tag:blogger.com,1999:blog-84800121868356938772024-03-21T13:18:05.763+00:00Mark RowanA research log for my cognitive neuroscience PhD, with a sprinkling of thoughts on transport, life in Birmingham, and travelling (when I get the chance).
<p>
<a href="http://www.tamias.co.uk">Back to www.tamias.co.uk</a></p>Mark Rowanhttp://www.blogger.com/profile/00065798700890744332noreply@blogger.comBlogger31125tag:blogger.com,1999:blog-8480012186835693877.post-17846314892886237512011-07-01T11:58:00.000+01:002011-07-01T11:58:03.635+01:00Letter to MP about bus franchising in BirminghamDear <mp>,<br />
<br />
I read a report in the Birmingham Post today:<br />
<a href="http://www.birminghampost.net/birmingham-business/birmingham-business-news/businesslatest/2011/06/30/rail-coach-and-bus-sales-drive-national-express-rise-65233-28969859/" target="_blank">http://www.birminghampost.net/<wbr></wbr>birmingham-business/<wbr></wbr>birmingham-business-news/<wbr></wbr>businesslatest/2011/06/30/<wbr></wbr>rail-coach-and-bus-sales-<wbr></wbr>drive-national-express-rise-<wbr></wbr>65233-28969859/</a><br />
which states in very factual terms that National Express have had a<br />
good year and driven up profits 6%. It then goes on to say that they<br />
did this primarily by charging passengers more (increasing the price<br />
of travelcards 20% at a time of great financial uncertainty for the<br />
people who rely most on the bus) and by cutting rural or less-popular<br />
services (again, hitting the poorest hardest).<br />
<br />
However, NXWM can get away with this as they run the vast majority of<br />
bus services in Birmingham and commercial competition is practically<br />
zero. Buses are important to people in this city (up to 1 million<br />
journeys per day according to NXWM's own literature) and those without<br />
access to cars, such as students, pensioners, and poorer households,<br />
rely on them the most. Surely the operator of such a vital public<br />
service shouldn't be allowed to hold the city to ransom for the sake<br />
of increasing its profits?<br />
<br />
Labour introduced the Local Transport Act in 2008 which allows<br />
transport bodies such as Centro to specify the routes and fares which<br />
should be run in an area, and to allow bus operators to bid for the<br />
exclusive right to run services on these routes. Bad operators can be<br />
fined if they fail on punctuality or fail to bring in agreed<br />
improvements. London was spared the disastrous deregulation of buses<br />
which occured during the Major years, and bus travel has continued to<br />
increase in that time far beyond the growth levels seen in Birmingham<br />
and other deregulated areas. However, Centro have continuously ignored<br />
these powers, preferring to work on a voluntary partnership basis<br />
which has led to a monopoly commercial operator holding the city to<br />
ransom, and frustratingly slow take-up of new technology (which is now<br />
standard in other areas of the country) such as smart card ticketing,<br />
reliable real-time bus information, and audible announcements of the<br />
next stop.<br />
<br />
Franchising of bus routes in Birmingham would be fairer for<br />
passengers, and fairer for other bus operators who are currently<br />
effectively shut out due to NXWM's monopoly. I would urge you to look<br />
further into this issue and do whatever you can to ensure the people<br />
of Birmingham can travel to work, college, and the hospital without<br />
being held to ransom by an out-of-control monopolistic operator.<br />
<br />
Best regards,<br />
<br />
Mark Rowan </mp>Mark Rowanhttp://www.blogger.com/profile/00065798700890744332noreply@blogger.com2tag:blogger.com,1999:blog-8480012186835693877.post-48889507659432396352011-04-18T16:12:00.000+01:002011-04-18T16:12:45.021+01:00Conference paper and RSMG4 reportBoth of these are now up on my <a href="http://www.tamias.co.uk/research/">research page</a>. The paper is to be presented at <a href="http://www.ijcnn2011.org/">IJCNN 2011</a> in San Jose, California, in August of this year.Mark Rowanhttp://www.blogger.com/profile/00065798700890744332noreply@blogger.com0tag:blogger.com,1999:blog-8480012186835693877.post-36611418864165330682011-04-16T14:00:00.000+01:002011-04-16T14:00:54.260+01:00Maths of the voting system referendumLet's be honest, there's a lot of ridiculous arguments coming out from both sides in the <span id="goog_173902651"></span><a href="http://www.yestofairervotes.org/"><span id="goog_172128622"></span>Yes to AV<span id="goog_172128623"></span></a><span id="goog_173902652"></span> and <a href="http://www.no2av.org/"><span id="goog_1971792449"></span>No to AV<span id="goog_1971792450"></span></a> camps. I decided to write this short guide to my understanding of the referendum so far, partly to clarify my thoughts, and partly to help anyone who may be thinking along the same lines as me. I welcome comments and other points of view, as well as any "yes" or "no" arguments I may have missed out.<br />
<br />
I've tried to be as fair as I can as I haven't yet decided myself which way to vote, although I'm currently hedging towards "yes" -- not because of any political allegiances, or indeed the strengths of any of the two campaigns' arguments as we'll see, but because of the maths.<br />
<br />
Acronyms (in case you needed to know) are First Past The Post, the current electoral system, and AV, the proposed new electoral system.<br />
<b><br />
</b><br />
<b>"No" campaign arguments</b><br />
<br />
<ol><li><i>"It's too expensive; the money should be spent on soldiers / children / sweets for midwives"</i><br />
The referendum is already taking place, so the argument is moot. In terms of the actual cost of running the elections, it's admittedly going to be more time-consuming to count the votes under AV. But talk of electronic voting machines being necessities is disingenuous; if they are ever introduced, they would cost pretty much the same if used for FPTP elections. This argument is quite a desperate one; the same argument could be used to say "the NHS is too expensive" or "the Royal Family is too expensive".<br />
</li>
<li><i>"It will let extremists get in"</i><br />
This is an important argument. The argument goes that more people are likely to vote for smaller parties with AV, so parties such as the BNP stand a real chance of getting in. Yet, because of the requirement in AV for candidates to reach 50% of voter support, this actually makes it <i>harder</i> for the likes of the BNP to win.<br />
<br />
For Nick Griffin to become an MP, at least 50% of all voters in his constituency must put him down as one of their choices, AND enough of them have to put him down as their <i>first</i> choice for him to be able to get through the first round (and so on for however many rounds it takes). Is that ever really likely to happen?<br />
<br />
And yet, if it did happen, then by the arguments of democratic representation he should win (especially as he would have won under FPTP too anyway; in fact he could win with just 20% of the vote under FPTP if the other 80% was split across a number of other candidates, each with less than 20%). Democracy is no good if you tell people that their majority-elected candidate can't be an MP, no matter how much of a dick he may be.<br />
</li>
<li><i>"It destroys the principle of one person, one vote"</i><br />
An important point. This is how I see it: if the result of a FPTP election was inconclusive, everyone would be polled again, and again, until the result was clear. But this isn't counted as voting multiple times, as everyone has the same opportunities to vote each time.<br />
<br />
AV sets the bar for winning at 50%, so it simply has the effect of increasing the likelihood that the first round of voting gives an inconclusive result. Everyone is therefore "re-polled", but the least successful candidate drops out. This would mean that anyone who voted for that candidate actually loses their vote; so these people's second choice vote is used instead. It's still only one vote per person that actually gets counted by the time a winner has been found.<br />
</li>
<li><i>"It's too complicated"</i><br />
It's clearly not so complicated that the Tories, Labour, and many other political bodies use it to elect their leaders. The Electoral Commission leaflet which dropped through everyone's doors recently explains it clearly with diagrams so I won't repeat it here. Needless to say, from the voter's point of view the only difference is that they can either still choose just one candidate, as under FPTP, or they make a second, third, fourth, etc. choice in addition should their first choice candidate drop out of the re-counting in subsequent rounds.<br />
</li>
<li><i>"We want to stick one up at Nick Clegg"</i><br />
The anger over the Lib Dems' U-turns is understandable, particularly over issues such as tuition fees and spending cuts, but using petty personal vindictiveness as a reason to vote for or against such a historic change to the way the country is run is shooting yourself in the foot.</li>
</ol><b>"Yes" campaign arguments</b><br />
<br />
<ol><li><i>"It will make MPs work harder for your vote"</i><br />
I think a lot of MPs already work very hard. Mine certainly does. By the implication of this argument, if one candidate works less hard, another candidate will get their votes by default, so that's no different from FPTP either. Ultimately, <i>someone </i>will win in each constituency under FPTP or AV, even if they're just the best of a bad bunch. A pretty weak argument, yet it's the main thrust of the "yes to AV" campaign.<br />
</li>
<li><i>"It maintains the principle of one person, one vote"</i><br />
