LymeNet Home LymeNet Home Page LymeNet Flash Discussion LymeNet Support Group Database LymeNet Literature Library LymeNet Legal Resources LymeNet Medical & Scientific Abstract Database LymeNet Newsletter Home Page LymeNet Recommended Books LymeNet Tick Pictures Search The LymeNet Site LymeNet Links LymeNet Frequently Asked Questions About The Lyme Disease Network LymeNet Menu

LymeNet on Facebook

LymeNet on Twitter




The Lyme Disease Network receives a commission from Amazon.com for each purchase originating from this site.

When purchasing from Amazon.com, please
click here first.

Thank you.

LymeNet Flash Discussion
Dedicated to the Bachmann Family

LymeNet needs your help:
LymeNet 2020 fund drive


The Lyme Disease Network is a non-profit organization funded by individual donations.

LymeNet Flash Post New Topic  New Poll  Post A Reply
my profile | directory login | register | search | faq | forum home

  next oldest topic   next newest topic
» LymeNet Flash » Questions and Discussion » Medical Questions » Look closely at 2 photos - short and long versions

 - UBBFriend: Email this page to someone!    
Author Topic: Look closely at 2 photos - short and long versions
Marnie
Frequent Contributor (5K+ posts)
Member # 773

Icon 1 posted      Profile for Marnie     Send New Private Message       Edit/Delete Post   Reply With Quote 
Short version:

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

(pink picture) Leishmania

and

http://www.iadvocatehealth.org/protozoal_infection0.aspx

(blue picture)

What do you think?

Do they look identical/extremely similar to you?

Leishmania (first picture) produces a biofilm and is a protozoa parasite.

It also lives within macrophages (think of them as "pac men" of our immune system).

"Leishmania as component of CVBD
= Canine Vector-borne Diseases (CVBD) covers diseases caused by pathogens transmitted by

ectoparasites such as

ticks, fleas, sand flies or mosquitoes.

Other microorganism-based diseases caused by ectoparasites include Bartonella, Borrelia, Babesia, Dirofilaria, Ehrlichia, and Anaplasma."

"Leishmania cells have two morphological forms: promastigote (with an anterior flagellum in the insect host, and

amastigote (without flagella) in the vertebrate host."

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

(read more about it in the above link)

It is *logical* that Leishmania could accompany Bb given the vectors.

And yes, that pathogen produces a biofilm too (so do some of our "good guys" in our intestine!). It serves a purpose:

http://www.ncbi.nlm.nih.gov/pmc/articles/PMC1563644/

How to treat (besides the obvious i.e., drugs)?

http://www.ncbi.nlm.nih.gov/pmc/articles/PMC3071726/


*********** Longer version for those who chose to continue reading.


Re: biofilms

(which are PRIMARILY ***polysaccarides and proteins***),

but do include some other things like DNA, lipids, and "humic" substances.

Here is a common infection - problem re: the trapping of minerals IN biofilm:

http://jmm.sgmjournals.org/content/54/9/807.full

In the above note it is not Mg (alone)in biofilms, but is

crystals of *magnesium ammonium phosphate*

and

*calcium phosphate*.

"Iron and zinc ions are both important in the formation of biofilms of sugar-coated
bacteria."

http://www.nasw.org/users/mslong/2009/2009_07/Biofilms.htm

Additional:

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


Bb�s LuxS gene which it uses for quorum sensing (i.e., �communication) is Fe (iron) dependent:

http://iai.asm.org/content/70/8/4099.abstractS-

Ribosylhomocysteinase (LuxS) Is a Mononuclear Iron Protein

http://pubs.acs.org/doi/abs/10.1021/bi034289j

I will separate the word above

(ribosylhomocysteinase) for a reason;

Ribosyl homocysteinase.

Now look closely at Bb's toxin:

BB0755, a 37 kD protein of unknown function.

They call it Bb tox1. It is a protein of UNKNOWN FUNCTION, but


it appeared (exhibited) to have ADP-

ribosyl transferase activity

�which makes the cells ***susceptible to *** death.

http://www.actionlyme.org/Donta.htm


(I suspect Bb�s toxin is like that of botulism i.e., C3-ADP-ribosyltransferase.)


