Looking at "natural remedies" the mineral boron has claims to remedy rheumatoid arthritis. Boron deficiencies have associations similar to rheumatoid arthritis Is it possible that the "tip organelle" of mycoplasmas bind where boron does? Do mycoplasmas use boron receptors to infect ? Is it possible that THF is meant to not only recruit neutrophils but to compete with mycoplasmas for these boron receptors?
RA and low boron levels (how does the RF factor fit in?)
http://www.scopemed.org/?mno=26288
Boron and red blood cells
https://www.researchgate.net/publication/50951788_Dietary_boron_affects_blood_cell_counts_and_hemoglobin_concentrations_in_humans
RA and anemia
https://www.ncbi.nlm.nih.gov/pubmed/2180049
if boron binds heme could this somehow explain the anemia and photosensitivity of RA patients?
https://www.ncbi.nlm.nih.gov/pubmed/20576510
heme deficiency causes photosensitivity (there is a genetic link between genetically faulty hemes and photosensitivity )
boron and mycoplasmas (do not eat borax it is toxic)
http://www.jbbardot.com/inexpensive-osteoporosis-mycoplasma/
This Borax article suggests that boron somehow acts against mycoplasmas. It is the hypothesis of this blog that mycoplasmas use the Boron receptor. The connection to boron can be found in every area of RA.
mycoplasmas and rheumatoid arthritis
https://www.ncbi.nlm.nih.gov/pmc/articles/PMC1006269/
Boron is used to produce bone (supplement is even given in osteoporosis)
https://medlineplus.gov/druginfo/natural/894.html
Rheumatoid and osteoporosis
http://www.webmd.com/rheumatoid-arthritis/rheumatoid-arthritis-and-osteoporosis#1
Boron and parathyroid
http://forums.phoenixrising.me/index.php?threads/boron-deficiency-causes-the-parathyroids-to-become-overactive.25880/
Rheumatoid and parathyroid
http://ard.bmj.com/content/71/Suppl_3/654.1
Boron is used by bones, joints, parathyroid, dental enamel, the thyroid, and the pancreas
Interestingly some forms of RA seems to affect the bones as osteoarthritis, overactive parathyroid, graves disease, and diabetes
mycoplasma's tip organelle
http://onlinelibrary.wiley.com/doi/10.1111/j.1574-6968.2001.tb10610.x/full
Mycoplasmas bind negative
https://www.researchgate.net/publication/51192733_Identification_of_Amino_Acid_Residues_Critical_for_Catalysis_of_Holliday_Junction_Resolution_by_Mycoplasma_genitalium_RecU
These tip organelles have a high concentration of adhesions which might function as a strong lewis acid because Boron is a strong lewis acid. Hypothesis: the mycoplasma are strong lewis acids. (this means they can accept an electron pair)
Boron and adhesives
https://www.researchgate.net/publication/266210033_Boring_Boron_and_Adhesives
Foods high in Boron : Raisins are the highest
https://www.algaecal.com/algaecal-ingredients/boron/boron-sources/
safer than the Borax
If TNF is the cytokine of warning of internal cell infections because it is released by macrophages:
Is it possible that THF is meant to not only recruit neutrophils but to compete with mycoplasmas for these boron receptors directly? When a macrophage itself is infected and can no longer function as the immune system vacuum it releases THF which suppresses FOXp3 which increases the Tcells looking for internal infections which would be viruses or mycoplasmas. TNF also recruits immune system macrophage like cells that do not have nucleuses like neutrophils. (no nucleus for a virus to infect) It is very likely that TNF would have developed a feature against mycoplasmas.
TNF high levels and lupus blood cell issues
http://lupusresearchinstitute.org/our-research/lri-researcher-discovers-cause-and-potential-treatment-approach-lupus-anemia
Does TNF alpha sort of fit into this too???
TNF is released by macrophages when they have succumbed to infection like mycoplasmas. Is it possible that a second action of TNF is to compete with mycoplasma binding? (not just to stimulate neutrophils)
TNF alpha bind negative
http://www.jimmunol.org/content/143/4/1192
TNF and bone
https://www.ncbi.nlm.nih.gov/pubmed/17350185
TNF and parathyroid
https://www.ncbi.nlm.nih.gov/pubmed/1325978
review of TNF drugs?
http://www.sciencedirect.com/science/article/pii/S1359610114000781
Enbrel (etanercept) binds the TNF alpha receptor
https://en.wikipedia.org/wiki/Etanercept
Humira (adalimumab) binds directly to the TNF alpha molecule and then floats around with it.