See point 3 in the "no" campaign. As well as maintaining one <i>counted</i> vote per person, AV would reduce the effect that a handful of marginal seats has on the overall make-up of Parliament. At the moment, sometimes the Tories or Labour win enough marginal seats from each other to give them an outright majority of MPs in Parliament. The majority of voters in the other "safe seats" under FPTP have a much smaller effect on the final national outcome, but AV increases the likelihood that elected MPs represent the constituents' preferences by eliminating tactical voting (see below).<br />
</li>
<li><i>"It's proportional"</i><br />
No it's not. It levels the playing field in constituencies with more than two candidates (i.e. pretty much all constituencies) but Parliament is still made up in exactly the same way: the biggest number of seats wins. So the electoral system is still FPTP at its heart, and it will still be possible for any party to win control of Government with less than 50% of the national vote.<br />
</li>
<li><i>"We want to stick one up at David Cameron"</i><br />
See number 5 in the "no" campaign....</li>
</ol><br />
<br />
<br />
<div style="margin-bottom: 0px; margin-left: 0px; margin-right: 0px; margin-top: 0px;"><b>The Maths</b></div><div>As you can see, neither camp has particularly killer arguments; certainly not strong enough to sway me one way or the other either way. The reason I'm hedging towards "yes" is not towards political allegiances of any kind, but because of the multi-party political system we use, and the maths behind it.</div><div><br />
</div><div>Let me explain:</div><div><br />
</div><div>Imagine a constituency, much like any other around the country today, where traditionally there is one party which does well (say the Tories) and another which is the main contender (say Labour). The electoral system is FPTP. If you're a left-of-centre voter (e.g. Lib Dem or Green) you have to vote tactically to stop the Tories winning; your vote has to go to Labour regardless of your true allegiences if you want a left-of-centre candidate to win. The system only allows for <i>two real contenders </i>and therefore <i>encourages tactical voting</i> whenever there are more than two candidates.</div><div><br />
</div><div>Now imagine the same constituency under AV. You might be a Green person at heart, but rather than having to vote tactically for Labour to stop the Tories, you can safely vote for the Greens knowing that if, as expected, hardly anyone else does, your vote isn't simply thrown away. If you put Labour as your second choice, and the Greens are eliminated early in the counting, then your vote still counts towards a left-of-centre candidate. AV allows a level playing-field for all parties in constituencies with <i>more than two contenders</i> whilst ensuring that a voter's true left/right preferences are recognised, which <i>eliminates the need for tactical voting.</i></div><div><i><br />
</i></div><div>(It's easy to imagine these scenarios for a right-of-centre voter too, eg. preferring UKIP whilst voting tactically under FPTP for the Tories to keep Labour out, before I get accused of bias).</div><div><br />
</div><div>So that's the maths behind the voting system. In a country with just two main parties, such as the USA, FPTP makes sense. In the UK, which prides itself on smaller and independent parties, FPTP squeezes them out in favour of the two biggest parties, whichever ones they may be (and they may not always be Conservatives and Labour). I guess your choice is between these two principles.</div>Mark Rowanhttp://www.blogger.com/profile/00065798700890744332noreply@blogger.com1tag:blogger.com,1999:blog-8480012186835693877.post-59207435485103616502011-02-11T16:49:00.002+00:002011-02-11T16:53:29.852+00:00First paper, next stepsLast week I submitted my first ever paper (yay!) to <a href="http://www.ijcnn2011.org/"><span id="goog_1966569836"></span>IJCNN</a> 2011 in San Jose, having found some interesting results using my implementation of the Ruppin and Reggia (1995) model, most notably that:<br />
<ul><li>Synaptic compensation using remote memories (which of course are easier to obtain in AD) actually accelerates cognitive decline due to the decreased variability in the data set used to calculate compensatory terms.</li>
<li>Where small-world connectivity occurs in the brain, this has the effect of increasing redundancy and resilience to damage, at the expense of lower overall capacity.</li>
<li>Selectively partially muting, rather than deleting, synapses in a spreading area of damage can be used as a simulation of tau pathology, in which vesicles become blocked and axons degrade. This type of lesioning offers a much more graceful decline in performance as the compensatory mechanisms keep up with the changes, but catastrophic damage occurs after a certain level of lesioning and the decline in performance is much more dramatic than with plain synaptic deletion.</li>
</ul><div>Once I get feedback from IJCNN and make any required changes, I'll put a copy of the paper up on my website. In the meantime, I need to think about next steps.</div><div><br />
</div><div>Firstly, my RSMG4 progress report is due in April. This will be a simple 2000-4000 word write-up of my progress over the last 6 months, including what I learned in Göttingen and Zürich on the neuroscience and reservoir computing courses, and of course the IJCNN paper.</div><div><br />
</div><div>Beyond that, I guess I will have the following tasks to choose from:</div><div><ul><li>[OPTIONAL] Continue work on the Ruppin and Reggia model -- design experiments to explore the above effects further.</li>
<li>[ESSENTIAL] Collate definitive medical data against which my models should be compared, and lay out the way in which my model can be shown to be a small part of the overall larger brain organisation (i.e. hippocampal vs neocortical organisation). This is hard and will require much thought!</li>
<li>Incorporate amyloid (including N-APP and anaesthesia) pathology simulations to test cutting-edge medical theories in computational networks.</li>
<li>Begin working on implementation of a reservoir computing network which incorporates synaptic compensation (very important, as the reservoir network's dynamics change dramatically with only slight changes in the internal reservoir).</li>
<ul><li>Can reservoir networks be shown to be better models than, or at least as accurate as, Hopfield-style associative networks (a la Ruppin and Reggia)? What are the differences in behaviour?</li>
<li>What other symptoms of AD can be represented in a reservoir network, other than just failure to accurately recall a stored pattern? As the computational power is much greater, could a basic model of degradation of language / motor skills or some other feature be implemented?</li>
</ul></ul><div>Lots to do!</div></div>Mark Rowanhttp://www.blogger.com/profile/00065798700890744332noreply@blogger.com3tag:blogger.com,1999:blog-8480012186835693877.post-32021958537574636302010-11-03T14:15:00.001+00:002010-11-03T14:21:47.107+00:00Birmingham Oyster cards on their way!According to <a href="http://centro.journalistpresslounge.com/centro/news/index.cfm/fuseaction/details/id/11D70E19-13D3-97AA-2D55BD3FB452C1BC/cnt/1/ref/main/type/News%20Releases/ses/1.cfm">Centro</a> the roll-out of smartcard ticketing machines on all the West Midlands buses* is now complete. Currently the card readers can only be used by national Concessionary passes, but plans for paid Oyster-style ticketing are apparently in the pipeline.<br />
<br />
Optimistically, it looks as if Centro might even be implementing some of the policies which I called for in my <a href="http://blog.tamias.co.uk/2010/08/west-midlands-smartcard.html">previous post</a>: "passengers [will] pre-load their card with cash which is then deducted as it is used on the public transport network, regardless of which bus company’s service they get on", indicating that the card will indeed be an integrated Network West Midlands-branded product rather than simply directly deducting different amounts electronic cash depending on which bus operator's vehicle a passenger gets on. The other piece of good news is that Centro "are also looking at giving Smartcard holders discounted fares" just like in London, which will be a massive boost for the ever-increasingly squeezed West Midlands public transport users.<br />
<br />
Let's just hope the roll-out occurs trouble-free, and before the short-sighted <a href="http://www.bettertransport.org.uk/campaigns/climate_change/spending-review-2010/buses">Tory cuts to bus services</a> drives a critical mass of passengers away from public transport forever.<br />
<br />
<br />
<br />
*Except for the smaller companies with rather dodgy-looking and shabby buses who, presumably, are just there to make money off the Concessionary scheme by under-cutting the established bus operators.Mark Rowanhttp://www.blogger.com/profile/00065798700890744332noreply@blogger.com1tag:blogger.com,1999:blog-8480012186835693877.post-87883520759557328132010-08-10T12:52:00.000+01:002010-08-10T12:52:04.622+01:00West Midlands SmartcardAccording to <a href="http://centro.journalistpresslounge.com/centro/news/index.cfm/fuseaction/details/id/5AF55E6C-13D3-97AA-2D3BB09EAD949948/cnt/1/ref/main/type/News%20Releases/ses/1.cfm">this story</a>, now one third of the buses in the West Midlands are fitted with Smartcard machines as part of the project to get the bus, metro and rail networks all onto Oyster card-style ticketing systems. This is fantastic news for passengers in the region, but at the moment in this trial phase the readers only accept free national concessionary passes.<br />
<br />
When the times comes for letting the wider public use paid-for smartcard technology, there are some serious considerations which Centro must make regarding how the issue of pay-as-you-go fare charging will be tackled.<br />
<br />
Obviously the easiest solution in terms of implementation of a fare structure would be simply to use the smartcard as a stored-value ticket, and subtract each journey's current cash fare from the balance on every use of the card. However I would strongly encourage against this for a number of reasons:<br />