When Bb is camped out in the tick's stomach, it does not produce a biofilm.

Bb expresses OspA = outer surface protein A, in the tick and this is what Bb needs:

cGMP = Cyclic di-GMP is Essential for the Survival of the Lyme Disease Spirochete in Ticks

http://www.ncbi.nlm.nih.gov/pmc/articles/PMC3128128/

The cyclic dinucleotide c-di-GMP regulates lifestyle transitions in many bacteria, such as

the change from a

free motile state

***to a biofilm-forming community. ***

***Riboswitches*** that bind this second messenger are important downstream targets in this bacterial signaling pathway.

http://www.ncbi.nlm.nih.gov/pmc/articles/PMC3257324/

cyclic di-GMP = a tiny cycle of RNA, containing only two guanine bases linked by ribose and phosphate.

In bacteria, certain signals are communicated by synthesizing or degrading cyclic di-GMP.

Degradation of cyclic di-GMP is effected by proteins with phosphodiesterase (PDE) activity.

http://en.wikipedia.org/wiki/Cyclic_di-GMP

I think the PDE�PDE6 is implicated because of this:

http://www.ncbi.nlm.nih.gov/pubmed/21439020

http://www.nature.com/ijir/journal/v16/n1s/full/3901212a.html


Riboswitches are conserved regions of mRNA (messenger RNA).

Riboswitches are widespread in bacteria, whereas they appear to be less common in eukaryotes.

So far, no riboswitches have been identified in animals, and due to their role in regulating vital cellular processes, they are potential targets for antimicrobial drugs.

http://www-abell.ch.cam.ac.uk/research/Riboswitches.html

curious what "vitamins" the researchers are looking at binding riboswitches!

***Cyclic di-GMP-II riboswitches*** are a *pseudoknotted structure* = a "folding" (sort of).

So when exposed to our blood as the tick feeds Bb uses what is called a "riboswitch" and

on "his" way out, expresses OspC which grabs onto of SALP15 (a "sugary" protein) and another really bad (for us) protein called p8 which prevents our immune system from fully chopping Bb all of Bb's proteins up (inhibits the lectin pathway).

That �riboswitch� maybe the way Bb alters �his� Osp(s)�perhaps.

RNA molecules form pseudoknots.

RNA is made up of a long chain of components called nucleotides. Each nucleotide consists of a nucleobase (nitrogen-based molecules), ***a ribose sugar,*** and a phosphate group.

The sequence of nucleotides allows RNA to encode genetic information. All cellular organisms use messenger RNA (mRNA) to carry the genetic information that directs the synthesis of proteins.

In addition, many viruses use RNA instead of DNA as their genetic material.

(Nucleobases include adenine, guanine, etc.)

GMP consists of the phosphate group, the pentose sugar ribose, and the nucleobase *guanine.*

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

The Tick Salivary Protein, Salp15, ***Inhibits the Development of Experimental Asthma***

Activation of Th2 CD4+ T cells is necessary and sufficient to elicit allergic airway disease, a mouse model with many features of human allergic asthma.

http://www.jimmunol.org/content/178/11/7064.abstract?ijkey=b45e1fd4f1b7afab4fa3654892fcc0e75352b194&keytype2=tf_ipsecsha


It would appear the activation of Th2 CD4+ T cells maybe inhibited because of SALP15.

What lyme patients *and* MS patients need to happen is a very specific antibody called IgG1k.

The "k" (kappa - light chain) is important...very. It doesn't happen.

The target for IgG1k is IgE � Fc region.

The fragment crystallizable region (Fc region) is the tail region of an antibody that interacts with cell surface receptors called Fc receptors and some proteins of the complement system.

This property allows antibodies to activate the immune system.

