Wednesday, June 27, 2012

HBOT after Blast Brain Injury, Study

Hyperbaric Oxygen Treatment after the Blast Injury of Rabbitbrain the Expression of AQP4 and PWI in the Study Phase

Hyperbaric Oxygen Treatment after the Blast Injury of Rabbit brain the Expression of AQP4 and PWI in the Study Phase
Objective:To establish explosive brain injury model in rabbits;To investigate the expression of aquaporin 4(AQP4) in model of explosive brain of rabbits injury,and perfusion changes in the expression, to explore the formation of brain edema after blast injury mechanism, and early hyperbaric oxygen treatment of traumatic brain edema formation and development of the role of early treatment for clinical hyperbaric oxygen provide the basis for traumatic brain edema.Method:30 New Zealand white rabbits, weighing 2.0 ~ 2.5kg, in accordance with the vertical distance between the detonators and the skull group, were randomly divided into groups 5.0cm, 6.5cm group, 8.0cm group, n = 10. 600mg TNT equivalent of paper detonators were used to explode respectively 5.0cm, 6.5cm, and 8.0cm vertical distance from the top of the rabbit head, observing animal survival after injury, and using magnetic resonance imaging methods to understand the pathology and brain damage in each group.150 New Zealand rabbits were randomly divided into non-treatment group, treatment group and control group, and 10 rabbits were in the latter. Explosive brain injury model was made by paper detonator. Injuryed rabbits were randomly divided into 1h6h12h24h72h7d14d ,14 groups according to a further killed time points after injury, and each group has 10 rabbits. Using dry weight to measure the content water in brain tissue, and using RT-PCR method and image analysis to detect the group at different time points aquaporin 4 (AQP4)mRNA expression, and Western blotting to measure the expression of AQP-4 in brain tissue. Using magnetic resonance perfusion imaging ( PWI) injury time points detected in brain tissue blood perfusion. Finally, it was used for statistical analysis.Results:5 rabbits died immediately after injury and 4 rabbits died within 3 days in group 5.0cm,and only one survived more than 7 days;The rabbit has appeared most extensive brain contusion, cortical surface vessel rupture occurs, and significant fragmentation in brain tissue, large subdural hematoma, and significant brain stem contusion. All rabbits in group 6.5cm survived more than 7 days,except that 1 rabbit died on the 4th day after injury because of inability eating. 4 rabbits occurred epilepsy and got paralysis of limbs; Pathology observed in the survival of the rabbits had cerebral cortex partial rupture of blood vessels, brain edema and obvious laceration and contusion lesions clear boundary with the surrounding brain tissue. All rabbits in group 8.0cm survived, but showed no significant changes in the brain.Blast injury after contusion brain 1h aquaporin 4 (AQP4) mRNA expression increased, and in turn increased, 72h peak (P <0.05), 7d pm down. Brain tissue aquaporin 4 (AQP4) began to express 1h after injury increases, and 72h reached its peak (P <0.05), it turned to down after 7d, but it still maintained on a high level. Brain tissue water content and water aquaporin 4 (AQP4) expression were the same. The correlation analysis, aquaporin 4 (AQP4) expression and brain tissue water content was positively correlated (r=0.8767,P<0.001). The hyperbaric oxygen treatment, aquaporin 4 (AQP4) expression at different time points are different degrees of decline, aquaporin 4 (AQP4) expression of injury group compared with control group at after 6h points were lower (P <0.05 ). Blast injury after contusion brain 1h AQP4 mRNA expression increased, and in turn increased, 72h peak (P <0.05), 7d pm down, but still maintain a high level. After intervention by hyperbaric oxygen, in 6h, AQP4 mRNA expression was significantly lower than the injury to 14d is still significantly lower (P <0.05). Post-traumatic cerebral contusion early peripheral blood perfusion decreased significantly to 6 hours after injury, blood perfusion decreased to the lowest (P <0.05), then gradually increased, and maintain a perfusion (close to the control group) for 2 weeks. The hyperbaric oxygen treatment group than in the early trauma group (1-6 hours after injury) perfusion decreased more significantly. 12 hours after infusion began to rise, and non-treatment group was essentially flat.Conclusion:Detonators and the vertical distance of the skull 6.5cm, can produce good stability, repeatability strong blast injury model of rabbit brain.The expression of post-traumatic brain aquaporin 4 (AQP4) in traumatic brain is closely related to the formation and development of injury and brain edema. Aquaporin 4 (AQP4) expression may be associated with brain ischemia and hypoxia in the Hyperbaric oxygen intervention aquaporin 4 (AQP4) expression was significantly reduced. Instead, the blood perfusion than the control group and non-treatment group decreased significantly, suggesting that brain tissue oxygen levels of early trauma and aquaporin 4 (AQP4) expression is closely related to early hyperbaric oxygen therapy on the relief plays an important role in traumatic brain edema. Early hyperbaric oxygen therapy can improve cerebral blood oxygen contusion, increased blood oxygen content, ease the secondary cerebral hypoxia caused by cerebral edema.

