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» LymeNet Flash » Questions and Discussion » Medical Questions » Yellow laser for lyme - Germany new treatment

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Author Topic: Yellow laser for lyme - Germany new treatment
Marnie
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Hitting MRC complex II with yellow laser for lyme:

http://www.webermedical.com/en/weber-medical-for-professionals/med-lasertherapy/the-new-yellow-laser/

[ 07-05-2014, 12:29 PM: Message edited by: Marnie ]

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Marnie
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Up...I get how it might indeed work...does anyone else?
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Catgirl
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Very cool!

--------------------
--Keep an open mind about everything. Also, remember to visit ACTIVISM (we can change things together).

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Marnie
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Yup...Mitochondrial respiratory chain, complex #2 (II)...OH, YEA!!!

We can do the same "medicinally" too!!!

I've studied colors, wavelengths, etc. and it is odd that "yellow" on a "clock numbered-color wheel" corresponds to the #2 and to the element Helium. Yellow is a primary subtractive color.

Lithium (for bipolar mitochondrial dysfunction) is our 3rd element (position #3 on the same clock-color wheel) which, like PQQ, promotes mitochondrial biogenesis!

This is long...stick with me nurses and researchers...this took me awhile to figure out!

Because I know lyme can (and has) triggered cancers, I am absolutely devoted to stopping that from happening.

Ready, set, go:

“In the initial onset/proliferative stage of a tumor, MnSOD appears to be a tumor suppressor.

Yet, once tumor progresses to a more aggressive and invasive phenotype and MnSOD is upregulated,

the role of MnSOD is that of an oncogene, since MnSOD level positively correlates with enhanced metastasis.

Further evidence for the role of MnSOD as an oncogene has been provided by studies showing that

overexpression of MnSOD in aggressive cancers is

related to

the increased level of H2O2.”

http://www.sciencedirect.com/science/article/pii/S092544391100280

So…getting H202 down is important.

Thus…

“As previously discussed, if Ab and aging are keys to the generation of H2O2 in AD neurons,

then mitochondrially targeted

catalase,

*glutathione*,

MitoQ (a derivative of ubiquinone targeted to mitochondria) (Kelso et al. 2001),

or MitoVit-E (a derivative of vitamin E targeted to mitochondria) (Smith et al. 1999)

may likely, rapidly convert *toxic H2O2* into H2O and O2.”

http://onlinelibrary.wiley.com/doi/10.1111/j.1471-4159.2005.03530.x/pdf

Those doing HBOT know Bb doesn’t favor a lot of O2. And by “stealing” our cysteine -> homocysteine (which Bb does not use) via the reverse transsulfuration pathway, WE have limited ability to use cysteine -> taurine, GSH = glutathione, and sulfate.

Down goes our ability to make glutathione.

Homocysteine and/triggered ROS -> increased p53, a tumor suppressor that translocates to the mitochondria.

“We now report that homocysteine can induce neuronal apoptosis and can increase neuronal vulnerability to excitotoxicity by a mechanism involving DNA damage, PARP activation, and

p53 induction.”

http://www.jneurosci.org/content/20/18/6920.full

p53 impacts…

Specifically cyclin E and cyclin B.

Cyclin E, if it was not blocked -> cell cycle arrest.

This link has an easy to understand picture (Yo, Bob...help pasting it here?):

http://atvb.ahajournals.org/content/29/9/1244.figures-only

The upside-down capital “T” means it is blocked.

Here’s another link to another picture (help please, Bob):

http://www.sabiosciences.com/pathway.php?sn=Cyclins_Cell_Cycle_Regulation

What happened to protective catalase?

A deficiency of catalase is linked to type 2 diabetes and a catalase deficiency can have an underlying genetic cause

and
there is a link between homocysteine levels, folate, and low catalase -> excessive H2O2.

http://www.sciencedirect.com/science/article/pii/S0891584903004350

Oh, no…I just found this:

Homocysteine Inhibits Hydrogen Peroxide Breakdown by Catalase

http://www.benthamscience.com/open/toeij/articles/V001/34TOEIJ.pdf

So…too little (if any) glutathione, catalase won’t work to lower H2O2 due to high homocysteine…

that only leaves MitoQ to lower H2O2 levels -> H2O and O2.

About p53 translocating to the mitochondria:
p53 translocation to mitochondria precedes its nuclear translocation and *targets* mitochondrial oxidative defense protein-*manganese superoxide dismutase*.

Thus, p53 translocation to mitochondria and subsequent ***inactivation of MnSOD*** explains the observed mitochondrial dysfunction, which leads to transcription-dependent mechanisms of p53-induced apoptosis.

http://www.ncbi.nlm.nih.gov/pubmed/15867370

p53 interacted with the mitochondrial antioxidant enzyme MnSOD that resulted in a

reduction in MnSOD activity and

propagation of oxidative stress.

http://www.hindawi.com/journals/jst/2012/101465/

(Manganese superoxide dismutase is a nuclear encoded primary antioxidant enzyme
localized exclusively in the mitochondrial matrix.)

Normally MnSOD (when it is working) converts superoxide to -> H2O2…thus with MnSOD lowered superoxide goes up.

“Superoxide is biologically quite toxic and is deployed by the immune system to kill invading microorganisms.

In phagocytes, superoxide is produced in large quantities
by the enzyme NADPH oxidase for use in oxygen-dependent killing mechanisms of invading pathogens.”

In a phagosome, ***superoxide can spontaneously form hydrogen peroxide*** that will undergo further reactions to generate reactive oxygen species (ROS).

It is presumed that superoxide kills bacteria directly, as the

virulence of many pathogens is dramatically attenuated

when

their superoxide dismutase (SOD) genes are deleted.

http://en.wikipedia.org/wiki/Superoxide

“Transcriptional analysis of a superoxide dismutase gene of Borrelia burgdorferi”

http://onlinelibrary.wiley.com/doi/10.1111/j.1574-6968.2000.tb08930.x/pdf

So much for superoxide being effective against Bb (who has a SOD gene).

Review…NADPH oxidase -> increased superoxide, but Bb has a SOD gene to protect itself from superoxide…so much for NADPH oxidase.

2014…

These data demonstrated that NADPH oxidase activation was an initiator in mitochondrial damage.

Once mitochondria entered the feed-forward cycle, cell fate was no longer controlled by NADPH oxidase.

Only antioxidants that targeted mitochondria such as MitoQ could break the cycle and release cells from death.

http://www.ncbi.nlm.nih.gov/pubmed/23804302

To produce glucose to make “his” glycoproteins, Bb uses a parallel pathway of glycolysis called the pentose phosphate pathway.