<ul><li>This does nothing to address the current unacceptable situation where bus fares are different, and unpredictable, depending on which operator a passenger uses and at what time of day, and which leads to passengers avoiding catching certain buses simply because they are run by the "wrong" operator. I strongly believe that individual operators' fares should not be taken into account for the smartcard; the product should strictly be a "Network West Midlands" travel smartcard, as this will present a much more coherent product to potential passengers.</li>
<li>Fares should be capped more intelligently than simply at a daily limit. e.g. A day's usage should be capped at the price of an nBus/nTrain/nNetwork daily smartcard rate, but if sufficient days' travel are undertaken during a week, the daily caps within that week should be replaced with the equivalent weekly ticket. Similarly, if enough days/weeks are used in any given month, the monthly rate should be charged instead. This will enable infrequent passengers to truly feel they can trust the smartcard product to give them value for money, instead of worrying in advance whether or not they need to purchase a one-off weekly/monthly ticket and whether they will get full usage out of it if they do so.</li>
<li>Use of public transport in the region is liable to increase with the added convenience of using a smartcard instead of requiring potential passengers to hunt for change or queue to buy tickets. Additionally the requirement to swipe a smartcard rather than flash a strip of paper to the bus driver will lead to a reduction in the current high levels of fraud seen on the region's buses. Incorporating the above recommendations will also lead to much greater uptake of the product by people who would not otherwise consider using the transport network (just look at the number of pay-as-you-go Oyster cards now in use in London). This increase in passenger volume should be reflected in lower overall fares for smartcard users, just like in London, with cash fares remaining as the most expensive option.</li>
</ul>At the moment I fear that Centro will just take the easy option and give us a poor excuse for an integrated smartcard ticketing system which basically just replaces cash with an electronic card and gives passengers no other benefits. What is really needed is a London-style universal fare structure and, ultimately, proper franchising of bus services to ensure that operators are not competing against each other and the trains and metro in a free-for-all at the basic passenger level, but at the more appropriate level of bidding against each other to run pre-determined routes.Mark Rowanhttp://www.blogger.com/profile/00065798700890744332noreply@blogger.com1tag:blogger.com,1999:blog-8480012186835693877.post-29688722829299228322010-07-28T13:15:00.000+01:002010-07-28T13:15:20.680+01:00Racism UKI don't normally blog on politics, but I'm so frustrated and angry at what our Government is proposing with regards to immigration that I feel I have to speak out on this one.<br />
<br />
In short, David Cameron is currently consulting on what level to set a non-EU migration cap above which workers - regardless of ability or skills - will be barred from entry to the country on the basis of their nationality.<br />
<br />
The policy which is about to be implemented is nothing short of outright racism. It says that once the cap is reached, "you can't come to this country if you are not European". If you're Indian, Pakistani, Australian, American, Chinese, even if you're a highly-trained medical practitioner or scientist, you can't come in. Because you're from the wrong country.<br />
<br />
Now, I appreciate that immigration can be a thorny issue when talking about sharing the UK's resources around its ever-growing population, and I would never argue for a free-for-all policy with wide-open borders, but it should be remembered that immigrant workers are also the ones who help run our hospitals, lead our scientific research, and even cook our curries for goodness sake. Similarly, many of us Brits become migrant workers when we head overseas to work or study. The head of my University department, a world-renowned scientist who pays his taxes to the UK Government, is Chinese and would have been barred from coming to this country if the arbitrary cap had been reached at his time of application.<br />
<br />
In addition I strongly believe that rather than achieving the stated aim of reducing the malaise often shown towards the foreign cultures present in the UK by reducing their numbers, this policy will actually foster greater suspicions and racial tensions amongst communities as people view foreigners with an air of "are you even meant to be here? Hasn't this year's cap been reached?"<br />
<br />
The best solution, as has already been shown in Australia and elsewhere, is to admit people based on their skills and what they can bring to the country's economy, NOT on the basis of the country printed on their passport. You'd rightly be appalled if a job was advertised based on nationality rather than skills, and the same should apply for entry to the country.<br />
<br />
To be fair, the Tories always proposed this policy during the election campaign and yet nearly a third of the voting population fell for their racist policies dressed-up as "support for the indigenous population" (now where have we heard that before, Nick Griffin?), but now it comes with the full support of the "Liberal" Democrats too.Mark Rowanhttp://www.blogger.com/profile/00065798700890744332noreply@blogger.com0tag:blogger.com,1999:blog-8480012186835693877.post-56032399114766673532010-05-24T16:01:00.001+01:002010-05-24T16:01:17.478+01:00A plan?Another meeting with John today, after getting some feedback from John Jefferys in Neuroscience. The current plan for a framework of modelling and experimentation is as follows:<br />
<ol><li>Take one of the older models of Alzheimer's disease from the mid-1990s (e.g. Willshaw, Tsodyks and Feigel'man, Hasselmo).</li>
<li>Update it with modern learning algorithms (e.g. LEABRA, Contrastive Hebbian Learning).</li>
<li>Use evolutionary computation to set parameters instead of calculating / guessing them (e.g. firing thresholds, Gaussian connectivity radius and density). Fitness function should be adequate "normal" functioning of the network with least amount of energy (= connections?) required.</li>
<li>Use this updated and evolved model to repeat the 1990s experiments of Ruppin and Reggia or Hasselmo (that's already potentially one small contribution to knowledge in the bag). (As a footnote, Ruppin and Reggia's synaptic deletion and compensation model uses biologically implausible uniform compensation values across the whole network instead of adjusting the remaining synapses using the learning algorithm. This is another change worth considering).</li>
<li>Use the model to attempt to dis/prove a more recent medical hypothesis, such as Nikolaev et al. (2009), which will require showing that up to a certain level of deletion the performance actually increases, and then after that level it degrades. (John argues that I should also dis/prove other hypotheses with the same model to be able to show that it's a valid contribution).</li>
</ol>This should be enough for a bare minimum PhD thesis, but also opens several avenues for further tinkering or completely different approaches:<br />
<ul><li>Starting from different network architectures in (1). e.g. more recent models of schizophrenia or general neocortex models.</li>
<li>Implementing other learning algorithms in (2).</li>
<li>Broadening the number of parameters which could be evolved in (3), e.g. the distribution of DR6 "death receptors" in (5).</li>
<li>Trying out various different things along these lines until I get bored or run out of time!</li>
</ul>Mark Rowanhttp://www.blogger.com/profile/00065798700890744332noreply@blogger.com1tag:blogger.com,1999:blog-8480012186835693877.post-39793096788360229802010-04-27T17:33:00.001+01:002010-04-27T17:37:34.023+01:00Next stepsAfter speaking with John Bullinaria today we've worked out the next steps I should be taking on the way to creating the Thesis Proposal: <br />
<ol><li> Continue implementing some of the <a href="http://archive.cnbc.cmu.edu/Resources/disordermodels/alzheimers.html">older models</a> (e.g. Ruppin and Reggia (1995)), and repeating the experiments to compare results.</li>
<ol><li>Try other lesions, such as adding noise to the connections.</li>
<li>What symptoms appear?</li>
<li>What do these symptoms represent? (This could lead to a basic paper).</li>
</ol>
<li>Identify weaknesses in the models, and gaps in what they can tell us.</li>
<ol><li>Be analytical: are the assumptions of ~15 years ago still correct? Is a Hopfield network still the best type of model?</li>
<li>Identify possible improvements (preferably the ones involving the minimum work and the maximum impact).</li>
<li>Identify a selection of plausible hypotheses from the medical literature, and investigate how these could be modelled in existing or new model classes.</li>
</ol>
<li> Investigate more recent classes of neural model which can be adapted for studying Alzheimer's disease; for example:</li>
<ol><li>Contrastive Hebbian learning.</li>
<li><a href="http://en.wikipedia.org/wiki/Leabra">LEABRA</a> <a href="http://grey.colorado.edu/emergent/index.php/Leabra">learning.</a></li>
<li>Work by John Jefferys, Rolls and Loh, etc.</li>
<li>Recent and more comprehensive models of normal working memory, particularly ones involving the two stages of hippocampal and long-term memory storage (e.g. by McLelland).</li>