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


Now�about the Fc region/fragment:

Our antibody to Bb�s Osp B was �damaged� (our "original" from which we make copies was not correct):

A confocal microscopy study was undertaken to characterize the bactericidal effects of the Fab fragments of CB2, an immunoglobulin

***G1kappa***

murine monoclonal antibody�

http://www.ncbi.nlm.nih.gov/pubmed/9125579


This I. scapularis (me = deer tick) sphingomyelinase-like (IsSMase) protein is a Mg+2-dependent, neutral (pH 7.4) form of sphingomyelinase.

Furthermore, a Th2 response (me�rash/allergic response) is superimposed onto a ***virally-primed Th1 response*** by IsSMase.

http://www.ncbi.nlm.nih.gov/pmc/articles/PMC2748904/


Oftentimes (but not always) a Th2 response happens first i.e., the typical lyme rash i.e., allergic response THEN the bad response...Th1 response in response to a viral protein.

It would appear p8 is a viral protein.

"Our findings show that basal p8 expression represses autophagy and

protects cells from autophagy-induced cell death."

http://www.landesbioscience.com/journals//KongAUTO6-5.pdf


Autophagy is an essential, homeostatic process by which cells break down their
own components.

If p8 is actually AKT8...

AKT8 = murine leukemia virus

which is a retroviral protein.

We know also for fact that MS is triggered by a �retroviral protein� called�
HERV-W-related retroelement, multiple sclerosis retrovirus (MSRV).

http://www.ncbi.nlm.nih.gov/pubmed/20696240 2011.

Look at the mention of anti-oxidants in the above link!

SOD is an anti-oxidant enzyme, a protein, with manganese attached.

I think a key one maybe Mn-SOD which Bb uses to protect �himself� from oxidative damage and OUR mitochondria (cell powerhouses) use too. Not enough Mn-SOD to go around � to protect our SELF?

ROS (reactive oxygen species) in cancer and other diseases:

http://online.liebertpub.com/doi/abs/10.1089/ars.2011.4414?journalCode=ars 2012.

NORMALLY our NK cells (natural killer) work by sort of �spitting� a free radical at pre-cancerous cells to kill them.

Unbelievable as it may seem�we make about 4 pre-cancerous cells every day (DNA damaged). BUT�NK cells can (and do) only work in an alkaline environment.

They shut off/numbers are decreased when we exercise and make a lot of acids�lactic, because it that case they are not needed.

While it is the job of NK cells to destroy DNA damaged pre-cancerous cells, AKT8 = anti-apoptotic kinase.

Anti-apoptotic = Something that prevents apoptosis. Apoptosis is a type of cell death in which a series of molecular steps in a cell leads to its death.

In many neurodegenerative diseases there are some bystander cells that take a hit.

They are called SY �undifferentiated cells� and they would have become wonderful cells if it were not for brain inflammation happening.

Bb is NOT TOXIC to brain cells, but inflammation IS. SY cells look to be�get this�STEM CELLS!

Taken together, these findings indicate that

B. burgdorferi is not directly toxic to SY cells;

rather, these cells become distressed and die in the inflammatory surroundings generated by microglia through a bystander effect.


http://www.plospathogens.org/article/info%3Adoi%2F10.1371%2Fjournal.ppat.1000659


The SY cells look to be undifferientated stem cells and as of this year, 2012�

Stem cells are now known to exist in the brain and heart too!

http://www.geosalud.com/stem_cell/adult_stem_cells.html

Probably not a good idea for brain inflammation to knock off brain stem cells!


Back to the beginning�Bb and Leishmania in macrophages.

Bb ferments glucose�to produce:

Borrelia can obtain energy from the fermentation of glucose to lactic acid, and the product of the BBB29 gene is presumably involved in transport of glucose into the cell..

http://www.ncbi.nlm.nih.gov/pmc/articles/PMC415784/

�were all found to produce ***L-alanine from glucose fermentation ***, in addition to acetate, lactate, CO2 and H2.

http://www.ncbi.nlm.nih.gov/pmc/articles/PMC168047/

(Lactate + H = lactic acid.)

In this study we have demonstrated for the first time the presence of the enzyme
***L-alanine***: 4,5-dioxovalerate transaminase in Leishmania donovani.