(humira is an IgG molecule)
TNFalpha if it is a lewis acid like boron would float around with humira and bind up Copper explaining the side affects of Humira.
Humira causes foot drop and copper deficiency
foot drop and copper deficiency (after bariatric surgery)
http://www.scielo.br/scielo.php?script=sci_arttext&pid=S1679-45082010000200232
Copper reacts with lewis acids
http://pubs.acs.org/doi/abs/10.1021/jo202624s
Nodules have been found with enbrel.
https://www.ncbi.nlm.nih.gov/pubmed/11920425
https://www.ncbi.nlm.nih.gov/pubmed/28357602
note that macrophages can also be infected by candida (fungal infections) which is why TNF occurs in Lupus, discord lupus and sj.
http://www.aspergillus.org.uk/content/how-does-candida-kill-macrophages
lupus vs. SJ ?
http://angelabiggs.blogspot.com/2014/09/lupus-vs-sjogren-can-you-seperate-them.html
This blog post is focused on the RA forms that are linked to mycoplasmas.
Considering Felty's syndrome and how this boron, THF, and mycoplasma competition could explain things.
boron: high in bone, thyroid, and.....spleen
Felty's syndrome : RA, splenomegaly, and neutropenia
https://www.ncbi.nlm.nih.gov/pubmed/21255689
https://www.ncbi.nlm.nih.gov/pubmed/10553980
Could the mycoplasma infect the spleen using boron receptors?
Neutropenia is the loss of neutrophils. THF released by infected macrophages triggers neutrophils.
Are the mycoplasmas infecting the neutrophils?
mycoplasmas and neutrophils
http://www.sciencedirect.com/science/article/pii/S0165242717302222
rheumatoid nodules are common in 75% of Felty patients
http://www.uptodate.com/contents/rheumatoid-nodules
Are the mycoplasmas blocking TNF receptors just like enbrel? but infecting using the boron receptors?
previous post
Dividing up the types of Rheumatoid arthritis further using HLAs and viruses
http://angelabiggs.blogspot.com/2016/12/cross-targeting-triggering-rheumatoid.html
Nodules are made up of excessive collagen. If nodules are caused by inflammation without TNF receptor activation what is happening? only the cytokine il-1 ?
cytokine il-1, RA nodules, and TNF
https://www.ncbi.nlm.nih.gov/books/NBK6288/
http://onlinelibrary.wiley.com/store/10.1002/art.10776/asset/10776_ftp.pdf?v=1&t=j41cc75s&s=3641ae28d7ef50302d0d55fdcc5fdafd65bc7b9f
Il-1 stimulates collagen growth in skin cells
http://www.sciencedirect.com/science/article/pii/0167488987901698
So the same thing must be happening in the tendon when the TNF receptor is blocked and only il-1 is seen by the tendon.
Hypothesis: When nodules form it is because the TNF receptor is blocked by anti-TNF receptor drugs or mycoplasma binding and the il-1 stimulates collagen growth unchecked
here humira caused nodules?
https://www.researchgate.net/publication/282068751_Adalimumab-induced_lupus_erythematosus_profundus_in_a_rheumatoid_arthritis_patient
does this mean that the floating complex adalimumab-THF still can bind the receptor?
panniculitis and enbrel study
http://factmed.com/study-ENBREL-causing-PANNICULITIS.php
review of TNF receptors (TNF R1 is the one involved with inflammation )
TNFR1 is involved in adipose cells
http://www.sciencedirect.com/science/article/pii/S0014579307011957
TNFR2 is on blood vessels cells
achilles tendon and THF alpha (TNFR1 seems involved)
https://www.researchgate.net/profile/James_Gaida/publication/224932188_Evidence_of_the_TNF-alpha_System_in_the_Human_Achilles_Tendon_Expression_of_TNF-alpha_and_TNF_Receptor_at_both_Protein_and_mRNA_Levels_in_the_Tenocytes/links/54ded6880cf2510fcee51da8/Evidence-of-the-TNF-alpha-System-in-the-Human-Achilles-Tendon-Expression-of-TNF-alpha-and-TNF-Receptor-at-both-Protein-and-mRNA-Levels-in-the-Tenocytes.pdf
Risk of heart failure is extremely high in RA patients
anti-TNF therapy seems protective against heart failure in RA patients
https://www.ncbi.nlm.nih.gov/pubmed/14984815
So what is happening in RA???? It starts as an infection of the tendons, mycoplasmas in at least 30%, and then a virus infects the tendon too trigger autoimmune cross-targeting.
