin & vWF. This leads to the platelet activation and further recruitment of platelet to the site of injury and infection. This serves two purposes, the first being haemostasis to stop blood loss and the second being frontline defence against microbial infection. Also, platelets express a number of chemokine receptors which detect signals for all four classes of chemokine generated at sites of infection. This leads to rapid accumulation of platelets to the site of injury & infection [12-13]. 

Platelets have been known to influence the innate immune response through regulation of macrophages, neutrophils and dendritic cells. They can also interact with bacteria, viruses, fungi and protozoa, they also demonstrate anti-microbial functions too! Growing evidence also suggests that platelets play a role in adaptive immunity, shaping the immune response [13]. Despite being anucleate cells, i.e. cells without a nucleus, platelets play vast and surprising roles in both haemostasis and immunity, which is something I might explore in a separate blog post – is there anything our platelets can’t do?!

As you can see our immune system is an extremely important and complex system, without it we wouldn’t be able to fight against pathogens that we come into contact with regularly. This has been an overview of blood and the immune system, I hope you enjoyed this post!

Let me know in the comments if you know any interesting facts about our immune system – I’d love to learn more about our fascinating immune system!

Thank you for reading!

See you in the next one, 

Beth x

References:

[1] Medicalnewstoday.com. 2020. The Immune System: Cells, Tissues, Function, And Disease. [online] Available at: <https://www.medicalnewstoday.com/articles/320101&gt;

[2] InformedHealth.org [Internet]. Cologne, Germany: Institute for Quality and Efficiency in Health Care (IQWiG); 2006-. How does the immune system work? [Updated 2020 Apr 23]. Available from: <https://www.ncbi.nlm.nih.gov/books/NBK279364/>

[3] Betterhealth.vic.gov.au. 2020. Immune System. [online] Available at: <https://www.betterhealth.vic.gov.au/health/conditionsandtreatments/immune-system&gt;

[4] LeBien, T. and Tedder, T., 2008. B lymphocytes: how they develop and function. Blood, 112(5), pp.1570-1580.

[5] TeachMePhysiology. 2020. T Cells – Production Of T Cells – Types Of T Cells – Teachmephysiology. [online] Available at: <https://teachmephysiology.com/immune-system/cells-immune-system/t-cells/>&nbsp;

[6] 2020. The Immune System. [online] Available at: <https://www.hopkinsmedicine.org/health/conditions-and-diseases/the-immune-system&gt;

[7] Encyclopedia, M. and response, I., 2020. Immune Response: Medlineplus Medical Encyclopedia. [online] Medlineplus.gov. Available at: <https://medlineplus.gov/ency/article/000821.htm>&nbsp;

[8] Immunology.org. 2020. Phagocytosis | British Society For Immunology. [online] Available at: <https://www.immunology.org/public-information/bitesized-immunology/systems-and-processes/phagocytosis&gt;

[9] Institute of Immunity and Transplantation. 2020. Coagulation & Inflammation. [online] Available at: <https://www.ucl.ac.uk/immunity-transplantation/research/gene-therapy/coagulation-inflammation&gt;

[10] Oikonomopoulou, K., Ricklin, D., Ward, P. and Lambris, J., 2011. Interactions between coagulation and complement—their role in inflammation. Seminars in Immunopathology, 34(1), pp.151-165. 

[11] Simmons, J. and Pittet, J., 2020. The Coagulopathy Of Acute Sepsis.

[12] Ali, R.A., Wuescher, L. M., & Worth, R. G. 2015. Platelets: essential components of the immune systems. Current trends in immunology, 16, 65-78.

[13] Semple, J., Italiano, J. and Freedman, J., 2011. Platelets and the immune continuum. Nature Reviews Immunology, 11(4), pp.264-274.

Beth talks blood: part 6

Let’s talk about fat…

Fats that circulate in the blood are called lipids (fat-soluble components of living cells). Cholesterol and triglycerides are both lipids that have essential roles in the body but in excess they can be harmful [1-3]. 

What is cholesterol?

Cholesterol is required to build cell walls and to produce hormones and vitamin D. Some of our cholesterol comes from our diet but most of our cholesterol is made in the liver. When cholesterol is broken down it is used to make bile acids which helps us to digest food [3].

What are triglycerides?

To answer that we need to take a look at fatty acids. A fatty acid is an important component of lipids. They are the building blocks of fat in our bodies and in the food that we eat. During digestion the body breaks down fats into fatty acids which can then be absorbed into the blood [1-3].