This enzyme catalyzes the synthesis of 5-aminolevulinic acid (ALA), the first committed step in *heme* synthesis.

http://www.ncbi.nlm.nih.gov/pubmed/8564368

Since Bb�s LuxS gene is

Ribosylhomocysteinase (LuxS) Is a Mononuclear ***Iron Protein*** (previously linked)

It would make sense they live in synergy and

it *maybe* that the anti-spirochetal, berberine (link follows) can also simultaneously knock off Leishmania which would be a really good thing.

http://lymepoland.com/pliki/LD-%20zio%C3%85%C2%82a.pdf


******************

Further links for any interested doctors or others:

***Nitric Oxide Regulated C-Di-GMP Synthesis and biofilm formation*** in�

http://www.nyas.org/Events/Detail.aspx?cid=00d694b2-227e-4e85-a125-78af2edff1d3

(hit next)

Structural Basis for c-di-GMP-Mediated Inside-Out Signaling Controlling Periplasmic Proteolysis.

http://www.plosbiology.org/article/info%3Adoi%2F10.1371%2Fjournal.pbio.1000588

See also:

http://jb.asm.org/content/194/16/4415.abstract

2012 and mention of tryptophan

http://jb.asm.org/content/early/2012/06/11/JB.00642-12.abstract

Pay close attention to the last sentence regarding which mineral to avoid/chelate -Using... concerning biofilm!

Find this (unable to link):

H-NOX regulation of c-di-GMP metabolism and biofilm formation in Legionella pneumophila


read the summary and keep in mind this regarding LuxS and Fe+2:

http://www.ncbi.nlm.nih.gov/pubmed?term=PMID%3A%2015450491%20

The Nitric Oxide-Cyclic GMP Pathway Regulates FoxO and Alters..

http://www.ncbi.nlm.nih.gov/pmc/articles/PMC3290610/

Then "Google": berberine FoxO

[ 08-06-2012, 07:14 AM: Message edited by: Marnie ]

Posts: 9481 | From Sunshine State | Registered: Mar 2001  |  IP: Logged | Report this post to a Moderator
Keebler
Honored Contributor (25K+ posts)
Member # 12673

Icon 1 posted      Profile for Keebler     Send New Private Message       Edit/Delete Post   Reply With Quote 
-
Yes, they certainly do look nearly identical.

1. Wiki site, take the L. photo, clinking to enlarge it and then pulling it off the site onto my desktop, opening then in a different window.

2. Same with the small blue photo at the Fry site, that transfers nicely to desktop.

3. Then both can be viewed, same size, side by side on computer screen.

Only major difference I see is the color stain, and a minor difference or two.

True, the clarity could improve with further magnification and other slide samples, etc. but it's a stunning similarity, indeed. Perhaps the same thing or a very close cousin?

If these could be see unstained, or with exact same color staining, wonder if they would have any color variations? Configuration, though, looks like twins.
-

Posts: 48021 | From Tree House | Registered: Jul 2007  |  IP: Logged | Report this post to a Moderator
Marnie
Frequent Contributor (5K+ posts)
Member # 773

Icon 1 posted      Profile for Marnie     Send New Private Message       Edit/Delete Post   Reply With Quote 
Yes, I too wish we had a more powerful magnification!

You do know about methylene blue (Rember - a drug) for Alzheimer's, right?

I asked Tom Grier...he said not safe.

Another piece of the puzzle "fits"...Tritec.

If citrates impact biofilms...Tritec is rantinidine bismuth CITRATE!

And a long time ago, researchers found Tritec is capable of destroying ALL FORMS OF Bb

in the GI tract only.

It is/was NOT SAFE to give any forms of bismuth (only 2 are safe for humans to take ORALLY) systemically. It was tried (for lyme).

Tritec is rantinidine (Zantac) bismuth citrate.

Zantac lowers the PRODUCTION OF our stomach acid...HCL.

By taking something that contains HCL, do we thus shut off our production of the same?