Cancer…

“…altered expression of phosphoglycerate dehydrogenase, phosphoglycerate mutase 1, and pyruvate kinase M2 has been shown to reduce the rate of glycolytic flux to pyruvate and
increase flux to biosynthetic pathways,

such as serine biosynthesis, and

the pentose phosphate pathway.

Interestingly, increased glucose metabolism and the Warburg effect *also* promote tumor cell survival through redox ***regulation of cytochrome c*** and

inhibition of apoptosis.(Me...remember cyclin E is blocked? The picture link helps.)

http://journal.frontiersin.org/Journal/10.3389/fonc.2013.00292/full

Mitochondria…

The mitochondrial respiratory chain (MRC) consists of ***five multi-subunit complexes*** embedded in the inner mitochondrial membrane.

Its function is to conserve the energy released by the oxidative metabolism

and use it to drive the phosphorylation of ADP to ATP.

Cytochrome C is in the mitochondria where it *transfers electrons* between complex III and complex IV.

Yellow laser therapy for lyme looks to impact complex II (linked in a separate post) while low level laser red light looks to impact complex III and IV.

http://en.wikipedia.org/wiki/Cytochrome_c

Odd… the enzymatic activity of MRC complex II, which is exclusively encoded by the
*nuclear* DNA..

Complex II (also known as Succinate Dehydrogenase (SDH) or Succinate Coenzyme Q Reductase (SQR)) is made up of only four subunits (SDHA, SDHB, SDHC and SDHD) and as such is the smallest mRCC.

It is the only complex to be fully encoded by nuclear DNA.

http://www.sciencedirect.com/science/article/pii/S0005272812010328

When isolated complex II (succinate dehydrogenase) was incubated with MitoQ10 the rate of ubiquinone reduction was identical to that for idebenone and decylQ (Fig. 1B).

***This confirms that MitoQ10 is a good substrate for this enzyme***

and is consistent with previous observations in bovine heart mitochondrial membranes (3).

http://www.jbc.org/content/282/20/14708.full

succinate dehydrogenase:

http://guweb2.gonzaga.edu/faculty/cronk/biochem/S-index.cfm?definition=succinate_dehydrogenase

Succinate dehydrogenase (SDH) oxidises succinate to fumarate

as a component of the tricarboxylic acid cycle

and

ubiquinone to ubiquinol in the mitochondrial electron transport chain.

http://www.sciencedirect.com/science/article/pii/S1369526613000277

A significant hint as to the triggers and

***advantages of

enhanced glycolysis *** (Me...Yes, I "get" the ICHT comparison!)

in tumours was supplied by the recent discovery that

***succinate dehydrogenase (SDH)*** and fumarate hydratase (FH) are

***tumour suppressors***

and which associated, for the first time,

mitochondrial enzymes and their dysfunction with tumorigenesis.

http://www.nature.com/onc/journal/v25/n34/full/1209594a.html

Whew.

I wish PQQ and especially MitoQ weren't so darn expensive.

Since they are both relatively "natural", they should be safe. PQQ is IN foods and is even in...get this...comets, etc. God supplies our "nutrients" in our UNIVERSE for mitochondrial biogenesis cause he likes reproduction.

How great is HE?!

P.S. Some of you know I have said I believe Rhodopsin levels in the WFL were capable of destroying Bb. I stand corrected:

Rhodopsin and retinoldehydrogenase served as markers for outer segment membranes,

whereas succinate dehydrogenase was a marker for

inner ones.

It is shown that NAD kinase and glucose-6-phosphate dehydrogenase are localized within inner segment membranes of the photoreception cell and that

the activity of these enzymes in the crude preparations is due to contamination of

the inner segments."

http://europepmc.org/abstract/MED/181877

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lymie_in_md
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The following is from the link below:

http://atvb.ahajournals.org/content/29/9/1244.figures-only

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Figure 1. An integrative view of cellular senescence and possible relationships to HDL signaling.

Many molecules involved in stress and senescence signaling have been shown to be activated by HDL in cultivated cells (mostly in a functional context unlike senescence; see also figure 2) and are underlined in this figure.

These molecules are typically activated upon acute cellular stress but are not often depressed in fully senescent cells.

The species-specific aging mechanism replicative aging (upper panel) may cooperate with other aging mechanisms to activate the senescence program.4,5

These signaling pathways are funneled down to activate the p53 protein, the Rb protein, or both. ATM and ATR are primary sensors of DNA double and single-strand damages induced by replicative senescence or other DNA damages.

Once activated ATM and ATR trigger checkpoint responses to bring about cell cycle arrest. p21, a target of p53, can cause the activation of Rb and induce G1 arrest.

Mitotic or mechanical stress (involving the small G proteins Ras, Cdc42, and Rac) will additionally activate the p16/INK4a gene, also leading to Rb activation.

JNK is activated by radical oxygen species, pathogens, and cytokines. Apoptosis signal–regulating kinase 1 (ASK1), RhoA, and Cdc42 are transducers of these signals.

C-jun, which is phosphorylated and activated by JNK, inhibits the CDK1/cyclin B complex, thus inducing a G2/M arrest.

A stronger stimulation of p53 may lead to apoptosis by mobilizing Bax, a cofactor of p53, to mitochondria and activating the mitochondrial pathway of apoptosis via apoptotic protease activating factor 1 (APAF1).

Once the senescence program is activated, a series of changes in morphology, cell function, and gene expression takes place, associated with autocrine and paracrine effects of secreted cytokines.

Telomere attrition or dysfunction may additionally modulate gene expression by a telomere position effect (TPE).

[ 07-09-2014, 12:23 AM: Message edited by: Robin123 ]

--------------------
Bob

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lymie_in_md
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the following is from the link below:
http://www.sabiosciences.com/pathway.php?sn=Cyclins_Cell_Cycle_Regulation
 -

Progress in the eukaryotic cell cycle is driven by oscillations in the activities of CDKs (Cyclin-Dependent Kinases).

CDK activity is controlled by periodic synthesis and degradation of positive regulatory subunits, Cyclins, as well as by fluctuations in levels of negative regulators, by CKIs (CDK Inhibitors), and by reversible phosphorylation.

The mammalian cell cycle consists of four discrete phases: S-phase, in which DNA is replicated; M-phase, in which the chromosomes are separated over two new nuclei in the process of mitosis.

These two phases are separated by two so called “Gap” phases, G1 and G2, in which the cell prepares for the upcoming events of S and M, respectively (Ref.1).

The different Cyclins, specific for the G1-, S-, or M-phases of the cell cycle, accumulate and activate CDKs at the appropriate times during the cell cycle and then are degraded, causing kinase inactivation.

Levels of some CKIs, which specifically inhibit certain Cyclin/CDK complexes, also rise and fall at specific times during the cell cycle (Ref.2).