A fatty acid consists of a straight chain of an even number of carbon atoms, with hydrogen atoms along the length of the chain and at one end of the chain, with a carboxyl group (-COOH) at the other end. The carboxyl group is what makes it an acid (i.e. carboxylic acid). Fatty acid molecules are usually joined together in groups of three, forming a molecule known as a triglyceride [2].

Triglycerides are the fats found in our food. During digestion any fat in our food is absorbed by our gut. It is then moved around the body in the blood as triglycerides. The liver also makes triglycerides, and they provide the energy that is needed for our muscles and organs, they also help to keep us warm [3].

Lipoproteins: 

Lipids such as cholesterol and triglycerides cannot circulate loosely in the blood, so they need to be packaged in lipoproteins to be able to travel in the blood. Lipoproteins contain a mix of fats and proteins which allow them to circulate in the blood [3]. 

There are 4 main lipoproteins [3-5]:
1. Chylomicrons

2. Very low density lipoproteins (VLDL)

3. Low density lipoproteins (LDL)

4. High density lipoproteins (HDL)


Chylomicrons:

These are the largest lipoprotein and they carry triglycerides from the intestine to the tissues where they are required as a source of energy [3, 5].

VLDLs:

These transport mainly triglycerides made by the liver to where they are used by our muscles or stored for later use [3, 5].  

LDLs vs HDLs:

LDLs are known as “bad cholesterol” whereas HDLs are known as “good cholesterol”. LDL carries most of the cholesterol in our body from the liver to our cells that need it, whereas HDL plays a vital role in removing excess cholesterol away from cells and artery walls, back to the liver for disposal and recycling. When LDL gets into the walls of arteries, this can cause atherosclerosis which forms a blood vessel disease that can lead to heart attacks or stroke, meaning it is a major risk factor in cardiovascular disease [3-5].

Fatty acids & platelets:

Excess fatty acids can exert a profound effect upon blood clotting and can produce hypercoagulability of the blood leading to thrombosis (platelet aggregates formed within the thrombi) [6].

LDL attaches to a protein on the surface of platelets called CD36 which causes platelets to become “stickier”. When this happens, platelets release chemicals that cause inflammation and can damage the walls of the blood vessels, creating hardened areas in the blood vessel called plaques, which can lead to cardiovascular events [7].

Hyperlipidemia:

Hyperlipidemia means your blood has too many lipids e.g. cholesterol and triglycerides. A specific type of hyperlipidemia called hypercholesterolemia means that you have too much LDL (bad) cholesterol and not enough HDL (good) cholesterol in your blood [8].

Hyperlipidemia primes platelets and increases platelet activation in response to various agonists. Plasma cholesterol levels appear to have a critical role in modulating platelet activity. Oxidised LDLs or oxidised phospholipids, which are increased in hyperlipidemia, serve as ligands of platelet CD36 and activate platelets [9]. Oxidised LDL can be a harmful type of cholesterol that is produced in our bodies when normal LDL is damaged by chemical interactions with free radicals. Free radicals are unstable molecules that a produced as result of normal metabolism, a disease or exposure to certain toxins. Free radicals cause oxidation which de-stabilises molecules such as LDL. Along with inflammatory responses, these free radicals can result in the hardening of arteries known as atherosclerosis. The interaction between (ox)LDL and platelets play an important role in the pathogenesis of atherosclerosis, which can lead to cardiovascular events such as heart attack or stroke [10-11]. 

As you can see excessive fatty acids can cause havoc on our cardiovascular system which can lead to cardiovascular disease. It’s most likely to be a multifactorial process with interactions between LDLs, platelets, blood vessel walls, inflammation and clotting factors, that all contribute to the development of cardiovascular disease.

Developing our understanding of the cardiovascular system and what goes wrong in incidences of cardiovascular disease will help us to provide better, preventative measures and/or more targeted treatments. 

Thank you for reading, I hope you enjoyed this post!

See you in the next one.