Bismuth is a very peculiar metal. It is used in...get this...magic acts for levitation! I studied it a long time ago in depth. It is the most diagmagnetic metal of all.

Oddly, silver can act similarly!

http://davidfiedler.com/levitation.htm


Apparently when Tritec was used, Bb forms ended up covered in "black".

I can dig for the link if anyone wants it.

We all know the black tongue and black stools that happen when we take Pepto bismol (a different form of bismuth).


Tritec, to my knowledge, though made by a U.S. company, is now only available in Europe, but could be compounded here by a compounding pharmacy.

It appears the company felt there was not enough demand for that drug here.

Back to AD...curious article!

http://www.psychologytoday.com/blog/complementary-medicine/201108/maybe-its-not-alzheimers

A friggin vitamin deficiency found in some patients dx'd with AD who did not actually have the protein tangles (autopsy)?

Uhm...about "riboswitches" and vitamins...the links being explored...same vitamin was mentioned! B12. Methyl...!

I'm going to have to take a very close look at B12 with relationship to c-di-GMP.

Benefits AND warnings as well as the THREE different forms of B12!

P.S. the difference between the 5 carbon sugar ribose and ribosyl is this:

Ribose = C5H10O5
Ribosyl = the radical C5H9O4 formed from ribose.

The difference is one hydrogen and one oxygen removed. OH? Hydroxide.

[ 08-06-2012, 09:26 AM: Message edited by: Marnie ]

Posts: 9481 | From Sunshine State | Registered: Mar 2001  |  IP: Logged | Report this post to a Moderator
Marnie
Frequent Contributor (5K+ posts)
Member # 773

Icon 1 posted      Profile for Marnie     Send New Private Message       Edit/Delete Post   Reply With Quote 
There is a reason why the color photos differ if the researchers are looking for leishmania (a protozoa parasite):

If the tap water is highly acidic, resulting in smear turning grossly pink

too fast or highly alkaline, resulting in the smear remaining too blue.

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


Leishmaniasis in rheumatoid arthritis:

http://www.ncbi.nlm.nih.gov/pubmed/17898884

http://www.blackwellpublishing.com/acrmeeting/abstract.asp?MeetingID=774&id=89345

Yes...that co-infection would potentially be a bad thing.

That said...my sis did not suffer the negative effects of Humira (TNF alpha inhibitor).

http://www.medicaljournals.se/acta/content/?doi=10.2340/00015555-0633&html=1 All you need to read is the first brief paragraph.

However, note the combination of drugs in the link above i.e., methotrexate, prednisone and the TNF-antagonist adalimumab (Humira).

Researchers from the Indian Institute of Technology, Guwahati found in lab studies that

the drugs killed the leishmania parasites by

inhibiting the activity of trypanothione reductase (TryR), the enzyme necessary for the survival of the parasite in host cells.

http://www.nature.com/nindia/2011/110321/full/nindia.2011.40.html

Further info. about that enzyme is here:

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

Posts: 9481 | From Sunshine State | Registered: Mar 2001  |  IP: Logged | Report this post to a Moderator
   

Quick Reply
Message:

HTML is not enabled.
UBB Code� is enabled.

Instant Graemlins
   


Post New Topic  New Poll  Post A Reply Close Topic   Feature Topic   Move Topic   Delete Topic next oldest topic   next newest topic
 - Printer-friendly view of this topic
Hop To:


Contact Us | LymeNet home page | Privacy Statement

Powered by UBB.classic™ 6.7.3


The Lyme Disease Network is a non-profit organization funded by individual donations. If you would like to support the Network and the LymeNet system of Web services, please send your donations to:

The Lyme Disease Network of New Jersey
907 Pebble Creek Court, Pennington, NJ 08534 USA


| Flash Discussion | Support Groups | On-Line Library
Legal Resources | Medical Abstracts | Newsletter | Books
Pictures | Site Search | Links | Help/Questions
About LymeNet | Contact Us

© 1993-2020 The Lyme Disease Network of New Jersey, Inc.
All Rights Reserved.
Use of the LymeNet Site is subject to Terms and Conditions.