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Spinal Cord Injury - Science topic

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I want to cite a clinical trial from clinicaltrial.gov of incertin mimetic exenatide in spinal cord injury. However i am unable to get the citation of the study. I also tried google Scholar searching the heading of the study but with no success. Please let me know how can I cite this study using endnote
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Hello, we applied Epidural Electrical Stimulation to a patient who had a Spinal Cord Injury for the first time in Turkey. As a result of my literature research, no information was given about the design of rehabilitation programs. How should the rehabilitation program be shaped for this patient? Also, how should epidural electrical stimulation mapping be?
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Thank you Ragab
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We hope to commence a study to develop a local rehabilitation guidelines for individuals who suffer spinal cord injury. However, to accomplish that we shall be glad to receive contributions from experts who have done some works in this area. We are also open to collaboration, however, we do not have funding as at present.
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Dear Lawal,
I am not worked with rehabilitation of spinal cord injury subject, now working with people don't have spinal cord issues but with neurons problems. i found one article sharing for your reference.
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Hello,
I will develop materials for the repair of nerve damages in my master thesis, and I am planning to use neural cells for cell culture experiments. I have cell culture knowledge, but I have never worked with any kind of neural cells. If you have experience on this subject, can you tell me which cell line would be more proper and easy to handle for me and what should be considered differently from basic cell culture in this process?
Thank you!
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I have no experience with neural cell cultures. Moreover, it will be extra difficult for me to obtain and purify a primary culture. I think it is better to prefer to buy cells commercially.
Thanks a lot for your answer!
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In the article - Pressure distribution analysis in three wheelchairs cushions of subjects with spinal cord injury. I know the brand names of the cushions but I was wondering if you could let e know what the specific model of each cushion was so I can exclude or include it in a literature search. I am looking into high specification foam cushions and I wondered if these were HSFC or whether they were active cushions - I know the Roho will be an aircell cushion but I wasn't sure about the other two.
Thank you, Sarah
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Thank you - I did think that but I might buy the article to see. I work both in the NHS and for a manufacturing company specialising in pressure redistributing devices in the uk so im
trying to evidence the products we manufacture. I saw an article about lateral pressure that I thought was interesting.
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I tried to perform SSEP test in rat SCI model but I had the problems in anesthesia. I used the thiopental (that we had in lab.) 30 mg/kg IP, but the rats hadn't good anesthesia or died.
What is the suitable method to anesthesia in somatosensory evoked potential test in rat spinal cord injury model?
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I am delighted to see that you are investigating spinal cord injury. I'm preparing to publish a book that explains the relationships of anesthesia, analgesia, and stress. I'll try to briefly explain the nature of your problem.
Firstly, general anesthetic agents such as Isoforane confer their benefits by inhibiting consciousness. They are no different than intravenous hypnotic agents such as propofol. Both are "hypnotic" agents. The only advantage of inhalation agents is that their effects can be maintained at consistent levels over time, and they are conveyed quickly from lung to brain during induction so that they take effect quickly, and their effects dissipate quickly when they are expelled from the lung.
Neither intravenous nor inhalation hypnotic agents has the ability to inhibit nociception. In fact, they exaggerate nociception pathway activity in the spinal cord. This is because consciousness generates inhibitory signals that descend to the spinal cord and reduce spinal cord nociception activity. This explains why your rats anesthetized rats die when you damage their spinal cords: they suffer exaggerated nociception during anesthesia.
If you administer spinal anesthesia to your anesthetized rats BEFORE you injure their spinal cords, then their death rates will decrease and the severity of their injury will be mitigated. You will achieve the same effect by treating the rats with generous doses of fentanyl BEFORE you injure their spinal cords. This is because both fentanyl and spinal "anesthesia" are genuine analgesics. The term "spinal anesthesia" is a misnomer; it should be called "spinal analgesia", because it has no effect on consciousness.
Optimal surgical outcome requires complimentary combinations of anesthesia AND analgesia. Try reading the attached copies of my previously published papers.
The key to preventing permanent spinal cord damage after spinal cord "shock" syndrome is to prevent the spinal cord inflammation that develops in the aftermath of injury. The spinal cord is trapped in a narrow canal, so that spinal cord inflammation causes spinal cord edema that compromises microvascular tissue perfusion in the injured tissue. This explains why spinal cord function persists fora time after the injury, but then deteriorates and patients ultimately suffer what amounts to spinal cord transection. In theory permanent damage can be prevented by treatment with magnesium sulphate, EDTA, or trisodium citrate, all of which bind to Ca+, which inhibits thrombin generation that causes inflammation.
I am preparing to publish a book via Amazon that will be entitled "50 Years Lost in Medical Advance" in April of this year. I am adding final materials while I await reviews from Nature, Scientific American, and Science.
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Hello,
i am working on a Spinal Cord Injury Model and in order to characterize the lesion I want to do a 3 D Reconstruction of a spinal cord. Therefore, I have cut a Spinal cord of 1 cm into 10 µm sections; 4 cuts on one slide.
I Have tried FIJI but i am not happy with it. I need a 3D Reconstruction with which I can interact and measure Volume trauma in the reconstruction.
Does anyone know how to solve this problem?
Every help is very much appreciated.
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Hello Nima,
I am curious about your need, what type of images do you acquire: brightfield, fluorescence of some kind, other...?
I am currently working on an automated serial block face system which allows image acquisition and 3D reconstruction of unstained samples based on autofluorescence signal. This system could typically be useful for the question you ask. Maybe we can discuss?
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Hi everyone
I'm having trouble with the high mortality rate of my zebrafish after surgery. ( the surgery is done based on this article:
Becker, C. G., Lieberoth, B. C., Morellini, F., Feldner, J., Becker, T., & Schachner, M. (2004). L1. 1 is involved in spinal cord regeneration in adult zebrafish. Journal of Neuroscience, 24(36), 7837-7842. Chicago)
They die in a day or less after surgery. Has anybody got experience with that? after surgery, they are maintained separately in aging water (28 ° C)in dark with no food.
Thank you
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Try feeding them after surgery
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I would like to collect the cervical spinal cord sample from rat following retrograde tracer injection in the forelimb muscles. After collecting the sample, I would like to find out the corticospinal tract changes. Can anyone please help me to find out a protocol for IHC and 3D-Z.1light-sheet microscopical view of the cervical spinal cord.