Beth x

References:

[1] Encyclopedia Britannica. 2020. Fatty Acid | Definition, Structure, Functions, Properties, & Examples. [online] Available at: <https://www.britannica.com/science/fatty-acid&gt;

[2] Kidshealth.org. 2020. Definition: Fatty Acids (For Parents) – Nemours Kidshealth. [online] Available at: <https://kidshealth.org/en/parents/fatty-acids.html&gt;

[3] Heartuk.org.uk. 2020. [online] Available at: <https://www.heartuk.org.uk/downloads/health-professionals/publications/blood-fats-explained.pdf&gt;

[4] Cox RA, García-Palmieri MR. Cholesterol, Triglycerides, and Associated Lipoproteins. In: Walker HK, Hall WD, Hurst JW, editors. Clinical Methods: The History, Physical, and Laboratory Examinations. 3rd edition. Boston: Butterworths; 1990. Chapter 31. Available from: https://www.ncbi.nlm.nih.gov/books/NBK351/ 

[5] Siri-Tarino, P., Sun, Q., Hu, F. and Krauss, R., 2010. Saturated Fatty Acids and Risk of Coronary Heart Disease: Modulation by Replacement Nutrients. Current Atherosclerosis Reports, 12(6), pp.384-390.

[6] HOOK, J., WARNER, E. and CONNOR, W., 1967. Platelets, Fatty Acids and Thrombosis. Circulation Research, 20(1), pp.11-17.

[7] Bhf.org.uk. 2020. How Do Cholesterol And Platelets Team Up To Cause Blood Vessel Damage?. [online] Available at: <https://www.bhf.org.uk/research-projects/characterising-the-thromboinflammatory-roles-of-platelet-cd36&gt;

[8] http://www.heart.org. 2020. Prevention And Treatment Of High Cholesterol (Hyperlipidemia). [online] Available at: <https://www.heart.org/en/health-topics/cholesterol/prevention-and-treatment-of-high-cholesterol-hyperlipidemia&gt;.

[9] Wang, N. and Tall, A., 2016. Cholesterol in platelet biogenesis and activation. Blood, 127(16), pp.1949-1953.

[10] Verywell Health. 2020. Understand How Oxidized LDL Cholesterol Affects The Body. [online] Available at: <https://www.verywellhealth.com/what-is-oxidized-ldl-698079&gt; [Accessed 28 November 2020].

[11] http://www.heart.org. 2020. Atherosclerosis. [online] Available at: <https://www.heart.org/en/health-topics/cholesterol/about-cholesterol/atherosclerosis&gt;

Beth talks blood: Part 5

We all know that I’m a platelet girl at heart but we mustn’t forget the blood coagulation cascade, it is a vital part of haemostasis. Platelets and coagulation factors work together to prevent bleeding in incidences such as vascular injury. So one can’t be without the other and like most systems in the body, it involves a lot of things happening at the same time so when we study it, it can be quite overwhelming!

Blood coagulation is a dynamic process and is called a cascade due to its similarity to a waterfall. The principle is a cascade of pro-enzymes (inactive enzymes), leading to activation of downstream enzymes. In the coagulation cascade, activated enzymes are denoted by the addition of an ‘a’ [1-4].

The numbering system of the enzymes involved in blood coagulation are in Roman numerals and like most things, are named in order of discovery. The aim of the coagulation cascade is haemostasis, which is the arrest of bleeding! Haemostasis is maintained by complicated interactions between coagulation, the fibrinolytic system, platelets and the vessel wall [1-3].

Coagulation is split into two pathways (intrinsic and extrinsic) that leads to a common pathway, ultimately leading to clot formation. Normal coagulation represents a tight balance between pro-coagulant and anti-coagulant mechanisms, to ensure normal working order. Any imbalance in the coagulation system can cause issues such as thrombosis (hypercoagulation) or bleeding, imbalances like this can occur during the preoperative period and critical illness [1-4].

Extrinsic pathway [1-3]:

  • First step in plasma mediated haemostasis 
  • Activated by Tissue Factor (TF) which is exposed during injury
  • TF binds with Factor VIIa and calcium to promote conversation of Factor X to Factor Xa 

Intrinsic pathway [1-3]:

  • Parallel pathway for thrombin activation by factor XII*
  • Begins with Factor XII, HK, Pre-kallekrein and Factor XI resulting in activation of Factor XI 
  • Factor XIa further activates, Factor IX which then acts with is cofactor (Factor VIII) to form the ‘tenase’ complex on a phospholipid surface to active Factor X

*Interestingly, a deficiency in FXII does not cause bleeding making the intrinsic pathway an attractive target for potential anti-thrombosis drugs

Common pathway [1-3]:

  • Activated Factor X, along with its cofactor (Factor V), tissue phospholipids, platelet phospholipids and calcium from the ‘prothrombinase’ complex, coverts pro-thrombin into Thrombin (AKA Factor IIa)
  • Thrombin cleaves circulating fibrinogen to insoluble fibrin and actives factor XIII forming covalent cross linked Fibrin polymers incorporated in the primary platelet plug
  • The fibrin network stabilises the clot and forms a definitive secondary haemostatic plug to allow the cessation of bleeding and to start the process of wound healing 

Blood clots [5]:

Without blood clots during injury, we would bleed out from even the smallest of injuries. Blood clots can also form inside the body at sites of injury within a blood vessel. When the clot’s job is done there are processes that cause the clot to dissolve (fibrinolysis) but sometimes this doesn’t occur, and it’s these kinds of clots that can have serious consequences. These unwanted clots have the potential to block blood supply to the heart, the brain or veins of the legs. They can also move, travelling through the bloodstream to different parts of the body. Unwanted blood clots can arise from plaque rupture and can be dangerous, leading to serious life-threatening conditions such as stroke or heart attack.

Fibrinolysis [1, 3, 6]:

Fibrinolysis is the enzymatic breakdown of the soluble fibrin in blood clots after clots are formed. Plasmin cuts the fibrin meshwork in various places leading to the production of circulating fragments. These fragments are then cleared by other proteases in the blood. There are two fibrinolytic processes; primary fibrinolysis is a normal body process whereas secondary fibrinolysis is the breakdown of blood clots due to medication or disorder. 

Anti-coagulants [6, 7]:

Anti-coagulant drugs are usually prescribed after a cardiovascular event or as a preventative measure. There are many different anti-coagulant drugs out there that target different parts of blood coagulation, including clotting factors, platelets or fibrinolysis (more on this in a future post). The aim of anti-coagulants are to prevent the formation of unwanted blood clots, a common side effect of this however, is bleeding. Anti-coagulants have to be tightly controlled to make sure that those that are on anti-coagulants are not at too high a risk of bleeding or clotting. Development of new anti-coagulants aim to prevent blood clots without risk of bleeding by targeting clotting factors such as FXII (no bleeding risk) or FXI (minimal bleeding risk).

Fun fact, I used to work on the blood coagulation cascade before moving to the platelet field. I think it’s definitely helped me having a background in blood coagulation prior to working with platelets, all of these processes are happening at the same time but they’re usually studied separately. 

For extra fun, let me know in the comments if you have any punny coagulation/clotting jokes. A personal fave of mine is:

“So I heard you two tied the clot”

-“We sure did”

“Coagulations!”

I’m aware that joke is terrible but you’ve got to love a good pun joke, right?

Thank you for reading, I hope you enjoyed this post.

See you in the next one,

Beth x

References:

[1] Palta, S., Saroa, R. and Palta, A., 2014. Overview of the coagulation system. Indian Journal of Anaesthesia, 58(5), p.515.

[2] Chaudhry R, Usama SM, Babiker HM. Physiology, Coagulation Pathways. [Updated 2020 Sep 3]. In: StatPearls [Internet]. Treasure Island (FL): StatPearls Publishing; 2020 Jan-. Available from: https://www.ncbi.nlm.nih.gov/books/NBK482253/

[3] Pilli, V., 2018. Understanding the Clotting Cascade, Regulators, and Clinical Modulators of Coagulation. Hematology – Latest Research and Clinical Advances,.

[4] Labtestsonline.org.uk. 2020. Coagulation Cascade. [online] Available at: <https://labtestsonline.org.uk/tests/coagulation-cascade&gt;.

[5] Strokecenter.org. 2020. Thrombus Formation III–Activation Of Coagulation Cascade | Internet Stroke Center. [online] Available at: <http://www.strokecenter.org/professionals/brain-anatomy/atherosclerosis-and-thrombus-formation/thrombus-formation-iiiactivation-of-coagulation-cascade/&gt;.

[6] Publishing, H., 2020. Blood Clots: The Good, The Bad, And The Deadly – Harvard Health. [online] Harvard Health. Available at: <https://www.health.harvard.edu/heart-health/blood-clots-the-good-the-bad-and-the-deadly&gt;.

[7] Weitz, J. and Fredenburgh, J., 2017. Factors XI and XII as Targets for New Anticoagulants. Frontiers in Medicine, 4.

