The BBC’s topical science programme, Horizon, aired last night (27-10-09) with a programme exploring the potential of stem cell technology and what the future might hold in store for those living with chronic conditions. Following three individuals with different medical conditions (amputation, chronic progressive heart disease and SCI) it was the usual intercut vignettes and interviews with scientific and medical experts. Overall, it was a pretty balanced treatment of the topic, despite a tendancy towards simplifying technical hurdles and foreshortening timelines, and was careful to provide cautionary and realistic editorial on such issues as the conflict of interest that must exist when there are offers of cash in exchange for (unproven) treatments, the need for properly controlled clinical trials and the general hype inevitably surrounding stem cells.
Of note was the meeting between the subject with SCI and someone who had paid for stem cell “treatment” in India. Having watched video testimony that suggested improvement in his function, she was disappointed to find he had, in his own words, “not felt any improvement” and that what he achieved could have been achieved through rehab. His condition remained as it was before his trip to India.
She came face-to-face with one of the few western researchers (Bruce Dobkin) to examine patients before and after such unverified treatments, who told her that there was no evidence that these treatments currently work. In his view, if they did “why would you not want to conduct a small clinical trial to prove it?”. Follow this link to see a position statement – which Spinal Research endorses – from a number of eminent clinical and basic researchers on this topic which you may find interesting.
The programme ended with her meeting Hans Keirstead who, along with Geron, have developed a human embryonic stem cell line that has gained FDA approval for clinical trial in SCI. I am not sure when the programme was recorded but my own understanding is that the trial is currently on hold pending further submission of safety data to the FDA. This in itself is not unusual and a trial is very likely.
It is important to note that the cells to be transplanted in the Geron trial are not at that point stem cells. They are the product of stem cells which have been taken down a development path in culture dish to a point of relative maturity where they will only form something called an oligodendrocyte. As explained in the Horizon programme, oligodendrocytes are the cells of the central nervous system that provide the insulating material enveloping axons. The rationale for this treatment is that paralysis is due to axons being present but not functioning properly because they have become de-myelinated. There is evidence for de-myelination on some axons after SCI, but it is fair to say it is a matter of some debate amongst scientists as to the extent and significance of this in humans and it is certainly not the only or perhaps even the major cause of parlaysis. Other mechanisms by which (precursor) oligodenrocytes could provide positive effects may and probably do exist. A point conceded by Geron themselves.
At the time of posting the BBC’s iPlayer provided access to the programme.
Wednesday 28 October 2009
Monday 26 October 2009
Are we seeing inside the black box of Glial scar inhibition?
Growing axons, whether damaged or sprouting from spared neuronal tissue, are needed to restore lost function after SCI. Unfortunately, they are inhibited by molecules found on the surface of myelin – the insulting material surrounding axons that is found everywhere within the central nervous system.
The idea goes that myelin is decorated on its surface with many molecules and when growing axons come into contact with myelin, these molecules “dock” with specific receptors on the growing axon triggering a cascade of signals within the neuron telling it to go no further or even retract. Interfering with this inhibitory interaction is fundamental to a number of experimental treatments that are at various stages of development.
The idea goes that myelin is decorated on its surface with many molecules and when growing axons come into contact with myelin, these molecules “dock” with specific receptors on the growing axon triggering a cascade of signals within the neuron telling it to go no further or even retract. Interfering with this inhibitory interaction is fundamental to a number of experimental treatments that are at various stages of development.
Crucially, there is another known potent inhibitor of axon grow, namely CSPGs [see earlier posts] which increases in concentration at the Glial scar and elsewhere after injury. Exactly how CSPGs repulse axons is poorly understood, however, creating a bit of a black box on the mechanism and thus making it difficult to develop drugs to overcome this inhibition. That is until now, perhaps.
This week, in what may be a very significant paper published in the journal Science, neuroscientists from Harvard Medical School, Boston and Case Western Reserve University, Ohio, appear to have identified a protein on the surface of the growing axon which has all the hallmarks of a receptor for CSPGs and therefore potentially important in the cause of regenerative failure.
In the paper Shen et al., develop their case thus;
(i) a protein PTPsigma (a member of a large family of transmembrane protein tyrosine phosphatases; PTPs) was known to bind other proteoglycans important in early development so it might also bind to CSPGs which structurally similar
(ii) they found that PTPsigma did indeed bind to CSPGs
(iii) they demonstrated that binding was a genuine biological interaction because binding sites could be saturated and the interaction was high-affinity – ie. it was not a non-specific interaction
(iv) pre-treatment with chondroitinase (cleaves side chains on CSPGs) renders CSPGs inactive as inhibitors and also abolishes much of the binding with PTPsigma – indicating the side chains are important to this receptor binding as they are also in inhibition
In cell culture, they found that PTPsigma bound to cells responsible for producing the Glial scar – astrocytes.