http://angelabiggs.blogspot.com/2016/10/rheumatoid-arthritis-hla-drb1-and_24.html
RA and low boron levels (how does the RF factor fit in?)
http://www.scopemed.org/?mno=26288
Boron and red blood cells
https://www.researchgate.net/publication/50951788_Dietary_boron_affects_blood_cell_counts_and_hemoglobin_concentrations_in_humans
RA and anemia
https://www.ncbi.nlm.nih.gov/pubmed/2180049
if boron binds heme could this somehow explain the anemia and photosensitivity of RA patients?
https://www.ncbi.nlm.nih.gov/pubmed/20576510
heme deficiency causes photosensitivity (there is a genetic link between genetically faulty hemes and photosensitivity )
boron and mycoplasmas (do not eat borax it is toxic)
http://www.jbbardot.com/inexpensive-osteoporosis-mycoplasma/
This Borax article suggests that boron somehow acts against mycoplasmas. It is the hypothesis of this blog that mycoplasmas use the Boron receptor. The connection to boron can be found in every area of RA.
mycoplasmas and rheumatoid arthritis
https://www.ncbi.nlm.nih.gov/pmc/articles/PMC1006269/
Boron is used to produce bone (supplement is even given in osteoporosis)
https://medlineplus.gov/druginfo/natural/894.html
Rheumatoid and osteoporosis
http://www.webmd.com/rheumatoid-arthritis/rheumatoid-arthritis-and-osteoporosis#1
Boron and parathyroid
http://forums.phoenixrising.me/index.php?threads/boron-deficiency-causes-the-parathyroids-to-become-overactive.25880/
Rheumatoid and parathyroid
http://ard.bmj.com/content/71/Suppl_3/654.1
Boron is used by bones, joints, parathyroid, dental enamel, the thyroid, and the pancreas
Interestingly some forms of RA seems to affect the bones as osteoarthritis, overactive parathyroid, graves disease, and diabetes
mycoplasma's tip organelle
http://onlinelibrary.wiley.com/doi/10.1111/j.1574-6968.2001.tb10610.x/full
Mycoplasmas bind negative
https://www.researchgate.net/publication/51192733_Identification_of_Amino_Acid_Residues_Critical_for_Catalysis_of_Holliday_Junction_Resolution_by_Mycoplasma_genitalium_RecU
These tip organelles have a high concentration of adhesions which might function as a strong lewis acid because Boron is a strong lewis acid. Hypothesis: the mycoplasma are strong lewis acids. (this means they can accept an electron pair)
Boron and adhesives
https://www.researchgate.net/publication/266210033_Boring_Boron_and_Adhesives
Foods high in Boron : Raisins are the highest
https://www.algaecal.com/algaecal-ingredients/boron/boron-sources/
safer than the Borax
If TNF is the cytokine of warning of internal cell infections because it is released by macrophages:
Is it possible that THF is meant to not only recruit neutrophils but to compete with mycoplasmas for these boron receptors directly? When a macrophage itself is infected and can no longer function as the immune system vacuum it releases THF which suppresses FOXp3 which increases the Tcells looking for internal infections which would be viruses or mycoplasmas. TNF also recruits immune system macrophage like cells that do not have nucleuses like neutrophils. (no nucleus for a virus to infect) It is very likely that TNF would have developed a feature against mycoplasmas.
TNF high levels and lupus blood cell issues
http://lupusresearchinstitute.org/our-research/lri-researcher-discovers-cause-and-potential-treatment-approach-lupus-anemia
Does TNF alpha sort of fit into this too???
TNF is released by macrophages when they have succumbed to infection like mycoplasmas. Is it possible that a second action of TNF is to compete with mycoplasma binding? (not just to stimulate neutrophils)
TNF alpha bind negative
http://www.jimmunol.org/content/143/4/1192
TNF and bone
https://www.ncbi.nlm.nih.gov/pubmed/17350185
TNF and parathyroid
https://www.ncbi.nlm.nih.gov/pubmed/1325978
review of TNF drugs?
http://www.sciencedirect.com/science/article/pii/S1359610114000781
Enbrel (etanercept) binds the TNF alpha receptor
https://en.wikipedia.org/wiki/Etanercept
Humira (adalimumab) binds directly to the TNF alpha molecule and then floats around with it.
(humira is an IgG molecule)
TNFalpha if it is a lewis acid like boron would float around with humira and bind up Copper explaining the side affects of Humira.