Tuesday, June 5, 2012

The Vitamin D Council: LINK? the autism epidemic and the vitamin D deficiency epidemic

The Vitamin D Council: LINK? the autism epidemic and the vitamin D deficiency epidemic
The Vitamin D Council’s free remote autism program is not only up and running, we now have some outcomes to report. First, as some readers may know, another paper appeared last month that recommended “urgent” research on the association of the autism epidemic with the vitamin D deficiency epidemic.
The senior author in the above review was Christopher Gillberg. I should say thee Christopher Gillberg, as he is famous as a prolific author, editor and the recipient of numerous awards. Dr. Gillberg is especially well known across the world for his autism research. When I saw his name, I knew it was just a matter of time before the entire theory was under the microscope, so to speak.
If you remember, we are offering a free autism program to help parents vigorously correct vitamin D deficiency in their children with autism. As long as the Council can afford it, everything is free for the families: the vitamin D blood tests, the vitamin D, the scales, and the help from me. Just email us at
The entire goal is to raise vitamin D levels from the very low levels that we find initially (5-20 ng/ml, if they’ve never supplemented), to high normal ranges (around 80 ng/ml). The “normal” range for most labs is 30-100 ng/ml, so all the parents are doing is raising their children’s levels to the same levels some lifeguards have at the end of summer. With our help, the parents use a combination of sunlight (when it is available) and supplements to do so.
The most common problem we have run into is parent’s unwillingness to give enough vitamin D to their child to obtain high normal levels. Too often, the child’s pediatrician tells the parents that the dose is too high – in spite of the normal blood levels – and the parents withdraw from the program. We never give advice contrary to the child’s doctor; in fact, we try to work with the doctor when possible.
If you remember, for more than 30 years, most of the infants in East Germany received 600,000 IU every 3 months. Many had a total dose of 3.6 million units by age 18 months, with transitory mild high blood calcium being the only side effect in one-third of the infants. The authors commented on how healthy the infants appeared. While the East German doctors gave way too much vitamin D, it demonstrates that even infants tolerate high doses of vitamin D with few serious side effects. Again, our kids are all older, receive much less vitamin D and are maintained in the normal range.
The second most common problem we have had is vitamin A. Vitamin A interferes with the action of vitamin D, probably at the receptor site. Unfortunately, some autistic children have taken 50,000 or 100,000 IU of vitamin A repeatedly or take cod liver oil. As vitamin A has no known catabolic (breakdown) pathway in the human body, these children may have subclinical vitamin A toxicity and in theory, vitamin D might not help. I try it anyway, but I have seen what I said; it does not help very much. The parents ask how long it takes to get the excess vitamin A out of the system, and I have no answer to their question.
However, in the children who obtain the high normal blood levels and who have not taken vitamin A, the response has been very satisfying. I believe the vitamin D’s mechanisms of action in these autistic children is through a combination of its antioxidant capabilities, glutathione and superoxide dismutase upregulation, increased Tregs (cells that help prevent autoimmunity), increased production of the proteins that repair DNA, and reduction of inflammation via multiple mechanisms. I have sometimes found that levels of 75 ng/ml work in most children while levels around 50 ng/ml do not. I can’t explain that and would welcome some theories why not?
Vitamin D appears to have beneficial effects in autism on meltdowns, tantrums and sleep (one mother, who works outside the home, was so thankful when her child no longer woke at 3 AM, wanting to play). Surprisingly, vitamin D also seems to benefit shyness, eye contact, speech and sometimes, compulsiveness. Several parents have commented on the neuromuscular improvements after vitamin D. Most of our children require around 5,000 IU/day to obtain a 25(OH)D of 80 ng/ml but all are different. We try to use D-Plus as studies show that many autistic children are deficient in magnesium as well as zinc.
Our autism program has been a great success, personally rewarding for all of us here at the Council, and is ongoing. So, if you have a child with autism and want to participate in it, contact us at As long as our money lasts, everything is free.

John J Cannell, MD
Executive Director

Office: (805) 439-1075