A breakdown in the regulation of this cycle leads to uncontrolled growth and contribute to tumor formation.

Defects in many of the molecules that regulate the cell cycle also lead to tumor progression.

Key among these are p53, the CKIs (p15 (INK4B), p16 (INK4A), p18 (INK4C), p19 (INK4D), p21, p27 (KIP1)), and Rb (Retinoblastoma Susceptibility Protein), all of which act to keep the cell cycle from progressing until all repairs to damaged DNA have been completed.

In mammalian cells, different Cyclin-CDK complexes are involved in regulating different cell cycle transitions: Cyclin-D -CDK4/6 for G1 progression, Cyclin-E -CDK2 for the G1-S transition, Cyclin-A -CDK2 for S-phase progression, and Cyclin-A/B-CDC2 for entry into M-phase.

Apart from these well-known roles in the cell cycle, several Cyclins and CDKs are involved in processes not directly related to the cell cycle.

Cyclin-D binds and activates the estrogen receptor. (Ref.6). The Cyclin-H -CDK7 complex is a component of both the CDK-activating kinase and the basal transcription factor TFIIH and can phosphorylate CDKs.

Other Cyclins and CDKs (Cyclin-C-CDK8, Cyclin-T-CDK9, and Cyclin-K) are also associated with RNA Polymerase-II and phosphorylate the carboxyl-terminal repeat domain.

Cyclin-G, a target of p53, recruits PP2A (Protein Phosphatase 2A) to dephosphorylate MDM2 (Mouse Double Minute 2) (Ref.3).

Cyclins associate with CDKs to regulate their activity and the progression of the cell cycle through specific checkpoints.

Disruption of Cyclin action leads to either cell cycle arrest, or to uncontrolled cell cycle proliferation.

Mitogenic signals that are received by cell surface receptors communicate to the nuclear cell cycle machinery to induce cell division through growth factor receptors that target Ras,

which signals to a number of cytoplasmic signaling cascades such as PI3K (Phosphatidylinositiol–3 Kinase), Raf and Rho.

These proteins connect to the nuclear cell cycle machinery to mediate exit from Go into G1 and S-phase of the cell cycle.

Activation of Ras leads to transcriptional induction of Cyclin-D1 in early G1 through a Ras-responsive element in the Cyclin-D1 gene promoter.

Cyclin-D associates with CDK4 and CDK6 to form active Cyclin-D/CDK4 (or -6) complexes. This complex is responsible for the first phosphorylation of tumor suppressor Rb in G1 (Ref.1).

Subsequently, Cyclin-E is synthesized. When Cyclin-E is abundant it interacts with the cell cycle checkpoint kinase CDK2 and allow progression of the cell cycle from G1 to S-phase.

One of the key targets of activated CDK2 complexed with Cyclin-E is Rb. When dephosphorylated in G1, Rb complexes with and blocks transcriptional activation by E2F transcription factors.

But when CDK2/Cyclin-E phosphorylates Rb, it dissociates from E2F, allowing E2F to activate the transcription of genes required for S-phase.

E2F activity consists of a heterodimeric complex of an E2F polypeptide and a DP1 protein (Ref.5).

One of the genes activated by E2F is Cyclin-E itself, leading to a positive feedback cycle as Cyclin-E accumulates.

In S-phase, Cyclin-A is made, which in complex with DK2 adds further phosphates to Rb.

Cyclin-B is made in G2 and M-phases of the cell cycle (Ref.4). It combines with CDK1 (also called CDC2 or CDC28) to form the major mitotic kinase MPF (M-phase Promoting Factor)

MPF causes entry of cells into mitosis and, after a lag, activates the system that degrades its Cyclin subunit.

MPF inactivation, caused by the degradation of Cyclin-B, is required for exit from mitosis (Ref.2).

14-3-3s bind to the phosphorylated CDC2–Cyclin-B kinase and exports it from the nucleus.

During G2-phase, CDC2 is maintained in an inactive state by the kinases Wee1 and Myt1 (Myelin Transcription Factor 1).

As cells approach M-phase, the phosphatase CDC25 is activated by PLK (Polo-Like Kinase). CDC25 then activates CDC2, establishing a feedback amplification loop that efficiently drives the cell into mitosis.

All Cyclins are degraded by ubiquitin-mediated processes, and the mode by which these systems are connected to the cell-cycle regulatory phosphorylation network, are different for mitotic and G1 Cyclins (Ref.2).

The decision by the cell to either remain in G1 or progress into S-phase is the result in part of the balance between Cyclin-E production and proteolytic degradation in the proteosome.

Cyclin-E is targeted for destruction by the proteosome through ubiquitination when associated with a complex of proteins called the SCF or F box complex.

During G1-phase, the Rb-HDACs (Histone Deacetylases) repressor complex binds to the E2F-DP1 transcription factors, inhibiting the downstream transcription.

Many different stimuli exert checkpoint control including TGF-Beta, DNA damage, contact inhibition, replicative senescence and growth factor withdrawal.

The first four act by inducing members of the INK4A family or KIP/CIP families of cell cycle kinase inhibitors.

TGF-Beta additionally inhibits the transcription of CDC25A, a phosphatase that activates the cell cycle kinases.

DNA damage activates the DNA-PK/ATM/ATR kinases, initiating cascades that inactivate CDC2–Cyclin-B.

Both synthesis and destruction of Cyclins are important for cell cycle progression.

The destruction of Cyclin-B by Anaphase-Promoting Complex/cyclosome is essential for metaphase-anaphase transition, and expression of indestructible Cyclin-B traps cells in mitosis (Ref.3).

Cyclins-E and A have been implicated in the DNA replication initiation process in mammalian cells.

In embryonic systems, Cyclin-E regulates replication in the absence of Cyclin-A.

For centrosome duplication, in somatic cells Cyclin-A is required to induce DNA replication and it has also been implicated in activation of DNA synthesis,

because of its appearance time relative to the onset time of DNA synthesis and its localization to sites of nuclear DNA replication.

Cyclin-E regulates the transcription of genes that encode the replication machinery but has also been implicated in the initiation process in mammalian cells (Ref.1).

Similarly, expression of indestructible Cyclin-A arrests cells in late mitosis. Overexpression of Cyclin-F also causes an accumulation of the G2/M (Ref.3).

[ 07-09-2014, 12:29 AM: Message edited by: Robin123 ]

--------------------
Bob

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Marnie
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The first picture can be made bigger by going to the link and enlarge it.

Okay, thanks Bob...asking for help posting another picture of what happens in cancer cells because we know for FACT that Bb attaches to and gets cholesterol from HeLa (immortal cancer cells). Bb can even INVADE those cells for refuge.

http://www.plosbiology.org/article/info%3Adoi%2F10.1371%2Fjournal.pbio.0050010

See H going OUT of the cancer cell and Na going IN?

