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