</ol></ol>This last point (3) is perhaps the most important, as the premise that <b>I need to work from recent and comprehensive models of memory</b> is vital. There is not much point in trying to incrementally improve basic 15-year old models of AD when neural modelling has moved on a great deal in that time. A better approach would be to take these more recent models and lesion them to study AD, using the lessons learned from the older research.<br />
<br />
John also recommended looking into <a href="http://grey.colorado.edu/emergent/index.php/PDP%2B%2B">PDP++</a> (now called <i>Emergent</i>), a neural network simulator which could save some implementation time, and that for the thesis proposal I shouldn't worry too much about drawing up a specific single hypothesis, but rather focus on the experimental methodology I'll be employing (i.e. applying past work on AD modelling to recent working memory models).Mark Rowanhttp://www.blogger.com/profile/00065798700890744332noreply@blogger.com0tag:blogger.com,1999:blog-8480012186835693877.post-68703777246473013462010-04-27T17:06:00.004+01:002010-04-27T17:09:12.484+01:00RSMG2 publishedWell I've successfully got my <a href="http://www.tamias.co.uk/research/rsmg2.pdf">first proper report</a> out of the door, which is the 5000 word progress report on what I've been doing so far throughout the year. It was accepted in my Thesis Group meeting with only minor changes to the prospective timetable being required, and it seems that I'm heading along the right track in terms of writing style in my literature reviews etc, which I'm quite pleased about. I've also managed to convince Prof. John Jefferys of the School of Neuroscience to join my Thesis Group unofficially so I can receive feedback from an experienced neuroscience researcher regarding the medical side of my work.<br />
<br />
Other discussion points from the meeting were that I'm starting to move away from the original ideas regarding creating a model of routine memory maintenance and trying to evolve schizophrenia and Alzheimer's disease out of this, for two main reasons:<br />
<ol><li>Any model of 'normal working' in the brain would have to be incredibly fine-grained for it to be able to degrade in all possible ways that I'd want to test in order to try to develop the disorders. That's a lot of effort for not very much gain.</li>
<li>Attempting to shoe-horn evolution into the system in this way "for the sake of it" wouldn't necessarily achieve much. It would be better to use the evolutionary algorithm to find ideal starting parameters (such as amount of synaptic plasticity) for the various models, as current modelling techniques tend to just pluck values out of the air with little justification. So this is one area of existing modelling which I can improve.</li>
</ol>I was also encouraged to decide on one specific disorder to investigate (most likely AD in my case), and to use the relevant research into other disorders (schizophrenia, epilepsy, etc) to draw ideas from.<br />
<br />
Finally, it would be beneficial to create a framework to be able to experiment on different hypotheses and models whilst keeping environmental conditions constant. This is essential for me to be able to argue that my model actually does (dis)prove a given hypothesis, rather than it simply being the case that my model is badly implemented and simply doesn't actually work.Mark Rowanhttp://www.blogger.com/profile/00065798700890744332noreply@blogger.com0tag:blogger.com,1999:blog-8480012186835693877.post-43643339515173936642010-03-16T10:25:00.001+00:002010-03-16T10:25:45.904+00:00Petrol prices<a href="http://news.bbc.co.uk/1/hi/business/8569525.stm"> Petrol prices set for record high, says AA</a> (BBC News).<br />
<br />
Petrol prices are not too high if they encourage people to get out of their cars and walk, cycle, or use public transport wherever possible. This country needs a sustainable transport future. Blindly following the American way with 30+ million drivers simultaneously exercising their "right" to use their cars on this small island for every little trip will lead to spiralling congestion, pollution, and numbers of road accidents, not to mention fuelling the obesity problem.<br />
<br />
Rant over -- discuss :)Mark Rowanhttp://www.blogger.com/profile/00065798700890744332noreply@blogger.com1tag:blogger.com,1999:blog-8480012186835693877.post-14476399709598311942010-03-12T16:27:00.000+00:002010-03-12T16:27:16.817+00:00CyclestreetsHere's a fantastic website for searching for safe, quiet alternative cycling routes between any two points in the country. It's based on OpenStreetMap so the coverage for Birmingham is very good, and much better than Google Maps as it takes into account footpaths, cycle tracks, traffic levels, and even gives you a 'hilliness' overview: <a href="http://www.cyclestreets.net/">http://www.cyclestreets.net</a><br />
<br />
I've tried a few of my usual routes to various places on the journey planner and already found a number of alternatives or small adjustments I can use, to make my commute that little bit less hellish and avoid some of the worst motor traffic blackspots.<br />
<br />
Now all I'd like is a GPS-enabled version as an application on my Nokia... please? :)Mark Rowanhttp://www.blogger.com/profile/00065798700890744332noreply@blogger.com0tag:blogger.com,1999:blog-8480012186835693877.post-44849828355085904382010-02-03T12:10:00.000+00:002010-02-03T12:10:33.061+00:00Antipsychotics and antidementia agentsIn a neuroscience lecture this morning given by James Reed of Birmingham and Solihul Mental Health Foundation Trust, we followed the progress of a number of "typical" mental health, including schizophrenia and Alzheimer's disease cases. One interesting point I noted was that in both cases there was administration of drugs (anti-pyschotics in the schizophrenia case and drugs such as <i>donepezil </i>("<i>Aricept</i>") in the Alzheimer's case). I feel there is something to be learned for my research from how antipyschotics and antidementia agents act on the brain to reduce the symptoms. It's clear in both cases that the drugs do not address the causes of the disorders, but only manage the symptoms of the suffers. A bit of Wikipedia trawling follows... (proper paper references to come when I properly research this!)<br />
<br />
Aricept is a type of <a href="http://en.wikipedia.org/wiki/Acetylcholinesterase_inhibitor" title="Acetylcholinesterase inhibitor">acetylcholinesterase inhibitor</a> (i.e. it inhibits the enzyme which breaks down acetylcholine), which ties in with the theories I've read in Stein and Ludik (1998) about the role of acetylcholine in memory management and prevention of runaway synaptic modification. The <a href="http://alzheimers.org.uk/site/scripts/documents_info.php?categoryID=200137&documentID=147&pageNumber=1">Alzheimer's Society</a> helpfully explain that "Aricept, Exelon and Reminyl prevent an enzyme known as acetylcholinesterase from breaking down acetylcholine in the brain. Increased concentrations of acetylcholine lead to increased communication between the nerve cells that use acetylcholine as a chemical messenger, which may in turn temporarily improve or stabilise the symptoms of Alzheimer's disease ... the action of Ebixa is quite different to, and more complex than, that of Aricept, Exelon and Reminyl. Ebixa blocks a messenger chemical known as glutamate. Glutamate is released in excessive amounts when brain cells are damaged by Alzheimer's disease, and this causes the brain cells to be damaged further. Ebixa can protect brain cells by blocking this release of excess glutamate."<br />
<br />
Most antipyschotic drugs appear to work by simply <a href="http://en.wikipedia.org/wiki/Dopamine_antagonist">blocking dopamine receptors</a> in the brain, typically the <a href="http://en.wikipedia.org/wiki/Typical_antipsychotic">D<span style="font-size: xx-small;">2</span></a><a href="http://en.wikipedia.org/wiki/Atypical_antipsychotics"> or D<span style="font-size: xx-small;">4</span> receptor</a>, and "atypical" antipsychotics also <a href="http://en.wikipedia.org/wiki/Atypical_antipsychotics">act on serotonin receptors</a>. James mentioned that <a href="http://en.wikipedia.org/wiki/Clozapine"><i>clozapine</i></a> is a particularly effective antipsychotic (although it is rarely used now as it has some severe side-effects), and no-one quite knows why, although apparently it acts on D<span style="font-size: xx-small;">2</span> less strongly than other antipsychotics. Developing a new drug which works in the same way, but without the side-effects, is a major part of clinical schizophrenia research which would be aided by knowing how clozapine actually works, and how it is different to other antipsychotics! This is potentially something I could attempt to model during my work.<br />
<br />
There is some interesting background to various medical and neurological theories about the <a href="http://en.wikipedia.org/wiki/Causes_of_schizophrenia">causes of schizophrenia</a> on Wikipedia too, with particular mention of the <a href="http://en.wikipedia.org/wiki/Glutamate_hypothesis_of_schizophrenia">Glutamate</a> (related to NMDA receptors; see Greenstein and Ruppin, 1998) and <a href="http://en.wikipedia.org/wiki/Dopamine_hypothesis_of_schizophrenia">Dopamine</a> (supported by the fact that antipsychotics work by blocking dopamine receptors) theories. Apparently the glutamate hypothesis "does not negate the dopamine hypothesis, and the two may be ultimately brought together by circuit-based models." (Lisman et al., 2008, as cited at <a href="http://en.wikipedia.org/wiki/Glutamate_hypothesis_of_schizophrenia">Wikipedia</a>).<br />
<br />
Interestingly, glutamate is mentioned in both schizophrenia and Alzheimer's disease, although for different reasons. In the <a href="http://www.stenmorten.com/English/essays/glutamate-theory-of-schizophrenia.htm">glutamate theory of schizophrenia</a> (non-Wikipedia link), treatment is performed by <i>increasing </i>the amount of glutamate available, whereas Ebixa attempts to <i>reduce</i> the amount of damage caused by glutamate in Alzheimer's disease.<br />
<br />