Yipee says Bb who uses Na for "his" ATPase and NaCl for motility.

And..about succinate dehydrogenase (that helps donate and transport electrons):

…the other ***genes that show a
delayed response in HeLa cells***

encode proteins linked to energy production,

such as NDH-1, cytochrome bo3, and

***succinate dehydrogenase.***

These data suggest that the HeLa cell cytosol is a more favorable environment for bacterial growth than the macrophage cytosol at the early stages of infection.

http://iai.asm.org/content/73/1/88.full.pdf

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springshowers
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Been using laser

Yeah there are different colors and what is the take on yellow vs red green blue ?

Concepts of wavelengths and affects on cells and body would be very much the same.

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steve1906
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-
-
Larger photo from above

 -

Steve

--------------------
Everything I say is just my opinion!

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MattH
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First I did read every word of the post and not to sound too stupid but I thought this was about the possible breakthrough with yellow laser IV. Does anyone have any experience with this light frequency?

Can it be replicated with a rife machine using a plasma tube?

If we did not do an IV would it penetrate enough to work in other places?

Spring how his your laser treatment going?

All the Best, MattH

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springshowers
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http://www.emred.fi/htmls_en/laser_blood_irradiation_therapy_en.html

Transcutaneous Laser Blood Irradiation Therapy

In addition to the invasive method of intravenous laser blood irradiation (IV LBI) non-invasive transcutaneous laser blood irradiation (TLBI) is also available.

This non-invasive and relatively simple method of blood irradiation has been taken into use only after development of bright enough red and infrared lasers.

It was shown that infrared radiation can go deep enough to reach vessels and irradiate blood. In addition, red laser light can also influence blood in superficial veins.

Currently semiconductor laser diodes with red (630-670 nm) or near infrared (800-1300 nm) light emission are used to perform TLBI therapy.

Recent studies suggested that the medical effects of HeNe laser TLBI are similar or very close to the effects of HeNe laser IV LBI.

It is believed, that the treatment results of 20 mW HeNe laser transcutaneous blood irradiation are similar to 1 mW HeNe laser intravenous blood irradiation.

Laser light is delivered to the skin in the area of a large vein or artery through a special light-guide. Contact of the light-guide with the skin with some pressure can increase penetration of the light.

The biggest advantage of TLBI is that this method of blood irradiation is painless. Another important issue is that the need for intravenous injection is completely eliminated.

This is why TLBI has the greatest advantage for the treatment of children. It can be also applied for the treatment of patients with small or difficult to find deep veins.

Unfortunately, not enough research exists to date directly comparing medical and biological effects of IV and transcutaneous LBI with each other.

G. Brill (1994) suggested that the effects of the laser therapy depend on the method of irradiation.

He considered, that the term «transcutaneous laser blood irradiation» is not quite correct, because it mentions only irradiation of blood and hides the irradiation of other nearby tissues,

including all layers of skin, possibly acupuncture points, nerves, lymphatic glands and vessel, and even muscle and bone tissues.

In case of IV LBI the main portion of the laser light is absorbed by blood, while in case of TLBI only minor part can reach blood.

So, it is better not only to mention TLBI, but also to specify the exact area of irradiation. Top

[ 07-09-2014, 12:32 AM: Message edited by: Robin123 ]

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springshowers
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This doctor explains in his videos how he treats and gets people recovered using Laser

http://hotspottherapies.com

The connection between lymphs and blood and nerves and facia and tendons and muscles and cells all equal the pain and fatigue and symptoms we all list.

I believe the infections get us out of wack causing a cascade and this all needs to be undone even after you treat the infections. Espc in those of us who have had years of the disease.

The videos are pretty short and to the point. I think worth hearing how he views and treats and views these illnesses and symptoms and how he unwinds them in about 4 to 6 months using laser and infa red laser primarily.

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Marnie
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I think the light (yellow laser) is functioning as a transport mechanism.

More in awhile that will, I promise, blow you away (as it did me)!

We are up against one SMART pathogen that is using our RESPONSE to invade.

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lymie_in_md
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Bob

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Marnie
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Bob and others:

Keeping in mind I believe succinate dehydrogenase is the key enzyme involved in Bb's destruction in the WFL...

Macrophages activated by the Gram-negative bacterial product lipopolysaccharide

switch

their *core metabolism from oxidative phosphorylation

to glycolysis.*

Here we show that *inhibition of glycolysis* with 2-deoxyglucose

suppresses lipopolysaccharide-induced interleukin-1β but not tumour-necrosis factor-α in mouse macrophages.

A comprehensive metabolic map of lipopolysaccharide-activated macrophages shows upregulation of glycolytic and

downregulation of mitochondrial genes,

which correlates directly with the expression profiles of altered metabolites.

Lipopolysaccharide strongly

increases the levels of

the tricarboxylic-acid cycle intermediate

*succinate.*

Glutamine-dependent anerplerosis is the principal source of succinate,

although the ‘GABA (γ-aminobutyric acid) shunt’ pathway also has a role.


Lipopolysaccharide-induced succinate stabilizes hypoxia-inducible factor-1α,
an effect that is inhibited by 2-deoxyglucose,

with interleukin-1β as an important target.

Lipopolysaccharide also increases succinylation of several proteins.

We therefore identify succinate as a metabolite in innate immune signalling, which

***enhances interleukin-1β production during inflammation.***

http://www.nature.com/nature/journal/v496/n7444/full/nature11986.html?message-global=remove

Now get this...

Succinate *dehydrogenase* is upregulated in some

biofilms!

http://www.ncbi.nlm.nih.gov/pmc/articles/PMC2863491/

Succinate is an electron donor.

Dehydrogenases transfer H- (= hydride = hydrogen that *has an extra electron*, normally H has one + and one -)


Succinate dehydrogenase is used in the

dehydrogenation of succinate.

Dehydrogenation is the removal of hydrogen.

Hydrogen out...Na in. Bb needs NaCl for motility and uses it for its Na-ATPase.

But if upon invasion there is a lot of succinate dehydrogenase present BEFORE Bb produces its biofilm,

a LOT of *removal* of hydrogen would happen.

The pH would go up...way up. As shown in the cancer cell picture.

This sort of goes along with the WFL that eats a lot of very acidic insects.

There has to be a way for it to counter those acids.

It is interesting that the latest cancer therapies involve PROTON therapy i.e., + charges, not - charges.

Now Bb can indeed live in a wide pH range, but there is a limit even for it.

Remember how IL 1B is upregulated (interleukin 1 beta)?

Well...

Caspase-1,is located inside the cells. Caspase-1 was known as an

interleukin-1β converting enzyme.

