Thinking I had typed all upper case and that might be the glitch, I re-entered "lyme" all lower case and got the same reply, in all upper case. So, it seems their search feature does not have any article to give me.
Do you have a link or at least the exact title of the article and maybe the author's name - for a better search?
Can you find that same article at their website?
They may not access their full paper on the web, I know, but just hoping to find out more. This is the only newspaper that some of my distant family members read. -
Posts: 48021 | From Tree House | Registered: Jul 2007
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Keebler
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posted
- Ah, Hah! A cross-search out of their site but through Google took me right back to them!
Fragments of Lyme Disease Bacteria Linger in Joints After Treatment
Excerpt:
. . . indicating the antibiotics eliminated the bacteria but not the residual debris. Spirochetes were found adjacent to ear cartilage in most of the mice.
These bacterial deposits were capable of triggering an inflammatory response but not a full-blown Lyme infection, the study showed. . . .
---------------------
It's so very sad that Yale's bottom line is still
"not a full-blown lyme infection" --- but that's about the best I'd expect from Yale, the great denier of chronic infection.
What we deal with is "JUST DEBRIS" in their eyes. -
Posts: 48021 | From Tree House | Registered: Jul 2007
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Keebler
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- The citation posted at the bottom of the WSJ article:
Published in Volume 122, Issue 7 (July 2, 2012) J Clin Invest. 2012;122(7):2652�2660. doi:10.1172/JCI58813. Copyright � 2012, American Society for Clinical Investigation
Research Article
Spirochete antigens persist near cartilage after murine Lyme borreliosis therapy
Linda K. Bockenstedt1, David G. Gonzalez2, Ann M. Haberman2 and Alexia A. Belperron1
1Department of Internal Medicine and 2Department of Laboratory Medicine, Yale University School of Medicine, New Haven, Connecticut, USA.
First published June 25, 2012
Received for publication October 24, 2011, and accepted in revised form April 24, 2012.
------------------------
Scroll all the way down � this appears to be the full research article. Read, copy & save now as access to this may be blocked soon. That often happens.
Still, it's not at all the kind of quality medical thought and research required for those who really want to learn about the chronic nature of borrelia infection.
They see only "DEBRIS" and think they are done. They've been done with lyme patients for years and are just trying to justify that. They still stop way short. -
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Keebler
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- Add to some of the thoughtful comments that have been posted here:
Some of us may have a standard "web name" (or alias) that we use and an email tied to that web name that we may use for such purposes where our privacy may matter. That may work here but I've not yet formulated a good reply to test it out.
The thing is, though, that readers of the actual hard copy paper won't see these comments unless one makes it as a "Letter to the Editor" later. -
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Keebler
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- Dan,
I forgot to say "Thank You" for posting this. Even if it's not good reporting, it's important that we know what they print.
We need to know so that we can hold a conversation about this with those in our lives who may think the WSJ is Cr�me de la Cr�me of truth. Sigh!
I was so hoping they might have gotten it right this time. -
Posts: 48021 | From Tree House | Registered: Jul 2007
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posted
Keebler, I had opened the journal link in a different window and just read it and came here to post - saw that you had found it and posted it - I should have done that from the beginning....sorry.
Posts: 277 | From NY | Registered: Jun 2005
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Keebler
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- No worries, Darlin' - I can barely do much else so consider this kind of tracing a brain exercise from time to time. I used to teach journalism so I really want to see what the media print -- it's just so sad, though. Still, your lead helps. Merci.
Wish I could formulate a proper comment to post but my brain just can't do that. Hope you and others can. -
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sparkle7
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I wonder if these bacterial deposits were forms of Lyme that can become active again in time... Maybe they didn't look at them long enough? With cysts, blebs, L-forms - the bacteria does seem to have many different forms.
It's kind of tiresome that they come out with these so-called scientific studies for something alot of people already know through experience. How many times are they going to reinvent the wheel before people are going to get proper care?
They have been studying this for a long time... I guess if it's in the WSJ, it means that someone is going to potentially make some money off of this info.
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RDaywillcome
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posted
It was also in the Hartford Courant in June.
Keebler
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posted
- Oh, no. RDay has spotted the first of the latest "take it and run" for news outlets. A rash will soon develop from this mis-information.
Sparkle, exactly, they are not looking at all the forms of lyme or considering anything besides their agenda of dismissal.
It's the over-used "artifact" reaction. If they don't know what it is or the full implications, it's just "noise" on the screen, so to speak.
Those poor mice did not need to suffer and die for this (you know they were killed to be able to inspect their deep ear structure as it can only be accessed by moving the brain)
but more people will suffer and die, too, if doctors really believe this poor attempt of a "study". -
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RDaywillcome
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So I was going to post a question very related to this so I'll do it here. I've been through several years of oral Abx and am left with the knee and lower back (facet) "arthritis" which feels like pain, stiffness and weakness in connective tissues (I guess its some kind of micro-inflammation that doctors say they can see on X-ray but I wonder). These are pretty much the only persisting Lyme symptoms I have and I'm contemplating trying IVs for several months (Rocephin + Mepron) to see if it will take care of this and get me back to 100%.
So can anyone comment on how effective IVs are for this kind of "cleanup". I'm worried about the yeast risks if there is low probability that IVs do what I hope.
Keebler
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posted
- Marshall,
The answer is likely very complex. There could still be infection connection, of course. Be sure to discuss this with an ILADS-educated LLMD.
