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  1. #1

    Stem Cell Research Forum

    This forum is for posing of scientific articles from journals and discussion of the articles. Please post news and other discussion articles about stem cells either to the Cure Forum (if you think that it is relevant to the cure) or to the Health & Science News forum (if you think that is is no relevant to the cure). I just moved a bunch of news articles and other commentary to the Cure forum. Thank you very much.

    Wise.

  2. #2

    Stem cell tracking

    Quote Originally Posted by Wise Young
    This forum is for posing of scientific articles from journals and discussion of the articles. Please post news and other discussion articles about stem cells either to the Cure Forum (if you think that it is relevant to the cure) or to the Health & Science News forum (if you think that is is no relevant to the cure). I just moved a bunch of news articles and other commentary to the Cure forum. Thank you very much.
    Wise.
    Do you know if the stem cell placement in China will be under ionizing fluroscopy, Ultrasound or interventional MRI Sir? I hope not conventional Fluro do to the cell division suseptability to xray. Thought you would look at these attatchments and tell me what you know. Thank You.
    Last edited by mckeownp; 03-25-2006 at 07:19 PM.

  3. #3

    Anyone?

    Quote Originally Posted by mckeownp
    Do you know if the stem cell placement in China will be under ionizing fluroscopy, Ultrasound or interventional MRI Sir? I hope not conventional Fluro do to the cell division suseptability to xray. Thought you would look at these attatchments and tell me what you know. Thank You.
    I wonder if anyone knows how the implanted stem cell is tracked during and after implantation?

  4. #4
    This week, for the first time in humans, a heart failure patient received adult stem cells—taken from his own adipose (fat) tissue—which were processed and injected directly into the heart muscle with a special catheter.
    The procedure involves removing adult stem cells from fat tissue just as in a liposuction procedure. The cells are processed with a proprietary process developed by Cytori Therapeutics, Inc. After about one hour of processing, the stem cells are injected directly into damaged but viable areas of the heart muscle through an investigational device called a NOGA catheter.

    This is the first time people have used adipose-derived stem cells in humans, and they had good results.

  5. #5
    Senior Member NEWPARA's Avatar
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    Quote Originally Posted by Hampton
    This week, for the first time in humans, a heart failure patient received adult stem cells—taken from his own adipose (fat) tissue—which were processed and injected directly into the heart muscle with a special catheter.
    The procedure involves removing adult stem cells from fat tissue just as in a liposuction procedure. The cells are processed with a proprietary process developed by Cytori Therapeutics, Inc. After about one hour of processing, the stem cells are injected directly into damaged but viable areas of the heart muscle through an investigational device called a NOGA catheter.

    This is the first time people have used adipose-derived stem cells in humans, and they had good results.
    That sounds very intresting!Im suprized this forum dosnt have very many post.Im getting the feeling alot of memberes have gave up on a cure for sci?Please tell me Im wrong.I personaly feel a cure is very close,and Im planing on walking agin soon!

  6. #6
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    Quote Originally Posted by NEWPARA View Post
    That sounds very intresting!Im suprized this forum dosnt have very many post.Im getting the feeling alot of memberes have gave up on a cure for sci?Please tell me Im wrong.I personaly feel a cure is very close,and Im planing on walking agin soon!
    Hi Newpara,

    I think that this is the most positive forum for issues of cure. I belong to two others, and scathing cynicism to apathy appears to be the norm. I can sympathise with this, as historically, the ground covered in SCI research has seemed pretty small compared to some other medical advancements. I think we all have our own ways of dealing with it. In fact, some paralised, tend to over compensate.

    No one should give up the hope of beating this scourge, and I suspect the folks who may over compensate have the same wish.

  7. #7

    Interesting read on the neuroprotective properties of Polyethyline glycol

    Sorry that I can't post the full text of the article, but here is the summary. It is a very interesting application of PEG internally, and in greater quantity than the potential amount of adverse radicals.