"MitoQ inhibits caspase-1 activation"

There are actually 3 types of cell death:

Apoptosis Pyroptosis Necrosis

In lyme disease, the middle one - pyroptosis - is in full swing with the inflammatory cytokines released and the Th1 pathway kicks in.

The activated macrophages resist dying (apoptosis) which makes them a nice "home" for Bb.

Berberine chloride triggers apotosis and lowers the inflammatory cytokines without involving capases (capase independent).

http://www.ncbi.nlm.nih.gov/pubmed/19669998

Now back to MitoQ and capase-1 (triggered by capase 11).

If we inhibit capase-1, does that permit the survival of Bb?

Be sure to read this to the end:

Pyroptosis acts as a defence mechanism against infection by inducing pathological inflammation.

The formation of inflammasome and the activity of caspase-1 determine the balance between pathogen resolution and disease pathology.

In a healthy cell, caspase-1 activation helps to fight infection caused by Salmonella, Shigella via introducing cell death to restrict pathogen growth.

When the ‘danger’ signal is sensed, the quiescent cells will be activated to undergo pyroptosis and produce inflammatory cytokines IL-1β and IL-18.

IL-18 will stimulate IFNγ production and initiates the development of TH1 responses.

(TH1 responses tend to release cytokines that direct an immediate removal of the pathogen).

The cell activation results in an increase in cytokine levels, which will augment the consequences of inflammation and this, in turn, contributes to the development of the adaptive response as infection progresses. The ultimate resolution will clear pathogens.

In contrast, persistent inflammation will produce excessive immune cells which will be detrimental.

If the amplification cycles persist, metabolic disorder, autoinflammatory diseases and liver injury associated with chronic inflammation will take place.

Metabolic disorder

The level of expression of NLRP3 inflammasome and caspase-1 has direct relation with the severity of several metabolic syndromes, such as obesity and type II diabetic mellitus (T2DM).

This is because the subsequent production level of IL-1β and IL-18, cytokines that impairs the secretion of insulin, is affected by the activity of caspase-1.

Glucose uptake level is then diminished, and the condition is known as insulin resistance.

The condition is further accelerated by the IL-1β induced destruction of pancreatic β cells.

Recent studies demonstrated that caspase-1-mediated pyroptosis

drives CD4 T-cell depletion and inflammation by HIV,

two signature events that
propel
HIV disease progression to AIDS.

Pyroptosis appears to create a pathogenic vicious cycle in which dying CD4 T cells release inflammatory signals that attract more cells into the infected lymphoid tissues to die and to produce chronic inflammation and tissue injury.

It may be possible to break this pathogenic cycle with safe and effective caspase-1 inhibitors.

These agents could form a new and exciting ‘anti-AIDS’ therapy for HIV-infected subjects in which

the treatment

targets the host instead of the virus.

Of note, Caspase-1 deficient mice develop normally, arguing that inhibition of this protein would produce beneficial rather than harmful therapeutic effects in HIV patients.

http://en.wikipedia.org/wiki/Pyroptosis

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Thanks for the post, it makes so much sense and can explain why certain mono-protocols do not work for chronic Lyme.

So if we lined them up and worked from best to modest, what reduces inflammation?

There are numerous approaches but can they be listed in order of effectiveness?

Can we actively reduce the inflammation or do we shave to reduce instances of becoming inflamed?

Infrared sessions, acupuncture, rife, lower sugar diets, heat packs, detox, and numerous other methods are available but are they significant enough to work with the bug and virus killers if we have been sick for quite a while?

All the Best, MattH

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In addition to the above...

Notice the yellow laser targets this complex:

Succinate Dehydrogenase (= Complex II)

The WFL's blue belly...

Blue ABSORBS yellow wavelengths!

Blue corresponds to #8 position on a clock and the element oxygen. Yellow corresponds #2 and the element helium. Yellow is a primary subtractive color and blue is a primary additive color.

Repeating...blue absorbs yellow.

Now about waves and the yellow laser wavelength,

594 nm.

Imagine you are a surfer and the wave transports you somewhere (to the coast) just as...

Light waves *transfer energy

to the electrons*.

Succinate is a electron donor.

Dehydrogenases transfers hydrides (= hydrogen with

one extra electron

i.e., normally hydrogen has one + and one -, but hydrides contain an extra electron making hydrogen negative, not neutral).

In the picture here:

http://en.wikipedia.org/wiki/Succinate_dehydrogenase

See "Q" in the picture of Complex II ?

Uhm...that is MitoQ which is "Q" plus a transporter that functions LIKE phosphatidylcholine.

This is all about electron transport and lightwaves that

transfers energy

to the electrons.


ATP synthesis is not an energetically favorable reaction: energy is needed in order for it to occur.

Nutrients provides *biochemical energy* that we use to make our ATP. Energy can be transferred or converted, but is never created or destroyed and it is always in balance with mass/matter.

That biochemical energy came from light energy.

It takes light to grow plants to feed animals which we need to survive.

Without light...no biochemical nutrients which we need to make OUR ATP.

And directly, sunlight helps us to make vitamin D and the absence of light (as night approaches) triggers the conversion of serotonin to melatonin,etc.


Gotta log off - big electrical storm.

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lymie_in_md
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Marnie,

Another reference.

http://cdn.intechopen.com/pdfs-wm/40930.pdf

copy the below table and use a courier font in word or wordpad. it doesn't display well otherwise.

quote:
Enzyme Clinical presentation
=================== =======================================
Fumarase Progressive encephalopathy
Hereditary leiomyomatosis and
renal cell cancer

Malate dehydrogenase Alzheimer’s disease

Citrate synthase No disease identified so far

Aconitase No disease identified so far

Isocitrate dehydrogenase Low-grade gliomas

-Ketoglutarate Congenital lactic acidosis
dehydrogenase

Succinyl-CoA ligase Encephalomyopathy with mtDNA depletion

Succinate dehydrogenase Encephalopathy (Leigh syndrome)
Pheochromocytoma and paraganglioma



--------------------
Bob

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Robin123
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Another interesting tidbit about light and us - our cells have a compound called neuromelanin in them, which absorbs light, just as plants have their chlorophyll compound that absorbs light for their photosynthesis.

The neuromelanin compound is similar in structure to silicon chips in that they're sandwiched.

Our bodies are actually operating at the speed of light in some ways...

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Matt, I know this is all fancy science here, but in answer to your question about reducing inflammation, yes, by all means, with anti-inflams. Turmeric, mangosteen juice, noni juice and grapeseed extract are all working very well for me.
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Marnie
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Photodynamic therapy = PDT
Hypericin = HY

However, the cellular and molecular mechanisms underlying the role of PDT in facilitating tumor cell

***apoptosis***

remain ambiguous.

