Re: UVEITIS-INFLAMMATION-CATARACTS-CLOUDINESS-FLOATERS

[Guest guest]

AQUEOUS HUMOR OUTFLOW

EYE DISEASES SUCH AS CATARACTS AND MACULAR

DEGENERATION HAVE INDENTIFIED OXIDATIVE STRESS

AS A POTENTIAL FACTOR INVOLVED IN THE

PROGRESSION OF THE DISEASE.

GLAUCOMA/OS,

SUGGESTING THAT CELLS WITHIN THE OUTFLOW

PATHWAY ARE UNDER OXIDATIVE STRESS.

WHAT IS CAUSE? HOW DOES THIS ALTER OUTFLOW

PATHWAY? COMPROMISED ANTIOXIDATIVE POTENTIAL?

ENABLING IMBALANCE OF FREE RADICALS AND DEFENCE

MECHANISMS? (AGE) PRODUCTS,ADVANCED GLYCATION

END-CARBS(REDUCEING SUGARS) AND PROTEINS-FOUND

IN LENS,CORNEA,VITREOUS,RETINA.

http://www.ncbi.nlm.nih.gov/pmc/articles/PMC2092444/

[Guest guest]

AGEs in the lens, humm, AGEs are end products of glycation reactions

where sugar molecules attach to a protein. aren't mycotoxins DNA adducts? and a

protein? or mistaken as protein?

>

> AQUEOUS HUMOR OUTFLOW

>

> EYE DISEASES SUCH AS CATARACTS AND MACULAR

> DEGENERATION HAVE INDENTIFIED OXIDATIVE STRESS

> AS A POTENTIAL FACTOR INVOLVED IN THE

> PROGRESSION OF THE DISEASE.

> GLAUCOMA/OS,

> SUGGESTING THAT CELLS WITHIN THE OUTFLOW

> PATHWAY ARE UNDER OXIDATIVE STRESS.

> WHAT IS CAUSE? HOW DOES THIS ALTER OUTFLOW

> PATHWAY? COMPROMISED ANTIOXIDATIVE POTENTIAL?

> ENABLING IMBALANCE OF FREE RADICALS AND DEFENCE

> MECHANISMS? (AGE) PRODUCTS,ADVANCED GLYCATION

> END-CARBS(REDUCEING SUGARS) AND PROTEINS-FOUND

> IN LENS,CORNEA,VITREOUS,RETINA.

>

> http://www.ncbi.nlm.nih.gov/pmc/articles/PMC2092444/

>

[Guest guest]

AGEs in the lens, humm, AGEs are end products of glycation reactions

where sugar molecules attach to a protein. aren't mycotoxins DNA adducts? and a

protein? or mistaken as protein?

>

> AQUEOUS HUMOR OUTFLOW

>

> EYE DISEASES SUCH AS CATARACTS AND MACULAR

> DEGENERATION HAVE INDENTIFIED OXIDATIVE STRESS

> AS A POTENTIAL FACTOR INVOLVED IN THE

> PROGRESSION OF THE DISEASE.

> GLAUCOMA/OS,

> SUGGESTING THAT CELLS WITHIN THE OUTFLOW

> PATHWAY ARE UNDER OXIDATIVE STRESS.

> WHAT IS CAUSE? HOW DOES THIS ALTER OUTFLOW

> PATHWAY? COMPROMISED ANTIOXIDATIVE POTENTIAL?

> ENABLING IMBALANCE OF FREE RADICALS AND DEFENCE

> MECHANISMS? (AGE) PRODUCTS,ADVANCED GLYCATION

> END-CARBS(REDUCEING SUGARS) AND PROTEINS-FOUND

> IN LENS,CORNEA,VITREOUS,RETINA.

>

> http://www.ncbi.nlm.nih.gov/pmc/articles/PMC2092444/

>

[Guest guest]

>

>

> AGEs in the lens, humm, AGEs are end products of glycation reactions

> where sugar molecules attach to a protein. aren't mycotoxins DNA adducts? and

a protein? or mistaken as protein?

>

>

> > http://www.ncbi.nlm.nih.gov/pmc/articles/PMC2092444/

> >

>

[Guest guest]

WELL,I'VE BEEN ON A MISSION.

once again I've found that if your looking for a answer to something of a

medical mystery, because you didn't get a answer from a doctor,

or know you were outright lied to, look for information to pausable cures

because they usually go into much detail that you are not going to find

otherwise.