    I also apologize if this has already been posted.


    Neuroprotection from secondary injury by polyethylene glycol requires its internalization
    Peishan Liu-Snyder1, Melissa Peasley Logan1, Riyi Shi1,2, Daniel T. Smith3 and Richard Ben Borgens1,2,*

    1 Center for Paralysis Research, School of Veterinary Medicine, Purdue University, West Lafayette, IN 47907, USA
    2 Weldon School of Biomedical Engineering, College of Engineering, Purdue University, West Lafayette, IN 47907, USA
    3 Department of Industrial and Physical Pharmacy, Purdue University, West Lafayette, IN 47907, USA

    * Author for correspondence (e-mail: cpr@purdue.edu )
    Accepted 13 February 2007
    Polyethylene glycol (PEG) is well known to both fuse and repair cell membranes. This capability has been exploited for such diverse usages as the construction of hybridomas and as a reparative agent following neurotrauma. The latter development has proceeded through preclinical testing in cases of naturally induced paraplegia in dogs. The mechanisms of action of polymer-mediated neurorepair/neuroprotection are still under investigation. It is likely that the unique interaction of hydrophilic polymers with the mechanical properties of cell membranes in concert with an ability to interfere with mechanisms of secondary injury such as the production of highly reactive oxygen species (ROS or `free radicals') is the basis for neuroprotection by polymers.
    Here we provide further evidence that the ability of PEG to reduce or limit secondary injury and/or lipid peroxidation (LPO) of membranes requires entry of PEG into the cytosol, further suggesting a physical interaction with the membranes of organelles such as mitochondria as the initial event leading to neurorepair/neuroprotection.
    We have evaluated this relationship in vitro using acrolein, a potent endogenous toxin that is a product of LPO. Acrolein can pass through cell membranes with ease, inducing progressive LPO in `bystander' cells, and the production of even more acrolein by inducing its own production. Immediate application of PEG (10 mmol l–1, 2000 Da) to poisoned neurons in vitro was unable to rescue them from necrosis and death. Furthermore, three-dimensional confocal microscopy of fluorescently decorated PEG shows that it does not enter these cells for up to 2 h after application. By this time the mechanisms of necrosis are likely irreversible. Additionally, severe oxygen and or glucose deprivation of spinal cord white matter in vitro also initiates LPO. Addition of potent free radical scavengers such as ascorbic acid or superoxide dismutase (SOD) is able to interfere with this process, but PEG is not. Taken together, these data are consistent with the hypothesis that PEG is able to rescue mechanically damaged cells, based on a restructuring of the damaged plasmalemma. Furthermore, in compromised cells with an intact cell membrane, PEG must first gain access to the cytosol where this same capability may be useful in restoring the integrity of cellular organelles such as mitochondria, though the intracellular concentration of the polymer must be significant relative to the concentration of toxins produced by LPO in order to rescue the cell.
    Key words: PEG, secondary injury, acrolein, endogenous toxins, CNS
    No one ever became unsuccessful by helping others out

  8. #8
    Here's another article on the heightened concentration of caveolin-1 in a clip-compression injury of the rat spinal cord. This escalation commenced 4 days post.


    Increases in the phosphorylated form of caveolin-1 in the spinal cord of rats with clip compression injury Taekyun Shin, a,
    aDepartment of Veterinary Medicine, Cheju National University, Jeju 690-756, South Korea
    Accepted 3 January 2007. Available online 9 January 2007.