However, for support, also consider some specific enzymes such as WOBENZYME . . . Lumbrokinase, boluoke . . . or serrapeptase. -
[ 07-31-2012, 06:18 PM: Message edited by: Keebler ]
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sparkle7
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Yeah, I know Keebler. They just keep regurgitating the same info in different formats. They need to leave the poor mice (or other animals) alone already.
Marshall62 - have you tried any anti-parasite protocols? Sometimes, they can help with residual pain. Alot of doctors are trying them now.
Posts: 7772 | From Northeast, again... | Registered: Oct 2006
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posted
I think what sparkle's referring to is parasite treatment with drugs like Ivermectin , Albenza, Biltricide or herb combinations using wormwood and cloves etc. A lot of people are having success adding these to their treatment. I was still having some stiffness and tightness and low-dose Ivermectin helps with that, so it must be hitting something.
There is also the traditional protozoa/parasite treatment with Mepron, Malarone, Lariam, Coartem etc.
Systemic enzymes are necessary for thinning the blood and dissolving biofilm. When I first started treatment, before antibiotics, and added systemic enzymes, the tightness in my legs immediately resolved. They're very important.
Something else that I've found recently is FlexNow. I've read a number of famous LLMD's recommend this product that was formerly known as BSP 201, made from shea. It down regulates cytokins and inflammation. I gave some to a friend with debilitating back pain, along with Metagenics Inflavanoid Intensive Care, and he had immediate improvement and sustains that recovery. He played golf and was jumping around like he hadn't in years.
Posts: 964 | From san diego | Registered: Oct 2009
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sparkle7
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Dr. K is recommending this from what I have gathered. I believe he designed a protocol in conjunction with Dr. Simon Yu. He's written a book about parasites & treatment called -
"A Vicious Cycle Involving Release of Heat Shock Protein 60 from Injured Cells and Activation of Toll-Like Receptor 4 Mediates Neurodegeneration in the CNS"
In contrast, SH-SY5Y (SY) neuroblastoma cells co-cultured with B. burgdorferi expressed
negligible amounts of inflammatory mediators and also remained resistant to apoptosis (cell death).
When SY cells were co-cultured with microglia and B. burgdorferi, significant neuronal apoptosis consistently occurred.
Confocal microscopy imaging of these cell cultures stained for apoptosis and with cell type-specific markers confirmed that
it was predominantly the SY cells that were dying.
Microarray analysis demonstrated an intense microglia-mediated inflammatory response to B. burgdorferi including up-regulation in gene transcripts for TLR-2 and NFκβ.
Surprisingly, a pathway that exhibited profound changes in regard to inflammatory signaling was triggering receptor expressed on myeloid cells-1 (TREM1).
Significant transcript alterations in essential p53 pathway genes also occurred in SY cells cultured in the presence of microglia and B. burgdorferi,
which indicated a shift from cell survival to preparation for apoptosis when compared to SY cells cultured in the presence of B. burgdorferi alone.
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.***
If, as we hypothesized, neuronal apoptosis is the key pathogenic event in Lyme neuroborreliosis, then targeting microglial responses may be a significant therapeutic approach for the treatment of this form of Lyme disease.
So the SY cells (which can convert glutamate to GABA) are destroyed because of the inflammatory surroundings � bystander effect � leading to their death.
These undifferentiated cells take a hit because of all the friggin� inflammation.
What would these SY �undifferentiated cells� have become?
Cell differentiation is associated with changes in metabolism and function.
Understanding these changes during differentiation is important in the context of stem cell research, cancer, and neurodegenerative diseases.
Differentiated cells exhibited greater stimulation of mitochondrial respiration with uncoupling and an increased bioenergetic reserve capacity.
�differentiated cells were substantially more resistant to cytotoxicity and mitochondrial dysfunction induced by the reactive lipid species 4-hydroxynonenal or the reactive oxygen species generator 2,3-dimethoxy-1,4-naphthoquinone.
�an increase in complex IV subunits, which we propose contributes to the increase in reserve capacity in the differentiated cells.
Furthermore, we found an increase in MnSOD (anti-oxidant enzyme) that could, at least in part, account for the increased resistance to oxidative stress
Bb needs and indeed uses MnSOD to protect �himself� from oxidative stress�the free radicals that might �fry� his lipoproteins.
Our mitochondria rely also on MnSOD to protect them.
When inflammation happens and the undifferientated cells (SY) cells are destroyed via a �bystander effect�, they can�t become differientated cells which utilize MnSOD?
Sneaky way to rob differientated cells of MnSOD�destroy the precursor undifferientated cells!!! Knock them off via upregulating inflammation.
So...the bottom line is how do we get rid of the remaining proteins of Bb esp. since it appears the macrophages can't complete their job?
Our delayed reaction to Bb may trigger this:
DTH (delayed-type hypersensitivity) is typically mediated by CD4 + T cells of the Th1 phenotype.
Naive donor CD4+ T cells recognize alloantigens on host antigen-presenting cells and differentiate into T helper (Th) subsets (Th1, Th2, and Th17 cells).
(Th17 cells are implicated in MS.)
Okay...so our CD4+T cells are supposed to recognize antigens = proteins that have been chopped off/cleaved from a pathogen. But remember, the p8 protein interfers with the initial cleaving and likely skews the immune response to Th1 humoral response instead of cell-mediated immunity (which would have been very beneficial!).
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If you look on Betterhealthy Guy's website, the second doctor down, Dr. A. C. recommends BSP 201.
"BSP-201 is helpful for inflammation and has been shown in placebo controlled double blind studies to reduce CRP and inflammatory cytokines."
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