Finally, the BBC has produced a <a href="http://news.bbc.co.uk/1/hi/in_depth/health/2010/dementia/">Dementia 2010</a> news feature focussing on dementia and Alzheimer's disease. Of particular interest, if only for soundbites as part of my introduction, are:<br />
<br />
<ul><li><a href="http://news.bbc.co.uk/1/hi/health/8493248.stm">Dementia 'losing out' to cancer in funding stakes</a> (The usual sob story, albeit justified, calling for more funding).</li>
<li><a href="http://news.bbc.co.uk/1/hi/health/8478901.stm">What is delaying a cure for Alzheimer's?</a> (The answer again is "funding", but the article at least acknowledges that much of the currently-reported Alzheimer's disease research progress in the media simply focusses on seemingly trivial findings, such as that eating cornflakes three times a day and tying your shoelaces immediately before attempting a crossword statistically lowers your chances of developing AD, without going deeper into <i>why</i>).</li>
<li><a href="http://news.bbc.co.uk/1/hi/health/8492918.stm">Indian village may hold key to beating dementia</a> (Nearly one of the aforementioned "trivial observations" reports, but at least they did some research into more specific factors such as a low-cholesterol, vegetarian diet, and lack of the APO4E gene which apparently predisposes people to AD. This also links to a paper by Sima and Li (2006) on a proposed connection between diabetes and Alzheimer's disease).</li>
</ul><br />
<b>References</b><br />
Greenstein-Messica, A. and Ruppin, E. (1998), "Synaptic runaway in associative networks and the pathogenesis of schizophrenia", in <i>Neural Computation</i> 10:451--465.<br />
<br />
<span class="citation Journal">Lisman JE, Coyle JT, Green RW, <i>et al.</i> (May 2008). <a class="external text" href="http://www.pubmedcentral.nih.gov/articlerender.fcgi?tool=pmcentrez&artid=2680493" rel="nofollow">"Circuit-based framework for understanding neurotransmitter and risk gene interactions in schizophrenia"</a>. <i>Trends in Neurosciences</i> <b>31</b> (5): 234–42.</span> <br />
<br />
Sima, A.A.F and Li, Z. (2006), <a href="http://www.ncbi.nlm.nih.gov/pmc/articles/PMC1828287/">"Diabetes and Alzheimer's Disease - Is There a Connection?"</a>. <i>The Review of Diabetic Studies</i> <b>3</b>(4):161.<br />
<span class="citation-abbreviation"></span><br />
<br />
Stein, D.J. and Ludik, J. (1998), <i>Neural Networks and Pyschopathology</i>, Cambridge University Press.Mark Rowanhttp://www.blogger.com/profile/00065798700890744332noreply@blogger.com1tag:blogger.com,1999:blog-8480012186835693877.post-45782993832560259352010-02-02T14:14:00.001+00:002010-02-02T14:16:41.755+00:00I've created a brain!And now it's going to take over the world, mwahahahahaa....<br />
<br />
Well not quite, but in the last two weeks I've implemented (in Java) the model by Ruppin and Reggia (1995) which creates a non-fully-connected Hopfield network, gets it to learn a number of patterns or 'memories', in an activity-dependent Hebbian manner ("<i>cells that fire together, wire together</i>"), and then tries to recall them.<br />
<br />
Up to a certain number of patterns (<i>n / 2 log n</i>, where <i>n</i> is the number of neurons in the network) it works beautifully and then, as expected, once its memory is 'full' recall performance drops dramatically. I'm yet to formally carry out any experiments along the same lines as Ruppin and Reggia, but initial results seem to indicate my implementation gives roughly the same behaviour as their model.<br />
<br />
Ruppin and Reggia were only able to create networks up to 1600 neurons in size, due to the limited computing power available at the time. With my implementation I've already successfully run networks of 100,000 neurons in size (=10,000 memories!) in the default Java heap space of 64MB. By increasing the heap space -- and being very patient as it will take a long time to run -- I hope to be able to demonstrate networks of maybe up to half a million neurons in size. Whether that will enhance the experimental results at all remains to be seen.<br />
<br />
Next steps are to implement network lesioning -- that is, damaging the network by deleting neurons and/or synapses, in an attempt to get it to develop symptoms similar to Alzheimer's disease, and recreate the experiments of Ruppin and Reggia (1995) on a larger scale.<br />
<br />
After that, the model will be extended further to try to imitate symptoms of schizophrenia, as in Ruppin et al. (1996). There is also an alternative model of Alzheimer's disease introduced by Horn et al. (1996) which I'd like to implement, and no doubt I'll find some others in the literature during that time as well (including hopefully some more recent than the mid-1990s). During that time I'll also have to write up my current reading for the RSMG2 report, due in May of this year.<br />
<br />
<b>References</b><br />
Horn, D., Levy, N., Ruppin, E. (1996), "Neuronal-based synaptic compensation: a computational study in Alzheimer's disease", in <i>Neural Computation</i> 8:1227--1243.<br />
<b> </b><br />
Horn, D., Levy, N., Ruppin, E. (1998), "Memory maintenance via neuronal regulation", in <i>Neural Computation </i>10:1--18.<b> </b><br />
<br />
Ruppin, E. and Reggia<b> </b>J. (1995), "A neural model of memory impairment in diffuse cerebral atrophy", in <i>British Journal of Psychiatry </i>166:19--28<br />
<br />
Ruppin, E., Reggia, J., Horn, D. (1996), "Pathogenesis of schizophrenic delusions and hallucinations: a neural model", <i>Schizophrenia Bulletin</i> (22)1:105-123Mark Rowanhttp://www.blogger.com/profile/00065798700890744332noreply@blogger.com0tag:blogger.com,1999:blog-8480012186835693877.post-86509110563353215832010-01-13T19:56:00.004+00:002010-01-14T15:17:14.102+00:00Memories that can last a lifetimeHow does your brain store childhood memories for your entire life, even after the actual neurons present in your brain when you first experienced that memory have long since died and been replaced, many times over?<br />
<br />
It's a fascinating question, and one which Horn et. al. (1998) attempt to answer using a computational model. Firstly, memories are not stored one-per-neuron: "Stored memories are not represented at specific neurons of the network, but their corresponding representations are distributed; many neurons participate in a given [memory], and a particular neuron participates in several different [memories] (Ruppin et. al., 1996). Horn et. al. (1998) show that by adjusting the strengths of the synapses between neurons whenever a neuron dies in order to keep the activation of all of the remaining neurons the same, the overall network is capable of retaining the stored memories for quite a while.<br />
<br />
Interestingly, this mechanism also counter-balances the 'pathological attractors' which tend to arise from the deletion or modification of synapses in this way during <i>activity-dependent learning</i>, and which represent symptoms of schizophrenia (Ruppin et. al., 1996).<br />
<br />
This got me thinking: what if I could create a copy of this model to show memories being retained in this way during the course of normal neuronal death, but implement some existing medical hypotheses e.g. <i>delayed NMDA receptor maturation</i> (Greenstein and Ruppin, 1998) or <i>excessive neuronal activity leading to excess glutamate production and neurodegeneration </i>(Good Brain, Bad Brain module semester 2) to try to model a change in the normal neuronal death process which leads to a disorder such as Alzheimer's or schizophrenia (or both, if it can be shown that they are sufficiently closely-linked)? Horn et. al. (1998) also suggest that "recent findings [listed] indicate that signaling molecules involved in neuronal regulation are altered in Alzheimer's disease", adding further weight to this idea.<br />
<br />
This would be taking a different angle to the research compared to the suggestion of simply trying to explain Rund (2009)'s findings that there may be a degenerative process in schizophrenia in the context of Alzheimer's disease (which is possibly looking like a very tenuous link to make).<br />
<br />
So it looks like I could currently take three paths:<br />
<ol><li>Model possibly <i>causes</i> of Alzheimer's and/or schizophrenia, in the context of memory maintenance (Horn et. al., 1998).</li>
<li>Model the shared elements of the <i>progress</i> of Alzheimer's and schizophrenia (i.e. synaptic runaway (Ruppin et. al., 1996; Greenstein and Ruppin, 1998; Hasselmo, 1994; Ruppin and Reggia, 1995; Horn et. al., 1996)).</li>
<li>Model a <i>degenerative process in schizophrenia</i> (possibly drawing from Alzheimer's disease modelling), to corroborate Rund (2009)'s findings.<br />
</li>
</ol><br />
<b>References</b><br />
Greenstein-Messica, A. and Ruppin, E. (1998), "Synaptic runaway in associative networks and the pathogenesis of schizophrenia", in <i>Neural Computation</i> 10:451--465.<br />
<br />
Hasselmo, M.E. (1994), "Runaway synaptic modification in models of cortex: Implications for Alzheimer's disease", in <i>Neural Networks</i> 7:13--40. <br />
<br />
Horn, D., Levy, N., Ruppin, E. (1996), "Neuronal-based synaptic compensation: a computational study in Alzheimer's disease", in <i>Neural Computation</i> 8:1227--1243.<br />
<br />
Horn, D., Levy, N., Ruppin, E. (1998), "Memory maintenance via neuronal regulation", in <i>Neural Computation </i>10:1--18.<br />
<br />
Rund, B.R. (2009), "Is there a degenerativeprocess going on in the brain of people with schizophrenia?" in <i>Frontiers in Neuroscience</i> (3)36:1--6. <br />
<br />
Ruppin, E. and Reggia<b> </b>J. (1995), "A neural model of memory impairment in diffuse cerebral atrophy", in <i>British Journal of Psychiatry </i>166:19--28<br />
<br />
