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IngeD
Member
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Posted: Fri Aug 31st, 2007 15:19 |
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Now there is another epidemic I was bang in the middle of. I was living in Malaysia during the SARS epidemic. Travelled through Singapore airport then Hong Kong where everyone was wearing masks. Coincidentally (??????) this was the time my 90 day cough emerged.....!!!!!! So I can be thankful that despite my Th1 illness I survived that epidemic!
Re diabetes and peripheral neuropathy. My father had diabetes and very shortly after diagnosis developed peripheral neuropathy. I was prediabetic with peripheral neuropathy. Both peripheral neuropathy incidences were labelled "diabetic peripheral neuropathy". I now understand the connection. Diabetes is a Th1 illness and many people with Th1 present with peripheral neuropathy. Hence the connection. Not that diabetes CAUSES the peripheral neuropathy. That interpretation is due to an incorrect interpretation of the statistics imo.
Thanks Trevor for your explanations. Hopefully things will get a lot clearer over the next few years! Inge.
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MP start Jan'07 | Rickettsiosis, gastric ulcers, peripheral neuropathy, chronic bronchitis, adhesions/IBS/Crohn's, pre-diabetes, hypertension | initial 125D=51, 25D=26 | last 25D= 8.4 ng/mL Mar '11 |9.2 ng/ml Feb 12
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eClaire
inactive member
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Posted: Fri Aug 31st, 2007 17:22 |
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Just a note about the peripheral neuropathy. I developed a wee bit of it in both feet and one hand in the year (or two, can't remember) before starting the MP. All but a smidge of it is gone (and I think that is a bit unusual so early in the MP--about 3 to 4 months in at the time). (My brother also had this and my mom just asked me the other day what could be causing the numbness in her hands--she has Th1 illness and if she had a biopsy for the lumps in her lungs, little doubt that the diagnosis would be sarc.) Hoping that the neuropathy is not leprosy related! And even if it is that a body without Th1 illness will be able to take care of it. Claire
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Dec 2006, Olmesartan break Feb - April 2007, ME/Fibro/PTSD/MCS/Hypermobility (since childhood; disabled 2003); 25D summer 2012 <4 (meaning unable to detect)
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Prof Trevor Marshall
Foundation Staff
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Posted: Fri Aug 31st, 2007 18:10 |
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No sign of leprosy in our cohort to this point Claire. You can relax 
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Russ
inactive member
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Posted: Sat Sep 1st, 2007 05:24 |
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| Where does Borrelia fit into the picture? Is it's persistance dependent on the VDR not functioning properly or do you suspect that like Mycobacteria and Rickettsia it has other ways of persisting?
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Aussie Barb
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Posted: Sat Sep 1st, 2007 07:47 |
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| see Post Treatment Lyme Disease Syndrome Definition, symptoms, transmission, testing, treatment
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♥Barb♥: Dx Inflammation - Endocrine Imbalance 2003| Depression| 24+ years not Dx| MP Aug04-Aug2010| barbliv @ hotmail.com | ABC of MP| Barb's Story|
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Frans
Member*
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Posted: Sat Sep 29th, 2007 13:50 |
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Dr Trevor Marshall wrote: Here is a graph from my Visiting Professor presentation to the FDA last year.
It depicts the concentration-dependent displacement of one ligand from a receptor by another. You might like to review my FDA presentation, or Google for "homologous binding" for for the details
Trevor, I hope I am not asking too much, but would it be possible for you to post the same graph, but one that shows the homologous binding of 25D vs 1,25D to the VDR? That should wrap things up 
Sincerely, Frans
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Burn-out/nervous breakdown Jan01 125D 48 25D8.48 Ph1Nov06 ModPh2Jan07 Ph2Apr08 Cipramil Seroquel NoIRs lite exp r/t work cover up 25D3.9(Oct07)
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Prof Trevor Marshall
Foundation Staff
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Posted: Sat Sep 29th, 2007 14:53 |
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Er, um, I give the formulae there. Can one of our maths buffs crunch the numbers for me? This took me several hours when I first did it, and right now every minute of my time is scheduled for the next several weeks
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Frans
Member*
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Posted: Thu Oct 4th, 2007 08:05 |
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Anyone up to it?