2008-NANOPARTICLES ARE SUITABLE FOR CROSSING BIOLOGICAL BARRIORS THROUGH TISSUE

DIFFUSION<<<

EXTRAVASATION AND ESCAPE FROM HEPATIC FILTRATION.<<<<<<<<

http://www.ncbi.nlm.nih.gov/pmc/articles/PMC2663893/

NEURODEGENERATIVE DISEASES

ABNORMAL PROTEIN IN BLOOD AND SPINAL FLUID<<<<<

http://biomed21.wustl.edu/IRC_HCPPFN.htm

--------------

2007-glycation,aggregation of lens proteins,leading to cataracts.

http://www.ncbi.nlm.nih.gov/pmc/articles/PMC2274899/

failure to control oxidative stress is closely related to ageing

and a diverse range of diseases.

oxidative stress,protein aggregation in the lens

what causes protein aggregation? folding,clumping

humm, FLUID?

PH,DENATURATION,ELECTROSTATIC,

ENVIRONMENTAL FACTORS,STRESSORS,

NANOPARTICLES<<<<<<<<<<(MYCOTOXINS)

NANOPARTICLES /AMYLOID DISEASE

http://icon.rice.edu/resources.cfm?doc_id=10866

cell to cell diffusion

http://www.ncbi.nlm.nih.gov/pmc/articles/PMC1483098/

http://www.iovs.org/cgi/content/full/48/7/3269

buildup of protein in the lens that makes it cloudy, why? no one

knows, toxin exposure listed as a cause. oxidative stress,meds.

protein fluid transport in the lens

fluid circulation,lens extracellular space,lens homeostasis and

transparency,nutrient transport

2009-oxidative stress,lens gap juntions, and cataracts.

homeostasis and transparency of the avascular lens depend on

an extensive network of gap junctions. communication through gaP

junction channels allows intercellular passage of molecules,(up to

1kDa) including antioxidants. lens gap junctions and their

constituent proteins, connexins (Cx43, Cx46,and Cx50), are also

subject to the effects of oxidative stress.these observations

suggest that oxidative stress-induced damage to connexins (and

consequent alted intercellular communication) may contribute to

cataracts formation.

http://www.ncbi.nlm.nih.gov/pubmed/18831679?ordinalpos=1 & itoo

l=EntrezSystem2.PEntrez.Pubmed.Pubmed_ResultsPanel.Pubme

d_DiscoveryPanel.Pubmed_Discovery_RA & linkpos=4 & log$=relat

edreviews & logdbfrom=pubmed

gap junctions are membrane channels formed by a array of

connexins which links adjacent cells realizing an electro-metabolic

synapse.<<<<<<

connexin-43 role in altered intercellular communication in the lung.

fibrosis in the lung.

mutations in Cx43 cause cataracts

dye transfer between cells of the lens.

patch voltage clamp technique, results-extensive dye

communication between fiber cells at the lens posterior surface,

anterior surface, and equatorial surface. dye tranfer between deep

fiber cells was also observed.

matabolic communication

physiological properties of the lens

gap junctions direct current, model predicts that fluid moves same

as ionic current, physiological role of the current is to create a

internal circulatory system for the avascular lens.

http://physrev.physiology.org/cgi/content/abstract/77/1/21?ijkey=5

048c7d6202934cf59ff568591b2d863134c6f41 & keytype2=tf_ipsecsha

MMPs AS MEDIATORS OF CATARACT

http://www.ncbi.nlm.nih.gov/pmc/articles/PMC2583795/

QUANTIFICATION OF DOLICHOL IN THE HUMAN LENS

WITH DIFFERENT TYPES OF CATARACTS.

http://www.molvis.org/molvis/v15/a167/

CATARACTS IN FISH ARE FUNGAL CATARACTS.

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> >

> >

> > http://www.ncbi.nlm.nih.gov/pmc/articles/PMC2092444/

> >

>

[Guest guest]

thought I'd mention, these AGEs are also produced by the browning of foods,

cooked foods without water, do you suppose a person might become sensitive to

these?

> >

> > AQUEOUS HUMOR OUTFLOW

> >

> > EYE DISEASES SUCH AS CATARACTS AND MACULAR

> > DEGENERATION HAVE INDENTIFIED OXIDATIVE STRESS

> > AS A POTENTIAL FACTOR INVOLVED IN THE

> > PROGRESSION OF THE DISEASE.

> > GLAUCOMA/OS,

> > SUGGESTING THAT CELLS WITHIN THE OUTFLOW

> > PATHWAY ARE UNDER OXIDATIVE STRESS.

> >