Experimental results showed that interleukin (IL)-6 was significantly increased
in
all HY-PDT-treated cells, especially in 1 μg/ml HY-PDT, resulting in cell death.

http://www.nature.com/cddis/journal/v4/n6/full/cddis2013219a.html

Mitoquinone (MitoQ) is a synthetically modified, redox-active ubiquinone compound that accumulates predominantly in mitochondria.

We found thatMitoQ is 30-fold more cytotoxic to breast cancer cells than to healthy mammary cells.

MitoQ treatment led to irreversible inhibition of clonogenic growth of breast cancer cells

through a combination of autophagy and

***apoptotic***

cell death mechanisms.

http://www.ncbi.nlm.nih.gov/pubmed/20805228

Remember I found this:

There are actually 3 types of cell death:

Apoptosis Pyroptosis Necrosis

In lyme disease, the middle one - pyroptosis - is in full swing with the inflammatory cytokines released and the Th1 pathway kicks in.

Macrophages are the ultimate hide-out too since they are very resistant to death and upregulate glycolysis.

Autophagy:

Autophagy also plays a housekeeping role in removing misfolded or aggregated proteins, clearing damaged organelles, such as mitochondria, endoplasmic reticulum and peroxisomes, as well as

eliminating intracellular pathogens

http://www.ncbi.nlm.nih.gov/pubmed/20225336

BTW...the alkaloid, berberine also triggers apoptosis!

http://www.plosone.org/article/info%3Adoi%2F10.1371%2Fjournal.pone.0036418

[ 07-09-2014, 10:49 AM: Message edited by: Marnie ]

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Marnie
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Bob, Figure 1 in the link...the TCA cycle is indeed upregulated as bacteria also look to use this cycle...succinate...

Before I go into this...the yellow laser maybe transporting 2 hydrogens...each with a proton and an electron. Basically the net is 2 protons and 2 electrons.

The ability to donate ONE electron (versus two) at a time maybe important.

"The isoalloxazine ring system of FAD or FMN

can accept *one or two* electrons,

in contrast to NAD, which can only be reduced by

two electrons at a time."

http://guweb2.gonzaga.edu/faculty/cronk/biochem/F-index.cfm?definition=FAD

Let's back up...

Bacteria use the isoprenoid-containing compounds ***ubiquinone*** and menaquinone in their electron transport chains (Gennis and Stewart, 1996).

SQR (succinate dehydrogenase) possesses three iron-sulfur clusters that mediate transfer of electrons

from FADH2

to ubiquinone (which bacteria use),

reducing the latter to ubiquinol (anti-oxidant):

FADH2 + Q (ubiquinone) → FAD + QH2 (ubiquinol)

Thus if Bb is dependent on ubiquinone and the WFL produces a LOT of succinate dehydrogenase this may =

ubiquinone deficiency for Bb

because the WFL's available ubiquinone would be converted

to ubiquinol (and FAD)


Without ubiquinone,

we can’t MAKE CoQ10...or more appropriately ubiquinol, in OUR mitochondria.

Now...get this...biofilms contain succinate dehydrogenase (complex II mitochondrial protein).

Now it seems odd we would TAKE a supplement containing ubiquinone (as MitoQ) since plasma levels of ubiquinone are already high and are an indication of oxidative stress

and especially since Bb looks to also need and use ubiquinone.

I think what we are doing is restoring a very critical nutrient that our mitochondria need, and Bb is depleting (among MANY others!).

The MitoQ formulation is quinone attached to a carrier (that functions like phosphatidylcholine - but isn't) that targets delivery of ubiquinone directly the mitochondria where they take it up and convert it to the anti-oxidant, ubiquinol.

This allows it (ubiquinol) to neutralize free radicals that accumulate

within the mitochondria.

In healthy persons the ratio of ubiquinol to ubiquinone is about 95/5 in human plasma.

In sick people ubiquinone is up as a marker of oxidative stress.

"A significant increase in the oxidized form (ubiquinone-10) content was observed in plasmas of patients with hepatitis, cirrhosis, and hepatoma when compared with normal subjects, suggesting increased oxidative stress in these patients.

http://www.ncbi.nlm.nih.gov/pubmed/9266509

Remember...

SQR (succinate dehydrogenase) possesses three iron-sulfur clusters that mediate transfer of electrons

from FADH2

to ubiquinone, reducing the latter to ubiquinol.

We can try to replace all the nutrients Bb is depleting from us...all the vitamins, several minerals, several amino acids,

but

it appears starving the mitochondria of ubiquinone (which it converts into ubiquinol) is extremely harmful to those cells that are infected. How can a cell do its job if its "engines"/ powerhouses aren't firing on all cylinders?

Just like our car engines don't work without oil, our mitochondria can't work without ubiquinone.

It is a transportation problem since one of Bb's proteins IS phosphatidylcholine. We had to come up with something that FUNCTIONS LIKE phosphatidylcholine, but isn't (as a carrier).

***

AD is now (2104) linked to a genetic mutation passed from family member to family member called
V44M and V44A.

The mutation V44M and V44A increase Aβ42/Aβ40 ratio.

V44M and V44A open up T48 for the initial
ε-cleavage
by γ-secretase.

The change in Aβ product line preference towards Aβ42 by FAD mutations increases Aβ42/Aβ40 ratio. (AB42 up)

Gamma secretase complexes have also been observed
localized to the mitochondria,
where they may play a role in promoting apoptosis.

One of the gamma secretase inhibitors is...get this...cortisone.

But cortisone depletes vitamin A and a vitamin A deficiency upregulates ...get this...liver ubiquinone levels.

Which is probably why taking cortisone (before antibiotics) isn't good if one has lyme.

The influence of feeding a fat-free diet, and of the administration of cholesterol, on the metabolism of ubiquinone in rat liver was investigated.

It was observed that in advanced essential fatty acid (EFA) deficiency

the concentration of ubiquinone was increased about twofold.

Administration of cholesterol in the diet resulted in a marked depression in ubiquinone con centration."

http://jn.nutrition.org/content/84/4/401.full.pdf

This link is really mind blowing (just read the beginning!!!):

http://www.ias.ac.in/jarch/jbiosci/11/391-397.pdf

Most types of cells can utilize fatty acid as a fuel except for the cells of the brain.

When the cells of the liver

utilize fatty acid in their mitochondria,

they generate chemicals called ketone bodies. The ketones then enter the blood stream.

And one ketone called BHB can cross the BBB and enter the cells' citric acid cycle to generate ATP.

Excess glucose -> "fatty liver" (seen sometimes on an ultrasound, but always on a CT scan).