Thanks in advance.
Regards,
Rakib
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Cholera toxin subunit B conjugated with Alexa Fluor 488 or 594 (Invitrogen-Molecular Probes, Eugene, OR, USA) is a proper choice. 3 days after injection is OK for observing the motor neurons in the spinal ventral horn.

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being working on a preclinical research studying spinal cord injury ..
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- Aneurysm clips having exact force and shapes are normally used for spinal cord compression models.
- However, spinal cord contusion (via weight drop) and hemi/sectioning seem to be more commonly used in SCI studies
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When treating patients with abnormal tone, I often find recurrent inhibition using a range of sensory modalities from cooling to electrical stimulation at low levels is very effective in some patients. Others respond best to reciprocal activity. Clearly, spasticity results from an inbalance of inhibitory and excitatory activity, but can we deduct or identify which? If so, does that have a direct influence on central or peripheral management of tone? While Botox and other end organ interventions work, I am looking for ways to alter the central activity related to the abnormal tone.
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I need to help me with your experience in application of stem cell in spinal cord injury clinically.
Thanks
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Stem cell therapy is a rapidly evolving and promising treatment for spinal-cord injuries. ... Mesenchymal stem cells (MSCs), most commonly harvested from bone marrow, can prevent activation of inflammatory responses that lead to cell death. Functional recovery using MSCs in spinal cord injury patients has been mixed.
for further information please check a link;
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I am trying to couple angiogenesis and osteogenesis in a rodent model of spinal cord injury. What I would like to do is take a bone which exhibits osteoporosis (bone loss) and couple this with the absence of type H vessels by staining for CD31 and Endomucin.
Is it possible to fix a bone in formalin, then microCT scan it the next day, and then decalcify the same bone and perform IHC / histology on it without compromising results?
Also, are there any better stains you would recommend to analyse bone vasculature?
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At least you can try once or twice to prove on. It is difficult task but not impossible
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Disabled people are considered under WHO recommandations for daily physical activity, but standard measures used for healthy people could them really be used at the same for disabled ?
In other way, for example, for a femoral amputee, walking at 4m/s speed is it under 3 MET (very low level activity) or over (low activity)?
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Emmanuelle Cugy Firstly, physical activity guidelines expressed using Metabolic Equivalent Tasks (METs) are not useful for the general public. The concept of METs is difficult to understand and few people are familiar with it. It is really challenging for the public to know the MET values for any/all the activities they do.
Secondly, The energy consumption in people with limb amputation would be certainly much higher for amputees. To my knowledge METs values and disability have not been worked on very much. See systematic review
Metabolic costs of activities of daily living in persons with a lower limb amputation: A systematic review and meta-analysis. https://www.ncbi.nlm.nih.gov/pubmed/30893346
Thirdly, there has been some work on METs and paraplegia which may help guide you.
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Autonomic dysreflexia (AD) is a life-threatening condition. AD is more frequently reported among SCI patients with higher lesions (e.g. cervical lesions). How about patients with lower lesions?
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The lowest level of SCI where AD was documented is T10.... Neurological level of injury not always correspond with autonomic level of injury....
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I did my research project on the assumption that the neuroma would somehow be influenced by the presence or absence of the communicating branch.  My sample was only 40 cadavers, but there was no apparent link that we found in that sample group.  I would be very interested in pursuing this further.
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Dear sir Patrick Frank ..nice project I am interesting to know the final results.... good luck...
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Does SCI-induced central NP or peripheral NP or both?
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Hossain, M. Z., Unno, S., Ando, H., Masuda, Y., & Kitagawa, J. (2017). Neuron–Glia crosstalk and neuropathic pain: Involvement in the modulation of motor activity in the orofacial region. International journal of molecular sciences, 18(10), 2051.
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Habitual behavior/Everyday habits in manual wheelchair users with spinal cord injury (and the impact on shoulder load)
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Dear,
impact depends on the level of the SCI.
Sarah
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I am considering using the EQ-5D-5L instrument (https://euroqol.org/wp-content/uploads/2016/09/EQ-5D-5L_UserGuide_2015.pdf) in people with spinal cord injury. The mobility item of the scale asks about the ability of the person to "walk about". Would anybody know if there is an adapted version for people using a wheelchair? Something that would potentially use the word "mobiling" or "moving from A to B" instead of "walking about"?
I would appreciate any guidance on this.
Anestis
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Thank you Tamrat Befekadu!
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Recently, i'd gone through an article of Clinical Biomechanics titled "Mechanomyography responses characterize altered muscle function during electrical stimulation-evoked cycling in individuals with spinal cord injury".
On page 24 (page 4 of the article), section 2.7 Data Analysis, line 3 to 7, it was mentioned "...were normalized to their respective peak values considering all the participants and trials....".
It seems the authors took the maximum value in the PRE condition from all the 6 subjects, and normalize the other data w.r.t that peak value. If someone can confirm whether the authors normalized each subject w.r.t that subject's peak value OR they took one peak value for all subjects and normalize all w.r.t that highest among all subjects peak value?
Is it really possible, i.e. to normalize w.r.t a single value for the whole experiment over different subjects?
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Thanks Dr. Ritzmann,
I'd gone through the document you mentioned above, I'd also seen few other articles on this very topic. It seems my understanding to the statement of the authors that i mentioned in the above question, is wrong. if you can please go through that document and comment on that particular statement.
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  • One of my concerns is the limitations available for people with disabilities, especially those with spinal cord injury and I want to help them.
  • My idea is to send brain orders to the organs via "WiFi", for this purpose a transmitter chip is embedded in the brain and a receiver chip also after the spinal cord injured.
  • Is it possible? What problems will there be for the implementation of this idea?
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Thank you for your answers.
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Hi guys,
i'm working on a spinal cord injury model. Basicall, I drilled a hole in the left hemisphere of spinal cord. Though this leads to a paralysis of the corresponding parts, many mice died in the first week or two. Does anyone have any ideas about what happened? What did I mess up?