Beth talks blood: Part 4

Platelets (or thrombocytes) are tiny blood cells that help our body to form clots to stop bleeding! Platelets are pretty important for normal haemostasis (arrest of bleeding), without platelets we’d bleed out from the smallest of injuries [1, 2].  

Max Schultze in 1865 first described platelets as “spherules” which he noted were much smaller than RBCs, sometimes clumped and found in fibrin material. Little did he know what these “spherules” were, it wasn’t until 1882 whereby Giulio Bizzozero described platelets as ‘little plates’ which overtime became to be known as ‘platelets’. Bizzozero went on to identify their function in coagulation and has been pivotal in our understanding of platelets through use of the microscope [3].

Platelet production [2}:

Platelets are produced by very large cells in the bone marrow called megakaryocytes. As megakaryocytes develop into larger cells they undergo fragmentation that results in the release of platelets. Once platelets are made and circulated into our blood stream they live for 8-10 days. Our bodies usually contain a lot of platelets, the normal platelet count ranges from 150,000-450,000 platelets per micro-litre of blood [2]. 

Platelet activation [4, 5]:

During vascular injury, blood vessels get damaged which sends out a signal to the platelets. The platelets are then drawn to the site of injury and through a series of tightly regulated cell signalling processes they become active, change shape to form tentacle-like protrusions, spread across the injury surface and aggregate together. In combination with clotting factors, platelets help to form a blood clot that is stable until wound healing has occurred. It’s the cooperation of platelets, cells of the endothelium and clotting factors that prevent us from bleeding out when we injure ourselves. Platelet activation is an extremely important process in haemostasis! [4, 5]In incidences such as cardiovascular disease we get unwanted platelet activation, this is where platelets can become activated without vascular injury, which can be a result of issues in platelet activation and/or platelet inhibition, as well as atherosclerosis and inflammation.

Platelet inhibition [6, 7, 8]:

Under normal circumstances to prevent spontaneous platelet activation, platelets are tightly regulated by inhibitors released from the endothelium. The endothelial cells produce naturally occurring inhibitors such as prostacyclin and nitric oxide to maintain the quiescent (resting) state of platelets in circulation. Prostacyclin and nitric oxide are constantly released by the endothelium in a manner that maintains platelets in an inactive state but while still allowing platelets to activate during vascular injury. 

Prostacyclin once bound to it’s IP receptor on the surface of platelets causes the activation of g-protein coupled receptors, which in turn activate adenylyl cyclases. Adenlyl cyclases are transmembrane proteins, once activated they lead to the production of cyclic adenosine monophosphate (cAMP). The intracellular concentration of cAMP increases and this then leads to the activation of protein kinase A (PKA). Kinases phosphorylate proteins, therefore the activation of PKA leads to the phosphorylation of proteins that ultimately lead to platelet inhibition. Nitric oxide works in a very similar fashion. Nitric oxide is cell permeable so doesn’t require a receptor like prostacyclin. Once inside the cell, NO activates guanylyl cyclases (GCs) which leads to the production of cyclic guanosine monophosphate (cGMP). Cyclic GMP, just like cAMP, goes on to activate protein kinases, in the case it activates protein kinase G (PKG). Protein kinase G then phosphorylates proteins that contribute to the inhibition of platelets [8]. 

The regulation of platelets in circulation is a strict balance between activation and inhibition. Platelets need to be inhibited enough to prevent spontaneous activation but not so much that they can’t activate during vascular injury. It’s a perfect example of how tightly controlled cell signalling processes in our bodies actually are, without this balance we could be at risk of spontaneous clotting or bleeding out from small injuries. 

Platelet disorders [1]:

Thrombocytopenia is a condition where the bone marrow makes too few platelets or the platelets are destroyed. If the platelet count becomes too low, bleeding can occur under the skin and can be seen as bruise or it can happen inside the body as internal bleeding. It can also happen outside the body through an injury that won’t stop bleeding. Thrombocytopenia can be caused by many conditions including several medicines, cancer, liver disease, pregnancy, infection and abnormal immune system.

Essential thrombocythemia is a condition where the bone marrow produces too many platelets. Those with this condition have platelet counts of over 1 million, which is a lot of platelets. Symptoms include the formation of blood clots which can potentially block blood supply to the brain oor heart. It has been said that the cause of this is yet to be determined. 

Secondary thrombocytosis is another condition whereby there are too many platelets, however this condition is much more common. In this case, it is caused by another disease or condition which causes the bone marrow to produce more platelets. The causes include, infection, inflammation, certain types of cancer and sometimes reaction to medicines. The symptoms are usually not serious and the platelet count usually returns to normal once the original condition is treated. 