So they had very strong evidence that PTPsigma binds to CSPGs. That in itself was not enough, so they next tested the theory that PTPsigma was functionally important to the failure of axons to grow. To do this they needed a mouse strain that did not posses a functional PTPsigma arguing that neurons cultured from such a mouse would grow better over CSPGs, which they did.
Their findings open the door on a potential new and exciting lead for drug design and treatment of SCI and other neural injury/diseases.
Notes:
CSPGs = chondroitin sulphate proteoglycans
Wednesday 21 October 2009
Restoration of bladder function
Bladder/bowel dysfunction is a major clinical/quality of life issue for those suffering a SCI. There are a few strategies being examined to recover bladder function including some drug interventions and functional electrical stimulation (FES). According to Lee (SfN2009 Program# 858.4) there has to date been far less focus on regeneration strategies to promote recovery of efficient bladder function.
Using a combinatorial approach that included treating with growth factor, a graft of peripheral nerve serving as a tissue bridge across the injury and chondroitinase to encourage regenerating axons to exit the graft, Lee and colleagues (Case Western Reserve University, Ohio) were able to demonstrate recovery of a more normal pattern of bladder emptying at one month post injury.
When they looked they found clear evidence of more extensive regeneration into the peripheral nerve graft and crucially beyond into the spinal cord itself.
The improvements in bladder reflexes they found may well be due to a newly formed circuitry via this nerve regeneration.
Using a combinatorial approach that included treating with growth factor, a graft of peripheral nerve serving as a tissue bridge across the injury and chondroitinase to encourage regenerating axons to exit the graft, Lee and colleagues (Case Western Reserve University, Ohio) were able to demonstrate recovery of a more normal pattern of bladder emptying at one month post injury.
When they looked they found clear evidence of more extensive regeneration into the peripheral nerve graft and crucially beyond into the spinal cord itself.
The improvements in bladder reflexes they found may well be due to a newly formed circuitry via this nerve regeneration.
Tuesday 20 October 2009
Successes in chronic injury
If you want to get injured axons to regenerate across the injury site it is pretty clear you need to adopt a combinatorial approach. Simply placing Schwann cells into the injury, for example, results in regeneration of axons into the graft but they refuse to come out again back into the cord. Even introducing “axon candy” – neurotrophins – to entice regenerating axons to leave the graft doesn’t always work (see earlier post).
The Tuszynski lab (UCSD, La Jolla, CA) presented findings on a 3-pronged combinatorial approach employing neurotrophins to attract axons, cellular grafts to act as tissue bridges across the injury and techniques (a peripheral nerve pre-conditioning injury, if you want to know) to stimulate the neurons to regenerate (SfN2009 Program# 365.6). And they did this is a 15 month old chronic injury rather than acute. They showed that you could achieve regeneration of sensory neurons – those neurons relaying information from the body back towards the brain – beyond the graft site even at these chronic time points, albeit to a lesser degree than if intervention were carried out acutely. Nevertheless, it did show that injured neurons could respond to treatment well after an injury.
Today (SfN2009 Program# 542.1), the group presented their findings on the capacity of descending neuronal fibres – those conveying signals from the brain to the body important for motor control – to respond to combinatorial therapy broadly similar to that described above. A couple of important differences are worth mentioning; (i) you can’t perform a pre-conditioning injury to the descending pathways so administration of a small molecule called cAMP is used as a pharmacological equivalent and; (ii) some of the animals where additionally treated with chondroitinase (see earlier post), the reason being chondroitinase should break down scar tissue where you want the regenerating axons to exit the cellular graft. They found significant improvements in function in the “full” combination group which included the chondroitinase even in the chronic injury.
The Tuszynski lab (UCSD, La Jolla, CA) presented findings on a 3-pronged combinatorial approach employing neurotrophins to attract axons, cellular grafts to act as tissue bridges across the injury and techniques (a peripheral nerve pre-conditioning injury, if you want to know) to stimulate the neurons to regenerate (SfN2009 Program# 365.6). And they did this is a 15 month old chronic injury rather than acute. They showed that you could achieve regeneration of sensory neurons – those neurons relaying information from the body back towards the brain – beyond the graft site even at these chronic time points, albeit to a lesser degree than if intervention were carried out acutely. Nevertheless, it did show that injured neurons could respond to treatment well after an injury.