Best,
Ling
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Hi, This is a very unfortunate issue. As you know, beside possible infections caused by the surgery itself, spinal cord injury also affect the urination system causing it to to also paralyzed. Therefore, if you don't "help" them to release the liquids in their urinary bladder, it inflate and explode causing their death. You should note also that by "helping" them, which is done by pressing the bladder, you need to be careful not to harm their internal organs as well.
I hope I helped you.
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We are recording muscle spasticity in rats after spinal cord injury when stimulation is applied. While recording, we see that there is more deflection in one direction (either positive or negative depending on the arrangement of the electrodes themselves) than the other. Just looking for any possible causes and solutions. I attached an example of this uneven deflection.
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I added a picture of our current setup. For the recording and ground electrodes, we are using patch electrodes that only make contact with the surface of the tail. The red and white clamps are the recording and the black is the ground. The stimulating electrode we are using is a cuff style electrode. This is the yellow electrode seen closer to the tip of the tail. We are acquiring the patch electrodes from Biopac, the same company that produces the clamps that the electrodes attach to and the hardware we are using to record and shock with. The stimulating electrode is made in our lab. It is made from 1/8 inch inner diameter tygon tubing that has silver wire threaded through that has been soldered to a conducting wire. The patch electrodes already come with adhesive on them but we use velcro cable ties to ensure that the electrodes are making contact with the tail. We have tried altering the placement of the clamps on the electrodes but nothing seems to eliminate the uneven deflection.
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Hi Chris,
I agree that the small spikes do look a little suspicious. Did you use surface or needle electrodes?
Nevertheless, in EMG you would usually expect deflections in both directions. Since there is no clear meaning to that you can simply rectify.
Have a look at this:
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Does anyone know if spinal cord injury is common due to blasts? I have a nice spinal cord model and thought it might be useful for that...
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In my clinical experience of 25 years as a orthopaedic trauma surgeon I have not seen any SCI related to blast in civilian population in Lothian, SE Scotland. However may be more commonly seen by military surgeons.
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Because of gliosis injured axons unable to regenerate which has become a crucial target for regeneration research in Spinal Cord Injury O(SCI). So, I want to know research specific mechanism. If, possible please give me an illustration of it.
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Dear Dewan,
Hercules has provided some of the classic reviews for the glial scar field.
However, in addition to the inhibitory nature of the glial scar, CNS axon regeneration is also inhibited due to developmental changes in the neurons themselves. The links below are to a couple of recent reviews:
These are just suggestions as to where to start your reading.
Best,
Jill
Please note, RG changed my links to the abstracts in PubMed to the articles in RG itself. I did not do this, and I am not trying to evade copyright protection of these articles.
Hercules, how did you get your links to stay as the original PubMed Central links? Inquiring minds want to know!
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After SCI, glial scarring by astrocytes inhibit axon regeneration. So, which intracellular components induce glial scar?
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Hello Dewan,
atrogliosis is a process which occurs after SCI and leads to expression of numerous signaling molecules. Two scar types form after SCI , the glial scar and the fibrotic scar. The fibrotic scar in the lesion core is packed with growth inhibiting molecules like NG2. The glial scar area also contains molecules which inhibit axon growth like NOGO. Beside these growth inhibiting structures there are multiple factors influencing axonal growth cones like immune cells etc. I guess I didn‘t answer your question on the molecular pathways causing astrogliosis, but I felt like adding this bit of general information might be useful. Best regards, Nicole
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Application of stem cell on Spinal Cord Injury animal model
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There are a handful of companies trying to solve this particular problem - how to use stem cells to treat SCI.  One of those is Q therapeutics in Salt Lake City, Utah.  See http://www.qthera.com/live/Technology/Our-Solution.aspx for more details.
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For people with central nervous system disorders, how much joint assistance or individual's effort is required for joint movement to restore motor function or better motor learning? What factor that defines The optimum assistance for reorganization of CNS is? Please tell me the papers or information on these.
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Hi Kenichi,
if the joint is assisted, the individual is learning to move the joint in an manner that does not activate the sensory and motor systems necessary for normal movement. The individual may learn to move in an assisted manner, but the carry over to normal movement will still require additional training.  As for restoring normal movement, we anticipate roughly 4000 repetitions, however the joint movements are task specific, therefore the carry over to similar movements may require additional training. 
Monica Rivera 
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Thank you for your reply in advance,
I've been having a trouble that rats were dying during contusive spinal cord injury.
When I make a contusive injury model, rats should be anesthetized with katamine(90mg/kg) and xylazine(5mg/kg), then laminectomy at the 10th thoracic vertebra.
As you well know,  before laminectomy, the lesion site should be incised of skin with blade then removed fat tissue. There has been happened in next step.
To detach of the muscle from bone on the spinal laminae, retractors are positioned to keep the incision widely open, in this the procedure,
the rats suddenly stopped breathing and be die after a couple seconds.
There was no bleeding. and specific problem during surgery, I guess something give a vital problem to rats to breath.
I don`t know what is the problem, I thought the problem might anesthetize, but even though the concentration of ketamine was increased, the problem was happend..
Anyone have a experience that the animals during surgery can not breath suddenly?
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I've used a dose of 2ml/Kg of a cocktail of: ketamine (25 mg/ml), xylazine (1.3 mg/ml) and acepromazine (0.25 mg/ml) and it worked ok. Are you using a heat pad during your surgery to keep the animals warm?
I'm now using isoflurane and it's much more convenient.
What level is your injury?
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Hello I am orthopaedic surgeon interested on spinal cord injury cases and studies! I was just wondering if  we can be involved in this study 
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Dear dr Mandari, Thanks for your interest. I am the coordinator of the Dutch participation of this international study. The overall organization is in hands of the Swisci. You can find information concerning this worldwide survey at the website. Here, you can also find contact information. The website is: https://www.insci.network/insci/T1/en/welcome.php
Best Regards, Karin Postma
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Hello!does anyone have experience with glycerol-induced muscle injury?I I have to assess the in vivo differentiation capability of my stem cells but I did not find any remark about the reference of glycerol used. I just need the reference to order it. Thank you!
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Ciao Cesare...mi potresti mandare per favore il protocollo...grazie mille!!