Platelet dysfunction is a condition where the platelet count is normal but the platelets do not work as they should. Many rare diseases can be linked to poor platelet function. Medicines such as Aspirin can cause, which is why in some cases such as cardiovascular disease, Aspirin is used to reduce platelet activation. It’s important to know how medicines can affect platelets, as taking certain medications that result in platelet dysfunction can increase the risk of bleeding. 

Thanks so much for reading, I hope you enjoyed this post!

Do you use platelets in your research? Let me know in the comments, I’d love to hear from you!

See you in the next one,

Beth x

References:

[1] https://www.nzblood.co.nz/news/2017/top-10-facts-about-platelets/

[2] https://www.stanfordchildrens.org/en/topic/default?id=what-are-platelets-160-36

[3] Brewer, D.B. (2006), Max Schultze (1865), G. Bizzozero (1882) and the discovery of the platelet. British Journal of Haematology, 133: 251-258. https://doi.org/10.1111/j.1365-2141.2006.06036.x

[4] Jonathan M. Gibbins. Journal of Cell Science 2004 117: 3415-3425; doi: 10.1242/jcs.01325

[5] Brass LF. Thrombin and platelet activation. Chest. 2003 Sep;124(3 Suppl):18S-25S. doi: 10.1378/chest.124.3_suppl.18s. PMID: 12970120.

[6] Moncada S. Prostacyclin and arterial-wall biology. Arteriosclerosis. 1982; 2: 193-207. doi: 10.1161/01.ATV.2.3.193

[7] Moncada, S., Gryglewski, R., Bunting, S. et al. An enzyme isolated from arteries transforms prostaglandin endoperoxides to an unstable substance that inhibits platelet aggregation. Nature 263, 663–665 (1976). https://doi.org/10.1038/263663a0

[8] Fukumoto S, Koyama H, Hosoi M, Yamakawa K, Tanaka S, Morii H, Nishizawa Y. Distinct role of cAMP and cGMP in the cell cycle control of vascular smooth muscle cells: cGMP delays cell cycle transition through suppression of cyclin D1 and cyclin-dependent kinase 4 activation. Circ Res. 1999 Nov 26;85(11):985-91. doi: 10.1161/01.res.85.11.985. PMID: 10571528.

Beth Talks Blood: Part 3

The blood circulatory system (cardiovascular system) delivers oxygen and nutrients to all the cells in the body. It is comprised of the heart and blood vessels that run through the entire body. Blood is circulated around the body through blood vessels by the pumping action of the heart [1].

In animals with lungs, arterial blood carries oxygen from inhaled air to the tissues of the body and venous blood carries carbon dioxide, a waste product of metabolism by cells, from the tissues to the lungs to be exhaled.

Functions of blood & circulation [2, 3]:

  • Supply of oxygen & nutrients to tissues 
  • Removal of waste such as carbon dioxide, urea and lactic acid
  • Helps to maintain body temperature
  • Messenger functions – transport of hormones and signalling of tissue damage
  • sends antibodies to fight infection 
  • Contains clotting factors to help blood to clot and the body tissues to heal

Blood vessels [2, 3]:

Arteries and arterioles:

  • Carry oxygenated blood away from the heart
  • Thick hollow tubes 
  • Highly elastic which allows them to dilate (widen) and constrict (narrow) as blood is forced through them by the pumping heart 
  • Branch and re-branch becoming smaller until they become all arterioles which are even more elastic 

Capillaries:

  • Distribute oxygen and nutrients to the body’s tissues
  • Remove deoxygenated blood and waste 
  • Extremely thin, only one cell thick 
  • Connect the arterioles to the venules 

Veins and Venules:

  • Very small veins
  • Merge into larger veins 
  • Carry blood back to the heart 
  • Vessel walls are similar to arteries but are slightly thinner and less elastic 
  • Carry deoxygenated blood towards the lungs to receive oxygen 

There isn’t only one blood circulatory system, it’s made up of two systems that are connected [1, 3]

1. The systemic circulation provides organs, tissues and cells with blood so that it can get oxygen and other vital substances. 

2. The pulmonary circulation is where the fresh oxygen we breath enters the blood and at the same time carbon dioxide is released from the blood. 