Today (SfN2009 Program# 542.1), the group presented their findings on the capacity of descending neuronal fibres – those conveying signals from the brain to the body important for motor control – to respond to combinatorial therapy broadly similar to that described above. A couple of important differences are worth mentioning; (i) you can’t perform a pre-conditioning injury to the descending pathways so administration of a small molecule called cAMP is used as a pharmacological equivalent and; (ii) some of the animals where additionally treated with chondroitinase (see earlier post), the reason being chondroitinase should break down scar tissue where you want the regenerating axons to exit the cellular graft. They found significant improvements in function in the “full” combination group which included the chondroitinase even in the chronic injury.
Monday 19 October 2009
More about inhibitors - beyond the glia scar
One poster presentation at the Society for Neuroscience meeting really caught my eye today, but we need a bit of background first. There are many inhibitors in the central nervous system (CNS) that prevent axonal regeneration after injury. Their function in healthy cord is likely to be related to preventing uncontrolled growth of fibres once the CNS matures after early development and the various circuits are functionally defined. But in the injury state this becomes a problem as we want to create new functional circuits. We’ve talked about myelin – the insulating material surrounding axons – before as one source of inhibition, but another very potent inhibitor comes in the form of an extracellular matrix. This matrix is produced by cells in the CNS and is composed of many different proteins that are covered in side chains. These side chains are responsible for the inhibition and presumably dock with receptors on growing axons signalling them to stop growing. Collectively they’re called CSPGs (chondroitin sulphate proteoglycans).
If this wasn’t bad enough, when the cord is injured the amount of CSPGs dramatically increases at the injury site (forming scar tissue) but also in regions at some distance from the injury site.
Overcoming the inhibitory scar is an important therapeutic target for which we have a potential treatment. The bacterial enzyme, chondroitinase, digests the CSPG side chains leaving them inactive as inhibitors and a great deal of evidence is now available that treatment with chondroitinase is beneficial in terms of improvements in function. Closer investigation of the mechanisms by which chondroitinase may be beneficial suggest that it may not only work by breaking down scar, as originally thought, but it may have other activities, such as increasing plasticity and neuroprotection.
So, what about this poster (programme#365.4)? Well according to Hunanyan (Stony Brook University, NY), after an injury to one side of the spinal cord there is an increase in CSPGs in regions of intact fibres on the other. What’s more, if you look at the signal conduction of these intact fibres you begin to see a decline in activity during the same period of increased CSPGs. The question is, are the two related, because obviously if previously undamaged nervous tissue begins to lose function after injury then preventing this could be important to retaining function.
Hunanyan and colleagues wanted to test whether it was the CSPGs that were causing the decline in activity. They knew adding chondroitinase to the cord after injury would breakdown the CSPGs and if they guessed right, they would see increased activity when they did this, which they did. So, CSPGs appeared to be culprit. But there is more than one type of CSPG and to cut a long story short, they added each individually, looked at activity and found just one was responsible – NG2 ……. but that’s a developing story.
So, chondroitinase may have yet another beneficial effect in addition to breaking down scar tissue, increasing plasticity and neuroprotection; it may also help to maintain good electrical activity in surviving neurons.
If this wasn’t bad enough, when the cord is injured the amount of CSPGs dramatically increases at the injury site (forming scar tissue) but also in regions at some distance from the injury site.
Overcoming the inhibitory scar is an important therapeutic target for which we have a potential treatment. The bacterial enzyme, chondroitinase, digests the CSPG side chains leaving them inactive as inhibitors and a great deal of evidence is now available that treatment with chondroitinase is beneficial in terms of improvements in function. Closer investigation of the mechanisms by which chondroitinase may be beneficial suggest that it may not only work by breaking down scar, as originally thought, but it may have other activities, such as increasing plasticity and neuroprotection.
So, what about this poster (programme#365.4)? Well according to Hunanyan (Stony Brook University, NY), after an injury to one side of the spinal cord there is an increase in CSPGs in regions of intact fibres on the other. What’s more, if you look at the signal conduction of these intact fibres you begin to see a decline in activity during the same period of increased CSPGs. The question is, are the two related, because obviously if previously undamaged nervous tissue begins to lose function after injury then preventing this could be important to retaining function.