Alessio
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In BrainQ, I've developed a therapeutic device that have shown to increase rehabilitation process in animal model after stroke, SCI, and TBI, where the major phenomena was to regenerate white matter of specific neural networks that lead to re-gaining lost functions. However, one of the main questions is the rate of degeneration of axons after stroke. In our paper we can see that after stroke, 2 weeks later to the stroke, the rat (stroke side) CC is invisible in the MRI/DTI image. I be be grateful to hear your opinion on this mater, which reflect on treatment of people after stroke.
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Dear Emmanuelle
BrainQ is a company that was created to resolve neurological deficits by means of enhancing natural rehabilitation processes of neural networks. It started where my son, Lear, was born with a rare genetic disorder that affect the CNS. In the process of understanding what is his exact "problem" I've discovered that many other nervous syndromes and impairments share similar characteristics to my son syndrome. Then I've developed a conceptual model for intensify rehabilitation processes in the brain (and spinal cord). Once pre-clinical trials have shown first signs that the concept is feasible, BrainQ (Brain cue to cure) was formed. The principle of the treatment is a very low intensity and frequency electromagnetic stimulation which sync to the way neural networks work, and by that, promote their re-growth, and by that, increase the chances and extent of rehabilitation after impairment. Since BrainQ have showed very impressive pre-clinical results (TBI, Stroke, SCI), BrainQ, as a compaby was formed. Right now we are conducting a clinical trial that is focused on spinal cord injury (were he people are about 6 months and longer after the injury, which brought me to ask how "post acute" .vs. "chronic" are they). We are seeking collaboration with researchers who are interested in clinical trials. We have published two papers about Stroke and SCI, and now in the process of publishing our paper about TBI.
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I am looking for any modul specifically for Occupational Therapy intervention following Spinal cord injury. 
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First of all - make sure optimum positioning is secured, using appropriately fitted wheelchair, supports and patient education about what is optimum so he/she can request modifications, if necessary.  Secondly, training in ProprioceptiveNeuromuscularFacilitation (PNF) is strongly recommended for achieving maximum conditioning for available musculature, including the diaphragm.  (That is one of my specializations and the most effective form of therapeutic exercise for any patient suffering muscle weakness for any reason.)  Hope that helps.
Vicki
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with reference to various research articles; relating to various spinal cord injury experiments, the spinal cord is preferred to be harvested from live animal (mouse, dog) for the purpose of western blotting and immuno cytochemistry, but circumstances are not every time favorable to collect the spinal cord from live animal. do the livability of animal affect the integrity of spinal cord? can it be harvested while the animal is dead during experimental period? 
i need to know the significance of spinal cord harvesting from live animal.
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The main puropose to investigate complete and fresh neural systems should be to learn more of the flexibility and other neuromechanical and neurodynamical characteristics .
In the period 1960-1985 the neuroscientist and neuroradiologist Milan Roth investigated the neuro-osseous growth realtions, that can be disturbed by internal factors ( lack of O2 at birth, poison, drugs) but it offers a good explantion too, how the sedenatary lifestyle of children hinders this groth by stretch of the CNS and priovide the western world with bad postures , early and seroious degenration, but also ( from own observations) very thight central cords that look  responsble for Arnold Chiari, syringomeylie and : skeletal deformations as scoliosis. A spinal fracture will give central cord injuries much easier as the cord is thight already.
Roth did fsh cadaveric studies to show that the cord stays in central position in bending the spine in a young  healthy boy, killed by accident ( to show the imortance of Holzer's Neuroprotective Mechanism )  In modern youth this would show inevitably a cord that will be pulled against the wall, if it is not already attached to it ( you can see this on many MRI's )
Focus on biochemic substances blurs the more important neuromechanic characteristics that make cords vulnerable for overstretch. If injures, the both parts of the cord will retract immediately, so sponteanous repair is impossible.  
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I have control rats that developed mechanical hypersensitivity over time that is comparable to my experimental rats (streptozotocin induced DM).
What filaments do female/male control/naive sprague dawley rats usually respond to and when does repetitive testing start to influence withdrawal thresholds, as described by Chaplan (J. Neurosci. Meth. 1994 53: 55-63)? 
Does anyone know of literature that supports the influence of anything other than an induced model (nerve injury, experimental diabetes, spinal cord injury etc) on withdrawal responses in rats?
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Just another thought: von Frey measures allodynia thus in an ideal setting there should be no response from a normal animal. The filament to be used very much depends on the strain, line, gender experimental setting.. thus you should best establish which one to use for your specific situation as the largest one that does not provoke a response. It might also be good to use different pain assessments in parallel e.g. spontaneous pain, thermal allodynia, mechanical or thermal hyperalgesia.., 
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I am a student occuaptional therapy and I am writing a thesis about the the interventions that can be used in therapy for patients with hand injuries because of spinal cord injury.
So I am searching for literature that gives the link between upper limb and hand rehabilitation after SCI and occupational therapy.
All suggestions about literature about this topic are welcome.
Thank you for your attention!
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What protocols training respiratory muscles used for patients with spinal cord injury?
I continue or interval training?
What training loads used?
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Thank you very much for your answer.
Regards!
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I read that syrinx formation may be associated with pain that develops after a year or so? What all the factors that may lead to syrinx formation in SCI? Is over-exercise a reason for that?
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please check it
www.ncbi.nlm.nih.gov › NCBI › Literature › PubMed Central (PMC)
www.ncbi.nlm.nih.gov › NCBI › Literature › PubMed Central (PMC
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Which model is best to start with? We are going to start up a SCI model, and also have seen that weight drop model outnumbers the baloon compression model at pubmed. Please advice what is the end point differece between these too. 
your advice's will be highly appreciated.
Thanks
Syed
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Hellow  Syed,
please check the pdf and links
www.nature.com › Journal home › Archive › Reviews
www.ncbi.nlm.nih.gov › NCBI › Literature › PubMed Central (PMC)
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Abdominal viszeral pain is an increasing problem in patients with neurogenic bowel desease after spinal cord injury. We try alwas to improve bowel function. But especially in patients with higher spinal cord lesions the pain remains. What is to do?
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patients with non-neurogenic bowel dysfunction such as IBS and functional constipation often experience abdominal pain without any change to bowel movements. The evidence suggests that this is due to perturbed gut-neuronal communication systems. I would presume (not evidence based of course) that the same is true for your patients.