Humira causes foot drop and copper deficiency
foot drop and copper deficiency (after bariatric surgery)
http://www.scielo.br/scielo.php?script=sci_arttext&pid=S1679-45082010000200232
Copper reacts with lewis acids
http://pubs.acs.org/doi/abs/10.1021/jo202624s
Nodules have been found with enbrel.
https://www.ncbi.nlm.nih.gov/pubmed/11920425
https://www.ncbi.nlm.nih.gov/pubmed/28357602
note that macrophages can also be infected by candida (fungal infections) which is why TNF occurs in Lupus, discord lupus and sj.
http://www.aspergillus.org.uk/content/how-does-candida-kill-macrophages
lupus vs. SJ ?
http://angelabiggs.blogspot.com/2014/09/lupus-vs-sjogren-can-you-seperate-them.html
This blog post is focused on the RA forms that are linked to mycoplasmas.
Considering Felty's syndrome and how this boron, THF, and mycoplasma competition could explain things.
boron: high in bone, thyroid, and.....spleen
Felty's syndrome : RA, splenomegaly, and neutropenia
https://www.ncbi.nlm.nih.gov/pubmed/21255689
https://www.ncbi.nlm.nih.gov/pubmed/10553980
Could the mycoplasma infect the spleen using boron receptors?
Neutropenia is the loss of neutrophils. THF released by infected macrophages triggers neutrophils.
Are the mycoplasmas infecting the neutrophils?
mycoplasmas and neutrophils
http://www.sciencedirect.com/science/article/pii/S0165242717302222
rheumatoid nodules are common in 75% of Felty patients
http://www.uptodate.com/contents/rheumatoid-nodules
Are the mycoplasmas blocking TNF receptors just like enbrel? but infecting using the boron receptors?
previous post
Dividing up the types of Rheumatoid arthritis further using HLAs and viruses
http://angelabiggs.blogspot.com/2016/12/cross-targeting-triggering-rheumatoid.html
Nodules are made up of excessive collagen. If nodules are caused by inflammation without TNF receptor activation what is happening? only the cytokine il-1 ?
cytokine il-1, RA nodules, and TNF
https://www.ncbi.nlm.nih.gov/books/NBK6288/
http://onlinelibrary.wiley.com/store/10.1002/art.10776/asset/10776_ftp.pdf?v=1&t=j41cc75s&s=3641ae28d7ef50302d0d55fdcc5fdafd65bc7b9f
Il-1 stimulates collagen growth in skin cells
http://www.sciencedirect.com/science/article/pii/0167488987901698
So the same thing must be happening in the tendon when the TNF receptor is blocked and only il-1 is seen by the tendon.
Hypothesis: When nodules form it is because the TNF receptor is blocked by anti-TNF receptor drugs or mycoplasma binding and the il-1 stimulates collagen growth unchecked
here humira caused nodules?
https://www.researchgate.net/publication/282068751_Adalimumab-induced_lupus_erythematosus_profundus_in_a_rheumatoid_arthritis_patient
does this mean that the floating complex adalimumab-THF still can bind the receptor?
panniculitis and enbrel study
http://factmed.com/study-ENBREL-causing-PANNICULITIS.php
review of TNF receptors (TNF R1 is the one involved with inflammation )
TNFR1 is involved in adipose cells
http://www.sciencedirect.com/science/article/pii/S0014579307011957
TNFR2 is on blood vessels cells
achilles tendon and THF alpha (TNFR1 seems involved)
https://www.researchgate.net/profile/James_Gaida/publication/224932188_Evidence_of_the_TNF-alpha_System_in_the_Human_Achilles_Tendon_Expression_of_TNF-alpha_and_TNF_Receptor_at_both_Protein_and_mRNA_Levels_in_the_Tenocytes/links/54ded6880cf2510fcee51da8/Evidence-of-the-TNF-alpha-System-in-the-Human-Achilles-Tendon-Expression-of-TNF-alpha-and-TNF-Receptor-at-both-Protein-and-mRNA-Levels-in-the-Tenocytes.pdf
Risk of heart failure is extremely high in RA patients
anti-TNF therapy seems protective against heart failure in RA patients
https://www.ncbi.nlm.nih.gov/pubmed/14984815
So what is happening in RA???? It starts as an infection of the tendons, mycoplasmas in at least 30%, and then a virus infects the tendon too trigger autoimmune cross-targeting.
http://angelabiggs.blogspot.com/2016/10/rheumatoid-arthritis-hla-drb1-and_24.html
No comments:
Post a Comment