Hunanyan and colleagues wanted to test whether it was the CSPGs that were causing the decline in activity. They knew adding chondroitinase to the cord after injury would breakdown the CSPGs and if they guessed right, they would see increased activity when they did this, which they did. So, CSPGs appeared to be culprit. But there is more than one type of CSPG and to cut a long story short, they added each individually, looked at activity and found just one was responsible – NG2 ……. but that’s a developing story.
So, chondroitinase may have yet another beneficial effect in addition to breaking down scar tissue, increasing plasticity and neuroprotection; it may also help to maintain good electrical activity in surviving neurons.
"Two" much of a good thing
We all know - don’t we? – that the insulating material (myelin) surrounding the axons in the nervous system helps the efficient transfer of signals from one neuron to the next. Unfortunately, this myelin also contains molecules that are inhibitory to regenerating axons that come into contact with it. So researchers have developed an antibody to masks these inhibitory molecules and help damaged axons to regenerate.
Given early after injury, antibody treatment produces functional improvement in animal models. Similarly, rehabilitative training produces functional improvements. So what happens when you combine treatment with rehab? Does the combination result in even better function? NO! In fact Michele Starkey (SfN2009 Program# 176.16) found combining the two treatments, of antibody and rehab, early after injury results in a far worse functional outcome than either of the monotherapies. Why this should be we don’t know but it is clear that you can never assume that combining two safe and effective strategies will always result in positive outcome.
[The anti-NOGO antibody is being developed by Novartis and is currently in clinical trial]
Given early after injury, antibody treatment produces functional improvement in animal models. Similarly, rehabilitative training produces functional improvements. So what happens when you combine treatment with rehab? Does the combination result in even better function? NO! In fact Michele Starkey (SfN2009 Program# 176.16) found combining the two treatments, of antibody and rehab, early after injury results in a far worse functional outcome than either of the monotherapies. Why this should be we don’t know but it is clear that you can never assume that combining two safe and effective strategies will always result in positive outcome.
[The anti-NOGO antibody is being developed by Novartis and is currently in clinical trial]
Sunday 18 October 2009
Cellular repair strategies need a helping hand
The use of cellular grafts or transplants to aid recovery of function after SCI is attractive for a number of reasons. They can potentially replace lost cells, act as cellular factories producing biological molecules to stimulate and support axonal growth or they could potentially repair the spinal circuitry that’s become disrupted by the loss of the insulating myelin sheath. All these strategies are being investigated by researchers around the world.
One particular cell type – the Schwann cell – is normally found in the peripheral nervous system (PNS) where it wraps the axons of neurons in a blanket of insulating myelin. The PNS is far better than the central nervous system (CNS) at repairing itself after injury and Schwann cells may be partly responsible for that. Schwann cells are also fairly easy to “harvest” from the body and grow in sufficient numbers for transplantations making them a clinically viable cell type. For these reasons Schwann cells have been investigated as potential therapeutic grafts. Indeed, grafting Schwann cells into SCI results in robust axon regeneration into the graft and remyelination. So far so good, but their contribution to repair is somewhat restricted by a failure of these same regenerating axons that enter the graft to re-exit; they find it very comfortable there.
One strategy being looked at to overcome this has been to introduce the equivalent of cellular candy. Neurotrophins stimulate growth and axons like it. So injecting some neurotrophins just outside the graft may entice the axons to come of the graft and form a connection with spinal cord below. Direct delivery of neurotrophins has caused (sensory) axons to leave the confines of the graft, but muscle control is provided by axons coming down from the brain in long tracts and little investigation of the graft/neurotrophin approach on descending axons has been carried out.
Oudega presented a poster at the meeting investigating this very thing. Schwann cells were grafted into the injury site and below the injury they injected a viral vector modified to carry the gene for D15A [a protein with 2 neurotrophin activities; NT-3 and BDNF]. The gene enters the cell carried by the viral vector and begins to produce the neurotrophins. Oudega and co-workers found some functional improvement in treated animals but when they looked surprisingly there was still no evidence of axons leaving the graft. So what’s the mechanism? It’s unclear to them and they continue to work on this problem.
One particular cell type – the Schwann cell – is normally found in the peripheral nervous system (PNS) where it wraps the axons of neurons in a blanket of insulating myelin. The PNS is far better than the central nervous system (CNS) at repairing itself after injury and Schwann cells may be partly responsible for that. Schwann cells are also fairly easy to “harvest” from the body and grow in sufficient numbers for transplantations making them a clinically viable cell type. For these reasons Schwann cells have been investigated as potential therapeutic grafts. Indeed, grafting Schwann cells into SCI results in robust axon regeneration into the graft and remyelination. So far so good, but their contribution to repair is somewhat restricted by a failure of these same regenerating axons that enter the graft to re-exit; they find it very comfortable there.
