microtwjc analysis 2. unique tweeters

When considering participants in #microtwjc, we can also measure the number of unique tweeters, tweeters who have not tweeter at a previous session. This allows a measure of growth of #microtwjc to new people. I have plotted unique 'new' tweeters over time for both the total tweeters and the engaged (n<1 tweeters per session) people. Again, both measures are different. But a major finding of this is that #microtwjc has continued to recruit engaged tweeters over the time. This is at a fairly constant rate, except for a couple of spikes. I've shown the cumulative growth of tweeters in the graph below. Total is growing at an average of 1.8 tweeters/session while engaged are growing at an average of 1.3 tweeters per session. Questions arising from this are: are these tweeters staying? What's the loss of engagement like? To do this I could plot tweeters per person per session. Let's try that. 

dark ale take 2.

Spoiler: it was great. The key to good and science (and good beer) is repetition. The act of doing an experiment again and again allows you to not only find weaknesses in your thinking and doing that you might not have realised but it allows you to act on those weaknesses and improve and rectify them. This is why I tried to make another porter/stout. This was mainly because the last one had some issues (too sugary sweet/ not mellow and not enjoyable to drink). This is a stout after all; it should be relaxing to drink. Guiness anyone? I had tried a similar recipe before (details here). The major differences between the two recipes that I planned are: lower original gravity and the addition of flavor elements that would mellow the beer out (oatmeal, coffee, dark chocolate). My thinking was that the worst aspects of the first beer were high OG and lack of complex elements (chocolate etc.). [never though of this but perhaps I shouldn't have used so much crystal]. Coffee was made in caffetiere, 4 squares of chocolate (Dark, tesco, cheap) were melted in the coffee + boiling water. Oatmeal was steeped.

#microtwjc analysis 1.

The microbiology twitter journal club (#micrtowjc) has been going since x. This 'group' was established to allow the easy discussion of microbiology papers, data and ideas. To do this, a session is planned every two weeks (roughly) on a Tuesday night at 8 pm UK time. One moderator picks a paper that has been recently published (and is usually open access) and then uploads a brief summary and questions to be discussed come the next Tuesday. 

This arrangement has been going on for about two years now and we have not had a chance to evaluate what we have done. In essence, we have conducted a two year experiment into using science communication. By doing a brief eye-balling online it looks like #microtwjc is longest running, functional twitter journal club. The original twitter journal (http://www.twitjc.com/) ran for 2.5 years (June 2011 - December 2013), with a half-year break between June 2013 and December 2013 (other breaks were taken). This means that #microtwjc affords an optimal chance of getting something useful out of its study. 

For the last few months we have been trying to gather as much data about #microtwjc as we can. This covers number of tweeters over time at each session, number of tweets per tweeter per session, papers discussed, journals most chosen etc., etc. These data can be used to assess the worth and potential for #microtwjc to be better in the future. It also serves as a model to understand the use of twitter and social media for science communication and public engagement with science in the future. 

In a series of posts I will try and analyse these data with a hope of finding some useful knowledge and wisdom about #microtwjc. You can view the data here.

A brief description of the methods to get the numbers discussed in this post. 1) each session was logged in storify or topsy format. 2) logged on to each site and searched for each session by date, name etc. 3) went through and counted number of tweeters and number of tweets they made. *this data collection was carried out by a number of the moderators of #microtwjc* . You know who you are. If any of you want to explore these data further, go do it. It's all open. 

Firstly, I took the numbers and divided them per session (fig 1. ). What I quickly realised is that many tweeters tweeted only once, advertising the session, apologising for not being there. I felt these people were not 'engaged' with the session and as we are primarily interested in 'engagement' I decided to clean up the data and remove them from later analysis (posts to come). The engaged tweeters are shown in magenta (fig. 1.). The average tweeters per session was higher in the non-engaged group (As expected) with an average of ~8 compared to ~6. The spread of tweeters was also greater, mostly accounted for by session 1 (fig. 2 green). 

fig 1. number of tweeters: total (green); tweeters tweeting more than once 'engaged' (magenta).

 Fig. 2. shows the data from fig. 1. shown over time for each session. This allows us to pick up peaks of troughs of activity and 'engagement'. 

fig 2. number of tweeters taking part in each session: total (green); tweeters tweeting more than once 'engaged' (magenta).

 Comparing the number of 'engaged' tweeters with total tweeters for each session we can come up with a map of engagement over each session (fig. 3.). This largely parallels fig. 2. but shows it better. 

fig. 3. percentage of tweeters who tweeted more than once per session (engaged) (orange).

I think two conclusions can be gleamed from this small analysis of #microtwjc tweets. 1) There is a more active 'engaged' community of tweeters and 2) tweeters and engaged tweeters changes over time. The reasons why are unknown. There looks to be a difference between years 1 and 2 (session 1 - 26). Your comments are welcome below. 

The hope is that these data can be compiled, analysed, uploaded onto a data repository (figshare) and then use this to publish (PLoS, for example). This process will be completely open and collaborative. 

basic liver biology - why things go wrong when it's infected

Being a virologist is hard. Not only do you have to know molecular biology but you also have to know cell biology and if you are interested in how viruses cause disease, you have to know anatomy and physiology. As you can imagine, while being extremely interesting, it is very time consuming This is why I have spent the last few days (weeks now) trying to come to terms with my liver. 