Best, Frans
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Burn-out/nervous breakdown Jan01 125D 48 25D8.48 Ph1Nov06 ModPh2Jan07 Ph2Apr08 Cipramil Seroquel NoIRs lite exp r/t work cover up 25D3.9(Oct07)
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bookdad
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| Location: | Riverdale, Utah USA |
| Posts: | 433 |
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Posted: Mon Apr 21st, 2008 14:30 |
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Dr Marshall. First I want to say how appreciative I am that your science is real and it works. My gradually elevated level of quality of life, and that I am living is proof of that.
Secondly I had a question. Since the beginning of this thread was devoted to the lipid generation of certain bacterial microbes found in joint transplant replacement surfaces (Capnine), and since I have RA along with Sarc, I was wondering if salinity might play a roll in microbial affinity or propagation of lipids.
Has anyone looked at a possible correlation between location/ concentration of microbes and or the ability of these microbes to produce Capnine with the levels of serum and cellular salinity?
The basis of my question is that I have noticed that any added intake of table salt from what occurs naturally in the food that I eat will cause a corresponding increase in inflammation and pain at the RA affected areas. This can be a pre-prepared meal or a can of soup. Unless I prepare it myself, there is always this risk. Once this salinity level is decreased to it’s normal level, the inflammation and pain subsides. I should also note that potassium chloride does not affect me the same way.
Last edited on Mon Apr 21st, 2008 14:33 by bookdad
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Sarcoidosis/lungs RA Ph1Nov05 Ph2Mar06 Ph3Aug06 lite exp r/t to work cover up NoIRs Ph5 Aug 09
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bookdad
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Posted: Mon Apr 21st, 2008 14:30 |
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My lady can crunch the numbers for you. Is all the data that she needs in the graph? I will give it to her tonight.
Last edited on Mon Apr 21st, 2008 14:32 by bookdad
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Sarcoidosis/lungs RA Ph1Nov05 Ph2Mar06 Ph3Aug06 lite exp r/t to work cover up NoIRs Ph5 Aug 09
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smsinger
inactive member
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Posted: Mon Apr 21st, 2008 22:13 |
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| dr. m, is there a relationship between surgical hip repair of torn labrum, reshaping and re-attaching of head of femur, and repair of ligamentum terres, as in hip prosthesis surgery; i.e. surgical tools, sutures,loosening of area by centimeters to allow for "repair work", and antibiotics.hank you for considering this thought. smsinger
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Fatigue, Hypervitaminosis D, Post-treatment Lyme Disease Syndrome, 25 Dihydoxyvitamin D 36ng/ml; 1,25 Dihydroxyvitamin D 62 pg/ml; ALT 499; AST 191; ACE 18. Benicar 20 mg Q4. Ambien as needed.
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Ruth Goold
Health Professional
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Posted: Fri May 23rd, 2008 19:59 |
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This paper http://jb.asm.org/cgi/reprint/JB.01444-07v1.pdf contains another example of a bacterial ligand (3OC12-HSL) that interacts with at least two host nuclear hormone receptors – PPARbeta/delta and PPARgamma. Possibly also with RXRalpha which, of course, heterodimerizes with both PPAR and VDR. Interstingly, the bacterial ligands are also signalling molecules in the bacteria themselves – quorum sensing molecules during biofilm development. The bacteria involved is an important lung pathogen for cystic fibrosis patients.
The authors of the paper were astute enough to realize that the host inflammatory responses that were induced in the presence of 3OC12-HSL were likely mediated by one or more Nuclear Hormone Receptors and tested 3OC12-HSL against a panel of the of NHRs (but not the VDR) in mouse and human cell lines. They found:
J Bacteriol. 2008 Jan 4; : 18178738 (P,S,E,B)
Peroxisome Proliferator Activated Receptors Mediate Host Cell Pro-inflammatory Responses to P. aeruginosa Autoinducer.