One strategy being looked at to overcome this has been to introduce the equivalent of cellular candy. Neurotrophins stimulate growth and axons like it. So injecting some neurotrophins just outside the graft may entice the axons to come of the graft and form a connection with spinal cord below. Direct delivery of neurotrophins has caused (sensory) axons to leave the confines of the graft, but muscle control is provided by axons coming down from the brain in long tracts and little investigation of the graft/neurotrophin approach on descending axons has been carried out.
Oudega presented a poster at the meeting investigating this very thing. Schwann cells were grafted into the injury site and below the injury they injected a viral vector modified to carry the gene for D15A [a protein with 2 neurotrophin activities; NT-3 and BDNF]. The gene enters the cell carried by the viral vector and begins to produce the neurotrophins. Oudega and co-workers found some functional improvement in treated animals but when they looked surprisingly there was still no evidence of axons leaving the graft. So what’s the mechanism? It’s unclear to them and they continue to work on this problem.
Saturday 17 October 2009
Scientists get new tools to play with.
The Allen Institute for Brain Science is a non-profit medical research organization dedicated to innovative basic research on the nervous system and distributing its discoveries to researchers around the world. The Institute takes on "far-reaching projects at the intersection of biology and technology" - not surprising, it being the brainchild of philantropist Paul G. Allen.
Launched in 2003 with seed funds from Allen, it aims to be sustainable by seeking federal and state funds, along with private contributions and foundation awards, as part of an ongoing public-private partnership. Its first major project was the Allen Mouse Brain Atlas, a three-dimensional map of gene expression in the adult mouse brain. Similar in scale to the Human Genome Project, the Atlas is a dataset of expression patterns of approximately 20,000 genes covering the entire adult mouse brain down to the cellular level. The Brain Atlas was completed in 2006.
Following on from this success and in response to a call for support, Spinal Research awarded a grant to the Allen Institute for a similar mapping of the mouse spinal cord. This has now been completed and again, like the brain atlas, provides a comprehensive interactive database of gene expression mapped at cellular resolution across all segments of the mouse spinal cord.
World-wide, experts from the spinal research community have been working to identify interesting neuronal and non-neuronal genes (more than 17,000), their locations and differences in expression levels between the juvenile and adult cord. It simple terms it revealed what genes are switched on at different times from birth to adulthood - and where they are being switched on. I understand from those closely involved, that a lot of the grunt work – cell identification and counting – had to be done manually by volunteer students and young scientists.
What’s this actually mean? Well, judging by the numbers of people listening at posters today, it appears to be a welcome new resource. But is it a new play thing for the neuroscientist or something that may help people? Jane Roskams (Univ. of British Columbia, Vancouver, Canada) provided an example of some of the earliest discoveries made possible by the Atlas. Roskams said, “we thought that stem cells were found only at the centre of the spinal cord around something called the central canal. But it turns out that there is a previously unidentified type of cell, very similar to stem cells, around the edge of the cord, surrounding the white matter." She continued, "We didn't know they existed until we analysed the spinal atlas." The white matter is the region of the cord that houses all the communicating axons up and down the spine. Damage to the white matter is the major reason for the resulting paralysis after injury. "Expecting stem cells from the centre of the spinal cord to repair white matter on the outside may be too much to ask but if we can understand more about these newly identified cells around the perimeter (close to the white matter) and learn how to manipulate them for therapeutic effects we may be on to something", said Roskams.
This is only the beginning of an analysis that will hopefully reveal other novel cellular pathways that may be manipulated to enhance repair of injury and spinal cord disease.
Launched in 2003 with seed funds from Allen, it aims to be sustainable by seeking federal and state funds, along with private contributions and foundation awards, as part of an ongoing public-private partnership. Its first major project was the Allen Mouse Brain Atlas, a three-dimensional map of gene expression in the adult mouse brain. Similar in scale to the Human Genome Project, the Atlas is a dataset of expression patterns of approximately 20,000 genes covering the entire adult mouse brain down to the cellular level. The Brain Atlas was completed in 2006.
Following on from this success and in response to a call for support, Spinal Research awarded a grant to the Allen Institute for a similar mapping of the mouse spinal cord. This has now been completed and again, like the brain atlas, provides a comprehensive interactive database of gene expression mapped at cellular resolution across all segments of the mouse spinal cord.