Ruppin, E., Reggia, J., Horn, D. (1996), "Pathogenesis of schizophrenic delusions and hallucinations: a neural model", <i>Schizophrenia Bulletin</i> (22)1:105-123Mark Rowanhttp://www.blogger.com/profile/00065798700890744332noreply@blogger.com0tag:blogger.com,1999:blog-8480012186835693877.post-11965744722457610192010-01-13T18:45:00.011+00:002010-01-13T19:58:07.637+00:00Some models to start off withIn a <a href="http://blog.tamias.co.uk/2009/12/skills-and-interests.html">previous post</a> I started to look at the possibility of modelling a shared overlap with Alzheimer's disease and schizophrenia.<br />
<br />
The first thing to mention is that, contrary to what I wrote previously, <i>synaptic runaway</i> appears to have very little to do with Alzheimer's disease, so we've lost that potential link with schizophrenia (which does have a lot to do with synaptic runaway).<br />
<br />
<b>EDIT: </b>Actually, maybe synaptic runaway <i>does</i> have something to do with Alzheimer's: Greenstein and Ruppin (1998) mentions "Hasselmo's [1994] hypothesis concerning ... synaptic runaway in the progression of Alzheimer's disease".<br />
<br />
There's a whole raft of papers by Ruppin, Reggia, Horn and Levy amongst others from the mid-90s on computational modelling of both Alzheimer's disease and schizophrenia. One such paper includes a very clear description of a model of Alzheimer's disease, in which they deleted synapses at random but also caused the remaining synapses to attempt to compensate for these changes, which caused older memories to be retained long after recent (short-term) memories were destroyed by the deletion process (Ruppin and Reggia, 1995), just like in Alzheimer's disease where patients forget things like turning off the cooker long before they forget older memories such as the names of their loved ones.<br />
<br />
They then took this model and re-spun it to model schizophrenia via synaptic runaway, such that the model retained <b>all</b> its memories for a long time, but interestingly also spontaneously retrieved parts of memories at random without any stimulus (Ruppin et. al., 1996), mirroring the hallucinations and delusions in schizophrenia and perhaps explaining the sensation that "someone else" (aliens, the CIA, etc.) is controlling the sufferer's thoughts.<br />
<br />
This appears to be the last paper in this particular strand of their research, and it contains some interesting proposals for future work, which could feasibly form part of my preliminary research:<br />
<br />
<ol><li>Putting several copies of the schizophrenia model together to simulate <i>cortical modules</i> communicating with each other, to see if this restricts hallicinogenic symptoms (the 'biased pathological attractors' in the jargon) to individual parts of the brain, or spreads them throughout.</li>
<li>Enabling the models to be reset each time they suffer a 'hallucination' so they can be repeatedly re-tested instead of forcing them to remain in the 'pathological attractor' state.</li>
<li>Simply running the models with far larger neural networks, now that improved computational power is available.<br />
</li>
</ol>Interestingly, another paper in this series by Greenstein and Ruppin (1998) potentially refutes Rund (2009)'s hypothesis that schizophrenia could be a neurodegenerative disorder like Alzheimer's disease. This indicates that I could be barking up the wrong tree if I try to "model degenerative processes in both disorders" as I <a href="http://wrote%20previously/">wrote previously</a>.<br />
<br />
Greenstein and Ruppin (1998) hypothesised that schizophrenia is due to <i>delayed NMDA receptor maturation</i> which leads to the neural network being "overloaded at an early stage, much before it reaches its explicit capacity limits" and therefore to synaptic runaway and schizophrenia, with no mention of unusual cell death -- so perhaps we'll have to find some other process to explain Rund (2009)'s observations of neurodegeneration in some schizophrenia patients.<br />
<br />
<br />
<b>References</b><br />
Greenstein-Messica, A. and Ruppin, E. (1998), "Synaptic runaway in associative networks and the pathogenesis of schizophrenia", in <i>Neural Computation</i> 10:451--465.<br />
<br />
Hasselmo, M.E. (1994), "Runaway synaptic modification in models of cortex: Implications for Alzheimer's disease", in <i>Neural Networks</i> 7:13--40. <br />
<br />
Rund, B.R. (2009), "Is there a degenerativeprocess going on in the brain of people with schizophrenia?" in <i>Frontiers in Neuroscience</i> (3)36:1--6.<br />
<br />
Ruppin, E. and Reggia<b> </b>J. (1995), "A neural model of memory impairment in diffuse cerebral atrophy", in <i>British Journal of Psychiatry </i>166:19--28<br />
<br />
Ruppin, E., Reggia, J., Horn, D. (1996), "Pathogenesis of schizophrenic delusions and hallucinations: a neural model", <i>Schizophrenia Bulletin</i> (22)1:105-123Mark Rowanhttp://www.blogger.com/profile/00065798700890744332noreply@blogger.com0tag:blogger.com,1999:blog-8480012186835693877.post-87559576771759286572010-01-12T15:51:00.001+00:002010-01-12T15:51:11.267+00:00Bus regulation is backHooray! I had no idea this was even in the pipeline, but <a href="http://www.telegraph.co.uk/finance/newsbysector/transport/6967077/UK-bus-companies-face-stricter-regulation-from-town-halls.html">according to The Times</a> our local authorities now have the power to force bus companies into line through <i>quality contracts</i> for routes, fares, timetables, and technological enhancements (including introducing cashless smart cards such as Oyster) in a move which "reverses the deregulation of the bus industry by the Conservative Government in the 1980s" -- much like the current system in London where routes and the contracts to run them are drawn up by the council, and operators bid to run the services under their terms.<br />
<br />
Hopefully now we'll finally begin to see some joined-up bus networks which truly integrate with each other and with other transport modes, and we can finally leave behind the ridiculous situation where passengers have to stand back and let buses going to their destination pass by simply because they're the wrong colour!<br />
<br />
Oh, and Oyster cards for the rest of the country would be nice too :)Mark Rowanhttp://www.blogger.com/profile/00065798700890744332noreply@blogger.com1tag:blogger.com,1999:blog-8480012186835693877.post-22539228904552516632009-12-23T22:41:00.001+00:002009-12-23T22:44:12.327+00:00Metro DevelopmentAfter my post on the <a href="http://blog.tamias.co.uk/2009/11/midland-metro-extension-finally-to-go.html">new Midland Metro extension proposal</a> I asked Centro about their confidence in the new proposals. Judging by their response they seem pretty up-beat about the chances of success this time around. Maybe after 10 years of swimming upstream against Government policies which <a href="http://www.bettertransport.org.uk/campaigns/public_transport/trams/whats_needed">discriminate against trams</a> it looks like we may at last be on the cusp of achieving a tram network to be proud of in the West Midlands.<br />
<div style="font-family: Arial,Helvetica,sans-serif;"><span style="font-size: small;"><br />
</span><br />
</div><div style="font-family: Arial,Helvetica,sans-serif;"><span style="font-size: small;">Metro Development<br />
<br />
Thank you for your email regarding the future Metro development projects to bring more tram services to the streets of the West Midlands.<br />
<br />
It was very encouraging to read that you fully support our proposals. Please follow the link below to our press release earlier this year, which sets out exactly what Centro is proposing:<br />
<br />
<a href="http://centro.journalistpresslounge.com/centro/news/index.cfm/fuseaction/details/id/A6C15BB3-13D3-97AA-2D049A95F30F7EA0/cnt/1/ref/main/type/news%20releases/ses/1.cfm" target="_blank">http://centro.<wbr></wbr>journalistpresslounge.com/<wbr></wbr>centro/news/index.cfm/<wbr></wbr>fuseaction/details/id/<br />
A6C15BB3-13D3-97AA-<br />
2D049A95F30F7EA0/cnt/1/ref/<wbr></wbr>main/type/news%20releases/ses/<wbr></wbr>1.cfm</a><br />
<br />
The decision to give this scheme the go-ahead is due in the new year and this decision will be taken by the Department for Transport (DfT). Centro are confident that the bid is extremely robust and that we have done everything possible to explain the benefits to the DfT of this scheme. Once a decision has been reached, I can assure you this will be widely publicised and full details will be available from Centro at the time.<br />
<br />
I hope the above information is helpful and would like to thank you for taking the time to contact Centro and for your interest in this project.</span><br />
</div>Mark Rowanhttp://www.blogger.com/profile/00065798700890744332noreply@blogger.com0tag:blogger.com,1999:blog-8480012186835693877.post-60596102451894542822009-12-16T17:22:00.004+00:002009-12-16T18:08:57.926+00:00Skills and interestsRight, time to focus a little more specifically on what I actually want to do (i.e. which techniques to use) during this PhD.<br />
<br />
I want to utilise:<br />
<ul><li>Evolutionary computation</li>
<li>Neural networks</li>
<ul><li>Hence --> evolving neural networks</li>
</ul>
<li>Methodical experimentation rather than "one great big long think"</li>
</ul>This lends itself to the idea of heuristically creating or refining a model to fit a certain fitness function (e.g. expected behaviour of the network under certain conditions).<br />
<br />
<br />
The fields in which I am particularly interested in using these techniques are:<br />
<br />
<ul><li>Understanding more about Alzheimer's disease</li>
<ul><li><i>Model of robustness of musical memory in AD?</i></li>
<ul><li>Nothing obviously defined in the literature, but it could be over-ambitious to hope to model musical memory sufficiently in the time available for the PhD.<br />
</li>
</ul>
<li><i>Models of progression?</i></li>
<ul><li>Already many models defined -- probably end up refining or combining existing models.</li>
</ul>
</ul>
<li>OR understanding more about schizophrenia</li>