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Hi, we work in a acute neurorehabilitation clinic admitting SCIs in the first 8 weeks of the injury onset and we have difficulties with the tetraplegic patients during upright positioning trials. Nonpharmachologic(ie: corset,pneumotic compression, fluid intake, meal,  urinary and GI tract  precautions) and pharmachologic (ie: midodrine up to 30mg) management strategies usually do not work in the first months. For example many patients do not tolerate upright positioning although they can be positioned 60 degree on the tilt table for 15-20 minutes or ortostatic hypotension problems do not resolve in complete tetraplegics up to 4-6 months. Can anyone have experience about ideal timing for upright positioning of tetraplegics and ideal pharmachologic (forexample fluidrocortisone?) treament strategies for ortostatic hypotension during the acute phase rehabilitation process?
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I am a rotating physiotherapist who has some recent experience in spinal cord injury. While working with the more senior experienced physios immediately have often put patients in tilt in space wheelchair as soon as tolerable. This can be as early as week 2 as long as they are haemodymanically stable. While the patient is at intensive care we try to sit them up or tilt bed to start the gradual process early as long as the spin is stable. Abdo binder pass 30 degrees is used to help with coughing and BP. It is important to start the process early so quite often when patients arrive at the acute wards from ICU they can start trialling to sit in wheelchair as mentioned above while monitoring BP, and slowly increasing the sitting time. This really helps with future standing practices.
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Very often I'm working with people that are impaired by a traumatic spinal cord injury. People elaborate this loss along some more-or-less-defined phases, that are very alike to the phases of grief.
Usually the period of grief ends with the possibility, for the person, to put his/her resources on new objectives.
However in the case of acquired disabilities the entity of the loss is enormous and may impair each future scenario.
Are there studies, based on a cognitive - behavioural framework, that may help me to better understand how to face these problems?
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Hi Michele,
it's great that you are looking into this. In addition to th literature mentioned above, I would suggest considering the rationale behind and techniques of Acceptance and Commitment Therapy (ACT, for example Hayes, S. C., Strosahl, K. D., & Wilson, K. G. (1999). Acceptance and Commitment Therapy: An experiential approach to behavior change. New York, NY: Guilford Press.).
Best regards
Franziska
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I am a student who is writing a thesis about the link between upper limb and hand rehabilitation after SCI and occupational therapy.
All suggestions about literature about this topic are very welcome!
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There are several activities and different treatment interventions you can use, it depends on your initial goals and what are the expectations for your client (patient). As a rehabilitation professional you may want to start with short term goals, these are important to engage you and your client. However it is important to emphasize that a long term goal may be something that will become more functional and improve the quality of life of this individuals. It is important to get these info from a proper book. A book will give a broad idea of your goals and what are the best intervention for your client, based on what he/she is capable of doing. (Remember Area of lesion and muscle function must be very sharp in your mind - it will help your to decide what activities you can re-introduce). When you say upper limb, you have to think whether his upper limb has some movement. Is there some elbow and wrist movement? is he/she able to make a fist? If yes, measure his/her strength with a handgrip dynamometer. http://www.topendsports.com/testing/tests/handgrip.htm
 All those things must be assessed first, once you have an idea of what he/she is capable of doing, then you can think about activities to enhance his abilities. Please, be careful as some activities could not be appropriate and may generate frustration. Scientific articles are great, when you start searching for specific concepts and activities. Mary Ann McCall is an Occupational Therapist with vast scientific publication in Spinal Cord. You can get a lot info, from her publications, even the old ones.  
Good Luck with your search,
Kamary
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Does anybody have some reference about this subject ?
Especially, I don't know if there's something about difference between paraplegic and tetraplegic patients, even if they're lying on a bed 24 hours a day to heel a pressure ulcer.
Many thanks
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Cher Anthony,
You'll find the (poor) available evidence about this topic here:
About pressure sores, look at this topic too:
For the treatment of PU in SCI, there is level 4 evidence (from one pre-post study; Brewer et al. 2010) for arginine supplementation for pressure ulcer Healing.
Notice the works of W.O.Seiler
Have also a look at this publication of our swiss cohort study on spinal cord injured patients (SwiSCI)
En restant à disposition pour en discuter!
X. Jordan
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i really confused about where is the best place to put the electrode for rehabilitation of hand, which the place for each muscle in hand is complex and have specific movement each. Example, to make circular wrist movement or extension and flexion elbow joint.
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Dear Erwin,
Look the materials that I sent to you. I believe that you should find your responses.
I hope this helps.
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I wondered wheter it is possible to merge axial and sagittal T2w images of spinal cord lesions (same field of view) into one image.  Does anyone know a software which has a pipeline included?
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Once I did some reconstruction of the image of an aortic dissection using Osirix but never attempted to do it with the brain. This may be possible, at least in the professional version.
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experimental spinal cord injuries studies
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In our experience, we've used quite a few histological techniques, such as quantifying the total lesion volume, monitoring adjacent tissue for activated microglia and reactive astrocytes, cell counting for NeuN, and Propidum Iodide staining post-SCI.
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Is monocytes (type 1 or 2) can be involved in this process?
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I am  sorry I do not k\now
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I am studying the effectiveness to avoid the muscle atrophy
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Are you talking about a lower or upper motor neuron lesion? Send me a private text if you want, i am currently doing my research in that area as part of my PhD.
Cheers!
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As you know the scar in the SCI patients and animal models forms inside  the spinal cord tissue and forms a cavity but there are a lot of investigations that applied electrospinning nanofibers for motor neuron recovery and astroglioal scar decrement. I think the sheets of electrospinning nanofiber just affects through mechanotransduction pathways and its effects is not direct and maybe hydrogel based scaffold is a true option instead of it. Electrospinning nanofiber is a good option for peripheral nerve regeneration not SCI. What is your opinion about it?
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thanks a lot Guillaume, but when you implant an aligned nanofiber in a site far from of SCI defect, out of cavity, how it directs cells around the cavity?
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The Trial & Error Prize is seeking spinal cord injury data so that the research community can learn from each other and not duplicate experiments.