[My paper] Aruna Jahoor, [url=http://lib.bioinfo.pl/auth atel,R]Rashila Patel[/url], Amanda Bryan, [url=http://lib.bioinfo.pl/autho,C]Catherine Do[/url], Jay Krier, Chase Watters, Walter Wahli, Guigen Li, Simon C Williams, Kendra P Rumbaugh
The pathogenic bacterium Pseudomonas aeruginosa utilizes the 3-oxo-dodecanoyl homoserine lactone (3OC12-HSL) autoinducer as a signaling molecule to coordinate the expression of virulence genes through quorum sensing (QS). 3OC12-HSL also affects responses in host cells, including the upregulation of genes encoding inflammatory cytokines. This pro-inflammatory response may exacerbate underlying disease during P. aeruginosa infections. The specific mechanism(s) through which 3OC12-HSL influences host responses are unclear, and no mammalian receptors for 3OC12-HSL have been identified to date. Here, we report that 3OC12-HSL increases mRNA levels of a common panel of pro-inflammatory genes in murine fibroblasts and human lung epithelial cells. To identify putative 3OC12-HSL receptors, we examined the expression pattern of a panel of nuclear hormone receptors in these two cell lines and determined that both peroxisome proliferator-activated receptor beta/delta (PPARbeta/delta) and PPARgamma were expressed. 3OC12-HSL functioned as an agonist of PPARbeta/delta transcriptional activity, an antagonist of PPARgamma transcriptional activity and inhibited the DNA binding ability of PPARgamma. The pro-inflammatory effect of 3OC12-HSL in lung epithelial cells was blocked by the PPARgamma agonist rosiglitazone, suggesting that 3OC12-HSL and rosiglitazone are mutually antagonistic negative and positive regulators of PPARgamma activity, respectively. These data identify PPARbeta/delta and PPARgamma as putative mammalian 3OC12-HSL receptors and suggest that PPARgamma agonists may be employed as anti-inflammatory therapeutics in P. aeruginosa infections.
To my untutored eye, the structure of 3OC12-HSL (shown in this publication: http://www.mrc-lmb.cam.ac.uk/genomes/awuster/wecb/Shiner_et_al_2005.pdf ) looks a lot like retinoic acid but perhaps Trevor, in his spare time, will find that it is also an agonist or antagonist of the VDR.
Ruth
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03/02/07 Ph 1 MP; 2001: Pulmonary sarc; 01/04/07: 125 D=110pmol/L(45.8 pg/ml)| 25D=20.8 ng/ml: 04/07 19.2: 07/07 11?: 09/07 16.5: 11/07 <10.0: 01/08 <10.0: 05/08 10 ng/ml. Ca. Elocom (ears). diphenhydramine 25 mg. Adidas EE glasses outside. NoIRs
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Frans
Member*
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Posted: Sat May 24th, 2008 05:39 |
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Ruth, good work !
Since PPARgamma is a type 1 nuclear receptor, just like the VDR, meaning they look structurally alike, I suspect you have, indeed, found another capnine.
I hope Trevor finds time to start the models to see if it does bind into the VDR with enough affinity and perhaps if it is actually an antagonist.
It is extremely interesting that it actually plays a role in biofilms.
Best, Frans
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Burn-out/nervous breakdown Jan01 125D 48 25D8.48 Ph1Nov06 ModPh2Jan07 Ph2Apr08 Cipramil Seroquel NoIRs lite exp r/t work cover up 25D3.9(Oct07)
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bookdad
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Posted: Mon May 26th, 2008 23:38 |
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Hey folks not to sound dumb, but my lady is willing to take a crack at your equation. Since she is a mathematician and not a medical person, we need to know what Ki is in the graph. Since Kd is based upon Ki, we need to know what that is. Also there is no reference for 25 d in the equation.