<ul><li><i>Model of ability of music to calm patients in both AD and schizophrenia?</i></li>
<ul><li>Nothing obviously defined in the literature, but it could be over-ambitious to hope to model musical processing sufficiently in the time available for the PhD.</li>
</ul>
</ul><ul><li><i>Models of hallucinations?</i></li>
<ul><li>Already many models defined -- probably end up refining or combining existing models.</li>
</ul>
</ul>
<li>OR investigating the overlap between aspects of AD and schizophrenia </li>
<ul><li><i>Model of potential degenerative processes in both disorders?</i></li>
<ul><li>Degenerative process in schizophrenia postulated in Rund (2009).</li>
<li>Possible supporting evidence for reduced cortical synaptic connection in schizophrenia (Hoffman and McGlashan (2001)) and reduced hippocampal synaptic connection in Alzheimer's disease (Duch (2007) and Wallenstein and Hasselmo (1997)) both leading to <i>runaway synaptic modification</i> (Hasselmo (1994)).</li>
<li>Would need to show how the runaway synaptic modification follows the same basic pathology but diverges to form the two separate disorders.</li>
<li>Needs further reading to investigate the initial feasibility of this hypothesis, or whether it's easy to disprove.<br />
</li>
</ul>
</ul>
</ul>Well, having written all that down, it looks like the above question (modelling degenerative processes in AD and schizophrenia) actually could present quite a good topic. (On an unrelated note, why is it that I can spend a day moping around, staring blankly at some papers and not really getting much done, but as soon as I sit down and start to write here, ideas come flowing forth?)<br />
<br />
For the time being, at least, if I read further into the possibility of a neuropathalogical overlap in AD and schizophrenia, I can get an idea for how feasible as a hypothesis this is (at the moment it's not much more than a hunch, having read through a few related papers).<br />
<br />
I'll also need to figure out how I'll actually go about testing any hypothesis in this area experimentally, as I still want to make use of the refine-and-repeat evolutionary computation technique for generating candidate networks according to the rules of whatever model I end up using / designing.<br />
<br />
<b>References</b> <br />
Rund, B.R. (2009), "Is there a degenerativeprocess going on in the brain of people with schizophrenia?" in <i>Frontiers in Neuroscience</i>.<br />
<br />
Wallenstein, G.V. and Hasselmo M.E. (1997), "Are there common neural mechanisms for learning, epilepsy, and Alzheimer's disease?", in Stein and Ludik (1997), pp. 314--316.<br />
<br />
Stein, D.J. and Ludik, J. (1998), <i>Neural Networks and Pyschopathology</i>, Cambridge University Press.<br />
<br />
Duch, W. (2007), "<b style="font-weight: normal;">Computational Models of Dementia and Neurological Problems", in </b><i><b></b>Methods in Molecular Biology</i>, pp. 305--336.<br />
<br />
Hoffman, R.E. and McGlashan, T.H. (2001), "Neural network models of schizophrenia", in <i>Neuroscientist</i> 7(5):441--454.<br />
<br />
Hasselmo, M.E. (1994), "Runaway synaptic modification in models of cortex: Implications for Alzheimer's disease", in <i>Neural Networks</i> 7:13--40.Mark Rowanhttp://www.blogger.com/profile/00065798700890744332noreply@blogger.com8tag:blogger.com,1999:blog-8480012186835693877.post-20454402497354269512009-12-15T17:59:00.001+00:002009-12-16T17:28:35.736+00:00So many questions, so little time!Argh!<br />
<br />
Now that I've got that out of the way, what is it that's so frustrating me?<br />
<br />
Whilst I've been (slowly) reading my way around the topic of modelling neurological disorders, I've come across some interesting articles. I've looked into models of schizophrenia and Alzheimer's disease, and analysed at least 6 models in the process. I've toyed with the idea of picking a model and refining it, or picking several models and merging them. Some models postulate key differences between themselves and other models, so I've considered trying to confirm or contradict these differences. I've thought about the nature of hallucinations in AD and schizophrenia, and the possibility of investigating differences in how damaged brains dream.<br />
<br />
As I read more, the number of questions one could ask grows ever longer. Whilst this is fantastic from a scientific point of view (no shortage of things to research, then), it really doesn't help when trying to narrow down a topic with the aim of writing a specific proposal 8 months from now!<br />
<br />
At the moment it feels like my reading is aimlessly meandering from sub-topic to sub-topic, with no clear goal in sight. I need to figure out a way to pick a question and stick to it, for the time being at least, so I can direct my reading around it.<br />
<br />
Any suggestions, anyone?Mark Rowanhttp://www.blogger.com/profile/00065798700890744332noreply@blogger.com0tag:blogger.com,1999:blog-8480012186835693877.post-58851367783507807732009-11-24T14:04:00.001+00:002009-11-24T14:04:28.922+00:00Midland Metro extension finally to go ahead?It looks like the Midland Metro Line 1 extension plans are back on the table! The Metro has been running for 10 years but currently suffers from low usage, which therefore makes it appear unattractive to extend it and to give Birmingham a world-class integrated transport system <a href="http://blog.tamias.co.uk/2009/05/integrated-transport-in-birmingham.html">such as Zurich's</a>. This is in no small part because <i>"Midland Metro Line 1 currently terminates at Snow Hill, short of (and beneath) the heart of the city centre. [...] Midland Metro is therefore not seen by many city centre visitors as the preferred public transport option to access city centre destinations. Indeed for many, Midland Metro is not seen at all. Being within Snow Hill Station and down an escalator the stop and the trams, the most obvious visual signal for the system, are out of sight from street level and out of mind for many." </i>(<a href="http://www.centro.org.uk/nmsruntime/saveasdialog.aspx?lID=2531&sID=4972">Centro Metro Strategic Case</a> document)<i>.</i><br />
<i><br />
</i><br />
Having spent time in Zurich and other European cities I am firmly convinced that trams should form the backbone of a city's transport network, with buses and heavy rail providing the secondary support network. This is due to the tram's high visibility, which encourages people simply to hop-on and off as needed, as even when a tram is not present the tram lines in the street indicate very clearly that "this is a tram route". This makes it far easier for passengers to plan their journeys, as buses by their nature follow the winding roads of a city and its suburbs and it can be difficult to work out which buses go where, or the best locations to change buses.<br />
<br />
With trams, passengers benefit from a relatively low (and therefore simpler) number of high-capacity routes [compare a 200-passenger tram with 50-80 seats on a bus] which are clearly denoted both on maps, due to the non-requirement to follow winding suburban roads, and of course on the streets themselves.<br />
<br />
Centro have updated their website with details of the <a href="http://www.centro.org.uk/metro/CityCentreExtension.aspx">city centre extension</a> we've already heard before, but with a brand new (October 2009) business case and strategy, showing a very clear proposal to bring the Metro right into the heart of Birmingham, thus making it a visible and attractive option for pedestrians and shoppers in the city centre to travel towards Wolverhampton, and indeed fulfilling the long-missing option of a transport link between Snow Hill station and the soon-to-be-redeveloped New Street station.<br />
<br />
<div class="separator" style="clear: both; text-align: center;"><a href="https://blogger.googleusercontent.com/img/b/R29vZ2xl/AVvXsEjRr22GTkGu9SwGXalwDTCuCCnAvhV74d4iAZO-VLRJ7epGFfgOPv97mnxZzt2Ih5pSnS-i9ihoOpgufZQt-dUKDNU3_1Ny472mVRtfTvNBO26OJAMx2XkmsEwoMQp-jR-Kmwll-no6xjdy/s1600/CityCentreExtn.png" imageanchor="1" style="margin-left: 1em; margin-right: 1em;"><img border="0" src="https://blogger.googleusercontent.com/img/b/R29vZ2xl/AVvXsEjRr22GTkGu9SwGXalwDTCuCCnAvhV74d4iAZO-VLRJ7epGFfgOPv97mnxZzt2Ih5pSnS-i9ihoOpgufZQt-dUKDNU3_1Ny472mVRtfTvNBO26OJAMx2XkmsEwoMQp-jR-Kmwll-no6xjdy/s320/CityCentreExtn.png" /></a><br />
</div> <br />
This should hopefully increase usage of the Metro by quite large levels, and in turn make future extensions along the Hagley Road, to the Airport, and elsewhere in the region more commercially viable.<br />
<br />
The Strategy document also shows an intriguing map of a proposed "West Midlands Rapid Transit Network". It denotes the existing rail network in green, as well as the proposals for re-opening links through Kings Heath and Moseley. But also, in purple, are new 'Rapid Transit' links which appear to follow the other proposed Metro extensions on Centro's site (such as the Quinton and Brierley Hill extensions). The proposed rapid transit network appears fairly comprehensive and it will be exciting to see a modern metro system finally running on the streets of Birmingham to destinations such as the University and hospital, M5 park and ride, Merry Hill, and the Airport.<br />
<br />
<div class="separator" style="clear: both; text-align: center;"><a href="https://blogger.googleusercontent.com/img/b/R29vZ2xl/AVvXsEjWpwEzn14CMRqobsWsRWlEsqVTSbfl-oSM2hhnMXAwWLI6Ud3nfY_BQf8OuaJSFPiMw8Wqvh6x5K0fQ11x3xxKXKW8iUpnjZSNHVIoKnIx9VlBQ4RBaeNuqBI41-Yf2W_NTM5IaCnTQcm7/s1600/rapidTransitMap.png" imageanchor="1" style="margin-left: 1em; margin-right: 1em;"><img border="0" src="https://blogger.googleusercontent.com/img/b/R29vZ2xl/AVvXsEjWpwEzn14CMRqobsWsRWlEsqVTSbfl-oSM2hhnMXAwWLI6Ud3nfY_BQf8OuaJSFPiMw8Wqvh6x5K0fQ11x3xxKXKW8iUpnjZSNHVIoKnIx9VlBQ4RBaeNuqBI41-Yf2W_NTM5IaCnTQcm7/s640/rapidTransitMap.png" /></a><br />
</div><br />
