(HOME) Subject: peripheral neuropathy
Ann Plast Surg 1998 Feb;40(2):156-9
Role of reactive oxygen species in optic nerve compression injury: a
preliminary study.
Babovic S, Im MJ, Angel MF, Manson PN
Division of Plastic, Reconstructive and Maxillofacial Surgery, The
Johns Hopkins University School of Medicine, Baltimore, MD, USA.
Optic nerve compression is one of the complications in craniofacial
surgery and blepharoplasty. We have shown previously that acute and
chronic nerve compression produce significant tissue injury in rat
sciatic nerve. In the present study the optic nerve was evaluated for
possible ischemia/reperfusion injury after acute compression in an
animal model. Male New Zealand White rabbits were used in the
experiment. The optic nerve was subjected to 2-hour compression
followed by reperfusion for 1 hour. Nerve compression was established
by banding the optic nerve with silastic tubing. The compressed optic
nerve was assayed for malondialdehyde, an indicator of lipid
peroxidation, measured as thiobarbituric acid reactive substances
(TBARS). The TBARS levels increased significantly to 2.5 times normal,
from 37+/-6 pmoles per milligram tissue (N=6) to 90+/-12 pmoles per
milligram tissue dry weight (N=5) in the compressed/reperfused nerve
(p < 0.05). Much of these increases were prevented by treatment with
deferoxamine, an iron chelator and antioxidant. The results indicate
that optic nerve is injured by acute compression followed by
reperfusion. The nerve compression injury appears to be due to
reactive oxygen species and can be ameliorated by treatment with free
radical scavengers.
PMID: 9495464, UI: 98154852
(HOME) _________________________________________________________________
Subject: diabetic neuropathy/vegan diet
DIABETIC NEUROPATHY/VEGAN DIET
Diabetic neuropathy symptoms of sharp, stabbing, burning and/or
shooting pains were entirely relieved in 17 of 21 patients placed on
an animal-product free (vegan), unrefined diet, and exercise at Weimar
Institute in Weimar, California. Improvement was noticed in four days
in some patients. (American Journal of Clinical Nutrition 48(3)Suppl
926, September 1988)
Subject: peripheral neuropathy
Ann Plast Surg 1998 Feb;40(2):156-9
Role of reactive oxygen species in optic nerve compression injury: a
preliminary study.
Babovic S, Im MJ, Angel MF, Manson PN
Division of Plastic, Reconstructive and Maxillofacial Surgery, The
Johns Hopkins University School of Medicine, Baltimore, MD, USA.
Optic nerve compression is one of the complications in craniofacial
surgery and blepharoplasty. We have shown previously that acute and
chronic nerve compression produce significant tissue injury in rat
sciatic nerve. In the present study the optic nerve was evaluated for
possible ischemia/reperfusion injury after acute compression in an
animal model. Male New Zealand White rabbits were used in the
experiment. The optic nerve was subjected to 2-hour compression
followed by reperfusion for 1 hour. Nerve compression was established
by banding the optic nerve with silastic tubing. The compressed optic
nerve was assayed for malondialdehyde, an indicator of lipid
peroxidation, measured as thiobarbituric acid reactive substances
(TBARS). The TBARS levels increased significantly to 2.5 times normal,
from 37+/-6 pmoles per milligram tissue (N=6) to 90+/-12 pmoles per
milligram tissue dry weight (N=5) in the compressed/reperfused nerve
(p < 0.05). Much of these increases were prevented by treatment with
deferoxamine, an iron chelator and antioxidant. The results indicate
that optic nerve is injured by acute compression followed by
reperfusion. The nerve compression injury appears to be due to
reactive oxygen species and can be ameliorated by treatment with free
radical scavengers.
PMID: 9495464, UI: 98154852
_________________________________________________________________
_____________________________________________________________
(HOME)