In this round of the Prize, there will be a total prize fund of $6,000 available, with up to $3,000 available for the top application.
The application deadline is January 21st 2016, and we welcome all interest and any questions. To view and enter the grants, please go to http://www.conquerparalysisnow.org/RibbonLinks/TEPrize/Overview.aspx 
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Hi Eric,
No special type of data or number of subjects are necessarily needed. However, please be aware of the following term and condition:
"8. All applications must be suitable for chronic SCI models. If acute models are used, the application must clearly state how and why the additional effort of using a chronic model is not justified and how the idea would be translated to a chronic model."
In essence, we are looking for lessons learned from chronic SCI-related research to help minimize the duplication of experiments and narrow down pathways of innovation.
Thanks,
Michael
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I need to analyze the fibrotic scar size in a mouse model of spinal cord injury and i used laminin-specific antibody,but it didn't work well.
Can anyone suggest a good antibody?
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Dear Zhu,
To stain for fibrosis it depends a lot on what you want to look for. In my experience, staining for alpha smooth muscle actin positive cells is a reflection of the activation of myofibroblasts, which are the main cells involved in fibrotic responses. Therefore, I would try to investigate their presence in the areas of lesion. Abcam has a very good antibody (ab7817). I have used it for IFHC using an alexa fluor 488 green antimouse as secondary and the staining was beautiful. For scar tissue, I think you should look at collagen deposition in the areas of lesion. Masson's staining or picro-sirius red can give you a very good staining for collagen and do not require use of antibodies. I personally prefer picro-sirius red that is also cheaper in terms of reagents. 
I hope this information is of help,
Good luck!
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if the fibroblast migration is arrested after spinal cord injury immediatelly by using some kind of drug such as taxol, will it migrate again toward the lesion site at the chronic stage after the drug delivery is stopped?
because i think the inflammatory molecules will be reduced at the chronic stage, if the inflammatory molecules are the reason that cause fibrosis, inhibition of fibroblast migration at the acute stage is enough to reduce the fibrotic scar and the fibrotic scar will not occur at the chronic phase,am i right?
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Perfect question about This subject. There are many reports about gliosis after spinal cord injury. however,  especially two of them have been  specially included This subject. One of these report authors have been suggested that gliosis which occurs following the spinal cord injury may a factor for poor recovery.  But  in the other report the authors have been showed that decreasing of gliosis does not improve the healing of the spinal cord after spinal cord injury. so that this subject is a dilemma for authors  
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Can we adapt the strategies in brain injured patients?
In a recent pilot study, Werndle et al. presented preliminary data of a new technique for the continuous monitoring of spinal cord pressure and the corresponding spinal cord perfusion pressure (Crit Care Med 2014;42:646–655). Their analyses revealed that the use of inotropic drugs for an increase of spinal cord perfusion pressure optimizes neuronal function measured by motoric evoked potentials and muscle strengths below the spinal level of injury.
Are we ready for a routinely monitored management of spinal cord perfusion? 
Which mean arterial blood pressure should be targeted in this context?
How long and how invasive should we monitor?
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Indeed, a fascinating topic. Thank you Dr. Sutter to bring this up. I came across a recent article by the Cambridge/London group that has enormous experience with ICP. Intra-spinal cord pressure seems to be closely matched to epidural pressure at the level of the lesion in spine-injured patients, which would make pressure monitoring less invasive and still reliable. Regarding spinal perfusion pressure, the evidence being gathered is most convincing for a principle analogous to CCP.
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There are unfortunately millions of paralyzed people around the world.
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Hi Emilio,
To the best of my knowledge: the China Spinal Cord Injury Network (ChinaSCINet) is the largest spinal cord injury clinical trial network in the world, comprising more than 20 leading spinal cord injury centers in Mainland China, Hong Kong, and Taiwan.
Since 2010, Dr. Wise Young of Rutgers Univ W.M. Keck Center for Collaborative Neuroscience "ChinaSCINet CEO" conducted Phase I/II trials in Hong Kong and Kunming to assess the safety and feasibility of umbilical cord blood mononuclear cell transplants, to regenerate the spinal cord and improve recovery in people with chronic complete spinal cord injury. One year follow-up assessments of 28 spinal cord injury patients who were treated with cord blood mononuclear cell transplants showed promising results. These results are being prepared for publication soon.  Based on these results, they are now planning to initiate phase III clinical trials in China, India, Norway and the USA to test 120 subjects with chronic complete spinal cord injury and to test different combinations of therapies.
please check this out;
hope this is what you are looking for
best wishes
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We want to evaluate temproal changes in the bladder function of rats with a spinal cord injury. In order to minimize costs we would like to have a clinical outcome measure, so we wonder if there are valid clinical tests to assess bladder function in rats.
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Thank you very much for your answers
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The SRS scores reported in scoliosis series are highly variable. Some authors use SRS22, others SRS30. Some papers report SRS as mean for each domain, and others report a total score. How can I convert these scores into a single one in order to do a meta-analysis? Do you have any reference?
Thanks,
Alisson R. Teles
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I found it at: 
Spine (Phila Pa 1976). 2011 Nov 1;36(23):E1525-33. doi: 10.1097/BRS.0b013e3182118adf.
Converting SRS-24, SRS-23, and SRS-22 to SRS-22r: establishing conversion equations using regressionmodeling.
Lai SM1, Burton DC, Asher MA, Carlson BB.
 
Abstract
STUDY DESIGN: 
Cross-sectional mail questionnaire.
OBJECTIVE: 
Assess the feasibility of translating total and domain scores from Scoliosis Research Society (SRS)-24, SRS-23, and SRS-22 to SRS-22r.
SUMMARY OF BACKGROUND DATA: 
Three successive editions of the original SRS-24 health-related quality-of-life questionnaire have resulted from efforts to improve its psychometric properties and validate its use in patients down to 10 years of age. This resulted in the need to establish, if possible, conversion equations to the last and most thoroughly validated version, SRS-22r.
METHODS: 
A consolidated questionnaire of 49 questions that incorporated the various questions in the four questionnaires was mailed to a consecutive series of 235 patients who had received primary posterior or anterior instrumentation and arthrodesis to treat adolescent idiopathic scoliosis. Regression modeling was used to establish conversion equations from the SRS-24, SRS-23, and SRS-22 to the SRS-22r.