Your liver is pretty amazing. Chances are you take it's special role for granted but you really shouldn't. This is something that I have been thinking about over the last few months after starting a postdoc into hepatitis C virus (HCV) biology, while I pondered on what it must feel like to lose the function of your liver. To appreciate what is happening during a disease like viral hepatitis, you have to understand how the liver does it job when it's not sick. This post will hopefully be the beginning of a series of blog posts aimed at trying to understand HCV infection and pathogenesis and how my research fits into it. FYI - I have not included any references in this post because what I am writing is established understanding in basic textbooks. This post will act as background as I continue my exploration of the liver and HCV.

You probably won't have seen your liver and your only experience of its metabolic work will have been after you've had a few drinks and you don't remain inebriated for too long. But it also does much, much more. Your liver carries out a complex array of functions, very difficult to summarise in a post like this (but I'll give it a go). Your liver operates a central role in keeping you alive by carrying out a 'biotransformative' role, lying between absorption (your intestines do this) and excretion (your kidneys do this). Biotransformation exists as two major metabolic functions: altering and breaking down molecules (catabolism) and synthesising them and releasing them into your blood stream to feed the rest of your body (anabolism). Another variation in this role is to break down toxins that can damage your body and it can even release hormones and bile, allowing it to function as a gland (again, variations of catabolism and anabolism). It can also store glycogen, an important carbohydrate storage vessel. What did I say, it is a complicated organ, so no wonder things go bad when it gets infected. The most important feature of your liver that allows it to function as a biotransformative organ is its close association with your blood stream and to do this, your liver employs some interesting physiological tricks. But it is these tricks that open it up to infections and disease

your liver, in relation to stomach and pancreas. Note the lobes and blood supply. (integrated.ca.com) 

Anatomically, your liver is a large (1.5 kg), triangular organ in the top right hand side of your chest, beside your stomach and your intestines.  It is divided into four sections, referred to as lobes. Allowing it to carry the job of breaking down and releasing important molecules into your bloodstream, is it's intimate relationship with your circulatory system, which is composed of blood and lymph fluids. Testament to this relationship is its reported blood flow of 1.5 litres per minute. Unlike other organs it has a dual blood supply made up of two major blood vessels run through your liver, the hepatic artery, which brings in oxygen-rich blood, and the the hepatic portal vein that brings in absorbed nutrients and toxins from your small intestine and allows the blood to flow back into circulation. What makes this dual supply even more impressive is the dense network of smaller blood-circulating endothelial cells that are in near-direct contact with your liver cells throughout your liver tissue. This anatomic arrangement allows maximisation of the surface area to volume ratio of you liver for optimal biotransformation.

hepatic lobules centred around a central vein (dnwalker.com)

The liver is a honeycomb mesh of four major cell types, which for ease of understanding are referred to either as parenchymal (hepatocytes) or non-parenchymal (endothelial, macrophage and fibroblast). Your liver parenchymal cells are largely made up of a single cell type, the hepatocyte, which are arranged into single-cell thick epithelial sheets. These cells are the business end of the liver and the one that is responsible for the majority of its metabolic activity (and mass). The main aim of the liver is to maximise the interaction between the hepatocyte and the blood. To do this, your liver employs endothelial cells to form the aforementioned dense network of blood supply between hepatocytes. These endothelial cells form hollow tracts, known as sinusoids, which line sheets of hepatocytes. Two other cell types, the macrophage-like 'kupfer' cells and the fibroblastic 'stellate' cells sit in close proximity to the liver sinusoids and serve immunological, filtering and healing roles, which I won't discuss here. But have covered elsewhere before. 

If you threw these four cell types into a pile together, very little would happen, but when arranged in the way that they are in your liver, they can efficiently interact with your blood. The patterns that these cell types are arranged in come in three flavours: classical hepatitic lobules, portal lobules and acini. Each pattern describes a different spatial interaction of hepatocytes with endothelial cells. The major structural unit of the liver is the classical hepatitic lobule. Within a single lobe of your liver there are many classical hepatitic lobules, each lobule is composed of a hexagonal arrangement of hepatocytes and endothelial cells. Both the hepatoyctes and endothelial cells are organised around a central vein with five-fold symmetry. At each point of the hexagon lies a 'portal triad' of hepatic arterioles, venules and bile ducts. The oxygen-rich blood coming from the hepatic artery and then moving through the liver lobules into the hepatic portal vein. Other patterns can be observed in your liver, and the lobules can also be divided into acini (with two-fold symmetry between portal triads and the other is the portal lobules, which is relevant for bile drainage. 

cells in the hepatic lobules: not hepatocytes, sinosoidal endothelial cell and kupfer cells

And so we come to the business end of the liver. Each cell has it's own role but it is the interactions between each of them allow the liver to carry out its important job. Importantly, the hepatocytes are the metabolic workhorses of the liver, and rightly, they make up the vast majority of the liver's mass. But in order to absorb and secrete, they must be in close contact with the blood supply and it is this interaction that is facilitated by the non-parenchymal cells, which essentially bridge the liver and the circulation. Most importantly, the endothelial cells form what are known as 'sinusoids', single-cell thick vessels with 'leaky' (fenestrated with no basement membrane) walls allowing extremely easy transport of blood fluid over the hepatocytes. But what happens inside the hepatocytes? I will explore this cell type in more detail in the next post.

the hepatocyte in relation to endothelial cells (hakeem-sy.com)