The circulation of blood starts when the heart relaxes between beats. The blood flows from both the atria into the ventricles which then expand, the following phase is called the ejection period which is where both ventricles pump the blood into large arteries

In the systemic circulation, the left ventricle pumps oxygen rich blood into the main artery (aorta). The blood then travels from the main artery to larger and smaller arteries and into the capillary network. The blood drops off the oxygen, nutrients and other important substances and picks up the carbon dioxide and waste. The blood is now low in oxygen and is collected by veins to travel to the right atrium and into the right ventricle, this is where the pulmonary system begins – the right ventricle pumps low oxygen blood into the pulmonary artery (branches off into smaller arteries and capillaries). Capillaries form a fine network around the pulmonary vesicles (grape like air sacs at the end of the airways). Carbon dioxide is released from the blood into the air inside the pulmonary vesicles and fresh oxygen enters the blood stream. When we breathe out, the carbon dioxide leaves our body [1, 3].

Thanks so much for reading, I hope you enjoyed this post!

If you have any questions, please feel free to drop them in the comments.

See you in the next one,

Beth x

References:

[1] https://www.ncbi.nlm.nih.gov/books/NBK279250/

[2] http://www.cancerindex.org/medterm/medtm8.htm

[3] https://www.innerbody.com/image/cardov.html

Day 2 of Lockdown 2.0

Here in England we went into a 4 week Lockdown yesterday (5th Nov 2020) and I’m feeling pretty anxious about it. This was inevitable really and I’m not going to go on about what we should have done and when, I’ll be here all day otherwise and I think I’m tired of the frustration about the whole thing to be honest. 

I found the last one exceptionally hard! It was a lot harder than I ever anticipated but I have to remember that I got through it. The last couple of weeks have been tough for me for a multitude of reasons that I won’t go into right now but it just feels like this second lockdown is really the final straw for me. I’m disappointed and angry. I’m not against a national lockdown but I do feel like this could have been earlier/prevented. I feel for all the independent businesses that will suffer through and my heart goes out to those who have lost someone due to the virus, I can’t even begin to imagine how’re they’re feeling throughout all of this! 

This time I know it will be different (at least for me), I can still go to the labs and at least try to move my project along in some way or another which is something positive at least. It may not be ideal but it’s certainly better than nothing and I’m really lucky that I’m still on my PhD programme and I’m still getting paid. While it may not be the PhD I thought I was going to get it’s still something and I know I will come out with my PhD in the end.

I think this time, I’m going to try and be more honest with myself and others about how this whole process has affected my mental health. I think in the first lockdown I was in a bit of denial and struggled through it whereas this time I’m going to keep tabs on my moods and how I’m feeling in order to manage my mental health. 

And let’s be honesty need to cut myself some slack, we all do! This won’t be productive, as much as I’d love it to be. It wasn’t last time and it won’t be this time and that’s totally ok. 

Things I’m going to ~try~ do to get through this 2nd lockdown:

  • Get up & get dressed every day 
  • Move my body in some way every day 
  • Create a routine (thankfully being in the labs will help with this)
  • Schedule in some down time 
  • Use app limits and productivity timers to help me avoid distraction (I feel like I’m on news overload and looking to social media for some escape)
  • Date nights with my bf 
  • Reduce screen time before bed
  • Drink water 
  • Early to bed 
  • Be kinder to myself 

What are you planning on doing to look after your mental health during lockdown 2? Let me know in the comments, I’d love to hear from you.

If you’re having a tough time at the moment and fancy a chat, my DMs are always open!

If you’re really struggling through this uncertain time please reach out to someone, you don’t have to go through this alone. There are several charities in the UK that are there to help during this crisis:

https://www.samaritans.org/how-we-can-help/if-youre-having-difficult-time/if-youre-worried-about-your-mental-health-during-lockdown/

https://www.mind.org.uk/information-support/coronavirus/

https://youngminds.org.uk/find-help/looking-after-yourself/coronavirus-and-mental-health/

https://www.headstogether.org.uk/coronavirus-and-your-mental-health/

Remember to look after yourself during this tough time ahead. This isn’t the time to be super productive so don’t feel bad if you can’t manage much, it’s ok! Self-care isn’t just a trend it’s really important to our mental health and is something we need to prioritise now more than ever. Make sure you schedule in some self-care time each day to take some time out of all the uneasiness that’s happening right now.

I hope you’re ok!

We’ll get through this, I know we will!

Stay safe,

Beth x