    Abstract The phosphorylation of caveolin-1, a lipid raft protein, alters cell shape, which is an important finding in the activation and migration of inflammatory cells. We studied the level of the phosphorylated form of caveolin-1 (p-caveolin-1) in the spinal cord of rats with a clip compression injury to determine whether the phosphorylation of caveolin-1 is involved in the pathogenesis of spinal cord injury. Spinal cords, sampled on days 0, 1, 4, 7, and 14 post-injury, were analyzed by Western blot and immunohistochemistry. Western blot analysis showed that the level of p-caveolin-1 significantly increased in the spinal cord at day 4 post-injury compared to the sham-operated control (p < 0.05), and its increased level remained in the elevated condition until day 14 post-injury. (emph. added) Immunohistochemistry showed that p-caveolin-1 was mainly localized in the macrophages/activated microglia in the injured spinal cords, even though caveolin-1 was immunodetected in neurons and reactive astrocytes as well as in inflammatory macrophages. Considering these findings, we postulated that the increased level of p-caveolin-1 is involved in intracellular signaling in affected cells, particularly macrophages/activated microglia, in the course of rat spinal cord injury.
    No one ever became unsuccessful by helping others out

  9. #9

    Possible intervention for UTI prevention

    Here is the abstract to an article in regards to research performed on paralyzed cats. An intervention helped the paralyzed cats hold more urine and have less residual urine after micturation. This can definitely help the fight against UTIs.

    Activation of the external urethral sphincter central pattern generator by a 5-HT1A receptor agonist in rats with chronic spinal cord injury

    Paul C. Dolber,1,2,3 Baojun Gu,1,2,4 Xiaoyang Zhang,1,2 Matthew O. Fraser,1,2,5 Karl B. Thor,1,2,5,6 and Jerome P. Reiter7

    1Department of Surgery, Veterans Affairs Medical Center, Durham; 2Division of Urology, Department of Surgery, Duke University Medical Center, Durham; 3Department of Pathology, Duke University Medical Center, Durham; 4Department of Urology, Affiliated 6th People's Hospital, Shanghai Jiaotong University, Shanghai, People's Republic of China; 5Urogenics Pharmaceuticals, Inc., Durham; 6Division of Gynecologic Specialties, Department of Obstetrics and Gynecology, Duke University Medical Center, Durham; and 7Institute of Statistics and Decision Sciences, Duke University, Durham, North Carolina
    Submitted 28 February 2006 ; accepted in final form 20 December 2006

    ABSTRACT TOP
    ABSTRACT
    MATERIALS AND METHODS
    RESULTS
    DISCUSSION
    REFERENCES

    We recently demonstrated that treatment with the 5-HT1A/7 receptor agonist [(R)-(+)-8-hydroxy-2-di-n-propylamino]tetralin (8-OH-DPAT) increases bladder capacity in chloralose-anesthetized female cats with chronic spinal cord injury. In the current study, we investigated the effects of 8-OH-DPAT on bladder capacity and external urethral sphincter (EUS) activity in urethane-anesthetized female rats (initial body mass 175–200 g) with chronic spinal cord injury (transsection at T10). Cystometric study took place 8–12 wk posttranssection. Intravesical pressure was monitored in urethane-anesthetized rats with a transvesical catheter, and EUS activity was assessed electromyographically. Spinal cord injury disrupts phasic activity of the EUS, resulting in decreased voiding efficiency and increased residual volume. 8-OH-DPAT induced a dose-dependent decrease in bladder capacity (the opposite of its effect in chronic spinal cord-injured cats) with an increase in micturition volume and decrease in residual volume resulting from improvement in voiding efficiency. The unexpected improvement in voiding efficiency can be explained by the 8-OH-DPAT-induced emergence of phasic EUS relaxation. Phasic EUS relaxation was also altered by 8-OH-DPAT in spinally intact rats, whereas the 5-HT1A receptor antagonist N-tert-butyl-3-[4-(2-methoxyphenyl)-piperazin-1-yl]-2-phenylpropanamide (WAY-100635), on its own, was without effect. It remains to be determined when phasic relaxation is restored after spinal cord injury, and indeed whether it is ever truly lost or is only temporarily separated from excitatory input.
    No one ever became unsuccessful by helping others out

  10. #10
    Damn, I just realized this was a forum for cure-related articles....sooorrryyy!
    No one ever became unsuccessful by helping others out

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