RESULTS: 
One hundred twenty-one of the 235 patients (51%), aged 23.3 ± 4.52 years (range 14.2-34.6 years), returned the questionnaire at 8.6 ± 4.00 years (range 2.3-15.9 years) following surgery. Estimation of SRS-22r questionnaire and nonmanagement domains total scores and mean scores from SRS-22 and SRS-23 scores is excellent (R2 scores of 0.97-0.99) and good for SRS-24 scores (R2 scores of 0.80-0.82, improving to 0.86 and 0.87 after minimal domain reconfiguration). Estimation of SRS-22r individual domain total scores and mean scores from SRS-22 and SRS-23 is good to excellent (R2 scores of 0.81-0.99). Minimal domain reconfiguration improves conversion from SRS-24 pain from R2 = 0.71 to 0.76, which are both fair; SRS-24 function from R2 = 0.69 and 0.74 to 0.83, from poor and fair to good; and SRS-24 satisfaction/dissatisfaction with management from R2 = 0.64 to 0.80, from poor to good. Conversion of SRS-24 self-image is poor (R2 = 0.60) despite the correlation being statistically significant.
CONCLUSION: 
With one exception, SRS-24, SRS-23, and SRS-22 questionnaire, nonmanagement domains, and individual domain total scores and mean scores can be translated to SRS-22r scores with fair to excellent accuracy, which is further improved in some instances by minimal domain reconfigurations. The sole exception is SRS-24 self-image, which translates poorly.
PMID:
 21289546
 [PubMed - indexed for MEDLINE]
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Is there a policy on early enteral feeding or is it a wait-and-see approach dependent on adequate oral intake? What factors influence the decision to transition from an nasogastric tube to a gastrostomy? Are patients involved in this decision making process?
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I enjoyed the well thought responses represented above. In my current position the decision is usually made prior to thier arrival in the Rehabilitation center. At my prior Institution it was different. 1.The patient and or family had some say. 2. reflexive cough was a highly valued indicator of transition to oral VS gastrostomy or duodenal tube placement. 3. FEES was also utilized frequently to assure clearance, especially in anterior approach fixations and high cervical levels. This was of particular value in complex cervical occipital dissasociation injuries. 4. Forced expiratory measurements add value to wait and see decision scenarios. Lastly we favored duodenal tubes for very high level p [rly responsive injuries when the decision was made to place a feeding tube. 
Nice reference for the inhaled citric acid, I am going to pass that on to our acute hospital team.
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I have been struggling lately with a rather peculiar problem with immunohistochemistry. My project entails transplantation of stem cells (engineered with an MSCV retrovirus), into a lesion model of spinal cord injury. I am seeing alot of "unspecific background" in the lesion animals in both fluorescence and DAB labeling due to the nature of performing IHC on injured tissue, this I have been able to control with appropriate blocking and treating of the tissue so unspecific binding is not my problem.
What remains a problem that is completely different from "unspecific background", is the fact that I am seeing  highly "specific" antibody staining of secondary antibody controls only in animals that A) received a lesion, and B) also received stem cells. Again, to reword, I have used transplant tissue as a secondary control and am seeing very specific cytoplasmic staining of only secondary antibodies that are made against mouse (Gt x Ms IgG). This problem does not exist with secondary antibodies made in other species. This remains a problem because our lab works on a system that uses predominately Ms and Rb primary antibodies, and many of the antibodies I need to use are made in Ms with almost no other option for buying IHC compatible antibodies in other species (e.g. IBA-1 or CD11b are almost exclusively made in mouse, or are not compatible with IHC when made in other species, if anyone can suggest a good substitute that would help alot too). More specifics of my protocols are the following. 4% PFA transcardial perfusion with overnight post-fixation, 25 micron sectioning, wash/ Peroxidase, avidin and biotin blocking if necessary/10% NGS/primary overnight/ 3x wash/ secondary 1 hour/ abc amplification and DAB development if necessary (main problem is in fluorescence).
To clarify species interactions, I use rat models and rat stem cells, but the problem appears localized to stem cell treated animals, ms secondary antibodies, and to regions within the needle track/ lesion epicenter making me think it is something going on with the transplanted cells. This problem does not exist in ICC cover-slipped stem cells, just transplanted ones. As one could imagine it remains impossible to make logically sound conclusions when this is a confounding variable. Please help if you know a solution or have experienced similar problems. I have exhausted alot of testing and controls into figuring this out and have stumped everyone else I have sought out help from.
Update: I know this question is many years old but the problem was, as Jan Johnson stated, Fc receptors present on some kind of inflammatory cell that reacted to the transplanted stem cells. If not Fc receptors, than something similar that arises in response to adaptive immunity, that rejected the transplanted cells.
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Non specific Fc receptor binding seems a plausible explanation since the lesion + stem cells probably triggers an inflammation response and rat Fc receptors might bind mouse Ig. The inflammation may also lead to the presence of many rat antibodies, so make sure your anti- Mouse secondary antibodies do not cross react with rat Ig. Since I have never heard of secondary antibodies made in mouse I have some doubt if you mean "X anti- Mouse secondary antibody" or "Mouse anti- Rabbit secondary antibody". Which one gives non specific staining?
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The Trial & Error Prize aims to incentivise the publication of ‘negative’ results, using crowdvoting and ResearchGate's open review system . Through this Prize, we hope to propel innovation in spinal cord injury (SCI) research through collaboration and information sharing.
The Trial & Error Prize is part of the ground-breaking CPN Challenge Program which will give up to $10 million in prizes and grants over the next 10 years for those who can provide significant improvements in the quality of life of people living with spinal cord injury. To increase the success of this Challenge, we believe that it is important to create a community whereby people can share their experiences and past research that might not have been successful as they hoped; researchers can learn from each other and thus narrow down pathways of innovation.
We currently have $3,000 available for our first round of prizes and the deadline is June 1st 2015.You can find out further information on how to enter please go to http://conquerparalysisnow.org/RibbonLinks/TrialandError/Overview.aspx
I have attached a useful infographic outlining the prize. If you have any queries, please do not hesitate to email trialanderror@conquerparalysisnow.org.  