All we now have to hope is that Centro can indeed raise the required money from the Government -- never an easy task at the best of times.<br />
<br />
<i>(Images in this post courtesy of Centro).</i>Mark Rowanhttp://www.blogger.com/profile/00065798700890744332noreply@blogger.com0tag:blogger.com,1999:blog-8480012186835693877.post-75557545054018957042009-11-23T18:43:00.001+00:002009-11-23T18:45:06.819+00:00Some questions to think aboutAfter chatting with John (my supervisor) briefly this evening, we've come up with a couple of potentially interesting questions to try to investigate, or at least to use to try to direct my research more specifically:<br />
<br />
Firstly, it is accepted that at least some hallucinogenic symptoms of schizophrenia "arise from pathological activation of neurocircuitry involved with ... perception" due to corticocortical (inter-cortical) connectivity disruption (Hoffman and McGlashan, "<i>Neural Network Models of Schizophreia</i>", 2009). Are these hallucinations related to (and could they arise from) the same low-level mechanisms as those which cause the hallucinations and altered personality in mid-to-late Alzheimer's disease, or in drug-induced hallucinations, e.g. following LSD ingestion?<br />
<br />
In other words, is it possible to create one universal low-level model for all types of hallucination and prove that all hallucinations, regardless of high-level disease/drug causes, arise from the same low-level activations of perceptive neurocircuitry?<br />
<br />
Secondly what, if any, differences there are there between dreaming in normal brains and dreaming in those with AD or schizophrenia? Have there been any studies comparing AD/schizophrenia dreaming with normal dreaming? What significances do any differences have, if there are any? This could start off quite a large body of research if interesting differences are found.<br />
<br />
In fact, there's a third question.. according to my <i>Good Brain, Bad Brain</i> neuroscience module, Down's Syndrome sufferers tend to develop AD at a much earlier age (sometimes in their 30's) -- what structural differences in the brain can cause this? Are these pointers to whatever structure it is that breaks down at the onset of AD?<br />
<br />
But for now, I'm still just practising implementing some different types of neural networks, so such thinking can wait til later :)Mark Rowanhttp://www.blogger.com/profile/00065798700890744332noreply@blogger.com0tag:blogger.com,1999:blog-8480012186835693877.post-25644384005647968432009-11-16T12:08:00.000+00:002009-11-16T12:08:41.604+00:00High Speed railMuchos respect for Lord Adonis (Transport Secretary) with his very clear and convincing case for European / Japanese-style high-speed rail in the UK, as recorded at <a href="http://news.bbc.co.uk/1/hi/programmes/politics_show/8361131.stm">http://news.bbc.co.uk/1/hi/programmes/politics_show/8361131.stm</a><br />
<br />
The crux of his argument is that, to provide sufficient capacity for future generations, the UK has three options:<br />
<br />
1) High-speed rail links between the major cities in England and Scotland, to put UK cities directly within reach of the rest of Europe<br />
2) Massive increases in the motorway network <i>[and therefore a massive increase in private car ownership, yet more traffic jams, and a further general decrease in the standard of living in congested cities]</i><br />
3) Massive increases in domestic aviation travel<br />
<br />
Of course, the fact that in each of the various high-speed route proposals "London to Birmingham is a given" is most welcome as well ;)<br />
<br />
The only downside is that it's unlikely we'll see any physical progress on this before 2025 or so, which is leaving it rather late to catch up with [poorer] countries like France, Spain, and even the Netherlands, who opened their first high-speed link only recently. Despite this, the long-term nature and benefits of the project are also its strengths.<br />
<br />
Hooray for long-termism!Mark Rowanhttp://www.blogger.com/profile/00065798700890744332noreply@blogger.com0tag:blogger.com,1999:blog-8480012186835693877.post-34490646812474833242009-11-04T12:23:00.000+00:002009-11-04T12:39:02.365+00:00Ambition or achievement?I have an abstract! I've just submitted my first report (<a href="http://www.cs.bham.ac.uk/resources/research_students/monitoring.php"><span style="font-style: italic;">RSMG1</span></a>)<span style="font-style: italic;"><span style="font-style: italic;"><span style="font-style: italic;"><span style="font-style: italic;"><span style="font-style: italic;"></span></span></span></span></span> stating that I will be working as follows:<br /><br /><span style="font-style: italic;">Computational Modelling of Neurological Disorders</span><br /> <br /><span style="font-style: italic;"> This work will begin with the undertaking of a general literature review to better understand and attempt to synthesize the field of computational modelling of neurological disorders, and recent developments within it. Disorders currently of particular interest are Alzheimer's disease and schizophrenia. The literature review is expected to identify a number of current computational models focussing on different aspects of the various disorders, as well as shortcomings of these models and potential ways forward. The main contribution of the work will be the development of improved and refined models that better represent the underlying biological processes. The work will involve testing of the improved models against empirical evidence (either from medical literature or specifically-commissioned experiments) to ascertain the level of support which can be given to them. The approach adopted will involve various techniques from the fields of neural computation and computational neuroscience, and possibly evolutionary computation.</span><br /><br />Next steps are a little unclear though, as officially I have nothing to submit until May 2010 now. By then I should have a "brief summary of work done so far, including literature reviewed, any coursework taken, programming languages learnt, talks given, etc." so that should give me some ideas where to start at least.<br /><br />You may notice I've added references to schizophrenia in my abstract. This is largely because a lot of the current computational modelling literature focusses in this area. Now, schizophrenia is a fascinating disorder, but the amount of attention being devoted to it seems disproportionately large given that a majority of people (thankfully) will not suffer from or be influenced by it; something which unfortunately cannot be said for dementia.<br /><br />I'm currently in two minds: I can either go down the currently-fashionable route of schizophrenia modelling, which could be easier given the current work being done in the field, and just try to achieve a PhD out of it as quickly as possible. Or I can stick with the less-fashionable field of dementia and Alzheimer's disease and ambitiously hope that I can come up with something really profound during my three years of research that might make a real difference to a lot of people.<br /><br />Ambition or achievement?<br /><br />Of course there is a third way... By studying the work being done in schizophrenia modelling I may be able to apply new models emerging from that field into the field of dementia, and through this contribute to both fields. This may prove difficult (not least because I'll have to learn about both disorders in great detail) but could be the most rewarding path to take.<br /><br />Well, in the meantime I have a handful of interesting papers to read, but it's probably about time I dusted off my programming gloves and neural networks books and bashed out a few multi-layer perceptron and Hopfield networks to get started.Mark Rowanhttp://www.blogger.com/profile/00065798700890744332noreply@blogger.com0tag:blogger.com,1999:blog-8480012186835693877.post-49781607361076349492009-10-20T16:19:00.000+01:002009-10-20T16:57:23.166+01:00First monthWell, my PhD is now officially underway. It's been about three weeks since I started, and I now have an official title, <span style="font-style: italic;">Computational Modelling of Neurological Disorders</span>, although work on an abstract for my Research Student Monitoring Group first report is progressing slowly (mainly due to my current seeming inability to sit still and read a paper for more than ten minutes at a time).<br /><br />The change of title is significant; my original proposal was under the title <span style="font-style: italic;">Modelling the Robustness of Musical Memory in Dementia</span>, however it's looking increasingly likely that -- although a valuable future route to take my research down, and certainly an interesting question in its own right -- it may be a bit too much to attempt for the duration of a PhD. By specifying "Computational Modelling" I create a stronger link with the Computer Science part of the PhD, and by broadening my scope to "Neurological Disorders" I can afford not to have to investigate the music question after all.<br /><br />The original question was along the lines of "How is it possible that an Alzheimer's sufferer can forget their own name and identity, yet still be able to sing along to songs heard in childhood?" but initial investigation shows that one of the principal reasons for this ability lies in the vastly distributed nature of music processing in the brain, and particularly music's strong links to emotion. Investigating and modelling this in itself is likely to take years of research, so whilst remaining an interesting question, I may have to limit myself to the old tried-and-tested model of scientific investigation for a PhD:<br /><ol><li>Read current knowledge</li><li>Implement a model from the literature</li><li>Test and improve model</li><li>Write thesis</li><li>Collect Nobel prize</li></ol>I'll let you know how it goes.Mark Rowanhttp://www.blogger.com/profile/00065798700890744332noreply@blogger.com0