World-wide, experts from the spinal research community have been working to identify interesting neuronal and non-neuronal genes (more than 17,000), their locations and differences in expression levels between the juvenile and adult cord. It simple terms it revealed what genes are switched on at different times from birth to adulthood - and where they are being switched on. I understand from those closely involved, that a lot of the grunt work – cell identification and counting – had to be done manually by volunteer students and young scientists.
What’s this actually mean? Well, judging by the numbers of people listening at posters today, it appears to be a welcome new resource. But is it a new play thing for the neuroscientist or something that may help people? Jane Roskams (Univ. of British Columbia, Vancouver, Canada) provided an example of some of the earliest discoveries made possible by the Atlas. Roskams said, “we thought that stem cells were found only at the centre of the spinal cord around something called the central canal. But it turns out that there is a previously unidentified type of cell, very similar to stem cells, around the edge of the cord, surrounding the white matter." She continued, "We didn't know they existed until we analysed the spinal atlas." The white matter is the region of the cord that houses all the communicating axons up and down the spine. Damage to the white matter is the major reason for the resulting paralysis after injury. "Expecting stem cells from the centre of the spinal cord to repair white matter on the outside may be too much to ask but if we can understand more about these newly identified cells around the perimeter (close to the white matter) and learn how to manipulate them for therapeutic effects we may be on to something", said Roskams.
This is only the beginning of an analysis that will hopefully reveal other novel cellular pathways that may be manipulated to enhance repair of injury and spinal cord disease.
Where's all this stuff heading?
Like a stream into a river into the sea; at Heathrow Terminal 5, you spot one, then another, then a few more. It is more obvious at departure gate A10 for BA flight 297 to Chicago, where it seems every third person is carrying one – a 3 foot long cylinder about the diameter of a couple of baguettes, usually black. The trick is to get on the plane early so that you can place your hand luggage overhead before these things start to jam the lockers.
Arriving at O’Hare International it is worse, most people are carrying these cylinders and by the time you arrive at the hotel you look out of place if you don’t have one slung over your shoulder – perhaps a tourist who has stumbled into the wrong town! Chicago, you see, is hosting this year's Society for Neuroscience meeting.
The cylinders are sturdy vessels that within hold rolled-up A0 sized posters depicting the research of a scientist or group. These posters are precious things, sweated over for many weeks or months. On such a limited canvas – the boards on which they will be placed are just 1.75 m x 1.11 m – you need to use the space wisely if you are to grab people’s attention and get then to stop and look at yours. You received your board number and session time when you will be expected to stand and be available to talk the interested through your work. And they survive only 4 hours before being cruelly replaced by a new one in the next session. Some posters will gather a crowd, others will be politely smiled at and walked past, a few, I’m afraid, will be largely ignored.
There are more than 15,000 posters being presented over the next 5 days and sessions run morning (8am-noon) and afternoon (1-5pm). There’s no time to waste and it all starts today.
Arriving at O’Hare International it is worse, most people are carrying these cylinders and by the time you arrive at the hotel you look out of place if you don’t have one slung over your shoulder – perhaps a tourist who has stumbled into the wrong town! Chicago, you see, is hosting this year's Society for Neuroscience meeting.
The cylinders are sturdy vessels that within hold rolled-up A0 sized posters depicting the research of a scientist or group. These posters are precious things, sweated over for many weeks or months. On such a limited canvas – the boards on which they will be placed are just 1.75 m x 1.11 m – you need to use the space wisely if you are to grab people’s attention and get then to stop and look at yours. You received your board number and session time when you will be expected to stand and be available to talk the interested through your work. And they survive only 4 hours before being cruelly replaced by a new one in the next session. Some posters will gather a crowd, others will be politely smiled at and walked past, a few, I’m afraid, will be largely ignored.
There are more than 15,000 posters being presented over the next 5 days and sessions run morning (8am-noon) and afternoon (1-5pm). There’s no time to waste and it all starts today.
Wednesday 14 October 2009
Chicago, here we come ....
Welcome to this new blog site created by Spinal Research. We will post regularly, providing comments on the latest research from around the world in the field of the repair of spinal cord injury.
Next week Spinal Research will be at the 39th Annual Meeting of the Society of Neuroscience in Chicago.
If you've never been or want to know what 30,000+ neuroscientists talk about when they get together then here's your chance to find out.
Next week Spinal Research will be at the 39th Annual Meeting of the Society of Neuroscience in Chicago.
If you've never been or want to know what 30,000+ neuroscientists talk about when they get together then here's your chance to find out.
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