Thanks
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Sarcoidosis/lungs RA Ph1Nov05 Ph2Mar06 Ph3Aug06 lite exp r/t to work cover up NoIRs Ph5 Aug 09
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caroldeleah
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Posted: Tue May 27th, 2008 09:18 |
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Dr Trevor Marshall wrote: Thanks, Jim, your link led me to
"Fat people harbour 'fat' microbes"
http://www.bioedonline.org/news/news.cfm?art=3017
and
"An obesity-associated gut microbiome with increased capacity for energy harvest"
http://tinyurl.com/2rfrzp PMID: 17183312
which was a very nice find indeed
I am not a scientist or anything close to it......But after reading this, I wondered if a reverse hypothesis might be relevant...... we know that losing weight cannot cause chronic inflammation......but could losing weight help expose Th1 more quickly? Weight gain is common for those who have hypothyroidism. My daughter was counselled by her doctor to reduce her weight and by the time she had lost about 30 lbs, she got uveitis. Have you found any correlation between weight loss and the appearance of Th1 symptoms? Just uneducated speculation. My mom had uveitis in the 30's or 40's--has never had a relapse. At some point in her life she lost a lot of weight, but I don't know the timeline. For being in her 80's now, she is fairly healthy, but all my siblings have multiple symptoms of Th1 and symptoms of Th1 have mushroomed in her grandchildren Thanks, Trevor, a lot, for all your work Carol
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Uveitis|HashimotosHypothyroidism|Thyroid Nodule|Arthralgias|RefractiveMyopia|1,25D34| Ph1Aug08|Ph2Nov08|Ph3Jun09|25D 11(06/09)|25D 6(02/09)|25D 9(12/08)|Combigan/Cytomel/RefreshPlusSgl/NoIRs
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Ruth Goold
Health Professional
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Posted: Wed May 28th, 2008 09:49 |
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And here is another one. Bacterial-Modulated Signaling Pathways in Gut Homeostasis. Lee, Won-Jae.
Sci. Signal., 27 May 2008
Vol. 1, Issue 21, p. pe24
[DOI: 10.1126/stke.121pe24]
You can see the abstract at :
http://stke.sciencemag.org/cgi/content/abstract/stke.121pe24
Ruth
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03/02/07 Ph 1 MP; 2001: Pulmonary sarc; 01/04/07: 125 D=110pmol/L(45.8 pg/ml)| 25D=20.8 ng/ml: 04/07 19.2: 07/07 11?: 09/07 16.5: 11/07 <10.0: 01/08 <10.0: 05/08 10 ng/ml. Ca. Elocom (ears). diphenhydramine 25 mg. Adidas EE glasses outside. NoIRs
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kingmom3
member
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Posted: Thu May 28th, 2009 11:32 |
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| Bless-You and your Knowledge. Lori
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Spino-Cerebellar degeneration w/ataxia, hyperthyroid, TMJ, 125D60, 25D40, MP 01/07, Modph2 11/07, Ph3 2/10 25D 7.3-2/10
25D9.0-2/13 (break on antibiotics; Benicar only as of 1/13)
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Bane
Research Team
| Joined: | Sat Jan 26th, 2008 |
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Posted: Fri Mar 26th, 2010 00:51 |
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'Clingy' bacteria causes infection
http://www.sciencealert.com.au/news/20100903-20692.html?utm_source=feedburner&utm_medium=feed&utm_campaign=Feed%3A+sciencealert-latestnews+%28ScienceAlert-Latest+Stories%29
Impact of Nanoscale Roughness of Titanium Thin Film Surfaces on Bacterial Retention
http://pubs.acs.org/doi/abs/10.1021/la902623c
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jlunn247
inactive member
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Posted: Sat Apr 3rd, 2010 06:20 |
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I think when i lost 30 pounds in 30 days it was more like a month long IP mega herx.
the little bugs and time of year gave me stomach flu symptoms cranked up to 11.
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Living in the land of the lost. JUST OLMECIP 5 x a day.Sarcoidosis Dx.
Bone disintegration,lungs,joint/muscle/stomach pain, diarrhea,incontinence. Weakness on my left side sweats,fatigue,neuropathy,headaches,mood swings,cognitive diss.
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Bane
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Posted: Sat Apr 3rd, 2010 07:58 |
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Biofilm Production Aids Campylobacter Survival
http://www.sciencedaily.com/releases/2010/03/100324184602.htm
Campylobacter cannot survive in the oxygen levels in the air, which forces the bacterium to adapt for survival in the food chain. One such a survival strategy is to form a biofilm, whereby the bacteria stick to a surface and encase themselves in a sticky 'slime' which protects them.
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