According to Wiki:

The ability of MitoQ to decrease mitochondrial oxidative damage and thereby improve the outcome of the pathology has been assessed

in vivo

in a number of murine disease model following the oral or intraperitoneal administration of MitoQ.[3]

These include models of the following disorders: Alzheimer’s Disease,[27]
Parkinson’s Disease,[28]
hypertension,[29]
type I diabetes,[30]
heart attack,[31]
sepsis,[32]
fatty liver disease,[26][33]
the metabolic syndrome,[34][35]
alcohol induced steatohepatitis,[36]
protection against doxorubicin[37]
and cocaine[38] cardiotoxicity
and in organ preservation for transplantation.[39]

These findings are consistent with mitochondrial oxidative damage being a potential therapeutic target in a range of human diseases and pathologies, particularly those degenerative diseases associated with ageing.

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Marnie
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Repeating a critical point:

Bacteria use the isoprenoid-containing compounds ***ubiquinone and menaquinone*** in their electron transport chains (Gennis and Stewart, 1996).

BACTERIA USE UBIQUINONE.

Keep reading to see where ubiquinone happens.

SQR (succinate dehydrogenase) possesses three iron-sulfur clusters that mediate

transfer of electrons

from FADH2 to ubiquinone (which bacteria use),

reducing the latter to ubiquinol (anti-oxidant):

FADH2 + Q (ubiquinone) → FAD + QH2 (ubiquinol)

In other words, bacteria use ubiquinone and convert it to ubiquinol to use as anti-oxidant protection.

But Bb and company effectively "robs" OUR mitochondria of ubiquinone.

If Bb is dependent on ubiquinone and the WFL produces a LOT of succinate dehydrogenase (ubiquinone to ubiquinol) this may =

***ubiquinone deficiency for Bb***

because the WFL's available ubiquinone would be converted

to ubiquinol (and FAD)via a LOT of succinate dehydrogenase.

Restore MITOCHONDIAL targeted ubiquinone using

MitoQ

which IS ubiquinone CONJUGATED TO a chemical that FUNCTIONS LIKE, but is not...phosphatidylcholine.

(One of Bb's proteins IS phosphatidylcholine.)

According to Wiki...the list of diseases MitoQ may help is amazing.

Talk to your doctor about this and if you decide to try it and your doc agrees, give it time (months) and go SLOWLY...follow the recommended directions as to dosage and timing.

[ 07-14-2014, 10:25 AM: Message edited by: Marnie ]

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lymie_in_md
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Marnie ... ubiquinone supplementation along with st john wort and this combination with the use of a Yellow LED ... also might include adding living foods and sungazing to the list. Would you recommend all this based on the science. I always believed if we found a holy grail, we could create a control study with a sponsoring LLMD.

Marnie please correct anything I've stated. It reminds me of when several folks went to Germany and discovered biophotons and some actually went into remission from the disease. (hi Six [Smile] )

I know not everyone is going to see any merit in this proposal. And many of the LLMDs are becoming more alternative every day. So I'm sure there is interest.

So my question to the site: is there any merit to taking the next step ? And how do we do it ? And who would want to do it ?

>> I can't participate, I'm already well

I would like to thank my great friend Marnie for the excellent work she did to piece this together. She is truly a lyme warrior.

--------------------
Bob

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Bob, I would NOT suggest St. John's Wort.

Potential photosensitivity = eye damage.

"Hypericin is known to cause phototoxicity."

The Yellow Laser + INTRAVENOUS hypericin (a component OF STJW) is far different than...

Swallowing St.John's Wort which contains some hypericin.

I'm not surprised they are using a light wave to hit Bb and I'm not surprise they are using yellow because cyan absorbs yellow and the WFL's blue belly is indeed cyan colored (unique).

Supposedly Bb is NOT photosynthetic.

Wanna bet?!!!

Follow this:

2013

Borrelia burgdorferi gene product BB0323 is required for cell fission and

pathogen persistence in vivo.

Here, we show that BB0323, which is conserved among globally prevalent infectious strains, supports normal spirochaete growth and morphology even at early phases of cell division.

http://www.ncbi.nlm.nih.gov/pubmed/23489252

BB0323 cyaC cyclolysin
-activating lysine-acyltransferase

membrane-bound adenylate cyclase CyaC…

(Adenylate cyclase does this: ATP -> cAMP + pyrophosphate or written like this: ATP → AMP + PPi)

The CyaC protein, a

***cyanobacterial***

adenylate cyclase,

has a unique primary structure composed of the catalytic domain of adenylate cyclase

and the conserved domains of bacterial two-component regulatory systems, one transmitter domain and two receiver domains

http://www.jbc.org/content/274/21/15167.full

Cyanobacteria also known as Cyanophyta, is a phylum of bacteria that obtain their energy through

photosynthesis.

Wiki.

Hypercinin is red...those who own red cars in Florida know how quickly that color fades (is oxidized). Ahh...those UVB damaging rays!

Hypericin is a naphthodianthrone, a

red-colored

anthra *quinone* (Q)

-derivative

Red corresponds to Magnesium and the #12 = 12th element.

(In fireworks, Mg can be lit to produce a very bright light. "Magnesium burns a very bright white, so it is used to add white sparks or improve the overall brilliance of a firework.")

On a color wheel that is numbered like a clock, #6 = ***cyan*** blue is directly opposite and
it corresponds to the element

Carbon.

“Because hypericin accumulates preferentially in cancerous tissues, it is also used as an indicator of cancerous cells.” Wiki

Now cancer cells use glucose for energy and glucose IS a

carbon chain....adding to the complexity...

"glutamate carbon

to fatty acid carbon via citrate"

That might account for red hypercinin accumulating in glucose-driven cells or those with high levels of glutamate?

About the yellow laser...work in progress...

Start with:

we KNOW, FOR FACT, Bb needs Na (sodium) for its ATPase and NaCl for motility...now look at this:

“New *589 nm* yellow laser pointers have been introduced using a more robust and secretive method of harmonic generation from a DPSS laser system.

***This 'sodium' wavelength,***

although only 4.5 nm away from the older 593.5 nm, appears more gold in colour compared to the more amber appearance of the 593.5 nm wavelength.

Ahh...remember how gold was used as a potential treatment for RA years ago?

Anyway...

Some weird facts about sodium, the element:

What's in a name? From the English word soda and from the Medieval Latin word sodanum, which means

"headache remedy."

Liquid sodium has been used as a *coolant* for nuclear reactors.

Cool/apply cold...as in anti-inflammatory...more alkaline, raise blood pH?

Bb looks to rely on losing and gaining electrons.

This is called redox = reduction and

oxidation. Here's how to remember it:


"LEO the lion says GER".

Lose Electrons in Oxidation (L, E, O)

Gain Electrons in Reduction. (G, E, R)

The above help Bb's protein folding which is absolutely necessary for replication.