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Hi Benoit, we are neuroscience researchers and carry out the histochemical and immunohistochemical studies in some rat models of central nervous system injury:  spinal cord (SC) injury caused by the SC hemisection; Alzheimer disease (AD) -  induced by the  beta-amyloid peptide injection; Parkinson disease (PD) - caused by the rotenone injection; vestibular nuclei injury - induced by the labyrintectomy; as well as immobilization stress. Many of these results are published.
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Patients and families can find BID enoxaparin injections difficult and INR monitoring with warfarin challenging after transitioning to home 6 weeks s/p acute sci.  
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you should look up clinical trial.gov
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ASIA is commonly used, however difficult to grade a muscle when it is spastic. Measures like FMA, Brunnstrome stages are available for cerebral lesions. They may not be appropriate here due to difference in pathology behind movement deficit.
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I would encourage you to do a search on rehabmeasures.org  If you entered the search term spinal cord injury - the site will come up with researched outcome measures and give you the validity, cut off scores etc.
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Information needed to compare 'slump sensitivity' between groups
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I think that the vertebral column might damage the blade or making it completely impossible. Has anyone ever tried to do this?
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Hi Matteo, without decalcification you can't cut the vertebrae in a cryostat. Quick decalcification protocols normally use acids which is not very good to the spinal cord, longer decalcification protocols with e.g. EDTA might work reasonably ok, but in my opinion the sectioning and the staining will never be as good as if you would process the spinal cord alone. My question is why would you need to do that?
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When a patient with complete SCI (T6- ASIA A) complains of pain (burning) in lower limbs, how can it be managed? Should exercises be modified if a person with SCI complains of central pain?
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At some point in the management of neuropathic pain after SCI it should be explored whether there is a role for surgical interventions. These should be considered when pharmacologic and other therapies have been thoroughly tested and the patient remains with a degree of pain that is still eroding their quality of life. There are several surgical options that range from reversible with low invasiveness to more invasive procedures. These include epidural stimulation, deep brain stimulation, cortical stimulation, radiofrequency lesions of the dorsal grey matter segments based on abnormal recordings from this area at and locally above the lesion level.  There are even more invasive treatments that should be reserved for unique cases.
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Hi all, I am in need of a software platform that can do PCA on a dataset that consists of the following:
41 subjects
1103 data points
41 categories of data (three hierarchical levels, 6 categories at highest)
674 pearson correlation coefficients (r values)
8 - 24 df; range of degrees of freedom between comparisons, with categories having values for 16-41 subjects
I'm looking to have a simple PCA analysis with determination of approximately three components, with simple plot of cumulative/proportional variability of each component, and 2 or 3 axis plots of the datasets.
With this data available, what are my best options for statistical software and graphing?
My sincere thanks, Jared
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Hi Dear Jared
I think Matlab too
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In my experiments, I perform a complete spinal cord injury, in a mice model, then I label the CST in motor cortex with FluoroRuby. Two weeks after, I investigate at thoracic segments (Thoracic 10) of the spinal cord, the regeneration of CST fibers in the lesion site. At the lesion site, I found fluorescente signal localized in the regenerated CST fibers and in others cells at the lesion site, the question is if exists the possibility that the FluoroRuby located in the CST fibers could be acquired by others cells at the lesion site?
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If your goal is anterograde labeling of CST axons, you might consider switching to BDA. There is a lot of literature on this tracer in models of spinal cord injury. I cannot comment specifically on the labeling patterns that you see with FR outside the CST axons. Perhaps pericytes or activated microglia responding to axonal die-back at the site of injury with subsequent incorporation of the dye. This is not something that is observed with BDA. I would recommend checking out PMID: 18596159
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What is the nursing care of spinal cord injured patient in the scene of the accident, in the emergency-intensive care unit and in the long-term rehabilitation? I would like related references or books about spinal cord injury nursing/neurological nursing/neuroscience nursing...thank you in advance!
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Should not move unnecessarily, Careful position in transferring the patient, prevent further damage, There are aides to assist with the moving of the
spine-injured patient. Then take him for surgery.
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We are using fast blue as retrograde tracer (in spinal cord tissue of rats) which is blue in color. So, we need some nuclear stain which is not blue in color.
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I have used propidium iodide (PI) and found it very reliable, easy to use, not-so-easily-fading, giving great contrast with FITC. The colour is red with a slight tinge of orange and the nuclear staining is very crisp.
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Some studies do suggest that, but I want to know of any recent studies on this topic.
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As far as I know no relaiable studies between SCI and able-bodied persons regadring RLS has been performed. In clinical practice, it is to my opinion not a major problem, spasticity is however, sometimes confused with RLS.
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Women with spinal cord injuries (SCI) represent a rising population. Unfortunately, there is limited information about labor care and delivery for women with SCI.
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These patients didn't feel labor pains so we must palpate them frequently .evacuate the bladder regularly as common associated with retention and uterine atony.good analgesia is needed to avoid autonomic dysreflexia .
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In studies in the area of Adapted Physical Activity among other limitations is the low n. An example can be seen in a recent publication by Kinoshita et al. (2013). One hypothesis leading to interesting results seemed to reduce this problem. What else may be done?
Reference:
Kinoshita et al. (2013). Increase in interleukin-6 Immediately after wheelchair basketball games in persons with spinal cord injury: preliminary. Spinal Cord. Spinal Cord, (12 February 2013) | doi: 10.1038/sc.2013.4
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The small n problem with SCI research has been around for decades. Traditionally, exercise research has been conducted using the student population attending the university, so a large n was usually achievable. With SCI, one of the issues is the number of spinal injuries in the population near to the research institution. If the population is low it is very difficult to recruit participants, especially if the research is looking for a homogenous sample. A way to combat this is to collaborate with local hospitals, therapy clinics, and other institutions to recruit subjects and possibly to assist with the research itself.
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I am assessing the response in spinal cord injury.
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Ependymal cells are generating neurospheres in cultures (Barnabe-Heider et al., 2011), hence behaving as neural stem cells. This is true for the intact spinal cord as well for the injured tissue. See Fiorelli et al., 2013, GLIA if you're interested in this technique.
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