Ronald F. Vetter wrote: > > Bev Steward wrote in part: > >Knowing what we do now about the brain being 80% damaged already > >when the first symptoms become noticable, I can trace several times > >in my life when I ran extremely high temperatures (105.8 & 106 > >degrees F)) with bouts of pneumonia, double pneumonia, infection and > >measles (at age 30). Encephalitis comes with high fevers, so I > >postulate that those fevers could have burned out cells in my > >substantia nigra. > > > >So, you can see why I agree with doing research in this direction. I > >wonder if it might lead to understanding why more people under 50 are > >being diagnosed as having PD. My personal thanks to Bill Langston > >and his crew! > > i have an unusual insight regarding this possibility. it comes from my > career as a solid propulsion rocket scientist/engineer. > > My solid propellant rocket experience included some failure investigation > research that determined that dark inclusions in translucent doublebase > propellant grains cause abnormal combustion. The flame zone normally exists > just above the regressing surface and is radiating heat with temperature and > pressure elevated. The regression of the surface is uniform unless the > portion of radiation passing through the unburned propellant is not > uniformly absorbed. Dark or opaque propellant or inclusions get warmer. At > times, burning initiates in subsurface hot spots resulting in > overpressurization rocket case rupture. > > I am curious if the darkness of the substantia nigra is a variable amongst > individuals with significance in radiation absorption. > > Dr. Jeffrey Tosk reported photon-phonon measurements which seem to add > credence to the possibility. > > It may be that the energy increase of the blacker loci is the proximate > cause of some overactivity during feverish illness that damages the neurons > sufficiently to induce apoptosis. > > It seems easy enough to make some sort of measurements of sunlight exposure > on animal cadavers perhaps. pathologists observations relevant to substancia > nigra damage and coloration of PD patients and fever-including lethal > diseases might provide clues that validate or deny any such energy > concentration due to pigment. > > I wonder if there is any test or measurement that can be done to ascertain > if the conjecture that I have "toyed" with might be shown as pertinent - or > not. The concept is somewhat related to the light sensitivity of the brain. > I have Parkinson's disease. One aspect of this is change in the blackest > portion of the brain, the substantia nigra. I know from numerous > translucent solid propellant rocket motor propellant investigations of > abnormal burning front progression - that the translucent or transparent > propellant can be heated in loci which are contaminated with dark inclusions > which absorb more of the radiant light energy; then, rise in temperature. > > The temperature rise can be nominal such that the portion heated is warm and > burns at a higher rate because of this - or, in some instances, the > localized heating is quite significant and actually causes ignition of the > heated portion - which will often cause pressure vessel rupture - id est, > the rocket bursts apart violently. > > The amount of radiant energy entering the brain is not known to me. > However, the substantia nigra being darkest might be warmest - which would > increase chemical activity. The Lewy bodies and neuromelanin are not > something I am visually acquainted with. In fact, I am unsure what the > normal substantia coloration is at birth, during development that is normal > and development of Parkinsonism. I think I have heard that the substantia > becomes whitened with disease, but I also remember reading that dopamine > gets combined into neuromelanin as part of the disease. Is not neuromelanin > black? > > ****** > excerpted from: > Zinc in pigmented cells and structures, interactions and possible roles > Jan Borovansk? > > Observations of Prota and his associates have recently revived attention to > the role of zinc in biosynthesis of melanins. They observed that various > transition metals including Zn2+ affected markedly the chemical properties > of melanin formed by the tyrosinase-catalyzed oxidation of L-dopa by > increasing the incorporation of 5,6-dihydroxyindole-2-carboxylic acid into > the pigment polymer [67,68]. Zn2+ can thus imitate function of dopachrome > oxidoreductase. When acting together the inhibition of > 5,6-dihydroxyindole-2-carboxylic acid decarboxylation was greater than that > produced by Zn2+ or dopachrome oxidoreductase separately [50]. The > suggestion that the presence of carboxylated indole units in natural > melanins is due to the intervention in the melanogenesis of metal ions can > be accepted. However, the role of Zn2+ namely in this respect appears to be > uncertain because the free Zn2+ cation is damaging to biological systems and > thus is associated with other molecules as Zn-ligand complex (see the > section 3) resulting in a actual free Zn2+ ion concentration that is 10-3 - > 10-6 that of the total zinc concentration [8,98]. Whether Zn2+-ligand > complexes can influence melanogenesis it has not been tested. Zn2+ ions were > shown to inhibit the