"These results provide direct in vivo evidence that correctly folded protein is achievable via cycles of oxidation and reduction."

http://www.ncbi.nlm.nih.gov/pubmed/19968787/

If DNA is the information of life, then proteins are the machines of life-- but they must be assembled

and correctly folded

to function.

A key step in the protein-folding pathway is the introduction of

***disulphide***

bonds between cysteine residues in a process called

oxidative protein folding.

Many bacteria use an oxidative protein-folding machinery to assemble proteins that are

essential for cell integrity

and to produce virulence factors.

http://www.researchgate.net/publication/23986118_DSB_proteins_and_bacterial_pathogenicity

The 2 proteins involved are: DsbA and DsbB...disulfide bond A and disulfide bond B.

Pay attention to ubiquinone and menaquinone...

"In bacteria, ubiquinone and menaquinone are involved in electron transport, while bactoprenols act as carbohydrate carriers in the biosynthesis of peptidoglycan."

"The oxidized form of the quinone

*electron carriers* ubiquinone and menaquinone..."

http://stock.cabm.rutgers.edu/blast/review.pdf


"On his turn, DsbB is reoxidized by

transferring electrons to oxidized *ubiquinone*,

which passes them to cytochrome oxidases, which finally reduce oxygen;

this is in aerobic conditions.

As molecular oxygen serves as the terminal electron acceptor in aerobic conditions,

oxidative folding is conveniently coupled to it through the respiratory chain.

In anaerobic conditions however,

DsbB passes its electrons to *menaquinone*, followed by a transfer of electrons to fumarate reductase or nitrate reductase.


In anaerobic conditions however, DsbB passes its electrons to *menaquinone*, followed by a transfer of electrons to fumarate reductase or nitrate reductase.

Because of the property of Ero1p to transfer electrons directly to molecular oxygen via a flavin-dependent reaction,

its activity may produce reactive oxygen species (ROS).

In bacteria, this problem is solved by

***coupling oxidative folding to the respiratory chain.***

There, the reduction of molecular oxygen to water is carried out by a complex series of proteins, which catalyse this reaction very efficiently.

In eukaryotes (us),

***the respiratory chain is

separated from oxidative folding***

since cellular respiration

takes place in the mitochondria

and the formation of disulfide bonds occurs in the ER.

Because of this, there is much more risk that ROS are produced in eukaryotic cells during oxidative folding.

As is known these ROS may cause many diseases such as atherosclerosis and some neurodegenerative diseases."

http://en.wikipedia.org/wiki/Oxidative_folding

About disulfides...that Salp 15 Bb picks up in the tick's saliva = alkaline phosphatase...

"Another example is alkaline phosphatase, which contains two essential *disulfides*…"

"serum alkaline phosphatase (SALP) [15]"


Ancora Imparo! Translation = I am still learning.

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lymie_in_md
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how about hypericin patches instead of IVs ? Seems like it would be more convenient... I hate IVs.

--------------------
Bob

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Edited...caution!!!

"Most readers will be aware that Hypericum is capable of causing photophobia of the eyes if ingested repeatedly in quantity

and that Hypericum can cause horrendous burns if it is used topically on the skin and is followed by exposure to strong direct sun.

Current research is revealing that the same mechanism responsible for photosensitivity may also lend Hypericum anticancer and antiviral properties (discussed briefly herein in the section on “Photosensitizing Coumarins and Antiviral Effects”).

Hypericin in Hypericum is the most potent natural photosensitizer known.

When rubbed into the skin, the absorption of UV light may increase dramatically

so as to induce third-degree burns.

The skin and eyes can also become more sensitive to light with oral ingestion if Hypericum flavonoids are consumed in quantity.

As with Lomatium and furanocoumarins of the Apiaceae family,

this photophenomenon may also lend Hypericum antiviral activity, as viruses can be subdued due to interactions with hypericin and viral protein as they pass through cutaneous blood vessels, close enough to the skin’s surface to be affected by UV light.

Furthermore, hypericin

generates large quantities of singlet oxygen

and other reactive oxygen species when exposed to UV light,

which is thought to be a mechanism by which this photodynamic therapy damages cells.

The topical use of Hypericum oil may also be combined with UV light as a complementary therapy for psoriasis and vitiligo, taking care not to overdue the UV light or natural sunshine and cause harm.

The research will be saved for a future article, but owing to these same mechanisms, Hypericum is also being explored for treatment of internal epithelial cancers where fiberoptic light can be delivered locally, such as bladder cancer and esophageal cancers.

In fact, many cancer cell types seem to intensely take up and concentrate hypericin.

Researchers have reported some initial success, and we can expect more investigations to be published in the coming decade.

One research group has described their success with pituitary adenomas in rats using simple visual spectrum light via the eyes."

https://ndnr.com/naturopathic-news/photosensitizing-coumarins-for-skin-diseases-and-cancers/

[ 07-14-2014, 10:31 AM: Message edited by: Marnie ]

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Marnie
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Up.

Read the warnings above about trying this yourself (topical) or even large doses of STJ'W.

Germany is a nice country to visit in the summer.

Yes, I know...we shouldn't HAVE TO.

But I bet there will be some LLMD's who will be going to Germany to learn...

[ 07-14-2014, 11:19 AM: Message edited by: Marnie ]

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Marnie
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Up...this is a REAL treatment that appears to be ***VERY SAFE*** (compared to ICHT) to treat MANY diseases, including cancers.

That is not to say there aren't other ways to accomplish the same!

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lymie_in_md
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If you use hypericum topically you could use it in areas of the body where the sun can't get to. I guess nudists would have to wear clothing for a while. [lol]

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aheadbehind
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I'm new to the forum. Just read through this thread and I'm intrigued by the hypericin + yellow laser concept. Does anyone have any updated info on this? Anyone tried it yet?
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poppy
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Well, I didn't understand a word of it, so you are ahead of me.
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bitbit99
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I'LL go for a big fat DUH on this..... and I have both cancer and lyme....So Not only should I stayed out of the woods but should have stayed in school to boot.
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Tincup
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I tried it. I saw no difference at all. Just my experience.

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tonesg
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quote:
Originally posted by Tincup:
I tried it. I saw no difference at all. Just my experience.

Short and to the point, kind of makes me wish they put your comment first, would have probably saved a lot of slogging through some of those War and Peace posts.
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Tincup
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Don't give up. I tried it again a couple of days ago. The doc said it can take several treatments to see a difference. We`ll see.

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lymeboy
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"So my question to the site: is there any merit to taking the next step ? And how do we do it ? And who would want to do it ?"


I'd do it if I had $$ but I do not. I'm willing to be a test subject if they'd have me.

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