initial rate-limiting reaction of melanogenesis - > tyrosine hydroxylation and thus to have a role in the regulation of > melanogenesis [50]. > > The frequent occurence of necroses in melanoma tissue [13] and the presence > of H2O2 [24] make the metal driven free radical processes in pigmented > tumours probable. Moreover, increased malondialdehyde levels found in the > livers of B16 and S91 melanoma-bearing mice [13,71] suggest that the tumours > alter host antioxidant defenses. Alteration of iron metabolism and increased > levels of lipid peroxidation are characteristic of substantia nigra in > Parkinson's disease [30] and the fact that also zinc levels in substantia > nigra are markedly increased under these circumstances may indicate a > physiological response to oxidative stress [29]. > > Evidence documenting that a number of catecholic melanin precursors, > including cysteinyldopas and dihydroxyindoles, are photochemically unstable > in vitro in the presence of biologically relevant ultraviolet radiation was > presented by Koch and Chedekel [52]. Definitive evidence of occurrence of > these reactions in vivo is currently unavailable, nevertheless these > photochemical processes are expected to have a role in the pathogenesis of > various pathological processes. The high level of zinc in epidermal and eye > pigment cells may again indicate a physiological defense against the > potential danger of oxidative stress. > > ******** > Some aspects of this disease are undoubtedly tied to the > de-pigmentation. I have not any reference information on the autopsy > findings. does anyone have such a thing as a source of some detail? > > some questions and conjectures: > Does the substantia nigra have the dark pigmentation in the fetus? or does > the pigmentation develop after birth? > > Have we measured the amount of light in the brain? I doubt that 'no' light > enters. Visible light might not be plentiful, nor other wavelengths of > electromagnetic radiation, but there must be quite a lot of cumulative > energy since some wavelengths of radiation pass through readily. Even if > the level of radiation is low, the black portion will tend to absorb - and > become warmer. > > Such warmth might accelerate activity and/or reactivity. Degradation might > accelerate as darkening increases. > > It seems easy enough to make some sort of measurements of sunlight exposure > on animal cadavers perhaps. pathologists observations relevant to substancia > nigra damage and coloration of PD patients and fever-including lethal > diseases might provide clues that validate or deny any such energy > concentration due to pigment. > > I wonder if there is any test or measurement that can be done to ascertain > if the conjecture that I have "toyed" with might be shown as pertinent - or > not. The concept is somewhat related to the light sensitivity of the brain. > I have Parkinson's disease. One aspect of this is change in the blackest > portion of the brain, the substantia nigra. I know from numerous > translucent solid propellant rocket motor propellant investigations of > abnormal burning front progression - that the translucent or transparent > propellant can be heated in loci which are contaminated with dark inclusions > which absorb more of the radiant light energy; then, rise in temperature. > > The temperature rise can be nominal such that the portion heated is warm and > burns at a higher rate because of this - or, in some instances, the > localized heating is quite significant and actually causes ignition of the > heated portion - which will often cause pressure vessel rupture - id est, > the rocket bursts apart violently. > > The amount of radiant energy entering the brain is not known to me. > However, the substantia nigra being darkest might be warmest - which would > increase chemical activity. The Lewy bodies and neuromelanin are not > something I am visually acquainted with. In fact, I am unsure what the > normal substantia coloration is at birth, during development that is normal > and development of Parkinsonism. I think I have heard that the substantia > becomes whitened with disease, but I also remember reading that dopamine > gets combined into neuromelanin as part of the disease. Is not neuromelanin > black? > > guess i am wanting to learn more - to see if this approach has some merit. > > my encounter with typhoid fever at the age of 11 may have done me some > damage. > > responses welcome; sincerely, ron > Ronald Vetter 1936, dz PD 1984, carbidopa/levodopa, Mirapex, selegiline > [log in to unmask] Ridgecrest, California > http://www.ridgecrest.ca.us/~rfvetter Hi ROonald Vetter, Your observations about high fever tie in with my experiences. First, my mother had a very hard labour when I was born, and stopped breathing and had to be given oxygen and I was reputedly born blue for lack of oxygen - postulated by some neurologists as the original trigger for my PD. Then at age 4 -- Scarlet fever with a 105 temperature, then at age 5, measles, again with a 105 temp. Then, at age 24, what I call my watershed year, 'cos it divides the healthy years from the later ones = that is when I contracted my mysterious still unsolved fever, also with a very high temp. ...it all starts to fall in place....... Hilary Blue